i

EFFICACY OF HOMOEOPATHIC TREATMENT IN MODULATION OF IMMUNOGLOBULIN E (IgE) LEVELS IN BRONCHIAL ASTHMA

(Thesis submitted in partial fulfillment for the award of

degree of Doctor of Philosophy in Homoeopathy)

by R SITHARTHAN

under the guidance of

Prof (Dr) T Abdurahiman

VINAYAKA MISSIONS UNIVERSITY

SALEM, TAMILNADU, INDIA

2015

ii

VINAYAKA MISSIONS UNIVERSITY

DECLARATION

I, R. Sitharthan, declare that the thesis titled “Efficacy of

Homoeopathic Treatment in Modulation of Immunoglobulin E (IgE) levels

in Bronchial Asthma” submitted to Vinayaka Missions University, Salem for

the award of degree of Doctor of Philosophy in homoeopathy, under the

guidance of Prof (Dr) T. Abdurahiman, that this has not previously formed

the basis for the award of any diploma,associateship, degree, fellowship in

this or any other University or other similar institutions of higher learning.

Place :Salem Signature of the Candidate

Date :

iii

VINAYAKA MISSIONS UNIVERSITY

CERTIFICATE

I, Dr. T.Abdurahiman do hereby certify that the thesis entitled

“Efficacy of Homoeopathic Treatment in Modulation of Immunoglobulin

E (IgE) Levels in Bronchial Asthma” submitted for the degree of Doctor of

Philosophy in homoeopathy by R. Sitharthan is a bonafide record of research

work carried out by him during the period from 2011 to 2015 under my

guidance and supervision and that this work has not formed the basis for the

award of any degree, diploma, associate ship, fellowship or other titles in this

University or any other University or institutions of higher learning.

Place: Salem Dr. T. Abdurahiman, MD (Hom), PhD

Date:

iv

ACKNOWLEDGEMENT

Success is the fruit of hard work. The thesis hereby prepared is not the

result of my own wisdom and experience but of collective effort of an expert

who guided me.

I am nothing in front of God Almighty, who laid his hand upon me and

provided me the wisdom and understanding to complete this dissertation.

It is my great privilege to express my sincere thanks and deep sense of

gratitude to the Dean research, Dr. Rajendran, PhD., Vinayaka Missions

University, Salem for his wonderful support and guidance for the successful

completion of this research.

It is my great privilege to express my profound gratitude and exclusive

thanks to my esteemed guide, Dr.T.Abdurahiman,MD(Hom),PhD., for his

constant valuable guidance, precious advice, highly instructive suggestion,

supervision, constant encouragement, and timely help during the entire

course of study as well as providing all possible facilities for successfully

carrying out this study. It is a matter of fact that without his esteemed

suggestions, highly scholarly touch and piercing insight from the inception till

the completion of the study, this work could not have been presented in the

manner it has been made.

I would like to extend my heartfelt thanks to our Director, Dr.Rajendran,

MD (Hom)., Vinayaka mission’s homeopathic medical college & hospital,

Salem for his warm and constant support, in most times in the path of this

research journey.

v

I express my respect and tribute to our Principal, Dr.Nagarajan,MD

(Hom)., Vinayaka mission’s homeopathic medical college & hospital, Salem

for his kind suggestions and support to complete this study.

I express my sincere thanks to the bio-statisticians

Dr.NandhaKumar,PhD (Stat) and Mr.Mani , M.Phil(stat) for helping me in

analyzing the data for this study.

I thank to all the Faculty members of Vinayaka mission’s homeopathic

medical college& hospital, Salem for their support and help during my study.

I extend my sincere thanks to the librarians, lab technicians, post

graduate students and interns who helped in my study.

I express my heartfelt gratitude to all the patients who have

participated and cooperated in the study. Without their co-operation, the study

would not have been possible.

Finally yet importantly, I express my gratitude to my family members

for their encouragement and support throughout the study.

(Sitharthan .R)

vi

INDEX

Sl No Contents Page No

1. Introduction 1 - 2

2. Review of literature 3 - 57

3. Statement of problem, need for study,

objectives and hypothesis

58 – 61

4. Materials and methods 62 – 74

5. Results and discussion 75 – 97

6. Summary, conclusion and recommendations 98 – 102

7. Bibliography

103 – 113

vii

LIST OF TABLES

Sl.No Table Page No

2.1 Severity of bronchial asthma 27

2.2 Key indications for diagnosing bronchial asthma 29

5.1 Assessment of significance of reduction in IgE

levels after treatment

84

5.2 Assessment of significance of reduction in absolute

eosinophil count after treatment

86

5.3 Assessment of significance of reduction in

FEV1/FVC after treatment

93

viii

LIST OF FIGURES

Sl.No Figure Page No

2.1 The inflammatory process in pathogenesis of

bronchial asthma

21

2.2 Activated mast cells in bronchial asthma 24

2.3 Pathophysiology of the inflammation and redox

abnormalities in asthma

25

5.1 Age wise distribution 76

5.2 Distribution of sex 76

5.3 Occupation wise distribution 77

5.4 Marital status wise distribution 77

5.5 Distribution of religion 78

5.6 Education wise distribution 78

5.7 Distribution of family history 79

5.8 Addiction wise distribution 79

5.9 Distribution of thermal relation 80

5.10 Miasm wise distribution 80

5.11 Distribution of IgE level before and after treatment 81

5.12 Distribution of remedies in reducing IgE levels 82

ix

5.13 Effective remedies in reducing IgE levels 83

5.14 Distribution of AEC before and after treatment 85

5.15 Distribution of remedies in reducing AEC levels 87

5.16 Effective remedies in reducing AEC levels 88

5.17 Distribution of FEV1/FVC levels before and after

treatment

89

5.18 Assessment of homeopathic treatment in relation to

results of pulmonary function tests

90

5.19 Effective remedies in modifying abnormal pulmonary

function

92

5.20 Distribution of remedies given among bronchial

asthma patients

94

5.21 Distribution of improved patients after treatment 95

x

Abbreviations

AEC Absolute Eosinophil Count

CD cells Cluster of Differentiation cells

FEV1 Forced Expiratory Volume in 1 second

FEV1/FVC Forced Expiratory Volume in 1 second/ Forced Vital

Capacity

FEV3 Forced Expiratory Volume in 3 seconds

FEV6 Forced Expiratory Volume in 6 seconds

FVC Forced Vital Capacity

Ho1 Null Hypothesis 1

Ho2 Null Hypothesis2

Ho3 Null Hypothesis3

HSS Higher secondary school

IFN-ϒ Interferon ϒ

IgE Immunoglobulin E

IL5 Interleukin 5

IL8 Interleukin 8

IQR Inter quartile range

N Number of patients

PFT Pulmonary function test

xi

T cells Thymus derived lymphocytic cells

T helper cells Thymus derived lymphocytic helper cells

Th2 cells T helper cells

TNF-α Tumor Necrosis Factor- α

VMHMC&H Vinayaka Missions Homoeopathic Medical College

and Hospital

1

I. INTRODUCTION

1.1. Serum immunoglobulin is a group of serum molecules which is

produced by B-lymphocytes and they are soluble secreted form of B-cell

receptors. They are produced to a maximum during invasion by an antigen, so

they are also called antibodies. The normal value of total serum

immunoglobulin less than 0.001%.

1.2. IgE is a mediator of allergic response. Usually it increases when there

is allergic conditions. It gives useful guideline for the clinical diagnosis of

atopic and non-atopic diseases. Higher levels of IgE are associated with

asthma in both adults and children. IgE also play a major role in modulating

the severity of asthma.

1.3. Several studies demonstrate that there is a link and relation between

IgE and asthma. There is a direct proportional fluctuation in IgE with the

severity of asthma. Increase in serum total and specific IgE levels indicate

atopic asthma. Burrows et al stated in his study says that prevalence of

asthma was closely related to serum IgE level which indicates allergic basis of

bronchial asthma.

1.4. Most common type of asthma is atopic asthma in which IgE mediated

hypersensitivity reaction is triggered by environmental allergens. It is

manifested by inflammation of the lungs, recurrent airflow obstruction, and

hyper responsiveness to environmental stimuli.

2

1.5. Eosinophils are important effector cells in asthma and allergic disease.

It is found in asthmatic airways. Their mediators are relevant to the disease

process as well as its removal is associated with an improvement in the

disease. Allergic asthma is commonly associated with eosinophilia.

1.6. Pulmonary function tests (PFT) are one of the important investigations

in the treatment of patients with bronchial asthma. It helps to diagnose and

monitor the response to treatment and guide the homeopathic physician

regarding treatment and intervention.

1.7. Spirometric patterns are seen usually by using FEV1, FVC and

FEVI/FVC.

1.8. Zhao Linlu and Bracken B Michael. (2011)1 observed that allergic

diseases have become a major public health problem over the past few

decades.

1.9. Adrian W Zuercher. et.al. (2006)2 observed that there is increased

prevalence of eczema, food allergy, and asthma dramatically, especially in

western society. Between 20% and 30% of individuals living in Western

countries suffer at least one form of allergic disease.

1.10. Nargues A. Weir et.al. (2012)3 define bronchial asthma is the

presence of intermittent symptoms such as cough, wheezing and difficulty in

breathing with tightness of chest.

3

II. REVIEW OF LITERATURE

2.1. Immune system is much important in protecting us from getting

infection. The main primary function of the immune system is to fight against

infection. It differentiates self from foreign bodies and stimulates other

protective responses.

2.2. We may inhale the allergen mostly or we may ingest also. Allergy is

the exaggerated response of immune system to foreign materials. Bronchial

asthma is a disease which primarily affects the immune system, the lungs and

the airways.

2.3. Immunoglobulin E:

Syed Ismal et al. (2009) 4 describes serum immunoglobulin as a cluster

of molecules synthesized by the B cell receptors of B lymphocytes which

counteracts against antigens, so they are termed as antibodies.

2.4. Raj Kumar et al (2006) 5 states there is relationship between serum

total IgE in the pathophysiology of asthma and the development of airflow

obstruction. He also states that serum IgE is having influence on

pathophysiological changes and air way obstruction in asthma.

4

2.5. Anatomy

2.5.1 Chest Wall and Diaphragm

Kennedy JW (2005) 6 demonstrate that according to Drake.RL the

thoracic wall consists of skeletal and muscular components, which extend

between first rib superiorly and twelfth rib, the costal margin and the xiphoid

process inferiorly. There are 12 ribs; out of which seven ribs articulate with the

sternum through costal cartilage and five ribs not connected anteriorly. On the

lower aspect of each rib there is a subcostal grove which contains a nerve,

artery and vein and known as neurovascular bundle.

He also says that the diaphragm divides thorax and abdomen.

Diaphragm helps in respiration. During inspiration diaphragm becomes

flattened and pushed down which gives more space for air entry into the

respiratory passages. Sternocleidomastoid and the scalene muscles of the

neck are the accessory muscles of respiration, where these muscles acts

more during severe difficulty in breathing and in conditions of severe air

hunger. So this becomes clinically important during asthma.

2.5.2.Upper respiratory tract

2.5.2.1. Nasal Morphology

Tu, Jiyuan et al (2013 ) 7 reveal that the nose is divided into external

and internal nose. It consists of nasal cavities on either side. It

5

is made up of a bony part and a cartilaginous portion. The opening of the nose

is called the nostrils and is separated by nasal septum cartilage. The nostrils

allow air to enter in to the nasal cavity. The nose and the nasal cavity provide

a pathway for the air to go to the lungs. It gives warmth and moistens the

inhaled air. It also filters the inhaled air.

2.5.2.1.2. Larynx

He also states that the larynx is commonly known as the voice box. It

has the vocal folds which are responsible for sound production. It functions as

a sphincter in transmitting air from the oropharynx to the trachea.

2.5.3. Lower Respiratory Tract

2.5.3.1. Trachea (windpipe)

Standring S. et.al. (2004) 8 demonstrates that the trachea is a hollow

muscular tube which is 11–14 cm long. Its cross-sectional diameter in normal

human adult males is 1.3–2.5 cm in the coronal plane and 1.3–2.7 in the

sagittal plane, whereas for women the diameters are slightly smaller which is

1.0–2.1 cm and 1.0–2.3 cm for coronal and sagittal diameters respectively.

6

2.5.3.2. Bronchial Tree

Kennedy JW (2005) 6 reveals that the bronchial tree starts superiorly

with the trachea, and made up cartilage rings with an open posterior wall

composed of smooth muscle. This bifurcates into the left and right main

bronchi. The right bronchus is more vertical and wider than the left. These two

main bronchi then split into lobar or secondary bronchi that supply a lobe

each, and then further divide into segmental or tertiary bronchi to supply

segments in each lung.

2.5.3.3. Lungs

Kennedy JW (2005)6 also states that lung is the primary organ of

respiration situated one on either side of the thoracic cage. Main structures

which lie closely to the left lung are the heart, aortic arch, thoracic aorta and

the oesophagus. The left lung is slightly smaller than the right due to the

predominantly left sided position of the mediastinum, and is split into an upper

and lower lobe by the oblique fissure.

2.5.3.4. Pleura

Kennedy JW (2005) 6 explain that according to Drake.RL the lungs lie

within the pleural cavities. Pleura are covered by a layer composed of

mesothelial cells and connective tissue. The pleura are subdivided into

parietal and visceral pleura. The parietal pleura attached to the thoracic

wall and the visceral pleura cover the lungs. In between

7

these two layers there is pleural space. A small volume of pleural fluid is

present in this space which acts to lubricate movement between the pleura

during respiration.

2.5.4. Pulmonary Vasculature

2.5.4.1. Arteries

Standring S. et.al. (2004) 8 shows that deoxygenated blood is carried out

by the pulmonary arteries from the right ventricle to the lungs. It enters the

hilum of both right and left lungs. It branches as lobal, segmental and sub

segmental arteries and ends as pulmonary capillaries. From the pulmonary

beds oxygenated blood is carried by the pulmonary veins to the left atrium.

2.5.4.2. Veins

Kennedy JW (2005) explains that according to Drake.RL oxygenated

blood is carried out from the lungs to the left atrium. The pulmonary veins

arise at the hilum of each lung as superior and inferior vein. Few bronchial

veins also join with these pulmonary vessels.

2.5.4.3 Lymphatic drainage

Also Drake RL et.al. reveals that the major lymphatic drainage of lungs

is through the thoracic duct. It begins superior to several lymph ducts, known

as the cisterna chyli, which drains the abdomen, pelvis

8

and lower limbs. The thoracic duct enters the thorax posterior to the aorta

through the diaphragm, and traverses superiorly through the posterior

mediastinum to the right of the midline. It then empties into the venous

circulation at the junction between the left subclavian and internal jugular

veins.

2.6. Physiology:

Jeffrey C. Smith A. (2009) 9 states that respiration includes both

inspiration and expiration. During inhalation air enters the nose to the pharynx

followed by larynx and then into the trachea and into the bronchi. From

bronchi air enters into bronchioles and end in air spaces known as alveoli

which are enriched with small minute blood vessels known as capillaries.

Finally oxygen transfers into the lungs through the capillaries of alveoli during

inspiration and carbon dioxide is expelled out from the lungs through the

capillaries of alveoli during expiration.

2.7. Definition of bronchial asthma

2.7.1. Valentin Prieto Centurion et al. (2012) 10 describes that asthma is

known as fast breathing. And also the other author Floyer defined asthma as

strained voluntary respiration associated with wheezing.

2.7.2. Adeniyi BO et al (2009) 11describes that asthma is a chronic, lung

disease characterized by recurrent breathing problems

9

such as cough, wheezing, and chest tightness. The narrowing of the air

passage in asthma is usually due to inflammation in the inner walls of the

trachea and also the bronchioles or smaller tubes letting in air to the lungs.

2.7.3. Thomas McCarter (2008) 12 define asthma as a chronic inflammatory

disease of the lungs, which typically presents with intermittent cough,

wheezing, shortness of breath or dyspnea, and chest tightness, commonly

occurring during the night and early morning. The underlying inflammation

leads to airway hyperresponsiveness and obstruction with some degree of

reversibility.

2.7.4. Nargues A. Weir and Stewart J. Levine et.al. (2012) 3

describe that asthma is a condition in which symptoms are commonly

triggered by exposure to allergens, irritants or cold air, viral infections and

exercise. So, when we consider this aspect we could be able to identify the

reality of this statement where most of the patients with asthma have any one

of the above reason for their illness.

2.8. Classification of asthma:

It is very clear that asthma is one of the diseases which affect the

immune system in the sufferer. Johansson SG. (2004) 13 stated that bronchial

asthma is immunologically broadly categorized into atopic (allergic) asthma

and non-atopic (non allergic) asthma.

10

2.8.1. As it is very well known that asthma patients has modification in

their immune cells due to atopic reactions. Atopy is the production of

increased levels of IgE in response to common environmental allergens and is

the strongest detectable predisposing factor for the development of

asthma.The study of Jain A, H. Bhat V, Acharya D. (2010) 14 shows there is a

strong association between family history of atopic disorder and the

prevalence of asthma.

2.8.1.1. Natalya V. Kukhtinova. (2012) 15 states that atopic asthma

begins before age 6, associated with atopy, and an increased severity of

bronchial hyper responsiveness, which persists into adulthood. It is a

hypersensitivity reaction provoked by environmental allergens, like endotoxin

and aeroallergens.

2.8.1.2. The common aetiological factors in the production of atopic

asthma are genetic and environmental factors explained below:

2.8.1.2.1. Genetic factors:

Some of the patients may be suffering from asthma, eventhough they

are not exposed to allegens. It might be due to genetic predisposition. Borish

L. (1999) 16 stated that studies have suggested that genes within the cytokine

gene cluster on chromosome, chromosome 11, chromosome 16, and

chromosome 12 may contribute to development of asthma and allergy.

11

2.8.1.2.2. Environmental factors:

2.8.1.2.2.1. Environmental factors much stimulating the occurrence of

asthma in many individuals. Constant exposure to these stimuli will initiate

the development of asthma. Trasande L and Thurston GD. (2005)17 states

that out door allergens constitute plant pollen and fungal spores. Pollens are

particles smaller than 100 nm, enter into the human immune system, spreads

to all organs of the body. When it lodges in the lungs it can cause respiratory

allergic reactions especially asthma. Similarly, Hansel NN et al. (2008)18 also

reported that the environmental tobacco smoke exposure has a causal

relationship with asthma. Along with these pollutants from the combustion of

natural gas and motor fuel, such as nitrogen dioxide (NO2) and particulate

matter with ozone also leads to asthma.

2.8.1.2.2.2. Occupational factors:

The other important factor which is to be considered in the cause of

asthma is the nature of work which is done by the patient. Definitely most of

the occupations have the provoking effect for asthma. International union

against tuberculosis and lung disease (2011)19 reveals that people working in

certain occupation can prone to get asthma.

12

2.8.1.2.2.3. Indoor allergens

The other aspect which is more crucial factor that is to be considered

more is indoor allergic exposure. Most of the patients with bronchial asthma

develop asthma mainly due to this problem. Pedro Giavina Bianchi et.al.

(2010) 20stated that exposure to indoor allergens, constitute proteins from

house dust mite, cockroach, dog, cat, and mice, animal secretions,molds,

perfumes, insecticides, paintings and distemper, fuels such as gas, kerosene

and liquid petroleum also provokes asthma.

Food allergies has been identified by Schroeder et al (2010)21 as a risk

factor of asthma in children independent from aeroallergen sensitization and

family history of asthma.Dietary changes with westernized life style also

noted in certain patients.In Finland, where low vitamin D intake, a short

exposure to sunlight have high prevalence of asthma.

2.8.2. Natalya V. Kukhtinova. (2012)15 defines non atopic asthma is a

recurrent airway obstruction that begins during the first two to three years of

life, following a lower respiratory tract illness caused by the spread of the

spectrum of the infecting organism. Respiratory syncytial virus induced

wheezing resolves in most children by 13 years of age.

2.8.2.1. Ana Lucia moncayo (2010)22 describes that the common

aetiological factors in the production of non atopic asthma are infection

13

induced allergic conditions like bacterial infections, viral infections such as

rhinitis, bronchitis, respiratory syncytial virus infection, broncho pneumonia,

chlamydia pneumoniae and mycoplasma pneumonia, epstein barr

virus, cytomegalo virus, measles virus, vaccination with whole virion influenza

vaccine, human rhinovirus infection, ascaris infections. It could be

understandable that any one of the above mentioned infection leads to

asthma. Shyam S. Mohapatra et al. (2008)23 states that according to World

Health Organization report, worldwide respiratory syncytial virus cause 64

million infections and 160,000 deaths annually. It usually infects persons by 2

years of age and can cause subsequent infections throughout life. Falsey et

al conducted a study and reported that respiratory syncytial virus infection is

the cause for 7.2% of hospitalizations due to asthma among aged 65 years

people.

14

Other causes:

Urbanization is also a main reason in the development of emotional

distubances and environmental pollution.

Lind beak M et al. (2003)24 reveals that socio economic factors like

indoor smoking, psychic disturbances, antibiotic use, parental asthma,

sedentary lifestyle, urbanization, dampness and exercises leads to asthma.

The most obvious reason here is that a patient suffering from asthma already

has an inflamed trachea.Thus the patient may not able to breath rigorously.

David J. Jackson et al. (2011) 25 observed that in children, seasonal

peaks in asthma exacerbations occur frequently in autumn, corresponding to

the weeks after the start of the school term. This has been termed the

September epidemic.In older adults a peak is seen in December to January.

Karthikeyan Ramaraju et al. (2014)26 noted that poor ventilation and

overcrowding at home, pet keeping, pregnancy, psychological factors

including mental stress, drug intake, gasteroesophageal reflux, maternal

distress, maternal exposure to farming activities and farm dairy products

provokes the risk of bronchial asthma. Rarely serum total cholesterol was

directly associated with the risk of asthma.

15

2.9. Incidence

As a researcher much importance should be given for the incidence of

bronchial asthma. It helps to analyse the various aspect of the disease.

2.9.1. Ranabir Pal et al. (2009)27 reports that asthma is less common

in developing countries when compared to developed countries.

2.9.2. Caroline Gouder et al (2013) 28 states that males have been

found to have a more risk of asthma than women. It was proved by a study

carried out in Delhi in two randomly selected schools and the results have

revealed that there was mild excess of asthma among men (54%). Gupta D.

(2006) 29 observed that exposure to environmental tobacco smoke was also

significantly associated with prevalence of respiratory symptoms such as

wheezing, cough and breathlessness. Environmental tobacco smoke

exposure during childhood is an important risk factor for asthma and

respiratory symptoms in non-smoking adults.

2.9.3. Mohan GR. (2008) 30 expressed that prior to puberty the

incidence is three times higher in boys than girls, whereas it is equal among

male and female during adolescence period. But in adult onset asthma

women are more affected than men.In children, asthma is more common

among the boys.

16

2.9.4. Pedro Giavina Bianchi et al. (2010) 20 reports that the worldwide

the estimated prevalence of asthma is 10%. It has drawn more reseach

concern among researchers. Ranabir Pal (2008) says that according to

Chhabra SK et.al. that there is high prevelance of asthma among children in

India.

2.9.5. Caroline Gouder et al (2013) 28 also reported that bronchial

asthma has prevalence of 7-10% worldwide. Scott.P. (2009)31 states that

asthma is high in the Caribbean with more than 20% of the general

population. Federico Fernandez Nievas I, et al. (2013)32 reported that

according to Akinbami LJ et.al. among patients with bronchial asthma in the

age group of 0 to 17 years, 11.3% males and 7.9% females have asthma.

Also, 9.6% children have asthma when compared to 7.7% in adults.

2.9.6. Jerry A. Krishnan et al. (2009) 33 reported that in the United

States, there are about 2 million emergency department visits and 500,000

hospitalizations for acute asthma each year.

2.9.7. Samuel J. Arbes, Jr. et al. (2007) 34 describes that the most

common asthma phenotype is atopic asthma, which accounts for 56% of

asthma cases in the United States. Lau S, Nickel R et.al. (2002) 35 stated that

according to German Multicenter Allergy Study atopy and asthma are usually

seen at age 7 years.

17

2.9.8. Parveen T et al. (2009)36 stated that among 260 patients of adult

asthma, 60% had reacted to house dust, 51% reacted to house dust mite.

2.9.9. Jindal. S.K. (2007)37 stated that there is a median prevalence of

asthma in about 2.4 percent of cases over 15 years of age. The prevalence is

higher in children. The total burden of asthma in India at an overall prevalence

of 3 per cent is estimated at over 30 million patients. Agam Vora (2012)38

stated that in India the incidence ratio of asthma and allergic rhinitis is about

20:26.

2.9.10. Ishita Mishra (2013)39 stated that asthma prevalence rate in

Chandigarh was 2.28 %, in Kanpur 2.05 % and 1.69 % in New Delhi. Ranabir

Pal et al. (2009)27 stated that the highest incidence was observed in

Bangalore and the prevalence rate was about 3.49 %. In recent studies it

shows that Bangalore had a prevalence rate of 29.5% of asthma in children

who are below the age of 18 years. Bloemen K, et al. (2007) 40 stated that

eosinophils are involved in the pathophysiology of allergic asthma with the

influence of mast cells, IgE and cytokines. Paramesh H. (2002)41 conducted a

study during 1979,1984,1989,1994 and 1999 among 20,000 who were below

18 years in Bangalore showed a prevalence rate of asthma which was 9% to

29.5%. Ramesh.R. (2011)42 conducted a study in Erode and reported that

there are 511 (95.15%) children had symptoms of asthma and Bhavani of

Tamilnadu had highest percentage.

18

2.10. Patho physiology of bronchial asthma

2.10.1. Adeniyi BO et al (2009)11 explains that the presentation of asthma

may be with following manifestaions like,

- Smooth muscle hypertrophy

- Bronchospasm

- Chest tightness

- Airway hyper-responsiveness to a wide range of common allergens

- Excessive mucous secretion and airway oedema.

2.10.2. Roopakala Mysore Subrahmanyam et al (2014)43 states that

serum levels of TNF-α and IFN-γ are higher in atopic asthmatics compared to

non atopic asthmatics.

2.10.3. Ramesh.R (2011) 42 states that bronchial asthma and allergic

rhinitis are thought to share a common pathogenesis in many patients.

2.10.4. Ingvild Bruun Mikalsen et al (2013)44 reveales that chronic

inflammation of the lower airways and bronchial hyper responsiveness (BHR)

are typical features of asthma, and markers of these factors are therefore

used for diagnostic purposes and to guide treatment.

19

2.10.5. Mudita arora (2008)45 stated that the airways undergo two type

of changes; the hypereactive response and the inflammatory response. In

hyperreactive response, smooth muscles in the airways of the lungs constrict

and narrow excessively in response to inhaled allergens.Inflammatory factors

cause the airways to swell, to fill with fluid and to produce a thick sticky

mucus.

2.10.6. Emanuel Sarinho and Alvaro Antonio Cruz (2006) 46stated that

one of the important main component is immunoglobulin E (IgE) which plays

an importanat role in allergic reactions. IgE is identified in the serum of blood

when there is any history of exposure to allergens.

2.10.7. David Prefontaine et al. (2012)47 reveals that asthma is a

chronic inflammatory disease of the airways characterized mainly by Th2

lymphocyte-mediated immune responses and associated with bronchial

hyperresponsiveness, airflow obstruction, and airway remodeling.

2.10.11. Cells involving in pathophysiology of bronchial asthma:

Adeniyi BO et al (2009)11 describes that the cells thought to play an

important part in the inflammatory response are mast cells, eosinophils,

lymphocytes, and airway epithelial cells, neutrophils, macrophages, etc. Each

of the cell types can help mediators and cytokines to irritate and

amplify both acute inflammation and long-term

20

pathologic changes.Presence of increased numbers of lymphocytes, mast

cells and eosinophils seen in allergic asthmatic individuals.

a. Role of IgE in pathophysiology of bronchial asthma:

IgE is the one of the important triggering factor which assists in the

mechanism of asthma. Kim Keun Chang (2001) in his study revealed that

immunoglobulin E is a type of immunoglobin which is the lowest percentage of

immunoglobulin present in the body comparing to other immunoglobulins. It

has short half-life below one day. It is constantly destroyed by endosomes, so

that the normal minimum level is maintained by the body. IgE binds with high

sensitive receptors on cells like mast cells and basophils during the process of

allergic conditions like Asthma. IgE antibodies are specific to a particular

group of allergens alone than to all allergens. Paolo Bellavite et al (2006)

found that during acute inflammation the first biological event occurs is

activation of basophils which is triggered by their binding to IgE antibodies and

due to sensitization it bound to high-affinity receptors.

Faoud T. Ishmael. (2011)49 observed that during allergic reactions

immunoglobulin E binds to receptors on the surfaces of mast cells and

basophils and it release mediators which stimulates bronchoconstriction and

and leads to inflammatory response. Production of IL-5 from Th2

cells increases eosinophil levels. Inflammatory mediators released

from eosinophils, T cells,

21

macrophages, and neutrophils produces damage to the airway and

bronchoconstriction.

Figure 2.1. The inflammatory response in the pathogenesis of

bronchial asthma.

Source: Faoud T. Ishmael. ( 2011). 49

22

b. Role of Absolute Eosininophil Count in pathophysiology of

bronchal asthma:

Biology of Eosinophil Activation: Adeniyi BO (2009)11 states that

eosinophils are responsible for inflammatory and allergic changes like broncho

constriction in asthma. There is production of thick, tenacious mucuos plugs

containing fibrin and eosinophils, which obstruct the airways due to impaired

mucociliary transport. Barnes PJ.(2003)50 in his study states that eosinophils

takes part in adhesion and migration into vascular endothelial cells of airways

which induces airway epithelial cells thus causes airway hyper

responsiveness and airway epithelial damage. Humbert M. Kay A.B. (2003)

51state that there is a strong assosiation of eosinophils in all atopic individuals.

There is a clear evidence that eosinophil secretes numerous lipid mediators

like eosinophil derived neurotoxin, eosinophil cationic protein and eosinophil

peroxidase which acts during the pathophysiology of asthma. Hamid Qutayba

et al. (2003)52 states that infiltration of mast cells, T cells, basophils, CD+(T

helper) cells, basophils, eosinophils and macrophages are seen in

pathophysiological process of Asthma. Covar et al, (2010)53 in their study

reveals that more prominent eosinophilic airway inflammation may be one of

the triggering factors for reduction in FVC level in asthma.

23

c. Changes in the Pulmonary Function in bronchal asthma

Bhattad Shital .S et al. (2013)54 states that in asthmatic children when

compared with normal children, there was no significant difference in both

study and control group in percent predicted values of FVC, but percent

predicted values of FEV1 and FEV1/FVC ratio in percent were decreased

significantly in asthmatic children as compared with healthy children.

Mohamed Faisal Lutfi (2011)55 conducted a study and found that FEV3 and

FEV6 are acceptable alternatives for FVC in the spirometric diagnosis of

bronchial asthma. And the study concluded that FEV3 and FEV6 may kept as

alternative for FVC.

d. Biology of Mast Cells Activation

Ulrich Blank et al. (2013)56 reveals that mast cells are cells which are

derived from hematopoietic origin which is present in the tissues that are in

contact with the external environment such as the skin, the gastrointestinal

tract, or the airways. When there is exposure of these tissues undergo an

allergic reaction mast cells comes into play. Mast cell mainly responsible for

type I hypersensitivity and allergies. Mast cells are released rapidly within a

few minutes upon activation a whole set of inflammatory products by cellular

degranulation including histamine and proteases, proteoglycans, lysosomal

enzymes, etc. Barnes PJ. (2003)50 states that mast cells are the cells which

initiates the acute bronchoconstriction to any allergens during exercise and

hyperventilation. Mast cells also release mediators like neutrophil,

24

proinflammatory cytokines and growth factors. .Humbert M. (2003)51 reveals in

his study that the mast cells are believed in airway remodeling through

fibroblast activation.

Figure 2.2: Activated mast cells in bronchial asthma.

Source: Heather J. Bax et.al.(2012) 57

Heather J. Bax et.al.(2012) 57 demonstrated that during allergenic

activation, the allergen enters the body and is captured by IgE antibody which

is bound to its high-affinity receptor, FcεRI, on the membrane of mast cells,

and basophils. Cross-linking of the IgE-FcεRI complex triggers mast cell

activation and the release of substances that cause the symptoms of allergy.

e. Biology of Basophil Activation: Paolo Bellavite et al (2006)48

states that basophil cells are cells which after activation binds with IgE ,

causing exocytosis and the release of mediators. Histamine in tissues

produces vasodilatation and permeability actions, thus causes wheals and

edema. Using homeopathic dilutions of Apis mellifica and

25

Lung histaminum has effect over allergic syndromes and by activating mellitin

and histamine, to activate basophils.

f. Biology of cytokines Activation: helps in manifestation of

symptoms in Asthma.

Figure 2.3: Pathophysiology of the inflammation and redox abnormalities

in asthma.

Source: Suzy A.A. Comhair and and Serpil C. Erzurum ( 2010)59

26

2.10.12. Mechanism of pathogenesis of Asthma:

Aldridge RE. et.al. (2002)58 expresses that activated eosinophils generate

oxidants. Production of reactive oxidant species by involvement of 2

pathways :

1st pathway is that Involvement of acquired immune system by

production of IL-5 and activation of eosinophils and

2nd pathway is that involvement of innate immune system by

production of IL-8 with activation of neutrophils are due to

respiratory bursting of cells.

2.11.Clinical features:

2.11.1. Monitoring and studying of asthma requires a consistent

terminology and defined bench marks.

2.11.2. Nargues A. Weir Stewart J. Levine (2012)3 stated that the major

complaints of asthma are episodes of wheezing, chest tightness, dyspnea and

cough. The frequency of asthma varies among individuals from frequent to

continuous symptoms. Asthma is most often worse at night usually in early

morning. At the beginning of an asthmatic attack, wheezing usually occurs

only while exhaling, whereas during severity, wheezing may be heard in both

inhalation and exhalation. As the time elapses the wheezing stops and the

bronchioles are completely

27

blocked, leads to a very serious condition. After the age of 11 years there are

chances of attack of wheezing due respiratory syncytial virus.

2.11.3. Michael E. Wechsler. (2009)61 explained about the severity of

asthma based on the symptoms are as follows.

Asthma classification Signs and Symptoms

Mild intermittent asthma Mild symptoms (up to 2 days /week and up to 2

nights per month)

Mild persistent asthma Symptoms more than two times a week, but not

more than one time in a day

Moderate persistent

asthma

Symptoms once in every day

Severe persistent

asthma

Symptoms throughout the day especially at night

Table 2.1: Severity of bronchial asthma

Source: Mudita Arora. (2008)45

2.11.4. According to Mudita arora. (2008)45 the first symptom of

asthma is non productive cough in some people.some may feel more

distressing than dyspnea.

28

2.11.5. Mudita arora. (2008)45 describes that the classic symptoms of

asthma attack is wheezing, shortness of breath, coughing, chest tightness,

rapid heart rate and sweating. One of the major sources of distress is

shortness of breath in the patients with asthma. Those at highest risk for this

effect trend to be older, female and those who have had the disease for a

longer period of time.

2.11.6. Sayeed Ahmad, D (2010)60 states that asthma usually begins

with mild chest pressure and dry cough. When the severity increases,

wheezing developes and increases in pitch.It follows development of

dyspnea, cough with expectoration.

2.11.7. Types of asthma:

Immunological classification of Bronchial asthma includes extrinsic asthma

and intrinsic asthma.

a) Extrinsic asthma- it is a type of asthma symptoms produced due to

influence of allergic reaction.

b) Intrinsic asthma- it is a type of asthma symptoms not produced due

to allergic reactions.

Intrinsic asthma is further divided into

Exercise induced asthma

Chemical induced asthma.

29

2.12. Diagnosis:

2.12.1. Asthma severity is confirmed usually by asthma exacerbations.

Wheezing- High pitched whistling sounds

History of the following

Cough

Recurrent wheeze

Recurrent dyspnea

Recurrent chest tightness

Worsening of symptoms during,

Exercise

viral infection

House-dust mites

Mold and pollen

Smoke

Climatic changes

Strong emotions

Table 2.2: Key indications for diagnosing Bronchial asthma

30

2.12.2. Adewole (2010)62 and Helen K. Reddel (2009)63 describes that

diagnosis of bronchial asthma can be made commonly by various tests which

includes; pulmonary function studies, total serum IgE level, absolute

eosinophil count, peak-flow metry, peak expiratory flow rate (PEF), skin

allergy testing with allergen, analysis of induced-sputum, chest X-ray, Pulse

oximetry. Among this test usual blood examination to determine atopic or

allergic nature is estimation of IgE and AEC.

2.12.3. Mudita arora, (2008)45 stated that estimation of IgE is done by

measuring the level of specific IgE antibodies in the blood serum. When there

is elevation of serum IgE level there is more chances of symptoms also.

According to Palm et al, IgE is thought to play an important role in the

bronchial asthma. Therefore it is a need to test IgE which will give the

therapeutic and prognostic guidance related to bronchial asthma. And also it is

necessary to test IgE in all patients having evidence of bronchial asthma.

2.12.4. Absolute eosinophil count is the number of eosinophils present

in the white blood cells. Normal Range of absolute eosinophil count is 50-

350/mm3. Eosinophils increased in allergic diseases like asthma.

2.12.6. Madan D (2010)64 reveals that the respiratory function of

patients with bronchial asthma can be assessed by spirometry measurements

which are usually termed as pulmonary function tests.

31

Pulmonary function tests are helpful in identification of the pulmonary function

mechanisms. They can guide in diagnosing and identifying complications. It

also helps to know the prognosis of treatment and to finalize the planning of

treatment. By voluntary airway exercise mechanism it is possible to assess

the normal and abnormal function of lungs through this test. And also the

parameters given below are important in assessment of lung function.

1. Forced Vital Capacity (FVC). 2. FEV1. 3. FEV1/FVC.

The main advantage of pulmonary function test is to diagnose asthma

from other lung impairments.

Valentin Prieto Centurion et al (2012)10 states that spirometry is one of

the parameter for conformation and prognostic assessment of asthma.

Exercise-induced asthma is diagnosed by the parameter like reduced FEV1.

2.13.Differential diagnosis:

Mudita arora (2008)45 have revealed that there are various differential

diagnosis for bronchial asthma such as cardiac asthma, chronic bronchitis,

obstruction of bronchi and bronchioles , broncho pneumonia, pulmonary

embolism, vocal cord dysfunction , chronic sinusitis, gastroesophageal reflux

disease, obstructive sleep apnea, and respiratory tract infections, allergic

bronchopulmonary aspergillosis,

32

allergic rhinitis, eczema, urticaria, atopic dermatitis and some parasitic

infections, food allergy and eosinophilic disorders of the gastrointestinal tract

,hyper-IgE syndrome and parasitic infections.

2.14. Complications

Das PC (2002)65 expresses that complications of bronchial asthma

includes status asthmaticus, emphysema of lungs, right heart failure, pneumo-

thorax, bronchiectasis, acute respiratory failure, reversible pulmonary artery

obstruction, angioedema, urticarial anaphylaxis, allergic rhinitis and

rhinosinusitis, pharyngitis, conjunctivitis, and dermatitis.

2.15. Prognosis

Porpodis K, Papakosta D (2009)66 have stated that long-term prognosis

of bronchial asthma was good and the outcome may be modified or delayed

due to factors like onset of asthma, male sex, presence negative history of

smoking.

2.16. Prevention

Preventive measures for asthma may include vaccination, patient

education and self-management, limiting their exposure to environmental

triggers and breastfeeding.

33

2.17. HOMOEOPATHY

2.17.1.Homoeopathy and bronchial asthma:

According to Lewith GT et al. (2002)67 homeopathy attempts to mitigate

disease by diluting the treatment without diluting the effect. Jawahar J Shah,

(2008)68 stated that homoeopathy is a system of medicine which is having

their unique characters based on principles of symptom similarity. The word

Homoeopathy is derived from two Greek words. Homois meaning similar and

pathois means suffering. Homoeopathic case taking is a process of collecting

relevant and important information about the symptoms, signs, clinical

categories, differential diagnosis, staging and complications related to the

case. These aspects are taken into consideration in treatment and prognosis

of bronchial asthma. Ullman D1, Frass M (2010)69 describes that

homoeopathic drugs are prepared either by crude or diluted substances. So

treatment is based on individually selected remedies for individual patient by

the process of individualization which shows more effect in treatment of

respiratory allergies like bronchial asthma. Anirban Biswas (2007)70 also says

that homoeopathy is based on individualization and symptom similarity which

makes regaining of healthy state by removing signs and symptoms. It is based

on the cause of each symptom.

34

In this study the main aim of the treatment is to treat allergy symptoms

and also to treat its underlying cause & individual susceptibility.

2.17.2. Paolo Bellavite et al (2006)71 states that immuno-allergology is a

unique branch which differentiates homoeopathy and modern medicine, that

homoeopathy has the concept that medicines are administered on the basis of

logic of similarity which is induced by ultra-low and high dilution doses which

acts on the immune system and makes changes in vital force and makes it

stronger to eradicate the disease force. Paolo Bellavite et al. (2005)48

expresses that homoeopathy is having a basic principle that the immunity in

the modern medicine is related with vital force’s self-healing power of an

individual.

2.17.3. Nature of classification of disease according to

Hahnemann:

Sarkar (2015) 72 stated that according to Hahnemann, health is a state

where life force governs the material, body in quiet equilibrium and

coordinating with mental, spiritual and physical planes of the body. Disease is

the altered state of health where the totality of symptoms observed outside as

abnormal sensations and functions which must be perceived by true physician

and to be treated properly in a systemic way following laws and principles of

Homoeopathy.

35

2.17.4 Hahenemann (1992)73 classified diseases into acute and chronic

in aphorism 72. Acute diseases are diseases which causes sudden alteration

in vital force which will have rapid process and ends less quickly. Chronic

diseases are diseases which alter the vital force dynamically and cause

gradual alteration in state of health and with its prolonged course. It is usually

associated with chronic miasms like Psora, Syphilis and Sycosis.

2.17.5. He also reveal that acute diseases are further classified into

individual, sporadic and epidemic in aphorism 73.

Hahenemann (1992) 73 reveal that individual diseases are diseases

which affects each and every individual separately by the exiting causes.

Exiting causes are the causes due to out side influences having capacity to

change or alter the vital dyamics to produce disease like cold exposure or

allergic exposure which may cause asthma.

Sporadic diseases are diseases which affects several people at same in

different localities due to meteoric and telluric causes.

Epidemic diseases affect more persons at same time with same cause

in vast area.

2.17.6. Hahenemann (1992)73 also defined drug diseases in aphorisms

74, 75, 76& 77. Drug diseases are diseases which are produced by the

administered drugs against the vital force. In patients with artificial diseases

produced by allopathic remedies the vital principle is weakened. The

weakened vital force either suppresses the disease

36

or it forms a complex disease with the disease force causing destructive

changes in the body. Homoeopathic system of medicine alone can cure any

disease Pseudo chronic diseases are diseases where patients continuously

exposed to some noxious agents with constant mental and physical irritation

will change the dynamic plane of vital force from health to disease, this state

will become be regained to healthy state when the person is removed from

exposure of that particular triggering agents.

2.17.7. True nature of chronic diseases are that arise from chronic

miasm in Aphroisms 78-82.True chronic diseases are diseases which

develops in side the body either due to improper treatment or due to wrong

treatment which makes the disease to grow very severe and makes more

pathological changes in both mental and physical planes with in complete

eradication of the disease. There are 3 important miasms namely psora,

syphilis, sycosis. Syphilis will end in incurabale state with termination of the

life of the patient. Syphilis shows its feature as destruction. On the other hand

sycosis will show its feature as external over growths which can only be

eradicated with proper homoeopathic medicines. Psora manifests by external

skin eruptions due to any suppressed major diseases. Psora is due the

suppressed effects of allopathic remedies from long back ago which exhibits

its manifestations as sudden expulsion when is having a tendency to produce

chronic disease. Specific antipsoic remedies for specific

37

individual who will guide through their totality of symptoms by strict process of

individualization and to trace the real hidden picture of disease, by which

helps to cure soon permanently also.

2.17.8 Hahenemann (1992)73 states that the acute disease or chronic

diseases will be presented with fully developed or one sided symptom in

Aphroisms 162- 178. Treatment given only with partially indicated medicines

in patients those who are having only partial totality of symptoms when exact

picture is not perceived. By the above method it will not give complete cure of

the disease but it shows the hidden state of the real disease which is

suppressed by that it guides for selection of exact similimum to make a

complete cure. The dose administered must be so minute one to just induce

the vital force. Even only few symptoms may be enough to make a quick

permanent cure provided if it has an uncommon, peculiar symptom of that

particular indicated remedy. If inappropriate, partial remedies without having

any peculiar, uncommon symptoms when it is prescribed will not make the

disease to be permanently cured due to unhomoeopathic laws. In such a

cases bad effects of that particular due to improper medication is reduced by

administering more number of similar remedies to compensate. Due to

imperfect homoeopathy remedy produced it will produce a new drug disease

which will be difficult to cure. If single medicine cannot make the restoration of

health when it is affected by a misguided disease by other improper methods

may be revaluated and

38

multiple drugs are needed to make a perfect cure. Improper case taking in the

first visit itself cause imperfect perception of portrait of disease will not cover

single remedy. So partial indicated remedy given first time, then after a few

period fresh case is taken and prescription is given based on the present

totality. First prescription with partial similimum followed by second

prescription with re fresh case taking makes path of cure to be clear and easy.

In non venereal chronic disease proper antipsoric remedies were given in

definite intervals to make a perfect cure. Difficulty in curing a patient when

they have only when a few symptoms alone will be perceptible. One sided

diseases are again difficult to cure as it has either physical or mental

symptoms alone with few symptoms. Exact cure takes place when well

selected similar remedies are given based on the homoeopathic laws.

2.17.9. Bronchial asthma is considered as a chronic miasmatic disease

which has different phases and different clinical presentations according to the

stage and miasm involved. So understanding the miasmatic background is

important in making a complete cure.

2.17.10. Miasmatic background of Bronchial Asthma

Gina Tyler (2012)74 describes that in Homoeopathy real cure is based

on the miasmatic treatment by which disease is completely eradicated from its

root cause. Miasms are otherwise known as a substance which cause

tendency to develop disease or the fundamental cause to develop a particular

disease. Aphorism 5 of Organon clearly

39

states that knowledge of fundamental cause that is miasm and totality of

symptoms are two important parameters to make effect of total cure. Dr.Kent

states that treating patients with totality of symptoms alone without

considering miasm may cause suppression or palliation of particular disease.

Thus the miasmatic approach becomes very important to ensure permanent

cure. Aphorism 78 of Organon states that the true natural chronic diseases

are due to chronic miasm which when untreated or with improper treatment

worsen the condition. It indicates that miasmatic temperament plays an

important role in development of disease. Miasm of a person can be modified

by factors like climate, abuses in life, mental abnormalities, dietary

abnormalities, habits, etc.

2.17.11. Gina tylor (2009) 74 stated that the miasms are classified as

Psora, Sycosis, Syphilis, and Tubercular.

2.17.12. Psora, is the main originating miasm among all with more

sufferings. 64

40

2.17.13. According to Mudita arora (2011)45 manifestation of signs and

symptoms of bronchial asthma in different miasmatic background includes:

a). Psora:

i. Hyper responsiveness of the tracheobronchial tree to any allergy.

ii. Family history or past history of allergies like rhinitis, eczema,

urticaria, or allergy to foods.

iii. Respiratory allergy with sneezing and cough.

iv. Throat congestion with much rattling mucus.

v. Scanty mucus secretions

b). Sycosis:

i. Family history of asthma.

ii. Non allergic Asthma.

iii. Cough with expectoration with dyspnea.

iv. <wet weather. >openair.

v. <early morning.> movement

vi. Greenish yellow expectoration

41

c). Syco syphilis:

i. Dyspnea

ii. <warmth

iii. Thread yellowish green discharge

iv. <midnight.

d). Tubercular:

i. Difficulty in breathing <climbing stairs.

ii. Mouth breathing with blockage in the nose.

iii. Foul smelling expectoration

iv. >in the open air.

2.17.14. Selection of medicine:

Close Stuart M. (2000)75 expresses that principles for selection of medicine

includes

Miasmatic totality , and

Totality of symptoms

Selection of medicine is the important part in homoeopathy where

individualization places a major role. No two individuals are alike, so each and

every individual needs a unique medicine for their presenting problem where

individualization takes place.

42

Close Stuart M. (2000)75 states that the important components in the

Homoeopathy system are potency, remedy and dose. In homoeopathy any

potency is related to any case. There is no fixed potency for a fixed case. A

well selected remedy may fail due to improper potency selection. Only the

exact similimum with minimum potency can bring an expected preferable cure.

2.17.15. Advantages of minimum dose are,

Minimum dose will not affect the physical plane; it just acts over the

spiritual vital plane to bring about easy curing of disease.

The diseased parts are so sensitive that even milder dose also reacts.

Lastly when single remedy is administered it has complete action and it

is not disturbed by other medicinal actions also.

2.17.16. Very minute dose or infinitesimal dose is the dose which divided and

redivideding the dose to cause minimum stimulation of vital force to exhibit a

cure. That also should be proper with proper direction and time. A proper dose

is very essential to promote cure.

43

2. 17.17. Choosing the Potency. -

Five considerations influence the selection of the dose:

i).The susceptibility of the patient: Susceptibility is the capable

reaction of an individual to a given stimuli. If susceptibility is found to be

more the potency of medicine also to be increased. Susceptibility is modified

according to age, temperament, constitution, habits, character of diseases

and environment.

ii). The seat of the disease: Low doses are necessary to treat fatal and

malignant diseases because the vitality is lost in these conditions.

iii). The nature and intensity of the disease. Low intensity in diseases

requires low potency but disease with higher intensity requires higher

potency.

iv). The stage and duration of the disease: early stage of disease requires

higher potency whereas end stage diseases requires lower potencies.

v). The previous treatment of the disease.Susceptibility can be altered by

treatment already taken for various diseases which helps in selection of

correct potency in prescription.

2.17.18. Repetition of Doses: If the remedy and the dose are correct

definitely there will be the result. The physician must want to

44

learn about wait and watch the medicinal action. Repetition of remedy is done

only when the improvement of patient stops.

2.17.19. In aphorism 245 Hahnemann quotes that if there is any

improvement in disease progress is one of the contraindication to repeat the

remedy. Hahenemann in Aphroisms 245-246 and 248 states that, Repetition

of dose of a particular medicine is required when that medicine action is

completely exhausted. In acute diseases it is necessary that repetition is

more frequent as every four, eight, twelve or twenty four hours, but in chronic

diseases it is enough to repeat even within forty to hundred days. If there is

stand still or reoccurrence of symptoms it is advisable to to give higher

potency of same remedy to induce the strong vital force. This is done by

potentiazing a medicinal solution and taking by teaspoon after several

successions between the 2 doses. This balances disease power and

medicinal power which acts over it. In case of homoeopathic aggravations the

dose is stopped and the sequence is observed.

2.17.20. Materia medica:

Mohanty Niranjan (2009)76 states that materia medica is a branch of

medical science deals with details like sources, preparation, effects on human

beings, dosage and method of administration of each and every individual

drug.

45

Homoeopathic materia medica is type of record which consists of

symptoms collections produced by a drug on healthy human being.

Preparation of materia medica is done by repeated proving of a particular drug

and collecting subjective and objective symptoms of that drug from the prover

and compiling into a systematic and schematic way.

2.17.21. Repertory:

Schroyens Frederik. (2011)77 states that the commonly used medicines

for bronchial asthma under various rubrics are given below:

1.RESPIRATION – WHEEZING: Aconitum Napellus, Agaricus

Muscarius, Ailanthus Glandulosa, Aloe Socotrina, Alumina, Ammonium

Carbonicum. Ambra Grisea, Anacardium Orientale, Arsenicum Sulphuratum

Flavum , Angustura Vera, Asafoetida, Apis mellifica, Apocynum cann, Aralia

racemosa, Arsenicum Album, Argentum metalicum, Arsenicum iodatum,

Argentum nitricum, Aurum metalicum, Arnica Montana,Bromium, Bitis arietans

arietans, Bovista, Blatta orientalis, Bryonia alba, Belladona,Cannabis sativa,

Calcarea, Camphora, Capsicum,Chamomilla,Calcarea sulphuricum, Carbo

animalis, Carbovegetabilis,Cicuta virosa, Chininum arsenicosum,Carboneum

sulphuratum, Causticum, China officinalis, Caladium Seguinum, Chloloralum

hydratum, Cina maritime, Cocculus indicus, Colocynthis, Conium maculatum,

Crocus sativus, Croton

46

tiglinum, Cuprum metallicum, Cyclamen europaeum, Desoxyribonucleium

acidum, Digitalis purpurea, Dolichos pruriens, Drosera rotundifolia,

Dulcamara, Euphrasia officinalis, Ferrum metalicum, Ferrum iodatum, Fluric

acid, Formica rufa, Graphites, Helleborus niger, Helodrilus caliginosus, Hepar

sulphur, Hydrocyanicum acidum, Hyoscyamus niger, Ignatia amara, Iodium,

Iodoformium, Ipecacuanha, Iridium metallicum, Kalium arsenicosum, Kalium

bichromicum, Kalium Carbonicum, Kalium iodatum, Kalium nitricum, Kalium

sulphuricum, Lac equinum, Lachesis muta, Laurocerasus, Ledum palustre,

Limestone burren, Loxosceles reclusa, Lycopodium clavatum, Lycopus

virginicus, Magnesium muriaticum, manciella, Manganum phosphoricum,

Melaleuca alternifolia, Mercuris solubilis, Mezereum, Moschus, Muriaticum

acidum, Murex purpurea, Naja tripudians, Natrum carbonicum, Natrum

muriaticum, Natrum nitricum, Natrum sulphuricum, Neon neon, Nitricum

acidum, Nitri spritus dulcis, Nux moschata, Nux vomica, Opium. Oxalicum

acidum, Paris quadrifolia, Phosphoricum acidum, Phosphorus, Plumbum

metalicum, Positronium, Pulsatilla pratensis, Ranunculus bulbosus,

Ranunculus sceleratus, Rhododendron chrysanthum, Rhus toxicodendron,

Ruta graveolens, Sabadilla, Sambucus nigra, Sanguinaria Canadensis,

Sanicula aqua, Sarsaparilla officinalis, Senega, Sepia officinalis, Silicea terra,

Spongia tosta, Squilla maritime, Stannum metallicum, Staphisagria,

Stramonium, Pancreas suis, Sulphricum acidum, Sulphur iodatum, Sulphur,

Bacillus

47

sycoccus, Syphilinum, Teucrium marum verum, Thuja occidentalis,

Tungstenum metallicum, Veratrum album, Veronica officinalis, Viscum album,

Zincum metallicum.

2. RESPIRATION – DIFFICULT: Abies canadensis, Abies nigra,

Abrotanum, Absinthium, aceticum acidum, Acetanilidum, Aconitum napellus.

Adonis vernalis. Aethusa cynapium, Agaricus muscarius, Agathis australis,

Agnus castus, Aids nosode, Ailanthus glandulosa, Allium sativum, Alloxanum,

Aloe socotrina, Alumina, Alumina silicate, Alumen, Ammonium carbonicum,

Ammonium muriaticum, Ambra grisea, Antimonium Crudum, Anacardium

orientale,Apocynum cannabinum,Angostura vera, Anhalonium Lewinii, ,

Antimonium tartaricum,Apis mellifica, Antimonium Arsenicosum, Aralia

racemosa.Arsenicum album,Arsenicum iodatum. Arsenicum sulphuratum

flavum, Argentum nitricum,Argentum metallicum, Arum triphillum, Arundo

mauritanica, Asarum europaeum, Asclepias tuberosa, argemone pleiacantha,

Asparagus officinalis, Aurum metallicum, Aurum arsenicum, Aurum iodatum,

Aurum muriaticum, Arnica Montana, Atrax robustus, Aurum muriaticum

natronatum, Aurum sulphuratum, Asafoetida, Astacus fluviatillis, Baryta

carbonica, Baryta iodate, Baryta muriatica, Baryta oxalsuccinata, Bacillinum

burnett,Belladona,Benzoicum acidum, Bismuthum, Blatta orientalis, Borax

veneta, Botulinum, Beryllium metallicum, Bufo rana, Bovista lycoperdon,

Brassica napus oleifera, Badiaga,Bromium, Brosimum

48

gaudichaudi, Bryonia alba, Buthus australis, Cadmium metallicum, Calcarea

carb,Cactus grandiflorus,Calcarea florica, Calcarea iodate, Calcarea

phosphorica,Calcarea sulphurica,Calcarea silicate, Camphora officinalis,

Calcarea arsenicosa, Cannabis indica, Cannabis sativa, Cannabis unknown

species, Corallium rubrum, Cantharis vesicatoria, Capsicum annuum,

Chininum sulphuricum, Carbolicum acidum, Causticum, Cedron, Carbo

animalis, Cainca, Cistus Canadensis, Caladium seginum, Carbo Vegetabilis,

Carboneum sulphuratum, Carboneum oxygenisatum, Cassia sophera,

Castoreum canadense, Chamomilla, Chelidonium majus, Carlsbad aqua,

China officinalis. Coca, Chininum arsenicosum, Chenopodium

anthelminticum, Cenchris contortrix, Collinsonia Canadensis, chloralum

hydratum, Chlorum, Chorda umbilicalis, Cimex lectularius, Chironex

fleckeri, Cina maritima, Coccus cacti, Cocculus indicus, Colchicum

autumnale, Colocynthis, Conium maculatum, Coffea cruda, Copaiva

officinalis, Convallaria majalis. Cordyceps militaris, Cortisonum, Cotyledon

umbilicus, Crotalus cascavella, Crocus sativus, Crotalus horidus, Croton

tiglinum, Cuprrum metalicum, Cicuta virosa, Cubeba officinalis, Cimicifuga

racemosa, Cuprum acteicum, Cuprum nitricum, Cuprum sulphuricum,

Cuprum arsenicosum, Curare, Cyclamen, Europaeum, Cytisus laburum,

Diitalis purpurea, Dipthero-tetano-typho-paratyphoidicum, Diptherotoxinum,

Dirca palustris, Dreaming potency, Drosera rotundifolia, Dulamara, Bacillus

dysenteriae, Eberthinum, Ephedra vulgaris, Equisetum

49

hymale, Eryngium aquaticum, Eupatorium perfoliatum, Euphornium

officinarum, Euphrasia officinalis, Falcon cherrug, Ferrum metalicum,

Ferrum asenicosum, Ferrum iodatum, Ferrum phosphoricum,Fluricum

acidum,Follicullinum, Fumaricum acidum, Galla quercina ruber, Gardenia

jasminoide, Gelsemium sempervirens, Geranium inodorum, Ginseng

qiuinquefolium,Glonoinum, Graphites,Grindelia robusta, Guajacum officinale,

Hamamelis virgiana, Helleborus niger, Helodrilus caliginosus, Hepar sulphur,

Hippozaeninum, Histaminum, Hura brasiliensis, Hura crepitans, Hydrastis

Canadensis, Hydrocynicum acidum, Hydrocotyle asiatica, Hydrogenium,

Hydrophis cyanocinctus, Hyoscyamus niger, Hypericum perforatum, Ignatia,

Indigo tinctoria, Iodium,Ipecac, Iridium metallicum, Iris versicolor, Ixodes

rcinus, Jaborandi, Jatropha curcas, juglans cinerea, Kalium

arsenicosum,Kalium bichromicum, Kalium bromatum, Kalium carbonicum,Kali

chloricum,Kalium Iodatum, Kalium muriaticum, Kalium nitricum, Kalium

phosphoricum, Kalium sulphuricum, Kalium silicicum, Kalium sulphuratum,

Kalmia latifolia, Ketoglutaricum acidum, Kreosotum, Lac equinum, Lac

caninum, Lachesis muta, Latrodectus haseltii, Lactuca virsa, Latrodectus

mactans, Laurocerasus, Lecithinum, Ledum palustre, Lilium tigrinum,

Limestone burren, Lavandula angustifolia, Lithium carbonicum, Lobelia

inflata, Lobelia erinus, Loxosceles reclusa, Lycopodium clavatum, Luna luna,

Lycopus virginicus,Lyssinum, Magnetis poli ambo, Magnetis polus arcticus,

50

Magnetis polus Australis, Magnesium muriaticum, Magnesium sulphuricum,

Magnesium carbonicum, Malaria nosode, Mandragora offcinarum, Manganum

act, Mancinella, Meddorrhinum, Melilotus officinalis, Menyanthes trifoliata,

Mercurius solubilis,Mercurius corrosivus,Mephitis putorius,Mercurius

cyanatus,Mercurius sulphuricus, Mercurialis perennis, Mezereum, Monilia

albicans, Bacillus morgan pure, Morphinum and salts, Bacillus morgan

gaertner, Moschus, Mucor mucedo, Muriaticum acidum, Murex purpurea,

Musca domestica, Mygale lasiodora, Naja tripudians, Natrium carb,Natrium

fluratum, Natrium arsenicosum, Natrium muriaaticum,Natriumnitricum,

atriumphosphoricum,Natriumsulphuricum,Natrium silicicum, Niccolum met,

nicotinamidum, Nitricum acidum,Nux moschata.Nux vomica, Oleum jecoris

aselli, Olibanum sacrum, Oenanthe crocata, Opium,Oxalicum acidum,

oxydendron arboretum, Osmium met, ozonum, Paris quadrifolia, Petroleum,

Phosphoricum acidum, Parabenzoquinonum, Phellandrium aquaticum,

Phosphorus pentachloratus, Phosphorus,Physostigma venenosum, Physala

pelagica, Phytolacca decandra, Pinus contorta, Pituitaria glandula, Placenta

humana, Plumbum metallicum, Plutonium nitricum, Platinum metallicum,

Podophyllum peltatum, Polystyrenum, Positronium, Bacillus proteus, Prunus

spinosa, Pseudotsuga menziesii, Psorinum, Ptelea trifoliata, Pulsatilla

pratensis, Pycnoporus sanguineus, Rananculus bulbosus, Rananculus

sceleratus, Raphanus sativus,

51

Ratanhia peruviana, Rauwolfia serpentina, Rheum palmatum,

Rhododendron chrysanthum, Rhus glabra, Rhus toxicodendron, Rumex

crispus, Ruta graveolens, Sabadilla, Sabina, Salix fragilis, Sambucus

nigra,Sanguinaria Canadensis, sarcolacticum acidum, Sarracenia Purpurea,

Sarsaparilla Officinalis, Scolopendra morsitans, Secale cornutum , Selenium

metallicum,Senega,Sepia officinalis,Silicea terra, Sinusitisinum, Spigellia

anthelmia, Spongia tosta,Squilla maritime, Stannum metallicum, Staphysagria,

Stramonium, Strontium carbonicum, Strophananthus sarmentosus,

Strychinum purum, pancreas suis, Sulphuricum acidum, Sulphur iodatum,

sulfanilamidum., Sulphur, Suprarenalis, Bacillus sycoccus, Syphilinum,

Tabacum, Taraxacum officinale, Tarentula hispanica, Taxus baccata,

Terebinthinae oleum, Thiaminum hydrochloridum, Thuja occidentalis,

Thymolum, Tilia europaea, Toxoplasma gondii, Tradescantia diuretica,

Trilum pendulum, Trinitrotolueum, Tuberculinum bovinum kent, Tuberculinum

avis, Tuberculinum residuum Koch, Tungstenium metallicum, Uva ursi,

Vaccinum, Valeriana officinalis, Veratrum album, Veratrum viride, Veronica

officinalis, Vespa crabro, Viola odorata, Vipera berus, Viscum album,

Xanthoxylum fraxineum, Serum yersiniae, Zincum metallicum, Zincum

phosphoricum, Zingiber officinale.

3. COUGH in general: Aconitum napellus, Agararicus muscarius,

Agnus castus, Alchornea cordifolia, Allium sativam, Alumina, Ammonium

carbonicum, Ammonium muriaticum, Ambra

52

grisea, Anacardium oreintale, Angustura vera, Antimonium crudum,

Antimonium tartaricum, Argentum metallicum, Argentum nitricum, Arnica

Montana, Arsenicum album, Asafoetida, Asaram europaeum, Aurum

metallicum, Bacillinum burnett, Baryta carbonica, Belladona, Bismuthum,

Bryophyllum proliferum Bovista lycoperdon, Bridelia atroviridis, Bromium,

Bryonia alba, , Borax veneta, Cadminum metallicum, Caladium seguinum,

Coffea cruda, Calcarea carbonica, Carbo animalis, Calcarea flurica,

Camphora officinalis, Cannabis sativa, Cannabis unknown species,

Colocynthis, Cantharis vesicatoria, Capsicum annuum, , Carbo Vegetabilis,

Carcinosinum, Causticum, Chamomilla,China officinalis, Cicuta virosa, Cina

maritime, Clematis erecta, Coccus cacti, Cocculus indicus, Colchicum

autumnale, Conium maculatum, Cortisonum, Crocus sativus, Cuprum

metallicum, Cuprum nitricum, Cyclamen europaeum, Dulcamara, Digitalis

purpurea, Drosera rotundifolia, Euphorbium officinarum, Euphrasia officinalis,

Ferrum metallicum, Ficus carica, Flavus, Galla quercina ruber, Glycyrrhiza

glabra, Graphities, Guajacum officinale, Helleborus niger, Hepar sulphur,

Heterotis rotundifolia, Hydrastis Canadensis, Hyoscyamus niger,Ignatia

amara,Iodium,Ipecacuanha, kalium bichromicum, kalium carbonicum, kalium

nitricum, Kreosotum, Lachesis, Lantana camara, Lantana trifolia, Latrodectus

mactans, Laurocerasus, ledum palustre, Lycopodium clavatum, Magnetis poli

ambo, Magnetis polus arcticus, Magnetis polus australis, Magnesium

carbonicum, Magnesium

53

muriaticum, Malaria nosode, Manganum act, Menyanthus trifoliate, Mephitis

putorius, Mercurius solubilis, Mezereum, Moschus, Muriaticum acidum,

Narcissus pseudonarcissus, Natrium carbonicum, Natrum muriaticum, Nitric

acidum, Nux moschata, Nux vomica, Ocimum santum, Olibanum sacrum,

Oleander, Opium, Paris quadrifolia, Pentadiplandra brazzeana, Petroleum,

Phosphoricum acidum, Phellandrium aquaticum, Phosphorus, Phytolacca

decandra, Piper guineense, pix liquida, Platinum metallicum, Plumbum

metallicum, Bacillus proteus, Psorinum,Pulsatilla pratensis, Pycnostachys

eminii, Quillaya saponaria, Rananculus bulbosa, Rananculus sceleratus,

Rheum palmatum, Rhododendron chrysanthum, Rhus toxicodendron, Rumex

crispus, Ruta graveolens, Sabadilla, Sabina, Salicylicum acidum, Sambucus

nigra, Sanguinaria Canadensis, Sarsaparilla officinalis, Secale cornutum,

Selenium metalicum, Senega, Sepia officinalis.Silicea terra, Spigelia

anthelmia, Spongia tosta,Squilla maritime,Stannum metallicum, Staphisagria,

Sticta pulmonaria, Stramonium, Strontinum carbonicum, Sulphuricum acidum,

Sulphur, Bacillus sycoccus, Tabacum, Taraxacum officinale, tetradenia riparia,

Teucrium marum verum, Thuja occidentalis, Toxoplasma gondii, Trema

orientalis, Ursinia tenuiloba, Variolinum, Veratrum album, Verbascum

Thapsus, Veronica officinalis, Xylopia aethiopica, Zincum metallicum,

Zizyphus mucronata.

54

4. CHEST – CONSTRICTION: Aesculus hippocastanum, Agaricus

muscaries, Aconitum napellus, agathis australis, Aids nosode, Aethusa

cynapium, Allium cepa, Alumina, Alumina silicate, Ailanthus glandulosa,

Ammonium carbonicum, Alumen, Ammonium muriaticum, Ambra grisea,

Ammonium phosphoricum, Angustura vera, Anhalonium lewinii, Anacardium

orientale, Anthraquinone, Antipyrinum, Antimonium tartaricum, Apis

mellifica, Aralia racemosa, Argentum nitricum, Argemone pleiacantha, Arnica

Montana, Arsenicum hydrogenisatum, Arsenicum Album, Arsenicum

sulphuratum flavum, Arsenicum iodatum, Asarum europaeum, Asclepias

tuberosa, Asparagus officinalis, Aurum metallicum, Asafoetida, Aurum

arsenicum, Aurum iodatum, Aurum muriaticum, Aurum muriaticum

natronatum, Baryta carbonica, ,Baptisia tinctoria, Baryta sulphurica, Baryta

iodate, Belladona, Bismuthum, Bitis arietans arietans, beryllium metallicum,

Borax veneta, Bovista lycoperdon, Bromium, Bufo rana, Bryonia alba,

Brosimum gaudichaudi, Cannabis indica, Cainca, Cannabis unknown

species,Cactus grandiflorus, Calcarea carbonica, Calcarea phosphorica,

Calcarea sulphurica, Calcarea silicate, Caladadium seguinum, Cadmium

sulphuratum, Camphora officinalis, Cantharis vesicatoria, Capsicum

annum, Carbolic acidum, Cannabis sativa, Carbo animalis, Carboneum

sulphuratum, Carcinosinum, Carbo vegetabilis, Cardiospermum

halicacabum, Carlsbad aquq, Chamomilla, Carbnoneum oxygenisatum,

Cheledonium majus,

55

Chininum arsenicosum, China officinalis, Chininum sulphuricum, Chlorum,

Chloralum hydratum, Causticum, Cicuta virosa, Cina maritima, Cimex

lectularius, Cinnabaris, Clematis erecta, Coffea cruda, Cocculus indicus,

Colchicum autumnale, Coccus cacti, Conium maculatum, Colocythis,

Crotalus cascavella, Copaiva officinalis, Crotalus horridus, Cuprum

metallicum, Croton tiglium, Cuprum sulphuricum, Cyclamen europaeum,

Cytisus laburum, Cuprum arsenicosum, Dulcamara, Digitalis purpurea,

Drosera rotundifolia, Dioscorea villosa, Elaps corallines, Euphorbium

officinarum, Ferrum phosphoricum, Ferrum metallicum, Ferrum arsenicosum,

falcon peregrinus disciplinatus, Ferrum iodatum, Gelsemium sempervirens,

Germanium metallicum, Gambogia, Ginseng quinquefolium, Graphites,

Glonoinum, Helleborus niger, Hedera helix, hydrocynaicum acidum,

Hypericum perforatum, Hepar sulphur,Hyoscyamus niger, Hydrogenium,

Ignatia amara, Iris versicolor, Ictodes foetida, Iridium metallicum,

Iodium,Ipecacuaha, Jatropha curcas, Kalium arsenicosum,Kalium

bichromicum,Kalium carbonicum, Kalium chloricum,Kalium iodatum, Kalium

muraiticum, Kalium nitricum, Kalium phosphoricum, Kalium sulphuricum,

Kalium silicicum, Ketoglutaricum acidum, Kola, Kreosotum, Lac humanum,

Lac loxodonta Africa, Lachesis muta, Lactuca virosa, Lapis lazuli, lappa

atrium, Latrodectus haseltii, Latrodectus mactans, Laurocerasus, Lavandula

angustifolia, Lecithinum, Ledum palustre, Lithium carbonicum, Lobelia inflate,

56

Loxosceles reclusa, Luna, Lycopodium calvatum,Lycopus

virginicus,Magnesium carbonicum,Magnesium muriaticum,Magnesium

phosphoricum,Mancinella, Mandragora officinarum, Manganum act,

Manganum phosphoricum, Melaleuca alternifolia, Menyanthes trifloiata.

Mercurius solubilis,Mercurius corrosivus,Mercurius iodatus ruber, Mezereum,

Monilia albicans, Bacillus Morgan gaertner, Morphinum and salts, Moschus,

Muriatum acidum, Naja tripudians,Natrium arsenicosum,Natrium carbonicum,

Natrium muriaticum,Natrium phosphoricum, Neon, Nitric acidum,Nux

moschata, Nux vomica, Olibanum sacrum, Oleander, Opium, Osmium met,

Oxalicum acidum, Ozonum, Petroleum, Phosphoricum acidum, Phosphorus,

Physostigma venenosum, Physalia pelagica, Picricum acidum, Pinus

contortaa, Pituitaria posterior, Placenta suis, Platinum metallicum, Plumbum

metallicum, Podophyllum peltatum, Positronium, Bacillus proteus, Psilocybe

caerulescens, Psorinum, Pulsatilla pratensis, Pycnoporus sanguineus,

Radium bromatum, Rananculus bulbosa, Ratanhia peruviana, Rauwolfia

serpentine, Rhododendron chrysanthum,Rhus toxicodendron, Ruta

graveolens, Sabadilla, Sabina, Salix fragilis, Sambucus nigra, Sarothamnus

scoparius, Sarsaparilla officinalis, Selenium metallicum, Senega,Sepia

officinalis, Silicea terra, Sinusitisinum, Spigelia anthelmia,Spongia tosta,

Squilla maritima, Stannum metallicum,Staphisagria, Stramonium, Strontium

carbonicum, Strychninum purum, Embryo suis, Hepar suis, Pancreas suis,

57

Sulphuricum acidum, Sulphur iodatum, Sulphur, Sumbulus moschatus,

Suprarenalis, Symphytum officinale, Tabacum, Tarentula hispanica,

Terebinthine oleum, thea chinensis, Thiaminum hydrochloridum, Thuja

occidentalis, Thyreoidinum, Trilium pendulum, Tuberculinum bovinum kent,

Tungstenium metallicum, Upas tieutu, Veratrum album, Verbascum Thapsus,

Veronica officinalis, Viscum album, Xanthoxylum fraxineum, Zincum

metallicum.

58

III. STATEMENT OF PROBLEM, NEED FOR STUDY, OBJECTIVES AND

HYPOTHESIS

3.1 STATEMENT OF PROBLEM:

Sae-Hoon kim et.al., (2011)78 states that asthma is a major health

problem which is highly prevalent in all countries throughout the world. Raj

Kumar et al. (2006) 6 stated that approximately 245 million individuals suffer

from asthma worldwide. Incidence of asthma is increasing day by day all over

the world including Asia. In India about 2-8% population is estimated to suffer

from bronchial asthma.

3.2. Allergic diseases have major health issue where asthma plays a

major role in allergic disorders. Bronchial asthma is a unique health related

issue which is usually associated with some of the occupations which needs

careful attention.

3.3 Incidence of Asthma increased in the past few years. It is also

having an impact on few occupations which needs careful attention.

3.4. Adeniyi BO et al (2009)11 states that asthma is one of the most

common chronic diseases worldwide affecting 300 million people and is thus

estimated to rise to 400 million by 2025. The global prevalence ranges from 1

to 18% in different population groups. Annual worldwide death is put at 250

000, mostly due to preventable causes.

59

3.5. Agam Vora. (2012)38 states that according to Indian Council of

Medical Research in India 2.38% suffer from asthma and 20 to 26% of people

suffer from allergic rhinitis. Symptoms of rhinitis were present among 75% of

children and 80% of asthmatic adults. At present there is enormous number of

cases of bronchial asthma in India. But asthma is still remains less

recognized, under-estimated and not treated accurately in India.

3.6. Nargues A. Weir Stewart J. Levine (2012)3 describes that

Homeopathy is cost effective, free from side effects and effective in treating

allergic disorders especially bronchial asthma. It is a system which treats the

patients individually based on their symptom similarity.

3.7. Paolo Bellavite et al (2006)48 states that homeopathic research has

great development now with implementation of clinical research works,

computerized based programs, and scientific proofs with investigatory

evidence than before.

3.8. Paolo Bellavite et al. (2006) 48 also states that according to the

study report given by Castellsagu after giving homoeopathic medicines like

Sulphur, Calcarea carbonica, Lycopodium and Pulsatilla at various potencies

for patients with bronchial asthma 58% of patients had complete cure, 23% of

patients had improvement and 19% of patients had failure.

60

3.9. NEED FOR STUDY

Assessment of IgE level during homeopathic management of bronchial

asthma demonstrates the effectiveness of homeopathic remedies in the

regulation of IgE.

3.10. No study is known to be conducted in bronchial asthma by

assessing the three parameters like IgE, absolute eosinophil count and PFT.

3.11. Hence the investigator has undertaken this study to assess the

modulation of IgE level, Absolute eosinophil count and the resultant

pulmonary function after homoeopathic treatment in bronchial asthma.

3.12. Objectives:

On this background it was proposed to conduct a prospective study at

Vinayaka missions homeopathic medical college and hospital and attached

peripheral centers with following objectives:

To find out the significant difference of Ig E level before and after

homoeopathic treatment in bronchial asthma

To find out the significant difference of AEC level before and after

homoeopathic treatment in bronchial asthma

To find out the significant difference of PFT before and after

homoeopathic treatment in bronchial asthma.

61

3.13 . Hypotheses.

This study was conducted with null hypotheses given below.

Ho1: There is no significant difference in the level of IgE before and

after homeopathic treatment among patients with bronchial asthma.

Ho2: There is no significant difference in the level of absolute eosinophil

count before and after homeopathic treatment among patients with

bronchial asthma.

Ho3: There is no significant difference in the level of pulmonary

function studies before and after homeopathic treatment among patients

with bronchial asthma.

3.14.The result of the study was stastically analyzed with Kruskal Wallis test

and Wilcoxon signed rank test for confirmation of the hypotheses.

62

IV. MATERIALS AND METHODS

4.1. This study was conducted in the patients who were attending the

outpatient, inpatient units and peripheral centers of Vinayaka missions

homoeopathic medical college hospital, Salem. Out of 171 patients 149

continued treatment and all 149 patients were selected for this prospective

study by using purposive sampling technique. Permission from ethical

committee of VMHMC&H was obtained before implementing the research.

Written consent was obtained from all the patients. The study was conducted

for a period from 01.03.2013 to 30.09.2014.

4.2. Criterias adapted for study:

a). Inclusion criteria: Patients with bronchial asthma and having the

symptoms such as daytime coughing, wheezing, and shortness of breath,

chest tightness; night-time coughing and wheezing were selected for the

study.

b). Exclusion criteria: Patients with status asthmaticus, patients who were

taking other system medicines for treating any illness (Allopathy, Ayurveda,

Siddha and Unani) and patients with other complications, uncooperative

patients.

63

4.3. Research design:

Patients

with

Bronchial

Asthma

Pre Test

Measuring

IgE,

AEC and

Pulmonary

function.

Treatment

Administer ing

Homoeopathic

medicines based on

total i ty.

Post test

Measuring

Absolute

Eosinophil

Count, IgE,

and

Pulmonary

function.

O 1 X1 X2 X3 X4 X5 etc O 2

E= O 2 - O 1

O 1 = Pre Test (pr ior to the treatment)

O 2 = Post test (at the end of treatment )

X1 X2 X3 X4 X5 etc = Treatment by using homoeopathic medicines

and measuring IgE level modulat ion.

E= effect iveness

The changes effected were evaluated by excluding the possibil i ty

of occurrence by f inding the p-value

4.4. Case selection, prescription and follow up: After obtaining

written consent, complete case recording was done. Blood sampling was

collected from each patient and sent for measuring IgE, AEC. Quantitative

Assay for total IgE antibodies by using BIORAD 680 Micro Plate Reader was

64

used to measure IgE level. Normal level of AEC is 40 to 440 cells/ cumm. By

using Swel lab 920 EO+ measurement of AEC was done. Pulmonary function

test was done by the researcher and recorded; Routine blood and urine

investigations also were done. Total WBC count, Differential count such as

polymorphs, lmphocytes, eosinophils, monocytes and basophils, erythrocyte

sedimentation rate and serum haemoglobin level. Blood sugar level done for

all patients except children. Urine test includes sugar, albumin, bile salts, bile

pigments, pus cells, blood, epithelial cells, casts and crystals. Each case was

analysed and evaluated and treatment was given according to the

homoeopathic philosophy. Patient’s history and clinical examination were

recorded in a standard case sheet performa. Analysis and evaluation as per

Hahemann’s method was done. Rubrics were selected from synthesis

repertory by Scroyens F., and repertorization was done to make a similimum.

Patients were asked to visit monthly once. Two doses of exact similimum

followed by plain saclac pills for one month were given and patients were

advised to report immediately if any discomfort they felt in between. Potencies

were selected according to the symptom similiarity, suceptability and

chronicity of disease. Drugs were repeated in conditions like reoccurance of

symptoms, no improvement in symptoms or when ever necessary. The results

were correlated with patient’s clinical history and suitable medicines with

accurate potency were selected. Various potencies like

65

30, 200, 1M, 10M, 50M were used based on the presentation. Repetition of

medicines was done when there is stand still of symptoms or when there is

recurrence of symptoms. Average period taken for repetition of medicines

ranges from 1 month to 3 months. 30th potency rarely used in this study. 200th

potency was given in the 1st visit of the patient as constitutional remedy or as

acute remedy for acute diseases due to maintaining cause. 1M potency was

given monthly once. 10M potency was given after exhaustion of action of

repeated doses of1m potency. 10M were given trimonthly or after the

exhaustion of action of previous dose. 50M potency was not used in any

patients. Patients were advised to approach the investigator if there is any

necessity. This procedure was repeated every month. Patient’s level of IgE

was monitored monthly, level of AEC was monitored once in 3 months and

readings of PFT were monitored monthly. Patients were observed for a period

from 6 months to 12 months. Evaluation and necessary investigation of the

secondary diseases was conducted simultaneously. Kruskal Wallis test and

Wilcoxon signed rank test were used for the statistical analysis. Prospective

study was be used to conduct the study.

4.5. The tools used for the study:

a). BIORAD 680 Micro Plate Reader

b).Total IgE ELISA Kit-Quantitative Assay for Total IgE Antibodies

c). Swel lab 920 EO+ for measuring AEC

d).RMS Spirometer Helios 401 for measuring PFT

66

e). Statistical Package for Social Science version 11.5

f). Case study proforma for collecting detailed history

g).Homoeopathic remedies used for prescription

a).BIORAD 680 Micro Plate Reader:

BIORAD 680 Micro Plate Reader is an instrument through which the

total IgE kit readings were recorded. It has inbuilt software for reading the

microplate. The software has three different protocol types: End-point

analysis, Kinetic analysis, and the checkmark validation protocols. The

software communicates through the 4-line, 20-character LCD and was

controlled through the instrument's membrane keypad and print out reports

were obtained by internal and external printer.

b).Total IgE ELISA Kit (Quantitative Assay for Total IgE Antibodies)

The total IgE kit is a method for detection of IgE antibodies by ELISA

method. It helps in diagnosis of allergic diseases. By this kit estimation of

serum IgE level was done.

Principle: Serum was diluted and incubated with anti human IgE which

is present in microtitre wells for 60 minutes. Un bound serum was washed and

added with antihuman IgE conjucated with horseradish peroxidase incubated

for 30 minutes. Again it was washed with 3,3’,5,5’- tetramethylbenzidine

(TMB) solution and enzyme substrate was added incubated for 10 minutes.

Stop solution (0.25M sulphuric acid) was added to finalize the pH for

development of color. Then positive results were read by microplate reader at

450nm.

67

c). Swel lab 920 EO+ for measuring AEC

Swelab instrument was used to measure the absolute eosinophil count.

It equipped with connectors for normal PC keyboards + USB printer port which

enables to take print out of the results.

The normal value considered for absolute eosinophil count in this study

was 40 to 440 cells/ mm3.

d). RMS Spirometer Helios 401 for measuring PFT

Helios 401 is a spirometer used by connected with computer.

1). Forced Vital Capacity (FVC): To perform the FVC maneuver, the

patient was asked to first breathe in deeply to his full extent. The patient was

instructed to place the transducer to the mouth with nose clip applied to the

nose and he expels the air in their lungs as quickly as possible. Once all the

air in the lungs has been expelled, the patient breaths in as quickly as

possible, still with the transducer to the mouth, until the lungs are full.

2).Slow Vital Capacity (SVC): The SVC test is a less strenuous

method of finding a patient’s Vital Capacity. The patient was asked to breathe

regularly through the mouthpiece. The patient should then take a deep breath

followed by a deep exhalation. Both inhalation and exhalation should be

performed to the maximum extent. After this slow maneuver the patient should

take a few gentle and normal breaths.

68

3).Maximal Ventilatory Volume (MVV): The patient was asked to

breathe deeply and quickly through the mouthpiece for 15 seconds. Breathing

should be as constant as possible.

Depending on where the values of FVC%Pred and (FEV1/FVC)%Pred

lie, the patient’s lung condition was suggested to be:

- Normal (NORM)

- Restrictive (RES)

- Mixed (MIXED)

- Obstructive (OBS)

e) Statistical package for social science version 11.5

Analysis for this study was done by software named as statistical

package for social science version 11.5.

Statistics included in the base software are descriptive statistics like

cross tabulation, frequencies, descriptives, explore, descriptive ratio

statistics bivariate statistics, means, t-test, ANOVA, correlation (bivariate,

partial distances), non parametric tests, prediction for numerical

outcomes: linear regression,prediction for identifying groups: factor

analysis, cluster analysis (two-step, K-means, hierarchical), discriminant.

Values in the study were coded and feed in this software and analytical

procedure was done.

69

f). Case study proforma for collecting detailed history

Patient’s complete history was obtained through a standard format of

case sheet. Analysis and evaluation of symptoms were done according to the

homoeopathic principles. The laboratory values like blood routine, urine

routine, IgE, AEC and PFT values were entered side by side in the prepared

format. Then the follow up symptoms of the patients with prescription were

recorded. This procedure was followed monthly once.

g). Homoeopathic remedies prescribed in this study

I). Arsenicum album: Debility, exhaustion, with restlessness, < night.

Constriction of air passages. Exhaustion < the slightest exertion.

Unquenchable and uncontolable thirst. Burning > by heat. <sea shore. <from

decayed foods; putrid discharge. Septic infections with low vitality. < lying

down, mid night. Fears suffocation. Cough < lying down on back.

Ii). Arsenicum iodatum: constant irritating discharges. Swelling of the nose.

Rapid pulse, with recurrent feverand sweats. Emaciation; diarrhœa.

Weakness of heart, emaciation and general debility; Amenorrhœa, with

anæmia and dyspnœa.dry cough with nasal obstruction. Aphonia.

Iii). Conium maculatum: Ascending paralysis. Painful stiffness of legs.

Weakness while walking.Weakness of memory memory.Complaints of

bachelors and old age peoples. Sexual debility. Mental and physical

70

weakness with trembling and palpitation. Cancerous tendency. Dry cough

more at evening and at night; itching in the chest and throat, < lying down,

talking and laughing.Expectoration < after long coughing. Dyspnea on least

exercise; oppressed breathing, pain in chest.

Iv). Ferrum iodatum: Glandular affections, and tumors. Emaciation of body.

Anaemia with Exophthalmic goitre followed by suppression of menses.

Debility due to lack of vital fluids.watery discharge from nose with oppression

of chest. Pressure in the retrosternal area.Heamoptysis.

V). Graphites: This is a great anti-psoric remedy, especially active, fair

complexion, with symptoms of skin affections and constipation. Delayed

menses with cold tendency.Absorption of the cicatricial tissue.Induration of the

tissue. Spasmodic type of asthma, dyspnea > eating. Constriction of the chest.

Hoarseness and rough of voice < after singing.Pain in themiddle of chest, with

cough, scraping and soreness.

Vi). Kali carboniucum: Dropsy with paralysis; prone to obesity. After loss of

vital fluids in anaemic. Great flatulence. < 3am to 4am. Dysmenorrhea.

Hoarseness of voice. Sensitive bronchitis < lying on right side. Dry cough

about 3 am, with stitching pains in pharynx. Scanty tenacious, expectoration <

morning, after eating; Hydrothorax < lying on painful side. Scanty

expectoration must want to be swallowed; cheesy taste, copious and

offensive, lump.

71

Vii). Kali iodatum: Desire for open air; fatigue > walking in open air.

Rheumatism of periosteum. Syphilitic manifestations <after overuse of

mercury. Swelling of glands. Severe cough< morning. Pulmonary and

laryngeal odema. Choking sensation of throat.Stitching type of pain starting

from lungs and extents to back. Soap like Expectoration. Dyspnea <

ascending with chest pain. Cold travels down towards chest.

Viii). Lobellia inflata: Indigestion. Alcoholic bad effects. Dyspnea < exertion.

Chest constriction; sensation of heaviness in chest better by rapid walking.

Complaints associated with weakness, Cramps, ringing cough with short

breath, as if catching at throat.

Ix). Lycopodium: Resembling Grauvogle's carbo-nitrogenoid constitution.

Malnutrition with atony. Symptoms start from right to goes to left, acts mainly

on right side. Compalints <from 4 to 8 pm. Craves warm things. Intellectual

keen person with physical weakness. Over sensitive to noise and odors.

Dyspnœa. Constriction and burning sensation in chest. Cough more while

going downhill. Night cough with thick expectoration. Catarrh with rattling of

mucus.

X). Medorrhinum: Suppressed gonorrhœa causing chronic ailments. Great

irritability of nervous system.Trembling all over the body with

collapse.Oedema of extrimities; dropsy and anasarca of serous sacs.Dyspnea

with oppression of chest.Hoarseness of voice while reading load. Soreness of

larynx dyspnea during exhalation.Nocturnal cough. Cough> by lying on

stomach.

72

Xi). Mercurius solubulis: Indicated in syphilis. Ulcerations of oral cavity and

throat, hair falling, the eruptions with ulcerations of mouth and throat.

Weakness and tremblings < from least exertion. Foul breath, foul excretions

and foul body smell. Sore sensation from throat to sternum. Complaints more

on right side. Cough more at night, from warmth of bed, tobacco smoke.

Catarrh, fear to go in air. Whooping-cough.

Xii). Natrum arsenicum: Catarrh with headache. Pain in eyes. Inflammation

of bronchus. Cough with greenish expectoration. Asthma in mine working

peoples. Dryness of eyes. Heaviness in chest.

Xiii). Natrum muriaticum: Anasarca, oedema and dropsy. Anaemia, gouty

diathesis. Neck emaciation. Stitching pain in chest. Dyspnea < while climbing

stairs. Bursting type of headache while coughing. Dyspnea more on going

upstairs. Whooping cough with lachrymation.

Xiv). Natrum sulphuricum: Headache due to head injury. Gouty diathesis.

Dyspnea < in damp wet weather. Holdings chest tightly during cough. Rattling

cough with asthma. All gone sensation in chest. Chest pain > pressure.

Xv). Nux vomica: Nervous, active and irritable persons. Indigestion. Portal

hypertension. Hypochondriasis. Epilepsy with consciousness; < open air,

spasmodic constriction in throat. Hoarseness and change of voice, Asthma,

assiosiated with fullness in stomach, < morning or after

73

eating. Suffocation of breathing. Cough with bursting type of headache and

bruised pain in epigastric region.

Xvi). Phosporus: Lean, tall persons with inflammation of mucous membranes

susceptible to external influences. Hoarseness of voice < evening. Aphonia

with Clergyman’s sore throat; pain in larynx while talking. Cough due to cold

air, reading, going from warm air into cold air. Sweetish taste of

sputum.Heaviness in chest.chest pain < lying on left side. Nervous coughs

due to strong odors< in the presence of strangers, lying upon left side and in

cold room.

Xvii). Psorinum: Wants warm covering of head even in summer. Increased

sweating.Discharges offensive.dyspnœa< sitting up; better by lying down and

keeping arms spread wide apart. Pain in chest with dry cough. Chest pain >

lying down. Cough < winter.

Xviii). Pulsatilla: Persons with changeable mood. Affections on who loves.

Thirst reduced. Upper lid styes. Toothache> holding cold water in the mouth.

Dry cough with hoarseness of mouth and throat. Dry cough <evening, night;

cough< early morning > sit up in bed. Copious expectoration. Expectoration

thick, profuse, greenish. Palpitation with Dyspnea < lying on left side.

Incontinence of urine.

Xix). Sanguinaria: Headache starts in occiput, periodic headache. Headache

at the climacteric; Circumscribed spots and red cheeks. Rheumatism of right

arm and shoulder. Aphonia, cough better by eructation. Odema of larynx.

Burning in the chest associated with

74

cough. Cough better in fresh air. Hæmoptysis due to suppressed menses.

Dyspnœa with constriction of chest. Offensive breath with purulent, putrid

expectoration. Asthma associated with gastric symptoms.

Xx). Sepia officinalis: Over sensitiveness. Indifferent Headache- Pulsating in

cerebellum. Herpes infection behind the ears on the nape of neck.Allgone

sensations not relieved by eating.Weakness of small of back. Pains extend to

back. Oppression of chest < morning and evening.Dry cough due to gastric

origin.Dyspnœa; immedialty after sleep better by rapid motion. Expectoration

Salty. Cough < morning, with profuse expectoration, Whooping-cough.

Xxi). Sulphur: Constant heat on top of head. Disagrees Milk. Early Morning

painless diarrhœa, drives out of bed, heat and burning all over body, itching

more from heat of bed. All gone sensation in stomach about 11 am.discharge

offensives. Itching; scratching turns into burning. Dyspnea association with

oppression and burning pain in chest better by open air. Chest pain < lying on

back or during deep breath. Flushes of heat in chest < rising to head.

Oppression in chest. Dyspnœa < middle of night, > by sitting up.

75

V. RESULTS AND DISCUSSION

The data obtained from this study are given below. These includes,

- Description of demographic variables of patients with bronchial

asthma

- Assessment of the effect of homeopathic drugs on level of IgE

- Assessment of the effect of homeopathic drugs on level of AEC

- Assessment of the effect of homeopathic drugs on changes in the

pulmonary function

- Test of significance on level of IgE, AEC, and PFT.

76

DESCRIPTION OF DEMOGRAPHIC CHARACTERISTICS OF PATIENTS

Figure 5.1. Agewise distribution

Highest percentage of 22.15% (33) were between 21-30 years, and the

lowest percentage of 2.68%(4) were in between 71-80 years.

Figure.5.2.Distribution of sex

Females were ( 53.02% ) more affected than males (46.98%)

10

27

33

22

19 20

14

4

0

5

10

15

20

25

30

35

1 to10 11to20 21- 30 31 - 40 41 - 50 51 - 60 61 - 70 71 - 80

Agewise distribution N

um

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Age

46.98% 53.02%

Distribution of Sex

Male

Female

77

Figure 5. 3. Occupationwise distribution.

28.19% of patients were coolie, 24.16% (36) were student, 15.44% (23)

were housewife, 12.08% (18) were weaver, 9.40% (14) were shopkeeper,

7.38(11) were government worker and 3.36% (5) of them were office worker.

Figure 5.4. Marital status wise distribution

64.43%(96) patients were married whereas 35.57%(53) patients were

un married.

15.44%

24.16%

12.08% 9.4%

3.36%

7.38%

28.19%

Occupationwise distribution

Housewife

Student

Weaver

Shopkeeper

Office worker

Govt worker

Coolie

64.43%

35.57%

Marital statuswise distribution

Married

Unmarried

78

Figure 5.5.Distribution of Religion

96.64% of patients belongs to Hindu religion, 2.68% were Christian and

0.67% patient was Muslim.

Figure 5.6 Educationwise distribution

26.17% (39) had completed primary education, 24.83% each had

secondary education, and no education. 16.11% (24) 4.70% (7) and 3.36%

(5) had completed under graduation, higher secondary education and post

graduation respectively.

96.64%

2.68% 0.67%

DIstribution of Religion

Hindu

Christian

Muslim

24.83%

26.17% 24.83%

4.70% 16.11%

3.36%

Educationwise distribution

Uneducated

Primary

Secondary

Higher secondary

Under graduate

Post graduate

79

Figure 5.7.Distribution of Family History

43.62 % of the patients had family history and 56.38% had no

family history.

Figure 5.8. Addiction wise distribution

88.59% (132) had no history of alcohol or smoking, 4.7% (7)

had history of consumption of alcohol, 1.34% (2) had history of smoking and

5.37 and (8) had history of both alcohol consumption and smoking.

43.62%

56.38%

Distribution of Family History

Yes

No

88.59%

4.7% 1.34 % 5.37%

Addiction wise distribution

None

Alcohol

Smoking

Both

80

Figure 5.9.Distribution of Thermal relation

48.32% (72) were hot patients , 25.5% (38) were chilly patients

and 26.17% (39) were ambi thermal.

Figure 5.10. Miasm wise distribution

52.35% (78) were psora, 25.5% (38) were tubercular and 22.15% (33)

were psorosycotic , but none of the patients were sycotic and syphilitic.

48.32 %

25.5 %

26.17%

Distribution of Thermal relation

Hot

Chilly

Ambi

78

0 0 38 33

0

10

20

30

40

50

60

70

80

90

Miasm wise distribution

Miasm

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81

Figure 5.11.Distribution of IgE level before and after treatment

All patients included in this study had IgE level of more than 188 IU/mL.

30 patients had range between 189 – 376 IU/mL, 31 patients had a level

between 377 – 564 IU/mL, 38 had a level of 565-752IU/mL, 42 had a level 753

– 940 IU/mL, 7 had a level of 941-1128 IU/mL and 1 had level of more that

1317 IU/mL before administration of drugs. After administration of indicated

homoeopathic drugs the results shows a shift to left with number of patients

with higher levels reducing to lower levels. 27 patients came to normal level of

less than 188 IU/mL, the number of patients increased to 47 from 30 in the

group 189 – 376 IU/mL. Total number of patients in the group 377 – 564

IU/mL increased to 41 from 31. The number of patients in 565 – 752 IU/mL

group reduced to 26 from 38. So also the number of patients in the group 753

- 940 reduced to 8 from 42. Those 8 patients who had a level of more than

940 IU/mL were all reduced to less than 940 IU/mL. This shift of IgE levels

from right to left shows study was significant and there is a

0

30 31

38 42

7

1

27

47 41

26

8

0 0 0

10

20

30

40

50

< 188 189 - 376 377-564 565-752 753-940 941-1128 >1317

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IgE Level Before After

Distribution of IgE level before and after treatment

82

definite evidence of action of homoeopathic medicines on the IgE level

reduction.

Distribution of remedies in reducing IgE levels

Figure 5.12. Distribution of remedies in reducing IgE levels

Sulphur was indicated in 56 ( 37.6%) patients. Of this 48 (32.2)

patients showed reduction in IgE and 5.4% not showed any reduction in IgE.

Arsenicum album was indicated in 27 patients of which shown good reduction

in IgE levels are 26 patients except in 1 patient where there is no reduction of

IgE. Pulsatilla was indicated in 10 patients out of which 9 of them showed

reduction in IgE and 1 patient shows no reduction in IgE levels. The remaining

drugs such as Conium maculatum, Ferrum iodatum, Graphities, Lobellia

inflata, Meddorrhoninum, Mercurius solubulis, Natrum arsenicum, Psorinum,

and Sangunuria given in lowest percentage (0.7%) of patients where patient

have shown reduction of IgE levels. This shows that study is

48

26

7 9 7 6 7

4 2 3 3 1 2 1 1 1 1 1 1 1 1 1

8

1 1 1 2 0 0 0 1 0 0 1 0 0 0 0 0 0 0 0 0 0

56

27

8 10 9

6 7 4 3 3 3 2 2 1 1 1 1 1 1 1 1 1

0

10

20

30

40

50

60

IgE improved IgE not improved Total

Nu

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Distribution of remedies in reducing IgE levels

Remedies given

83

significant and the result will be effective only when single indicated remedy

with proper potency is selected.

Figure 5.13. Effective remedies in reducing IgE levels

Highest percentage (37.58%) of remedies administered to reduce IgE

level was Sulphur and in 18.12% of patients Arsenicum album was used.

Arsenicum iodatum, Pulsatilla and Phosphorus were used in 5.37%, 6.71%

and 6.04% respectively. Least percentage (0.67%) used were Conium

maculatum, Ferrum iodatum, Graphites, Lobelia inflata, Medorrhinum,

Mercurius solubulis, Natrum arsenicosum, Psorinum, and Sanguinuria.

37.58

18.12 5.37

6.71

6.04 4.03

4.7

2.68

2.01

2.01 2.01

1.34

1.34

0.67

0.67

0.67

0.67

0.67

0.67 0.67

0.67 0.67

Effective remedies in reducing IgE levels

Sulphur Arsenicum album Arsenicum iodatum Pulsatilla

Phosphorus Kali iodatum Natrum sulph Lycopodium

Ferrum arsenicum Natrum mur Sepia Kali carboniucum

Nux vomica Conium maculatum Ferrum iodatum Graphites

Lobelia inflata Medorrhinum Mercurius solubulis Natrum arsenicosum

Psorinum Sanguinaria

84

IgE N Median

IQR

3rdquartile -1st

quartile

Difference

in

median

z value p

Before 149 627 794.72- 428

251 9.381 < 0.001**

After 149 376 546 -224

Table 5.1: Assessment of significance of reduction in IgE levels after

treatment.

The inter quartile range between 3rd and first quartile for IgE levels

before treatment was 794.72-428 whereas after treatment it was reduced to

546-224 and the p value was <0.001 shows highly significant reduction. This

shows that homoeopathic medicines are having effective role in reducing the

IgE levels in bronchial asthma patients.

85

Figure 5.14: Distribution of absolute eosinophil count before and

after treatment.

109 patients had the absolute eosinophil count value <440 before

treatment, which was increased to 140 patients after treatment. 4 patients had

the absolute eosinophil count level of 641-840 and 2 patients had the level of

841-1040 before treatment but none of them had these values after treatment.

This proves that homoeopathic medicine has effect on reducing the absolute

eosinophil count levels when it is administered on the strict basis of

homoeopathic principles.

109

34

4 2

140

9 0 0

0

20

40

60

80

100

120

140

160

< 440 441-640 641-840 841-1040

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Absolute eosinophil count Level Before After

Distribution of absolute eosinophil count before and after treatment

86

Absolute

Eosinophil

count

N Median

IQR

3rdquartile

-1st

quartile

Difference

in

median

z value p

Before 149 312 451-204 68 7.071 < 0.001**

After 149 244 328-176

Table 5.2: Assessment of significance of reduction in absolute

eosinophil count after treatment.

The inter quartile range between 3rd and first quartile for absolute

eosinophil count value before treatment was 451-204 whereas after treatment

it was reduced to 328-176 and the p value was <0.001 shows highly

significant reduction. This result reflects that homoeopathic medicines are

having excellent effect over reducing the Absolute eosinophil count levels in

asthma.

87

Figure 5.15: Distribution of remedies in reducing AEC levels

Sulphur was given for most of the patients with bronchial asthma

shown good improvement in reducing the level of Absolute eosinophil count.

43 patients had Absolute eosinophil count level within normal limit and 12

patients have shown improvement, whereas only one patient does not have

improvement while under treatment by using the drug Sulphur. Next to

Sulphur, Arsenicum album was found to be effective in reducing Absolute

eosinophil count level. The other drugs also found to be effective in reducing

Absolute eosinophil count level which shows effectiveness of homoeopathic

remedies on reducing Absolute eosinophil count levels. This shows that single

indicated medicine will have the ability to reduce the absolute eosinlphil count

level when it is prescribed on basis of symptom similarity.

43

16

6 7 7 4 6

3 2 2 3 1 2 1 0 1 0 0 1 1 1 1

12 11

2 3 2 2 1 1 1 1 0 1 0 0 1 0 1 1 0 0 0 0

56

27

8 10 9 6 7

4 3 3 3 2 2 1 1 1 1 1 1 1 1 1

0

10

20

30

40

50

60

AEC within normal limit AEC improved AEC not improved Total

Distribution of remedies in reducing AEC levels N

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Remedies

88

Figure 5.16: Effective remedies in reducing AEC levels

Sulphur was given in highest percentage of patients (37.60%),

followed by Arsenicum album (18.10%). Next least commonly administered

remedies were Pulsatilla (6.70%), Arsenicum iodatum (5.40%), Phosphorus

(6%), Kali iodatum (4%), Natrum sulph (4.7%), Lycopodium (2.7%), Ferrum

arsenicum, Natrum mur and Sepia were given in 2% of patients. Kali carb and

Nuxvomica given in 1.3% of patients. The least percentage (0.7%) used

remedies were Conium maculatum, Ferrum iodatum, Graphities, Lobelia

inflata, Medorrhinum, Mercurius solubulis, Natrum arsenicum, Psorinum and

Sanguinaria.

37.6

18.1 5.4

6.7

6

4

4.7

2.7 2

2 2 1.3

1.3

0.7

0.7

0.7

0.7

0.7

0.7

0.7

0.7

0.7

Effective remedies in reducing AEC levels

Sulphur Arsenicum album Arsenicum iodatum Pulsatilla Phosphorus

Kali iodatum Natrum sulph Lycopodium Ferrum arsenicum Natrum mur

Sepia Kali carboniucum Nux vomica Conium maculatum Ferrum iodatum

Graphites Lobelia inflata Medorrhinum Mercurius solubulis Natrum arsenicum

Psorinum Sanguinaria

89

Figure 5.17: Distribution of FEV1/FVC level before and after treatment.

27 patients had FEV1/FVC value of < 60 [V (L)] before homoeopathic

treatment whereas after homoeopathic treatment 68 patients had improved in

the level of FEV1/FVC in the range of 91-100 [V (L)]. This indicates

significance of homoeopathic treatment in improving FVC, FEVI and

FEV1/FVC levels and also shows evidence of improvement in the pulmonary

function.

27 24 23

31

44

0 5

9

20

46

68

1 0

10

20

30

40

50

60

70

80

<60 61-70 71-80 81-90 91-100 >100

Before Treatment After Treatment

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FEV1/FVC level

Distribution of FEV1/FVC level before and after treatment

90

Figure 5.18. Assessment of homeopathic treatment in relation to results

of pulmonary function tests

Distibution of patients

with bronchial asthma according to overall result of PFT before and after

treatment depicts that before treatment only 32 patients had the result of

within normal limits which was shown significant increase by showing the

value among 59 patients after treatment. 25 patients had mild restriction

during before treatment increased to 43 patients during after treatment. 13

patients had moderate restriction before treatment increased to 15 patients

during after treatment. 12 patients had severe restriction before treatment but

32 25

13 12 6

12 5

44

59

43

15

3 5 7 0

17

0

10

20

30

40

50

60

70

Withinnormallimits

Mildrestriction

Moderaterestriction

Severerestriction

Mildobstruction

Moderateobstruction

Severeobstruction

Mixedblockage

Pulmonary function test Before treatment

Pulmonary function test After treatment

Assessment of homeopathic treatment in relation to results of pulmonary function tests

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PFT interpretation

91

only 3 patients were there during after treatment. Before treatment 6 patients

had mild obstruction but only 5 patients had during after treatment. 12 patients

had moderate restriction during before treatment butonly 7 patients were there

during after treatment. 5 patients were there during before treatment in

severe restriction came as nil patients during after treatment. 44 patients had

mixed blockage before treatment whereas it was reduced to 17 patients during

after treatment. This shows significane of homoeopathic treatment in

improving the pulmonary function tests.

92

Figure 5.19 Effective remedies in modifying abnormal pulmonary

function

Sulphur was given for the highest number of patients (56) in modifying

abnormal pulmonary function to normal pulmonary function where it showed

good improvement in 29 patients and no improvement in 27 patients.

Arsenicum album was indicated in 27 patients where it shows 14 patients

were improved and 13 patients were not improved. 8 patients improved and 2

patients were not improved in total number of (10) patients were pulsatilla

prescribed. In 8 patients Arsenicum iodatum prescribed patients 4 patients

showed improvement and 4 patients not shown any improvement. Conium

maculatum, ferrum iodatum, graphities, lobelia inflata, medorrhinum,

mercurius solubulis,

29

14

8 6

4 3 1 2

0 1 1 0 1 0 1 0 1 0 1 1 0 0

27

13

2 3 4 4 5 2 3 2 2 2 1 1 0 1 0 1 0 0 1 1

56

27

10 9 8 7 6 4 3 3 3 2 2 1 1 1 1 1 1 1 1 1

0

10

20

30

40

50

60

Improved Not improved Total

Effective remedies in modifying abnormal pulmonary function N

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Remedies

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natrum arsenicum, psorinum and sanguinaria were prescribed in lower

frequencies in which ferrum iodatum, lobelia inflate, mercurius solubulis and

natrum arsenicum showed improvement where as conium maculatum,

graphities, medorrhinum, psorinum and sanguinaria showed no improvement

in the study.

FEV1/FVC N Median

IQR

3rdquartile

-1st quartile

Difference

in

median

z value P

Before 149 81.045 91.085-

63.895 8.625 5.02 < 0.001**

After 149 89.67 93.675-

80.845

Table 5.3: Assessment of significance of reduction in FEV1/FVC

after treatment.

The inter quartile range between 3rd and first quartile before treatment

for FEV1/FVCwas 91.085-63.895 whereas after treatment it was increased to

93.675-80.845 and the p value was <0.001 shows highly significant

improvement in FEV1/FVC.

94

Figure 5.20.Distribution of remedies given among bronchial asthma

patients.

Remedies mostly used in higher frequency was sulphur (37.58%),

followed by arsenicum album (18.12%).The remedies used with least

frequency (0.67%) were sanguinaria, psorinum, natrum arsenicum, mercurius

solubulis, medorrhinum, lobelia inflata, graphites, ferrum iodatum and conium

maculatum.

48

26

7 9

7 6 7 4

2 3 3 1 2 1 1 1 1 1 1 1 1 1

8

1 1 1 2 0 0 0 1 0 0 1 0 0 0 0 0 0 0 0 0 0

56

27

8 10 9

6 7 4 3 3 3 2 2 1 1 1 1 1 1 1 1 1

0

10

20

30

40

50

60

improved not improved total

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Remedies given

Distribution of remedies given among patients with bronchial asthma

95

Figure.5.21.Distribution of improved patients after treatment.

The overall study report reveals that 89.9% (134) patients were

improved and only 10.1% (15) patients were not improved.Totally 15 patients

have not shown improvement. Out of this 7 patients had no improvement in

lgE, PFT level whereas 8 patients had no improvement in IgE level and they

had normal AEC, PFT readings. Arsenicum album given for 1 patient had

maintaining cause as mechanic. Arsenicum iodatum given for 1 patient of

housewife had exposure to fumes while cooking. Ferrum ars prescribed for 1

student who had constant mental stress. Kali carb prescibed in 1 patient had

maintaining cause of textile worker. Phosphorus given in 2 patients had

history of excess intake of sweets and cold drinks and electrician by

profession. Pulsatilla has not given improvent in 1 patient probably due to

continuous intake of allopathic drugs. 8 patients given Sulphur had not

shown improvement

10.1%

89.9%

Improved patients after treatment

Not Improved

Improved

96

because of reasons like chronic complaint, short duration of treatment,

immunological defence mechanism, low susceptibility, and weever as

occupation.

DISCUSSION

A prospective study was conducted to assess the efficacy of

homoeopathic medicines in reducing the IgE level, reducing the AEC level and

modifying the lung function in bronchial asthma patients with the help of

investigatory procedures like assessment of serum IgE level, serum AEC level

and pulmonary function test which includes FEV1/FVC.

The patients selected for this study has shown a tremendous

increase in serum IgE levels in all patients with allergic bronchial asthma.

Homoeopathic treatment has shown statistically significant reduction in IgE

along with the clinical improvement.

In the present study it was found that AEC also has an important role in

influencing the mechanism of bronchial asthma where among most of the

patients there is considerable increase in AEC count. And there is a classical

reduction in AEC levels after homoeopathic remedies. Thus it is found that the

study is significant in modulating the AEC levels through homoeopathic

treatment in bronchial asthma. This study result is correlated with the study of

Bames BJ who found that there is reasonable correlation is there between

eosinophils and

97

pathophysiology of allergic bronchial asthma. Another study by Roismam et al.

also proves that there is a definite evidence of AEC in relation with asthma.

This supports that homoeopathy also has effect in modulating the AEC levels.

PFT is one of the important aspect which was considered in the

present study shown modification in all patients with allergic bronchial asthma.

So evaluation of FEV1,FVC and FVC/FEV1 was done in all patients in the

study. The results definietly points out the improvement of these three factors

with the help of proper homoeopathic treatment. A study by Strunk et al.,

proves that there is a reduction in FEV1 levels in patients who suffer from

bronchial asthma. Also study by Noha S. Elshaer et al. states that there is a

definite evidence that asthma has role in reducing FVC,FEV1 and FVC/FEV1

which can be modified or brought back to normal with indicated

homoeopathic remedies. This again proves that homoeopathic remedies are

effective to modify the lung volumes and capacities.

In the present study Sulphur was used in higher percentage of

patients, to modulate IgE,AEC and PFT based on the laws and pricinples of

homoeoapthy. This is proved with Castellsagu’s study that Sulphur was most

commonly indicated remedy in asthma.

98

VI. SUMMARY, CONCLUSION AND RECOMMENDATIONS

Summary

149 patients with bronchial asthma attending the outpatient,

Inpatient units and peripheral centres of Vinayaka Missions Homoeopathic

Medical College Hospital, Salem were selected by using purposive sampling

technique for this prospective study. Permission from ethical committee of

VMHMC&H was obtained before implementing the clinical study. Written

consent obtained from patients before starting treatment. The study was

conducted from 01.03.2013 to 30.09.2014. The data analysis was done by

using descriptive and inferential statistics.

Sulphur was used in highest percentage (37.58%) to reduce IgE level,

in 18.12% of patients Arsenicum album was used. Arsenicum iodatum,

pulsatilla and phosphorus were used in 5.37%,6,71% and 6.04% respectively.

Least percentage (0.67%) used were conium maculatum, ferrum iodatum,

graphites, Lobelia inflata, Meddorrhinum, Mercurius solubulis, Natrum

arsenicum, Psorinum, and Sanguinaria.

This study shows highly significant reduction in IgE with the z value of

9.381 with the p value at the level of <0.001 based on The Wilcoxon signed

rank test.

99

Predominant drug indicated and prescribed in this study was Sulphur

(37.6%), next to this Arsencicum album (18.1%) which was found effective in

reducing the Absolute eosinophil count levels

The z value of 7.071 with the p value of < 0.001 reveals the highly

significant reduction of AEC after homoeopathic treatment.

The results of PFT shows that before treatment 32 patients had values

of within normal limits which is increased to 59 patients after treatment. And

44 patients with mixed blockage before treatment reduced to 17 patients after

treatment. This demonstrates the evidence of significant improvement in

pulmonary functions after treatment.

Sulphur improved the pulmonary function in 19 patients and Arsenicum

album showed improvement in 14 patients with higher frequency. Remedies

mostly used in study in higher frequency were Sulphur (37.58%), followed by

Arsenicum album (18.12%).

The Wilcoxon signed rank test z value of 5.02 with p value <0.001 indicates

the significance of efficacy of homoeopathic treatment in improving pulmonary

functions after treatment.

The study demonstrated stastically significant improvement of 89.9%

(134) bronchial asthma patients after homoeopathic treatment.

100

CONCLUSION:

This study demonstrates the efficacy of homoeopathic treatment in

reducing the IgE and AEC levels and improving the pulmonary functions in

bronchial asthma with z values 9.381,7.071 and 5.02 respectively with p

value at the level of <0.001.

Sulphur, arsenicum album and pulsatilla are found to be more

effective in reducing IgE in this study. By sulphur 48 (32.2) patients showed

reduction in IgE . Arsenicumalbum showed improvement in 26 patients,

pulsatilla reduced IgE in 9 pateints. The remaining drugs such as conium

maculatum, ferrum iodatum, graphities, lobellia inflata, meddorrhoninum,

mercurius solubulis, natrum arsenicum, psorinum, and sangunuria reduced

ige in lowest percentage (0.7%) of patients, This shows that study is

significant in reducing the IgE levels.

Sulphur reduced absolute esoinophil count among 43 patients to

normal limits and 12 patients got mild improvement after treatment.

Arsenicum album showed improvement in 16 patients out of 27 patients. This

shows that homoeopathic treatment is effective in reducing the AEC count

levels.

Sulphur modified abnormal lung to normal in 29 patients and no

improvement in 27 patients. Arsenicum album showed result in 14

101

patients and no improvement in 13 patients. This shows that homoepathic

treatment can bring back abnormal lung fuction to normal.

This study establishes the significant reduction in IgE, AEC and

improvement in PFT along with clinical improvement in bronchial asthma

under homoeopathic treatment.

102

RECOMMENDATIONS:

A similar study can be replicated with a large sample, for longer period

of observation.

A comparative study should be conducted to evaluate the effectiveness

of different medicines in modulating IgE level among the patients with

bronchial asthma.

A comparative study of the duration taken for effecting the reduction in

IgE, AEC, and improvement in PFT may be attempted for speedy recovery.

A comparative study of cost effectiveness in relation to other modes of

treatment may be conducted.

103

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