review on gout disease and their treatment

www.wjpps.com │ Vol 10, Issue 8, 2021. │ ISO 9001:2015 Certified Journal │

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Bansode et al. World Journal of Pharmacy and Pharmaceutical Sciences

REVIEW ON GOUT DISEASE AND THEIR TREATMENT

Sandhya Gorakh Bansode*, Prof. K. N. Tarkase, Sagar Babasaheb Khedkar, Disha

Vikas Kamble, Akshay Nagnath Bhalekar

Dr. Vithalrao Vikhe Patil Foundation, College of Pharmacy, Viladghat, Ahmednagar.

ABSTRACT

Gout is a paiful condition that occurs when uric acid produced by the

body is stored as crystals in the joints and soft tissues. It is a

disturbance of uric acid in the body. Gout is a disorder of purine

metabolism, and occurs when it final metabolite, uric acid, crystallizes

in the form of monosodium urate, precipitating and forming deposits

(tophi) in joints, on tendons, and in the surrounding tissues. It is a

important to recognize that it is a systematic disorder caused by either

overproduction or underexcretion of uric acid. High serum uric acid, or

hyperuricemia, is the causative agent in gout; however, hyperuricemia

is not pathomnemonic of gout. Affecting factors – such as alcohol

abuse, obesity, and genetics determine a predisposition to developing a gout. There are

different types of gout such as Asymptomatic gout, Acute gout, Interval gout, Chronic gout

and Pseudogout. Alcohol consumption, age, postmenoupausal, diet, dehydration, kidney and

thyroid disorders, diuretics and cyclosporines intake, etc are the reasons of causes gout.

People with gout can develop more severe conditions, such as: Recurrent gout, Advanced

gout and kidney stone. Joint fluid test, blood test, x-ray imaging, ultrasound, dual- energy

computerized tomography (DECT) these test are help to identifying the characterization of

gout. Other important points in its management includes patient education, diet and life style

changes, as well as the drug used in the treatment of gout attack.

KEYWORDS: Gout, Hyperuricemia, Uric acid, Monosodium urate crystals, Purine

metabiltes, Pathophysiology of gout, Allopurinol.

INTRODUCTION

Gout is a painful condition that occurs when uric acid produced by the body is stored as

crystals in the joints and / or soft tissues. Located in the joints, these uric acid crystals

WORLD JOURNAL OF PHARMACY AND PHARMACEUTICAL SCIENCES

SJIF Impact Factor 7.632

Volume 10, Issue 8, 540-551 Review Article ISSN 2278 – 4357

*Corresponding Author

Sandhya Gorakh Bansode

Dr. Vithalrao Vikhe Patil

Foundation, College of

Pharmacy, Viladghat,

Ahmednagar.

Article Received on

27 May 2021,

Revised on 16 June 2021,

Accepted on 06 July 2021,

DOI: 10.20959/wjpps20218-19496


541


precipitate, causing inflammatory arthritis, which, in turn, cause swelling, redness, heat

sensation, pain and functional impotence at the articular level. Although gout is a disease

with a long history (with the description of the syndrome as "pruning" first described by the

ancient Egyptians and later by Hippocrates), the relationship between the disease and uric

acid was only demonstrated in the 19th century by Sir Alfred Baring Garrod, while only in

1909 the gout was assimilated by Sir Archibald Garrod to the acquired metabolic disorders.

Gout, referred to as "disease queen" and "disease of the kings," is a chronic condition, closely

linked to high-value uric acid metabolism, which can form monosodium urate crystals,

identified by Mc Carthy and Hollander in synovial fluid in inflamed joints, becoming gold

standard in the diagnosis of gout, crystals are deposited in the joints, causing joint

inflammation episodic or persistent, having key role in understanding of the disease.

Consecutively has instead increased local temperature, pain and tenderness in the joints

increased (most or at the joint of the hallucus), associated with a very intense night pain. Gout

is not just a metabolic disease in which uric acid is deposited in the joints or tissues, it can,

over time, cause diabetes, atherosclerosis, but also kidney complications. Unfortunately, it is

an invalidating disease, because the deposition at the level of the uric acid causes the joint to

be affected, which changes its appearance and becomes dysfunctional. The increased

production of uric acid is usually determined by purine-rich diets, high-fructose foods or by

increased alcohol consumption. Causes of increased uric acid are increased production,

decreased renal clearance, or a combination of these two mechanisms. The appearance of

gout is influenced by factors such as: sex (men make gout more often than women), age (the

risk increases after age 65); race, nutrition. Some lymph and myeloproliferative

haematological diseases, hemolytic anemia, cutaneous psoriasis, characterized by marked

cellular degradation, are associated with hyperuricemia and gout. Gene mutations of some

enzymes involved in the metabolism of purines (hypoxanthinguanine-phosphoribosyl-

transferase deficiency or increased phosphoribosylpyrophosphate-synthetase activity) are

known genetic causes, but fortunately, rare, hyperuricemia and gout. The elimination of uric

acid from the body is largely by renal elimination, which involves several processes, initially

glomerular filtration, then proximal tubular reabsorption, secretion and finally a new

postsecretory reabsorption.

There are three periods of disease evolution: the period of asymptomatic hyperuricemia - the

crystalline uric acid deposition takes place at the tissue level; acute attacks - the crystals

deposited in the joints cause inflammation, usually at the veil of a single joint; chronic gout -


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manifests with persistent joint pain and swelling, uric acid deposits in the soft tissues, called

tofi, usually located intra or periarticularly at the elbows, fingers and toes or at the ears. In

addition to joint manifestations and tofu formation, renal impairment is one of the most

common complications of hyperuricemia.

Gout is a heterogeneous group of sufferers sufferers characterized by hyperuricemia,

recurrent attacks of arthritis (in which synovial fluid contains monosodium urate crystals, and

in leukocytes phagocytosis occurs), tofu formation, especially around the extremity joints

(which sometimes lead to deformities and mutilation) or on the ear flag, parenchymal renal

disease affecting the renal interstitium, nephrons and vessels, uric renal lithiasis. In more than

half of the patients, the metatarsal-phalangeal joint of the hallucinus is damaged. The onset is

usually abrupt, the most frequent at night. Fever is preceded by chills. In chronic form, gouty

stews are almost characteristic. All these symptoms are a major clinical manifestation of

purine metabolism, which increases the amount of uric acid in the body (over 7 mg% in

serum).

Gout is also called as gouty arthritis. A form of arthritis characterized by severe pain, redness

and tenderness. Gout is a general term for a variety of conditions caused by a buildup of uric

acid. This buildup easily affects on feet. Gout is a form of inflammatory arthritis

characterized by recurrent attack of red, tender, hot, and swollen joint. Pain typically comes

on rapidly, reaching, maximal intensity in less than 12 hours. The joint at the base of big toe

is affected in half cases. It may also result in tophi, kidney stones, or kidney damage. Gout is

due to persistently elevated levels of uric acid in the blood. This occurs from a combination

of diet, other health problems, and genetic factors. At high levels, uric acid crystallizes and

the crystals deposit in joints, tendons, and surrounding tissues, resulting in an attack of gout.

Gout occurs more commonly in those who regularly drink beer or sugar-sweetened beverages

or who eat foods that are high purines such as liver, shellfish, or anchovies, or are

overweight. Diagnosis of gout may be confirmed by the presence of crystals in the joint fluid

or in a deposit outside the joint. Blood uric acid levels may be normal during an attack.

Pathophysiology and Treatment of gout

Gout is a disorder of purine metabolism, and occurs when it final metabolite, uric acid,

crystallizes in the form of monosodium urate, precipitating and forming deposits (tophi) in

joints, on tendons, and in the surrounding tissues. Although gout affects peripheral joint, it is

a important to recognize that it is a systematic disorder caused by either overproduction or


543


underexcretion of uric acid. High serum uric acid, or hyperuricemia, is the causative agent in

gout; however, hyperuricemia is not pathomnemonic of gout. According to studies, 60-95%

of individuals with hyperuricemia do not progress to gout. Therefore researcher posit that

other factors – such as alcohol abuse, obesity, and genetics determine a predisposition to

developing a gout. Additionally many patients with gout will not present with hyperuricemia

in the clinic. It is a important to reiterate, however, that all individual with gout must have

had hyperuricemia at some point in order to develop the disease.

As stated earlier, uric acid is a normal byproduct of purine metabolism. The purine

nucleotides AMP and GMP are broken down into hypoxanthine and xanthine respectively.

Xanthine is converted directly to uric acid by the action of xanthine oxidase (xo). Treatment

of gout target the enzyme xanthine oxidase by inhibiting its production of uric acid, and thus

raising the concentrations of more soluble uric acid precursors, which can be excreted. The

major drug is used to treat gout is Allopurinol, a structural analogue of hypoxanthine. The

action of allopurinol at XO is via another molecule, alloxanthine. Alloxanthine is a structural

analogue of xanthine made by a reaction between allopurinol and XO. Alloxanthine is a

active agent that act as a competitive inhibitor on the XO active site.

There are two principle ways that an individual can achieve hyperurecemia.

Overproduction or underexcreting uric acid. Uric acid is a normal metabolite of purine

catabolism. If purines such as AMP, GMP, or adenine are overproduced, uric acid level rise

consequently. Purine synthesis begins with ribose-5-phosphate and contains many steps that

are highly feedback regulated by purine end products. PRPP synthetase and PRPP

amidotransferase are the major rate determining enzymes of purine biosynthesis, and

consequently, they are high regulated. Mutations in either of thesetwo enzymes could lead to

a loss of feedback control, and thus cause overproduction of purines and eventually uric acid.

Deficiency of other enzymes in the purine synthetic pathway can cause hyperuricemia.

Hypoxanthine-guanine phoshoribosytransferase (HGPRT), for example, is an enzyme that “

salvages” excess purine byproducts and covert them back into nucleotides by the following

reactions:

Hypoxanthine + PRPP ↔ IMP + PPi

If HGPRT is deficient, the body is unable to recycle hypoxanthine back into purine

nucleotides. As a result, hypoxanthine levels build up and forms uric acid. Uderexcretion of

uric acid is other causative factor for hyperucicemia, and therefore gout. Underexcretion of


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uric acid typically occurs secondary to kidney disease and accouns for the minority of gout

cases. The vast majority of gout is caused by overoroduction of uric acid by the mechanisms

outlined above.

Although gout has been recognized and treated for centuries, the pathophysiology of gout has

only been elucidated in recent years. It has long been known that gout is associated with

hyperuricemia and monosodium crystals in joints, but it is known known that the

polymorphonuclear cells (PMNs) that has ingested uric acid crystals. The jagged crystals rip

open the plasma membrane of PMNs, releasing cytokines and other factor that initiate

chemotaxis of more PMNs cells. The process is represented pictorially in figure 1.

Figure 1: PMNs ingest uric acid crystals and rupture, causing release of chemotaxic

factors that promote inflammation.

Types

There are various stages through which gout progresses, and these are sometimes referred to

as different types of gout.


545


Asymptomatic hyperuricemia

It is possible for a person to have elevated uric acid levels without any outward symptoms. At

this stage, treatment is not required, though urate crystals may deposit in tissue and cause

slight damage.

People with asymptomatic hyperuricemia may be advised to take steps to address any

possible factors contributing to uric acid build-up.

Acute gout

This stage occurs when the urate crystals that have been deposited suddenly cause acute

inflammation and intense pain. This sudden attack is referred to as a “flare” and will normally

subside within 3 to 10 days. Flares can sometimes be triggered by stressful events, alcohol

and drugs, as well as cold weather.

Interval or intercritical gout

This stage is the period in between attacks of acute gout. Subsequent flares may not occur for

months or years, though if not treated, over time, they can last longer and occur more

frequently. During this interval, further urate crystals are being deposited in tissue.

Chronic tophaceous gout

Chronic tophaceous gout is the most debilitating type of gout. Permanent damage may have

occurred in the joints and the kidneys. The patient can suffer from chronic arthritis and

develop tophi, big lumps of urate crystals, in cooler areas of the body such as the joints of the

fingers.

It takes a long time without treatment to reach the stage of chronic tophaceous gout – around

10 years. It is very unlikely that a patient receiving proper treatment would progress to this

stage.

Pseudogout

One condition that is easily confused with gout is pseudogout. The symptoms of pseudogout

are very similar to those of gout, although thr flare-ups are usually less severe.

The major difference between gout and pseudogout is that the joints are irritated

by Calcium pyrophosphate crystals rather than urate crystals. Pseudogout requires different

treatment to gout.


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Symptoms

The signs and symptoms of gout almost always occur suddenly, and often at night. They

include.

1) Intense joint pain – Gout usually affects the big toe, but it can occurs in any joint. Other

commonly affected joints include the ankles, knees, elbows, wrists and fingers. The pain is

likely to be most severe within the 4 to 12 hours after it begins.

2) Lingering discomfort – After the most severe pain subsides, some joint discomfort may

last from a few days to a few weeks. Later attacks are likely to last longer and affect more

joints.

3)Inflammation and redness – The affected joint or joints become swollen, tender, warm and

red.

4) Limited range of motion – As gout progresses, then may not be able to move joints

normally.

Causes of gout

1. The buildup of uric acid in the blood from breakdown of purines causes gout.

2. Certain conditions, such as blood and metabolism disorders or dehydration, make a body

produce too much uric acid.

3. A kidney or thyroid problems, or an inherited disorders, can make it harder for body to

remove excess uric acid.

4. More likely to get gout if:

a) A middle aged man or postmenopausal woman

b) Have a parents, siblings, or other family members with gout

c) More consumption of alcohol

d) Take medications such as diuretics and cyclosporine

5. Have a condition like high blood pressure, kidney disease, thyroid disease, diabetes, or

sleep apnea also causes a gout.

Risk Factors

More likely to develop gout if high level of uric acid in a body, Factors that increases the uric

acid in a body includes:

1. Diet: Eating a diet rich in red meat and shellfish and drinking beverages sweetened with

fruit sugar (fructose) increase levels of uric acid, which increase the risk of gout. Alcohol

consumption especially of beer, also increases the risk of gout.


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2. Weight: If overweight, then body produces more uric acid and then kidney have more

difficult time eliminating uric acid.

3. Medical conditions: Certain disease and conditions increase the risk of gout. These include

untreated high blood pressure and chronic conditions such as diabetes, obesity, metabolic

syndrome, and heart and kidney diseases.

4. Certain medications: Low dose aspirin and some medications used to control hypertension-

including thiazide diuretics, angiotensin-converting enzyme (ACE) inhibitors and Beta

blockers- also can increase uric acid levels. So can the use of anti-rejection drugs prescribed

for people who have undergone an organ transplant.

5. Family history of gout: If other member of family have had gout, then more likely to

develop the disease.

6. Age and Sex: Gout occurs more often in men, primarily because women tend to have a

lower uric acid levels. After menopause, however, women’s uric acid levels approach those

of men. Men are also more likely to develop gout earlier usually between the ages of 30 and

50 whereas women generally develop signs and symptoms after menopause.

7. Recent surgery or trauma: Experiencing recent surgery or trauma can sometimes trigger a

gout attack. In some people, receiving a vaccination can trigger a gout flare.

Complications

People with gout can develop more severe conditions, such as.

1. Recurrent gout : Some people may never experience gout signs and symptoms again. Other

may experience gout several times each year. Medications may help to prevent gout attack in

people with recurrent gout. If left untreated gout can cause erosion and destruction of a joint.

2. Advanced gout: Untreated gout may cause a deposits of urate cryatals to form under the

skin in nodules called tophi (TOE- fie). Tophi can develop in several areas, such as fingers,

hands, feet, elbows or Achilles tendons along the backs of ankles. Tophi usually are not

painful, but they can become swollen and tender during gout attacks.

3. Kidney stones : Urate crystals may collect in the urinary tracts of people with gout, causing

kidney stones. Medications can help reduce the risk of kidney stones.

Diagnosis

Doctors usually diagnose gout based on the symptoms and the appearance of the affected

joint. Tests to help diagnose gout may include.


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Joint fluid test. Your doctor may use a needle to draw fluid from your affected joint.

Urate crystals may be visible when the fluid is examined under a microscope.

Blood test. Your doctor may recommend a blood test to measure the levels of uric acid in

your blood. Blood test results can be misleading, though. Some people have high uric

acid levels, but never experience gout. And some people have signs and symptoms of

gout, but don't have unusual levels of uric acid in their blood.

X-ray imaging. Joint X-rays can be helpful to rule out other causes of joint inflammation.

Ultrasound. This test uses sound waves to detect urate crystals in joints or in tophi.

Dual-energy computerized tomography (DECT). This test combines X-ray images

taken from many different angles to visualize urate crystals in joints.

Treatment of gout

1. If left untreated, gout can eventually lead to arthritis. This painful condition cal leave a

joint permanently damaged and swollen.

2. The treatment plan recommends will depends on the stages and severity of gout.

3. Medications to treat gout work in one of two ways.

Relieve pain and bring down inflammation

b) Or prevent future gout attacks by lowering uric acid levels.

a) Drugs to relieve gout pain include:

(1) Nonsteroidal anti-inflammatory drugs(NSAIDs), such as aspirin(Bufferin),

ibuprofen(advil, Motrin), and naproxen(Aleve)

(2) Colchicines(Colcrys, Mitigare)

(3) Corticosteroids

b) Drugs that prevent gout attacks include:

(1) Xanthine oxidase inhibitors, such as Allopurinol (Lopurin, Zyloprim) and febuxostat

(Uloric).

(2)Probenecid (Probalan).

4. Along with medications, lifestyle changes to help manage a symptoms and reduce the risk

of future Attacks. For example, reduce the alcohol intake, lose weight, quit smoking, etc.

medications and lifestyle are not the only way to manage gout. A few alternative therapies

have also shown promise.

CONCLUSION

The appearance of gout is favoured by a food containing large amount of nucleic, alcohol and

lead poisoning, probably due to the fact that all these substances have a harmful influence on


549


renal function. A clear diagnosis is the first step for a correct therapeutic approach. The

diagnosis of gout is made by identifying the monosodium urate crystals at the articular level

and based on the specific clinical signs and hyperurecemia.

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review on gout disease and their treatment

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