DR IRSHAD ALITMO, Med-B UNIT LRH

CASE HISTORYCASE HISTORY A 45 yrs old female,named xyz, from Peshawar presented to A 45 yrs old female,named xyz, from Peshawar presented to

our unit on 15-10-10 with the c/c of fever for the last one our unit on 15-10-10 with the c/c of fever for the last one month.month.

The fever was low grade, continuous, associated with The fever was low grade, continuous, associated with

generalized bodyaches esp: arms & neck.generalized bodyaches esp: arms & neck. Systemic inquiry regarding the cause of fever was not Systemic inquiry regarding the cause of fever was not

significantsignificant

Further questioning revealed that she had a flu and dry Further questioning revealed that she had a flu and dry cough one month back,both of which have settled now but cough one month back,both of which have settled now but still she is c/o ongoing low grade fever.still she is c/o ongoing low grade fever.

She claims to have some degree of weight loss in the last 1 She claims to have some degree of weight loss in the last 1

monthmonth. .

PAST HISTORYPAST HISTORY

She has diabetes for 5-6 yrs for which she is taking Glimepride 2mg …OD.

There was no history of previous hospitalization or

surgery.

DRUGS HISTORYDRUGS HISTORY

She was treated with Quinolones and Antimalarials for She was treated with Quinolones and Antimalarials for the said problem,but she the said problem,but she didn't show any improvement show any improvement with any of these medications.with any of these medications.

Her RBS at arrival was 402mg%.Her RBS at arrival was 402mg%.The dose of Glimepride was increased from 2mg to The dose of Glimepride was increased from 2mg to 4mg and her RBS & FBS on the following days were 4mg and her RBS & FBS on the following days were 201,180,130,138. 201,180,130,138.

Menstrual history:

She has amenorrhea for the last 3 months

Marital status:

She is not married.

Family history:

Her mother had pulmonary TB 10 yrs back for which she

took ATT for 8 months and according to the pt her mother is doing well now.

General Physical ExaminationGeneral Physical Examination

GPE revealed;

Pulse…..100/min,regular,high vol.

B.P…….140/90.

Temp….101 F

Lymphadenopathy…none

THYROID:

Enlarged, firm & tender.

Not adherent to nearby structures.

Regional lymph nodes not enlarged.

No hoarseness of voice.

FUNDI:

Normal.

LOWER LIMBS EXAM: revealed no signs of diabetes dermopathy or neuropathy

CVS:

CNS:Unremarkable

RESP:

GIT:

LAB :

1) TFT,S: F.T3….1.99. F.T4….16.31.

TSH….0.01.

A picture suggestive of primary hyperthyroidism.

2) Plasma glucose level: RBS…..402mg% FBS…..201,180,128,130.

3) Urine R/E: Albumin …..nill Sugar …..3+ Pus cells …..4-6 RBC,s ……nill

Epithelial cells…1+4) Special Smear:

HB…..11%TLC…..8500Plts…..4,25,000

ESR……35

5) U/S Abdomen Normal

6) CXR: Normal

So, keeping in view this History, Physical examination findings, and available lab data what do you think, is the most likely diagnosis and what further test should be performed to reach to the

diagnosis?

The D/Ds in this case include;

1) Grave’s disease

2) Hashimoto’s thyroiditis

3) chronic Lymphocytic thyroiditis

4) Sub acute thyroiditis

5) Toxic mutinodular goiter

6) Struma ovarii

RAIU Scan:

Markedly reduced RAIU by the thyroid gland.

The correct diagnosis is…

SUB ACUTE THYROIDITIS.

NOTE:It is very important to note here is that in any pt with an enlarged

thyroid and the TFT,s favouring a hyperthyroid picture,you should not straight away consider the dx of primary hyperthyroidism such

as grave’s disease and put the pt straightaway on antithyroid medications; BUT instead; U must have to go for the RAIU scan of the

thyroid & then decide whether the pt has grave’s dz, toxic MNG or sub- acute thyroiditis.

The above mentioned point is noteworthy bcoz the Rx of these conditions differ vastly such as sub acute thyroiditis needs not to be

treated with antithyroid medications.

DIAGNOSTIC EVALUATIONDIAGNOSTIC EVALUATION

CAUSES OF HYPERTHYROIDISM:

1) Grave’s dz (60—80% of thyrotoxicosis)

2) Thyroiditis: Thyrotoxic phase of sub acute thyroiditis , postpartum thyroiditis & painless sporadic

thyroiditis. 3) Toxic adenoma: (single or multinodular goiter) or, rarely functioning thyroid carcinoma. 4) TSH- secreting pituitary tumor or pituitary resistance to thyroid hormone( high TSH,high f.T4)

5) Miscellaneous: such as; amiodarone, iodine induced, struma ovarii(3% of ovarian dermoid tumor &

teratoma), hCG-secreting tumors e.g. choriocarcinoma.

RAIU SCAN & THYROID:

RAIU scan is a very useful test to differentiate between various causes of hyperthyroidism.

1) Increased Uptake:

a) Homogenous…….Grave’s disease

b) Heterogeneous……Toxic MNG c) 1 focus of inc: uptake with supression the rest of the gland……….Hot nodule.

2) No/Low Uptake:

a) Sub-acute painful thyroiditis

b) Silent painless thyroiditis

c) Exogenous thyroid hormones

d) Anti-thyroid drugs e) Struma ovarii f) Recent iodine load

Radioactive Iodine Uptake Radioactive Iodine Uptake ScansScans

Normal uptake in 30yo woman with postpartum painless thyroiditis

Increased uptake in 52yo woman with Grave’s disease

Decreased uptake in 42yo woman with subacute granulomatous thyrdoitis

THYROIDITIS:

includes disorders of different etiologies characterized by inflammation of the thyroid gland.

These disorders have different clinical courses & each can be associated at one or another time with euthyroid,thyrotoxic,or hypothyroid state.

MECHANISMS OF AUTOIMMUNE THYROID MECHANISMS OF AUTOIMMUNE THYROID DESTRUCTIONDESTRUCTION

The mechanism for autoimmune destruction of the thyroid The mechanism for autoimmune destruction of the thyroid probably involves both cellular immunity and humoral probably involves both cellular immunity and humoral immunity.immunity.

Lymphocytic infiltration of the thyroid gland by equal Lymphocytic infiltration of the thyroid gland by equal numbers of B cells and cytotoxic T cells is a numbers of B cells and cytotoxic T cells is a commoncommon

histological feature of all forms of autoimmune thyroiditishistological feature of all forms of autoimmune thyroiditis..

NORMAL THYROIDNORMAL THYROID

colloid

Thyroid epithelial cells

T4 90%T3 10%

TSH

Hashimoto’s Thyroiditis, andHashimoto’s Thyroiditis, and

Painless Postpartum ThyroiditiPainless Postpartum Thyroiditi

Painful Subacute ThyroiditisPainful Subacute Thyroiditis

SUBACUTE THYROIDITIS – PATHOLOGYSUBACUTE THYROIDITIS – PATHOLOGY

Multinucleated giant cell

GENETIC SUSCEPTIBILITYGENETIC SUSCEPTIBILITY

The genetics of autoimmune thyroid disease are The genetics of autoimmune thyroid disease are complex.complex.

Association of Hashimoto’s thyroiditis and painless Association of Hashimoto’s thyroiditis and painless postpartum thyroiditis with HLA-DR3, HLA-DR4, and postpartum thyroiditis with HLA-DR3, HLA-DR4, and HLA-DR5 has been reported in white persons, but HLA-DR5 has been reported in white persons, but other associations have been observed in other other associations have been observed in other racial and ethnic groups.racial and ethnic groups.

ENVIRONMENTAL FACTORSENVIRONMENTAL FACTORS

Among patients with Hashimoto’s thyroiditis, hypothyroidism Among patients with Hashimoto’s thyroiditis, hypothyroidism is more likely to develop in smokers than in nonsmokers,is more likely to develop in smokers than in nonsmokers, a a finding that may be related to the presence of thiocyanates in finding that may be related to the presence of thiocyanates in cigarette smoke.cigarette smoke.

An increased prevalence of painless postpartum thyroiditis An increased prevalence of painless postpartum thyroiditis has also been noted among smokershas also been noted among smokers

In addition, geographic variations in the incidence of In addition, geographic variations in the incidence of Hashimoto’s thyroiditis, painless postpartum thyroiditis, and Hashimoto’s thyroiditis, painless postpartum thyroiditis, and painless sporadic thyroiditis suggest that dietary iodine painless sporadic thyroiditis suggest that dietary iodine insufficiency may be protective against autoimmune insufficiency may be protective against autoimmune thyroiditis.thyroiditis.

CLINICAL AND BIOCHEMICALCLINICAL AND BIOCHEMICALCHANGES IN THYROIDITISCHANGES IN THYROIDITIS

The various forms of thyroiditis may cause The various forms of thyroiditis may cause thyrotoxicosis, hypothyroidism, or both.thyrotoxicosis, hypothyroidism, or both.

THYROTOXICOSISTHYROTOXICOSIS

In painless sporadic thyroiditis, painless In painless sporadic thyroiditis, painless postpartum thyroiditis, and painful subacute postpartum thyroiditis, and painful subacute thyroiditis, inflammatory destruction of the thyroiditis, inflammatory destruction of the thyroid may lead to transient thyrotoxicosis as thyroid may lead to transient thyrotoxicosis as preformed thyroid hormones are released from preformed thyroid hormones are released from the damaged gland.the damaged gland.

As in other forms of thyrotoxicosis, the serum As in other forms of thyrotoxicosis, the serum concentration of thyrotropin is suppressed, concentration of thyrotropin is suppressed, and concentrations of total and free and concentrations of total and free triiodothyronine (Ttriiodothyronine (T33) and thyroxin (T) and thyroxin (T44) are ) are elevated.elevated.

The signs and symptoms of thyrotoxicosis The signs and symptoms of thyrotoxicosis due to thyroiditis are usually not severedue to thyroiditis are usually not severe..

HYPOTHYROIDISMHYPOTHYROIDISM

The hypothyroid phase of thyroiditis results from the The hypothyroid phase of thyroiditis results from the gradual depletion of stored thyroid hormones.gradual depletion of stored thyroid hormones.

Although chronic hypothyroidism is most closely Although chronic hypothyroidism is most closely associated with Hashimoto’s thyroiditis,all types of associated with Hashimoto’s thyroiditis,all types of thyroiditis may progress to permanent thyroiditis may progress to permanent hypothyroidism.hypothyroidism.

This outcome is more likely in patients with higher This outcome is more likely in patients with higher serum concentrations of thyroid antibodies or in serum concentrations of thyroid antibodies or in patients in whom a more severe hypothyroid phase patients in whom a more severe hypothyroid phase develops.develops.

TYPES OF THYROIDITISTYPES OF THYROIDITIS

HashimotoHashimoto’’s thyroiditiss thyroiditis Painless postpartum thyroiditisPainless postpartum thyroiditis Painless sporadic thyroiditisPainless sporadic thyroiditis Painful subacute thyroiditisPainful subacute thyroiditis Suppurative thyroiditisSuppurative thyroiditis Drug-induced thyroiditisDrug-induced thyroiditis RiedelRiedel’’s thyroiditiss thyroiditis

HASHIMOTOHASHIMOTO’’S THYROIDITISS THYROIDITIS

Hashimoto’s thyroiditis , which is characterized by the Hashimoto’s thyroiditis , which is characterized by the presence of high serum thyroid antibody presence of high serum thyroid antibody concentrations and goiter, is the most common type of concentrations and goiter, is the most common type of thyroiditis.thyroiditis.

A firm, bumpy, symmetric, painless goiter is frequently A firm, bumpy, symmetric, painless goiter is frequently the initial finding in Hashimoto’s thyroiditis.the initial finding in Hashimoto’s thyroiditis.

About 10 percent of patients with chronic autoimmune About 10 percent of patients with chronic autoimmune hypothyroidism have atrophic thyroid gland(rather hypothyroidism have atrophic thyroid gland(rather than goiter), which may represent the final stage of than goiter), which may represent the final stage of thyroid failure in Hashimoto’s thyroiditis.thyroid failure in Hashimoto’s thyroiditis.

High serum thyroid peroxidase antibody concentrations High serum thyroid peroxidase antibody concentrations are present in 90 percent of patients with Hashimoto’s are present in 90 percent of patients with Hashimoto’s thyroiditis, and high serum thyroglobulin antibody thyroiditis, and high serum thyroglobulin antibody concentrations are present in 20 to 50 percent of these concentrations are present in 20 to 50 percent of these patients.patients.

Once overt hypothyroidism is present, levothyroxine Once overt hypothyroidism is present, levothyroxine sodium is the treatment of choice for Hashimoto’s sodium is the treatment of choice for Hashimoto’s thyroiditis.thyroiditis.

In patients with Hashimoto’s thyroiditis and a large goiter, In patients with Hashimoto’s thyroiditis and a large goiter, thyrotropin-suppressing doses of levothyroxine sodium thyrotropin-suppressing doses of levothyroxine sodium can be given over the short term (i.e., six months) to can be given over the short term (i.e., six months) to decrease the size of the goiter.decrease the size of the goiter.

PAINLESS POSTPARTUM THYROIDITISPAINLESS POSTPARTUM THYROIDITIS

Painless postpartum thyroiditis causes Painless postpartum thyroiditis causes lymphocytic inflammation of the thyroid within lymphocytic inflammation of the thyroid within the first few months after delivery.the first few months after delivery.

The disease is most common in women who The disease is most common in women who have high serum thyroid peroxidase antibody have high serum thyroid peroxidase antibody concentrations during the first trimester of concentrations during the first trimester of pregnancy or immediately after delivery and in pregnancy or immediately after delivery and in those with other autoimmune disorders, such as those with other autoimmune disorders, such as type 1 diabetes mellitus, or with a family history type 1 diabetes mellitus, or with a family history of autoimmune thyroid disease.of autoimmune thyroid disease.

In only one third of patients with painless post-partum In only one third of patients with painless post-partum thyroiditis will the classic triphasic thyroid hormone pattern thyroiditis will the classic triphasic thyroid hormone pattern develop .develop .

Thyrotoxicosis typically begins one to six months after Thyrotoxicosis typically begins one to six months after delivery and lasts for one to two months. delivery and lasts for one to two months.

That phase may be followed by a hypothyroid phase starting That phase may be followed by a hypothyroid phase starting four to eight months after delivery and lasting four to six four to eight months after delivery and lasting four to six months.months.

Eighty percent of women recover normal thyroid function Eighty percent of women recover normal thyroid function within a year; in one follow-up study, however, permanent within a year; in one follow-up study, however, permanent hypothyroidism developed within seven years in 50 percent hypothyroidism developed within seven years in 50 percent of the women studied.of the women studied.

Chronic hypothyroidism is more likely in multiparous Chronic hypothyroidism is more likely in multiparous women or in those with a history of spontaneous women or in those with a history of spontaneous abortions.abortions.

After a first episode of painless postpartum thyroiditis, After a first episode of painless postpartum thyroiditis, there is a 70 percent chance of recurrence with there is a 70 percent chance of recurrence with subsequent pregnancies.subsequent pregnancies.

Mild thyrotoxicosis rarely requires therapy, but when the Mild thyrotoxicosis rarely requires therapy, but when the disease is severe, it is treated with beta blockers.disease is severe, it is treated with beta blockers.

Antithyroid drug therapy is contraindicated, because Antithyroid drug therapy is contraindicated, because there is no excess thyroid hormone production.there is no excess thyroid hormone production.

Treatment of the hypothyroid phase may not Treatment of the hypothyroid phase may not be necessary, but if this phase is prolonged be necessary, but if this phase is prolonged or if the patient is symptomatic, levothyroxine or if the patient is symptomatic, levothyroxine sodium should be given, then withdrawn after sodium should be given, then withdrawn after six to nine months to determine whether six to nine months to determine whether thyroid function has normalized.thyroid function has normalized.

PAINLESS SPORADIC THYROIDITISPAINLESS SPORADIC THYROIDITIS

Painless postpartum thyroiditis and painless Painless postpartum thyroiditis and painless sporadic thyroiditis are indistinguishable except sporadic thyroiditis are indistinguishable except by the relation of the former to pregnancy.by the relation of the former to pregnancy.

Painless sporadic thyroiditis may account for Painless sporadic thyroiditis may account for about 1 percent of all cases of thyrotoxicosis.about 1 percent of all cases of thyrotoxicosis.

The clinical course is similar to that of painless The clinical course is similar to that of painless postpartum thyroiditispostpartum thyroiditis..

A low or undetectable concentration of A low or undetectable concentration of 123123 I at I at 24 hours can be diagnostic, and the test 24 hours can be diagnostic, and the test should be performed when the cause of the should be performed when the cause of the thyrotoxicosis is unclear, in order to avoid thyrotoxicosis is unclear, in order to avoid inappropriate treatment with Antithyroid inappropriate treatment with Antithyroid drugs.drugs.

Therapy is the same as that for painless Therapy is the same as that for painless postpartum thyroiditispostpartum thyroiditis..

PAINFUL SUBACUTE THYROIDITISPAINFUL SUBACUTE THYROIDITIS

Painful subacute thyroiditis , which is a self-limited Painful subacute thyroiditis , which is a self-limited inflammatory disorder, is the most common cause inflammatory disorder, is the most common cause of thyroid pain.of thyroid pain.

It occurs in up to 5 percent of patients with clinical It occurs in up to 5 percent of patients with clinical thyroid disease.thyroid disease.

It frequently follows an upper respiratory tract It frequently follows an upper respiratory tract infection, and its incidence is highest in summer, infection, and its incidence is highest in summer, correlating with the peak incidence of enterovirus.correlating with the peak incidence of enterovirus.

Subacute thyroiditis begins with a prodrome of generalized Subacute thyroiditis begins with a prodrome of generalized myalgias, pharyngitis, low-grade fever, and fatigue. myalgias, pharyngitis, low-grade fever, and fatigue.

Patients then present with fever and severe neck pain, Patients then present with fever and severe neck pain, swelling, or both.swelling, or both.

Up to 50 percent of patients have symptoms of Up to 50 percent of patients have symptoms of thyrotoxicosis. thyrotoxicosis.

In most patients, thyroid function will be normal after In most patients, thyroid function will be normal after several weeks of thyrotoxicosis, and hypothyroidism will several weeks of thyrotoxicosis, and hypothyroidism will subsequently develop, lasting four to six months, as in subsequently develop, lasting four to six months, as in painless sporadic thyroiditis and painless postpartum painless sporadic thyroiditis and painless postpartum thyroiditis.thyroiditis.

The hallmark of painful subacute thyroiditis is a markedly elevated The hallmark of painful subacute thyroiditis is a markedly elevated erythrocyte sedimentation rate.erythrocyte sedimentation rate.

The C-reactive protein concentration is similarly elevatedThe C-reactive protein concentration is similarly elevated

The leukocyte count is normal or slightly elevated.The leukocyte count is normal or slightly elevated.

Peripheral-blood thyroid hormone concentrations are elevated,, Peripheral-blood thyroid hormone concentrations are elevated,, and serum concentrations of thyrotropin are low or undetectable.and serum concentrations of thyrotropin are low or undetectable.

Serum thyroid peroxidase antibody concentrations are usually Serum thyroid peroxidase antibody concentrations are usually normal.normal.

The 24-hour The 24-hour 123123 I uptake is low (<5 percent) in the toxic phase of I uptake is low (<5 percent) in the toxic phase of subacute thyroiditis, distinguishing this disease from Graves’ subacute thyroiditis, distinguishing this disease from Graves’ disease.disease.

The treatment for painful subacute thyroiditis is to provide The treatment for painful subacute thyroiditis is to provide symptomatic relief only. Nonsteroidal medications or symptomatic relief only. Nonsteroidal medications or salicylates are adequate to control mild thyroid pain.salicylates are adequate to control mild thyroid pain.

For more severe thyroid pain, high doses of glucocorticoids For more severe thyroid pain, high doses of glucocorticoids (e.g., 40 mg of prednisone daily) provide immediate relief; (e.g., 40 mg of prednisone daily) provide immediate relief; doses should be tapered over a period of four to six weeks.doses should be tapered over a period of four to six weeks.

Corticosteroids should be discontinued when the Corticosteroids should be discontinued when the 123123I uptake I uptake returns to normal. Beta-blockade controls the symptoms of returns to normal. Beta-blockade controls the symptoms of thyrotoxicosisthyrotoxicosis..

Therapy with levothyroxine sodium is rarely required, because Therapy with levothyroxine sodium is rarely required, because the hypothyroid phase is generally mild and transient, but it is the hypothyroid phase is generally mild and transient, but it is indicated for symptomatic patients.indicated for symptomatic patients.

SUPPURATIVE THYROIDITISSUPPURATIVE THYROIDITIS

Suppurative thyroiditis is usually caused by Suppurative thyroiditis is usually caused by bacterial infection, but fungal, mycobacterial, or bacterial infection, but fungal, mycobacterial, or parasitic infections may also occur as the cause.parasitic infections may also occur as the cause.

The thyroid is resistant to infection, because of The thyroid is resistant to infection, because of

its encapsulation, high iodide content, rich blood its encapsulation, high iodide content, rich blood supply, and extensive lymphatic drainage, and supply, and extensive lymphatic drainage, and Suppurative thyroiditis is therefore rare.Suppurative thyroiditis is therefore rare.

Patients with suppurative bacterial thyroiditis are Patients with suppurative bacterial thyroiditis are usually acutely ill with fever, dysphagia, dysphonia, usually acutely ill with fever, dysphagia, dysphonia, anterior neck pain and erythema, tender thyroid anterior neck pain and erythema, tender thyroid mass, TLC and ESRmass, TLC and ESR

Thyroid function is generally normal in patients with Thyroid function is generally normal in patients with suppurative thyroiditis, but both thyrotoxicosis and suppurative thyroiditis, but both thyrotoxicosis and hypothyroidism have been reported.hypothyroidism have been reported.

The therapy for suppurative thyroiditis consists The therapy for suppurative thyroiditis consists of appropriate antibiotics and drainage of any of appropriate antibiotics and drainage of any abscess.abscess.

The disease may prove fatal if diagnosis and The disease may prove fatal if diagnosis and treatment are delayed.treatment are delayed.

DRUG-INDUCED THYROIDITISDRUG-INDUCED THYROIDITIS

Many medications can alter thyroid function or Many medications can alter thyroid function or the results of thyroid-function tests. the results of thyroid-function tests.

However, only a few are known to provoke However, only a few are known to provoke autoimmune or destructive inflammatory autoimmune or destructive inflammatory thyroiditis. (thyroiditis. (Amiodarone; Amiodarone; Lithium; Interferon Alfa Lithium; Interferon Alfa and Interleukin-2and Interleukin-2))

LITHIUMLITHIUM INDUCED THYROIDITIS INDUCED THYROIDITIS

In patients with preexisting thyroid autoimmunity, In patients with preexisting thyroid autoimmunity, lithium may increase the serum thyroid antibody lithium may increase the serum thyroid antibody concentrations and lead to subclinical or overt concentrations and lead to subclinical or overt hypothyroidism.hypothyroidism.

In addition, thyrotoxicosis has been reported In addition, thyrotoxicosis has been reported after long-term lithium use, possibly caused by after long-term lithium use, possibly caused by lithium’s direct toxic effects on thyroid cells or by lithium’s direct toxic effects on thyroid cells or by lithium-induced painless sporadic thyroiditis.lithium-induced painless sporadic thyroiditis.

INTERFERON ALFA AND INTERLEUKIN-2INTERFERON ALFA AND INTERLEUKIN-2 INDUCED THYROIDITISINDUCED THYROIDITIS

High serum thyroid peroxidase antibody High serum thyroid peroxidase antibody concentrations in such patients and in patients concentrations in such patients and in patients receiving interleukin-2 therapy may be receiving interleukin-2 therapy may be associated with overt or subclinical associated with overt or subclinical hyperthyroidism (Graves’ disease) or hyperthyroidism (Graves’ disease) or hypothyroidism.hypothyroidism.

Interferon alpha has also been reported to cause Interferon alpha has also been reported to cause destructive inflammatory thyroiditisdestructive inflammatory thyroiditis..

While treatment with interferon alpha or interleukin-2 is While treatment with interferon alpha or interleukin-2 is continued, the Thyrotoxic phase of inflammatory thyroiditis continued, the Thyrotoxic phase of inflammatory thyroiditis can be treated with beta-blockers and, if necessary, with can be treated with beta-blockers and, if necessary, with Nonsteroidal anti-inflammatory drugs or corticosteroids, Nonsteroidal anti-inflammatory drugs or corticosteroids, and the hypothyroidism can be treated with Thyroxine.and the hypothyroidism can be treated with Thyroxine.

Although thyroid function usually normalizes when Although thyroid function usually normalizes when cytokine therapy is discontinued, affected patients are at cytokine therapy is discontinued, affected patients are at increased risk for autoimmune thyroid dysfunction in the increased risk for autoimmune thyroid dysfunction in the future. future.

Ideally Thyroid-function tests and measurements of serum Ideally Thyroid-function tests and measurements of serum thyroid antibodies should be performed before and during thyroid antibodies should be performed before and during therapy with interferon alpha or interleukin-2 is initiated therapy with interferon alpha or interleukin-2 is initiated and every six months thereafter.and every six months thereafter.

RIEDELRIEDEL’’S THYROIDITISS THYROIDITIS

Riedel’s thyroiditis, a local manifestation of a Riedel’s thyroiditis, a local manifestation of a systemic fibrotic process,systemic fibrotic process, is a progressive fibrosis of is a progressive fibrosis of the thyroid gland that may extend to surrounding the thyroid gland that may extend to surrounding tissues. tissues.

The prevalence of this disease is only 0.05 percent The prevalence of this disease is only 0.05 percent among patients with thyroid disease requiring among patients with thyroid disease requiring surgery, and its cause is unknown. surgery, and its cause is unknown.

High serum thyroid antibody concentrations are High serum thyroid antibody concentrations are present in up to 67 percent of patients, but it is present in up to 67 percent of patients, but it is unclear whether the antibodies are a cause or effect unclear whether the antibodies are a cause or effect of the fibrotic thyroid destruction.of the fibrotic thyroid destruction.

Patients with Riedel’s thyroiditis present with a rock-Patients with Riedel’s thyroiditis present with a rock-hard, fixed, painless goiter.hard, fixed, painless goiter.

They may have symptoms due to tracheal or They may have symptoms due to tracheal or esophageal compression or hypoparathyroidism due esophageal compression or hypoparathyroidism due to extension of the fibrosis into adjacent parathyroid to extension of the fibrosis into adjacent parathyroid tissue. tissue.

Most patients are euthyroid at presentation but Most patients are euthyroid at presentation but become hypothyroid once replacement of normal become hypothyroid once replacement of normal thyroid tissue is nearly completethyroid tissue is nearly complete..

A definitive diagnosis is made by open biopsy. A definitive diagnosis is made by open biopsy.

The treatment is surgical, although therapy with The treatment is surgical, although therapy with glucocorticoids, methotrexate, and tamoxifen has glucocorticoids, methotrexate, and tamoxifen has been reported to be successful in the early stages of been reported to be successful in the early stages of the diseasethe disease..

T3

Hypothalamus

Anterior pituitary

Thyroid

TRH

TSH

T4

Remember this?

Iodide

TAKE HOME MESSAGE TAKE HOME MESSAGE

Subacute granulomatous thyroiditis is usually self-limited Subacute granulomatous thyroiditis is usually self-limited diseasedisease

The whole process of Hyper, normo, hypothyroid phases The whole process of Hyper, normo, hypothyroid phases last over a period of 6-9 monthslast over a period of 6-9 months

Treat with propranolol, +/- steroids, NSAIDsTreat with propranolol, +/- steroids, NSAIDs

Think of this diagnosis in patients who have FUO and Think of this diagnosis in patients who have FUO and tender thyroid.tender thyroid.

Hyperthyroid work-up should include TSH, free T4, RAIU Hyperthyroid work-up should include TSH, free T4, RAIU at minimum.at minimum.

ReferencesReferences Slatosky J, , Shipton B, , Wahba H. . Thyroiditis: differential diagnosis and Thyroiditis: differential diagnosis and

management. management. Am Fam Physician 2000 Jul 15;62(2):318. Am Fam Physician 2000 Jul 15;62(2):318. Pearce E, Farwell A, Braverman LPearce E, Farwell A, Braverman L. . Current Concepts: Thyroiditis Current Concepts: Thyroiditis

NEJM 2003; 348: 2646-55NEJM 2003; 348: 2646-55 Nishihara E, , Ohye H, , Amino N, , Takata K, , Arishima T, , Kudo T, , Ito M, , Kubota S, ,

Fukata S, , Miyauchi A. . Clinical characteristics of 852 patients with subacute Clinical characteristics of 852 patients with subacute thyroiditis before treatment. thyroiditis before treatment. Kuma Hospital, Center for Excellence in Thyroid Kuma Hospital, Center for Excellence in Thyroid Care, Kobe. Care, Kobe. nishihara@kuma-h.or.jp Intern Med. 2008;47(8):725-9. Epub 2008 Intern Med. 2008;47(8):725-9. Epub 2008 Apr 16.Apr 16.

Benbassat CA, , Olchovsky DOlchovsky D, , Tsvetov GTsvetov G, , Shimon IShimon I. . Subacute thyroiditis: clinical Subacute thyroiditis: clinical characteristics and treatment outcome in fifty-six consecutive patients characteristics and treatment outcome in fifty-six consecutive patients diagnosed between 1999 and 2005.diagnosed between 1999 and 2005.Endocrine Institute, Rabin Medical Center, Endocrine Institute, Rabin Medical Center, Beilinson Campus, Petach Tikva, Israel 49100. Beilinson Campus, Petach Tikva, Israel 49100. carlosb@netvision.net.ilcarlosb@netvision.net.il J J Endocrinol Invest. 2007 Sep;30(8):631-5.Endocrinol Invest. 2007 Sep;30(8):631-5.

Swinburne JLSwinburne JL, , Kreisman SHKreisman SH.. A rare case of subacute thyroiditis causing A rare case of subacute thyroiditis causing thyroid storm. Thyroid. 2007 Jan;17(1):73-6.thyroid storm. Thyroid. 2007 Jan;17(1):73-6.