THYROID DISORDERS

Dr. Gagan V

Anatomy and Histology

• 15 – 20 g• Two lobes and isthmus, pyramidal lobe• Right lobe more vascular than left lobe• Blood supply– Sup. Thyroid Artery – Ext. Carotid Artery– Inf. Thyroid Artery – Subclavian Artery

• Follicles – closely packed spherical units• Rich capillary network• Interior of follicle – thick proteinaceous colloid• Diameter – 200 µm• Follicular cells– Cuboidal – inactive– Columnar - active

Regulation of Thyroid Axis

• TSH – – Thyrotrope cells of ant. Pituitary– 31 kDa hormone α and β subunits– α subunit similar to LH, FSH and hCG– Stimulated by TRH– TSH, TRH supressed by Thyroxine– Pulsatile secretion– Long half life (50 minutes)

• Iodine primarily derived from diet• RDA of iodine• Adults – 150 µg• Children – 90 – 120 µg• Pregnancy – 200 µg• Urinary iodine is >10 g/dL in iodine-sufficient

populations• Plasma iodide partly replenished from thyroid

loss, peripheral deiodination

CLASSIFICATION

• Primary hypothyroidism with Goitre – Acquired Iodine deficiency(MCC)

• Hashimoto’s (autoimmune type 2A)• Drugs synthesis or release of T4

(lithium,ethionamide,sulfonamides,iodide)• Food goitrogens or as endemic substances or pollutants• Thyroid infiltration (Reidels struma,cystinosis,scleroderma)• sarcoidosis,amyloidosis,hemochromatosis.

– Congenital • Iodide transport or utilization defect• Iodotyrosine dehalogenase deficiency• Organification disorders• Defects in thyroglobulin synthesis or processing

• Atrophic hypothyroidism– Acquired

• Hashimoto’s disease (autoimmune thyroiditis type 2B)• Post ablative-follows surgery,I131 radiation

• Congenital• Thyroid agenesis or dysplasia (80-85% of neonatal

hypothyroidism)• TSH receptor defects• Thyroidal Gs protein abnormalities• Idiopathic TSH unresponsiveness

• Transient (post thyroiditis) hypothyroidism– Following subacute.painless, or post partum

thyroiditis• Consumptive hypothyroidism– D3 over expression in hemangiomas

• Central hypothyroidism– Acquired

• Pituitary origin (secondary)• Hypothalamic disorders (tertiary)• Bexarotene (RXR receptor agonist)• Dopamine and or severe illness

– Congenital • TSH deficiency or structural abnormality• TSH receptor defect

Thyroid Hormone Resistance

• autosomal dominant disorder

• characterized by elevated thyroid hormone levels and inappropriately normal or elevated TSH

• . do not, in general, exhibit signs and symptoms that are typical of hypothyroidism because hormone resistance is partial and is compensated by increased levels of thyroid hormone

• . The clinical features of RTH can include goiter, attention deficit disorder, mild reduction in IQ, delayed skeletal maturation, tachycardia, and impaired metabolic responses to thyroid hormone.

• mutations in the TR receptor gene.

• . The diagnosis is suspected when unbound thyroid hormone levels are increased without suppression of TSH.

• RTH must be distinguished from other causes of euthyroid

hyperthyroxinemia (e.g., FDH) and inappropriate secretion of TSH by TSH-secreting pituitary adenomas (Chap. 333).

.

RTH

• In most patients, no treatment is indicated; the importance of making the diagnosis is to avoid inappropriate treatment of mistaken hyperthyroidism and to provide genetic counseling

euthyroid hyperthyroxinemia

• These disorders result in increased total T4 and/or T3, but unbound hormone levels are normal.

• Usually caused by mutations that affects TBG,Tranthyretin, or albumin

CLINICAL FEATURESMechanism

Symptoms Signs

Slowing of metabolic processes

Fatigue and weakness

Cold intolerance

Dyspnea on exertion

Weight gain

Cognitive dysfunction

Mental retardation (infant)

Constipation

Growth failure

Slow movement and slow speech

Delayed relaxation of tendon reflexes

Bradycardia

Carotenemia

Accumulation of matrix substances

Dry skin

Hoarseness

Edema

Coarse skin

Puffy facies and loss of eyebrows

Periorbital edema

Enlargement of the tongue

Other Decreased hearing

Myalgia and paresthesia

Depression

Menorrhagia

Arthralgia

Pubertal delay

Diastolic hypertension

Pleural and pericardial effusions

Ascites

Galactorrhea

CLINICAL FEATURES

SKIN AND APPENDAGES

• Dry coarse skin• Pale cool extremities• Carotenemia• Poor wound healing • Easy bruisability• Dry brittle hair&nail

• Accumulation of hyaluronic acid, hygroscopic• Mucinious edema, boggy, non pitting• Eyes, dorsa of hand and feet, supraclavicular

fossae• Tongue enlargement, thickening pf pharyngeal

and laryngeal membranes• Decreased secretion of sweat and sebaceous

glands

• Skin wounds heal slowly• Increase capillary fragility – easy bruisability• Hair lost from temporal aspect of eyebrow –

Queen Annes sign

CARDIOVASCULAR SYSTEM• Decreased cardiac output at rest– Decreased stroke volume, heart rate– Increased peripheral vascular resistance

• Pericardial effusions(myxedema heart)– Protein rich, glycosaminoglycans

• Reversible diastolic hypertension• Asymmetric septal hypertrophy

Angina may appear/worsen during treatment initiation

ECG◦sinus bradycardia,◦PR prolongation,◦ low amplitude complexes,◦altered ST segment◦CHB

◦Echo◦Resting LV diastolic dysfunction

• Combination of large heart, hemodynamic and electrocardiographic changes and serum enzyme changes – myxedema heart

• Thyroid replacement reverts to normal• Increased Total and LDL cholesterol– Reduced on thyroxine initiation– No change in HDL levels

RESPIRATORY SYSTEM• Hoarse voice• Pleural effusion– Radiological – Rarely cause dyspnoea

• Myxedematous involvement of resp muscles and depression of respiratory drives– Decreased alveolar ventilation – Carbon dioxide retention

• Obstructive Sleep Apnoea common

ALIMENTARY TRACT• Decreased apetite• Modest weight gain(fluid retention) 10% of

body weight• Constipation(myxedema megacolon)• Myxedema ileus• Ascites(raised protein glycosaminoglycans)• Pernicious anemia(autoimmune)• Raised CEA, raised aminotranferases due to

decreased clearance

CNS & PNS

• Decreased CBF• Defective

memory,lethargy,somnolence

• A/C psychiatric illness• Headache,syncope• Night blindness,• SNHL(PENDRED)

• Cerebellar ataxia• CTS• Reversible dementia• Infancy-MR• Delayed

relaxation(hung up reflex)

MUSCULO SKELETAL SYSTEM• Weakness,cramps worsened by cold• Arthralgia• Increased muscle mass-firm• Role in bone maturation• Short limb dwarfism(Bone age<chr age)• Epiphyseal dysgenesis(x ray)• Myoclonus

RENAL • Decreased RBF &GFR• Increased uric acid • Decreased urine flow • Reversal of (n)diurnal pattern of urine

excretion• Mild proteinuria

HEMATOPOIETIC• Decreased RBC mass(low EPO)• NN anemia(macrocytic,microcytic)• Decreased factor8,9-bleeding

tendency

PITUITORY & ADRENOCORTICAL FN.• Enlarged pituitary, hyperplasia of thyrotropes,

rarely mass effect• Raised prolactin(galactorrhea)• Urinary cortisol decreases,plasma level normal• Long standing primary hypothyroidism,

adrenocortical insufficiency may be precipitated by thyroxine/stress

REPRODUCTIVE SYSTEM• Sexual immaturity• Delay in puberty, Anovulaton• Menorrhagia, amenorrhea• Impotence, oligospermia• Precocious sexual development -rarely in

primary hypothyroidism

ENERGY & METABOLISM• Low BMR• Positive nitrogen balance• Decreased secretion of GH• Serum proteins increase• Decreased glucose uptake by adipose

tissue and skeletal muscles• Insulin response to glucose delayed• Increased sensitivity to exogenous insulin

• True obesity is rare in hypothyroidism• Raised LDL & TG,low HDL• Hyperhomocystinemia-lead to

atherosclerosis• Hyponatremia• Hypoglycemia

DIAGNOSIS• Decreased freeT4,raised TSH : primary

hypothyroidism• Decreased TSH, Decreased Free T4, in

secondary(central)• Degree of TSH elevation correlates with severity.• Free T4 is done in pregnancy • Anti thyroglobulin and anti TPO Ab: Hashimoto’s• Absence of TPO Ab: post undiagnosed

subacute/viral thyroiditis/ post hyperthroid hpothyroidism

• TSH may take several months to reach normal

INDIVIDUAL CAUSES

• Hashimotos thyroiditis– Most common cause of hypothyroidism in

areas with sufficient dietary intake– There is mononuclear cell infiltrate and

destruction of follicles– Chronic thyroiditis defined as evidence of

intrathyroidal lymphocytic infiltration.mainly Tcell mediated destruction

– Occurs more commonly in women,prevalence increases with age

– Auto immune thyroiditis leads on to thyroid cell apoptosis leading to follicular destruction

– Almost 90% destruction before symptoms manifest

– HLA DR-3 ,HLA-DR5,seen with Downs syndrome and gonadal dysgenesis,polymorphisms in CTLA4

– Pregnancy ,drugs,low doses of irradiation,certain viral infections may increase risk

– Goiter hallmark finding,moderate size firm,freely mobile,lymph node enlargement unusual

– Increased prevalence of thyroid carcinoma– Diagnosis confirmed by autoantibodies,TPO AB more

common than TyAb

• Iodine deficiency– Thyroid iodine clearance rates and RAIU are

increased– Decreased urinary excretion of stable iodine– Results in cretinism

• Drugs – Lithium inhibits thyroid hormone release and

in high conc. can inhibit organic binding reactions

– Underlying autoimmune disease increase susceptibility

DRUGS

• Lithium• Propylthiouracil• Methimazole• Amiodarone• Interferon alfa• Interleukin 2

FOOD GOITROGENS

• Turnip • Cassava• Selenium deficiency

• Atrophic hypothyroiodism– (primary myxedema)– More common in women between ages of

40 and 60– May represent end stage of an autoimmune

thyroiditis in which goiter did not devolop or went unnoticed

– May be associated with TSH receptor blocking antibodies

• Post ablative hypothyroidism• Following total/subtotal thyroiodectomy• Subtotal resection of the diff.goiter of gravesor multinodular

goiter• Radioiodine treatment

– Manifests during the first yr after surgery– FT4I is low in patients with postablative

hypothyroidism,serum TSHlevels may be anomalously low for several months

• Transient hypothyroidism defined as period of reduced fT4I with supressed, normal or elevated,TSH levels that are eventually followed by a euthyroid state

• Seen with post viral,postpartum thyroiditis,painless lymphocytic thyroiditis

– Mild to moderate symptoms of hypothyroidism

– May have a transient period of hyperthyroidism

• Consumptive– Seen with hemangiomas– Due to increased expression of D3deiodinase

enzyme– Serum reverse T3 elevated– Thyroglobulin >1000 ng/ml

• Central hypothyroidism– Due to TSH deficiency caused by acquired or

congenital pituitary(secondary hypothyroidism) and hypothalamic origins (tertiary hypothyroidism)

– Decreased secretions of other hormones– Hypothyroidism due to central cause milder

than primary

• Subclinical hypothyroidism • Asymptomatic pt with – low normalT4– slightly elevated TSH(5.5-15MIU/L)

• Seen in hashimoto/graves after treatment with Sx/Radioiodine

• Asso.with Type I DM,PBC,pernicious anemia.• Presence of TPO Ab will require therapy• If no therapy ,patients to be monitored 6 -12

monthly both clinically and biochemically• Treat with T4(low dose)

Sick Euthyroid Syndrome

• Any acute, severe illness cause abnormalities of circulating TSH or thyroid hormone levels in the absence of underlying thyroid disease

• A decrease in total and unbound T3 levels (low T3 syndrome) with normal levels of T4 and TSH(MC)

• The magnitude of the fall in T3 correlates with the severity of the illness.

• increased reverse T3 (rT3)

• (low T4 syndrome) has a poor prognosis

TREATMENT OF HYPOTHYROIDISM

• T4 is the choice• Replacement dose-1.6 – 1.8 µg/kg bwt(lean body

mass)• Start with replacement dose initially except in elderly

and CAD• R/o adrenal insufficiency before Rx• Hypothyroidism after graves-lower doses(as there is

underlying autonomous function)• Dose adjusted on basis of TSH levels and clinical

assessment• the goal of treatment being a normal TSH, ideally in

the lower half of the reference range ( 0.4-2.5 )

• TSH measured after 2 months• Clinical effects may lag behind(3-6 mon)• Increments in 12.5-25microgram dose• Over Rx-AF, osteoporosis,pseudotumour

cerebri in children• Once TSH stable-yearly checkup with TSH• T3 not used because of short t1/2

Advice to patients

• Levothyroxine has a t1/2 of 7 days &it will take a week or more to start feeling better. If one tablet is missed out there will be no noticeable effect

• If muscle stiffness, weakness, or cognitive defects are present these may take upto 6 months to fully resolve

• Levothyroxine should be taken in empty stomach to maximise absorption

• Treatment is generally lifelong

• Early clinical response in moderate to severe hypothyroidism is a diuresis of 2-4Kg

• Serum sodium level rises • Thereafter pulse rate ,pulse pressure increases,

appetite improves and constipation disappears.• Psychomotor activity increases, delay in reflexes

disappears• Hoarseness abates slowly and skin changes

clears late.

• For rapid control T4 intravenous 500 microgram single dose

• Or orally T3 25 microgram orally every 12 hrs

Hypothyroidism and pregnancy

• Increased requirements(also during estrogen Rx)

• Increase dose by 30%• TSH meaured once every trimester• Try to achieve euthyroidism prior to

conception

Special considerations

• ELDERLY-Start with lower dosage• CAD-Start at 25-50 and gradually increase

every 2-3 months• EMERGENCY Sx-safe(routine sx-defer until

euthyroid)

Potential causes of TSH elevation in thyroxine-treated patients with primary hypothyroidism

• Suboptimal dosing • Inadequate prescribed dosage • Noncompliance • Dispensing error (incorrect dose or

formulation change)

Progressive decrease in endogenous thyroxine production

• Autoimmune thyroiditis • Previous thyroid irradiation

Reduced thyroxine absorption

• Iron• Calcium carbonate • Cholestyramine • Aluminum hydroxide gel • Sucralfate • Dietary soy and fiber

Co morbid conditions

• Disorders causing malabsorption - eg, coeliac disease

• Previous small bowel surgery

Drug interactions

• Phenytoin • Carbamazepine • Phenobarbital • Rifampin

Coexisting conditions

• Pregnancy • Nephrotic syndrome • Other systemic illnesses

MYXEDEMA COMA

• Ultimate stage of severe long standing hypothyroidism

• Mostly in older patients• Hypothermia is charecterestic• All manifestations of hypothyroidism are florid

seizures can occur• Delayed relaxation may be lackinf if areflexic• Alveolar hypoventilation ,narcosis and SIADH

MYXEDEMA COMA• PPTED BY • Infection• CHF• MI• GI bleed• CVA• Drugs-

sedatives,anaesthetics,antidepressants

CLINICAL FEATURES• Hypotension• Hypothermia• Hypoglycemia• Hyponatremia• Hypoventilation&

hypercapnia• Seizures

MYXEDEMA COMA• Levothyroxine 500-800microgram iv

bolus(nasogastric route also) followed by 50-100 microgram daily

OR• T3 10-25 microgram BD (Side effect :arrhythmia)

• Hydocortisone 5-10 mg/hr 50 mg Q6H• Combined T4 200 +T3 25 iv bolus followed by 25 T3

and 100 T4 after 24 hrs and 50 T4 daily• Supportive treatment and mechanical ventilation

Thyrotoxicosis refers to the clinical syndrome in

which free triiodothyronine (T3), free thyroxine

(T4), or both are elevated and the peripheral

tissues are hypermetabolic, irrespective of the

source of the excess hormones.

• Primary hyperthyroidism – Graves' disease (60-80%)– Toxic multinodular goiter – Toxic adenoma – Functioning thyroid carcinoma metastases – Activating mutation of the TSH receptor – Activating mutation of Gs (McCune-Albright

syndrome)– – Struma ovarii – Drugs: iodine excess (Jod-Basedow

phenomenon) • Thyrotoxicosis without hyperthyroidism

– Subacute thyroiditis – Silent thyroiditis – Other causes of thyroid destruction:

amiodarone, radiation, infarction of adenoma

– Ingestion of excess thyroid hormone (thyrotoxicosis factitia) or thyroid tissue

• Secondary hyperthyroidism – TSH-secreting pituitary

adenoma – Thyroid hormone

resistance syndrome: occasional patients may have features of thyrotoxicosis

– Chorionic gonadotropin-secreting tumours

– Gestational thyrotoxicosis

Heat intolerance, palpitations,anxiety, fatigue, weight loss, and irregular menses.

Tremor, tachycardia, wide pulse pressure, lid lag, and warm, moist skin

Gynecomastia, and spider angiomas.

Hyperglycemia, hypercalcemia, elevated ALP

Leukocytosis, and elevated liver enzymes

Polycythemia

Osteopenia & fracture

Alopecia

Onycholysis , pruritis , diffuse hyperpigmentation.

Normochromic normocytic anemia

Serum ferritin may be high

Grave’s disese

– ITP , spleenomegaly, lymphadenopathy

– Pernicious anemia

– Anti-neutrophilic antibody

Urinary frequency and nocturia

Graves’ disease –

Diffuse, nontender, symmetric goiter

Ophthalmopathy, consisting of protrusion of the orbits,

periorbital soft tissue swelling, inflammation, and

extraocular muscle dysfunction

Graves’ dermopathy with characteristic thickened skin

plaques, usually over the lower extremities, accompanied

by nonpitting edema

Thyroid Acropachy

Investigation

TFT : TSH by ICLA and T3 & T4 by RIA

Anti TPO antibody , TSI

USG thyroid & FNAC

RAIU

Radioiodine scan

With Graves’ disease and toxic nodular goiter, there tends

to be a higher proportion of T3, with a T3/ T4 ratio of

greater than 20.

With thyrotoxicosis caused by thyroiditis, iodine exposure,

or exogenous levothyroxine intake, there is generally a

greater proportion of T4, with a T3/ T4 ratio of less than

15

TSHR antibodies are detectable only in

autoimmune thyroid disease.

Persistence after treatment is predictive of

treatment failure.

Indication : Euthyroid exophthalmos

Pregnancy

During therapy

Doppler USG

Typically, a thyroid gland secreting excessive

hormones would be enlarged and have enhanced

Doppler flow.

In subacute, postpartum, or silent thyroiditis, or

exogenous causes of hyperthyroidism, the

thyroid gland would be expected to be small, with

decreased Doppler flow.

Therapeutic approaches

Antithyroid drugs

Radioiodine

Surgery

Thionamides

Inhibiting the iodination of tyrosines and coupling of the

iodotyrosines to form T3 and T4 in the thyroid.

Decreases concentrations of thyroid stimulating antibodies in

Graves’ disease

Decreases peripheral conversion of T4 to the active hormone

T3

Titration regimen

Starting doseMMI 20 mg to 30 mg dailyPTU 100 mg three times daily

Dose titrated based on unbound T4

Thyroid function tests are repeated every 4 to

6 weeks for the first 4 to 6 months .

On average, 30% to 40% of patients treated

with antithyroid drugs go into remission

lasting 10 years or more

Treatment with PTU or MMI for 12 to 18

months or longer results in long-term

remission in 40% to 60% of patients with

Graves’ disease, but the remission rate is lower

in patients treated for a shorter period of time

Franklyn JA. The management of hyperthyroidism. N Engl J

Med 1994;330(24):1731–8.

Larger goiter size, younger age, and higher

pretreatment serum T3 levels predict a longer

duration to euthyroidism with MMI treatment,

and poorer long-term remission rates Allahabadia A, Daykin J, Holder RL, treatment for Graves

hyperthyroidism. J Clin Endocrinol Metab 2000;85(3):1038–42.

Block-replace regimen*

The initial dose of antithyroid drug is held

constant and the dose of L thyroxine is adjusted

to maintain normal unbound T4 levels. Here starting dose is high

Maxi remission rate are achieved by 6 mon *BMJ 332 1369 - 2006

The doses of these drugs do not need to be

altered in children, the elderly, or persons

with renal failure

Adverse effects

Fever, rash, urticaria, and arthralgias occur in

1% to 5%, more common at higher doses.

Change the patient to another thionamide.

Arthralgias, classified as a “minor” reaction,

should prompt drug discontinuation, since this

symptom may be a harbinger of a severe

transient migratory polyarthritis known as

“the antithyroid arthritis syndrome.”

Agranulocytosis occurs in 0.5% of patients treated

with methimazole or PTU . The effect appears to be

dose-mediated for methimazole, with an increased

risk for agranulocytosis in patients taking more than

40 mg daily

PTU-associated agranulocytosis is not dose-related .

If agranulocytosis develops, thionamide

medications must be immediately discontinued

Most cases of agranulocytosis occur within the

first 90 days of treatment, but this

complication can occur even a year or more

after starting therapy

Drug discontinued if the granulocyte count is

less than 1000/mm3

Close monitoring of the granulocyte count if it

is between 1000-1500 /mm3

Prospective monitoring of the WBC count on

follow-up visits is not recommended, since the

onset of agranulocytosis is typically acute and

not detected by periodic surveillance.

PTU-induced hepatotoxicity manifests as acute

hepatitis which resolves with removal of the

PTU; may progress to fulminant hepatic failure

Patients taking methimazole may develop a

reversible cholestasis

ANCA, primarily p-ANCA, is present in 20% of patients on PTU

therapy

Taking PTU for a longer duration are more likely to develop ANCA

positivity , and titers may decrease after discontinuation of PTU.

ANCA-positive vasculitis is rare (arthralgias, skin lesions, renal

manifestations, fever, and alveolar hemorrhage)

Sato H, Hattori M, et al. High prevalence of ANCA positivity in Graves’ disease treated with PTU. J Clin Endocrinol Metab 2000;85(11):4270

Methimazole has been associated with rare

occurences of cutis aplasia , oesophageal &

choanal atresia.

Indications for thionamides

Graves disease for long term remission

Toxic nodular goitre prior to surgery to control

toxicity

Prior to Radioiodine therapy to prevent crisis

Pregnant and lactating women

Inorganic iodide ( SSKI or Lugol’s solution)

decreases thyroid hormone synthesis in the

short term (Wolff-Chaikoff effect)

Iopanoic acid, an iodine-rich oral

cholecystographic agent, is a potent inhibitor of

the conversion of T4 to T3

Beta blockers

Glucocorticoids (inhibit conversion of T4 –T3)

Cholestyramine (more rapid decrease in

circulating hormone levels.)

Potassium perchlorate competitively inhibits

transport of iodide into the thyroid.

Radioactive iodine

I 131

5-15 mCi

Post procedure prevent spread of RaI

Oral contraceptives

80% to 90% of patients become euthyroid

within 8 weeks of a single dose ; remaining

10% to 20% require a second, or even a third

dose of radioactive iodine

Complications

Ultimately causes permanent hypothyroidism

in over 90% of treated patients .

Depends on the dosage.

10 % in first year; 5% per year thereafter.

Radiation thyroiditis

Worsened thyrotoxicosis

Development or progression of Graves’

ophthalmopathy (prevented by cotreatment

with glucocorticoids)

Precautions

Most radioactive iodine is eliminated in the

urine, saliva and feces in 4-8 weeks.

Have double flushing of toilet and frequent hand

washing for several weeks

No close contact with children and pregnant

patients for 48-72 hours

Follow up Thyroid function returns to normal in 2 to 6

months.

Hypothyroidism occurs within 4 to 12 months as

a natural complication of the radioiodine; as a

consequence, lifelong therapy with L-

thyroxine is routine

Indications for RaI

Graves disease in elderly, even adolescents

Hyperfunctioning nodule.

Surgical

Subtotal thyroidectomy results in a rapid cure

of hyperthyroidism in over 90% of cases

Patients are frequently treated with inorganic

iodide for 10 to 14 days before thyroidectomy.

Transient hypocalcemia is seen in up to 25% of

post-thyroidectomy patients

Hypothyroidism may develop in upto 80% of

patients in the year following surgery

Indication for Surgery

Graves disease with large goitre, not

responding to drugs, associated

ophthalmopathy , pregnancy

Toxic nodular goitre

Considerations in the treatment of hyperthyroidism

Cause & Severity of hyperthyroidism

Patient preference

Patient age

Goiter size

Patient compliance

Presence of ophthalmopathy (in Graves’disease)

Pregnancy (current or planned) ; Lactation

Subacute thyroiditis

• Aspirin or NSAIDS

• Glucocorticoid therapy: prednisone 40 to 60

mg OD for a week, followed by gradual

tapering over 4 weeks.

• Thyrotoxicosis generally resolves

spontaneously

• THANK YOU