Thyroiditis refers to inflammation of the thyroid gland and can be caused by various factors such as viruses, bacteria, fungi, autoimmune disorders and medications. The document discusses the different types of thyroiditis including acute infectious, subacute, Riedel's, postpartum, autoimmune and amiodarone-induced thyroiditis. It provides details on symptoms, diagnostic testing, treatment and prognosis for each type. Genetic and environmental risk factors for developing autoimmune thyroid disease are also reviewed.

1. Thyroiditis

2. Topics
• Definition
• Acute Infectious Thyroiditis
• Subacute thyroiditis
• Riedel thyroiditis
• Postpartum thyroiditis
• Autoimmune thyroid disease
• Amiodarone Induced Thyrotoxicosis

3. Definition
• Thyroiditis is a term indicating the presence of thyroid inflammation and thus
comprises a large group of diverse inflammatory conditions.
• These conditions include the following:
1. autoimmune
2. viral or postviral conditions
3. infections- bacterial and fungal origins
4. Riedel thyroiditis
5. miscellaneous -
• radiation-induced
• Granulomatous cause- sarcoidosis
• lithium

4. Acute Infectious Thyroiditis
• Resistant to infection
• congenital abnormalities of the piriform sinus, underlying autoimmune disease, or immunocompromised
• bacterium-Staphylococcus, Pneumococcus, Salmonella, or Mycobacterium tuberculosis.
• certain fungi- Coccidioides immitis, Candida, Aspergillus, and Histoplasma.

5. • Repeated childhood infectious thyroiditis- internal fistula extending from the piriform sinus to the thyroid.
This sinus is the residual connection following the path of migration of the ultimobranchial body from the
fifth pharyngeal pouch to the thyroid gland.
• The predominance of thyroiditis of the left lobe- right ultimobranchial body is often atrophic whereas this is
not the case for the left side.
• Extremely rare disease even as a complication of direct puncture such as in fine-needle aspiration.
• In individuals with midline infections, persistence of the thyroglossal duct should be considered

6. • Clinical Manifestations - local pain and tenderness ,fever and chills may also accompany the condition.
• Ultrasonographic examination- Abscess in the thyroid gland or evidence of swelling,
• Needle aspiration may help pinpoint the responsible organism.
• Gallium scan will be positive
• barium swallow -fistula connecting the piriform sinus and left lobe .

7. • Needle aspiration,surgical drainage .
• If a piriform sinus fistula can be demonstrated- removed to prevent recurrence of the problem.
• Antibiotics, Fungal infections should be treated appropriately especially – immunocompromised
• Endemic organisms - Echinococcus and Trypanosomiasis infections
• Prognosis is excellent.

8. Subacute thyroiditis
• Painful (DeQuervain’s; Granulomatous) thyroiditis, (PFSAT) typically present with painful swelling of the
thyroid.
• Transient vocal cord paresis may occur.
• "creeping thyroiditis".
• Pain may radiate to the jaw or the ears.
• Malaise, fatigue, myalgia and arthralgia are common.
• A mild to moderate fever is expected, and at times a high fever of 104°F may occur.

9. • The disease process may reach its peak within 3 to 4 days and subside and disappear within a week but
more typically onset extends over 1 to 2 weeks and continues with fluctuating intensity for 3 to 6 weeks.
• The thyroid gland is typically enlarged, smooth, firm and tender to palpation, sometimes exquisitely so.
• Approximately one-half of the patients present during the first weeks of the illness, with symptoms of
thyrotoxicosis.
• Subsequently patients often experience hypothyroidism before returning to normal .
• lasts for a week to a few months, very high ESR ,CRP levels and has a tendency to recur.

10. • Painless (silent, autoimmune) subacute thyroiditis occurs spontaneously or following pregnancy when it is
referred to as postpartum thyroiditis [PPT]).
• Autoimmune thyroiditis is histologically similar to Hashimoto's thyroiditis and occurs following 3.9-10% of
pregnancies.
• The combination of thyroid enlargement usually without discomfort and positive anti-thyroid antibodies
associated with typical thyroid function test abnormalities over a 9-12 month course - PLSAT.

11. • painful form of the disease to follow upper respiratory tract infections or sore throats has suggested a viral
infection.
• An autoimmune reaction is possible as patients with PFSAT often manifest HLABw35 and those with PLSAT
are frequently TPO or TG-ab positive.
• In both forms, clinical thyroid symptoms result from either the initial release of thyroid hormone from the
inflamed tissue during the thyrotoxic phase or the lack of circulating thyroid hormones in the hypothyroid
phase

12. • Subacute thyroiditis is a diagnosis made clinically.
• Anterior neck pain, preceded by an upper respiratory inflammation- classic PFSAT.
• Differential diagnostic considerations include acute thyroiditis which is usually a painful nodular enlargement
of the thyroid or unusual presentations of Graves’ or nodular thyroid disease with pain generated by
capsular stretching.
• Thyroid function tests during the painful (initial) phase of SAT often reveal a suppressed TSH and elevation
of total T4 and T3 levels consistent with the thyrotoxic state. T3 (ng/dl) to T4 (ug/dl) ratio is less than 20 in all
forms of SAT.

13. • ESR greater than 50 ,WBC counts and CRP levels - PFSAT.
• PLSAT -TPO-ab, Tg-ab antibodies, both of which are usually absent or present only in low titers in PFSAT.
• TRAb are usually positive in Graves' disease and absent or low level in patients with PFSAT as well as PPT.
• Low RAIU - PFSAT and PLSAT
• Thyroid ultrasound- heterogeneously hypoechoic pattern and has a suppressed vascular pattern in SAT while
patients with Graves’ disease demonstrate hyper-vascularity. The presence of thyroid nodules supports the
presence of a toxic nodular goiter. Localized PFSAT can be suggestive of thyroid cancer.

14. • In some patients, no treatment is required.
• Analgesic therapy
• If this fails- prednisone 20-40 mg one to 2 weeks tapered over a period of 6 weeks.
• Recrudescence of symptoms- dose must be increased again.

15. • Recurrence rate of painful subacute thyroiditis after cessation of prednisone therapy is about 20%.
• Beta blocking agents- thyrotoxic symptom.
• Levothyroxine administration- transiently
• Surgical intervention is not the primary treatment for subacute thyroiditis but is safe and with low morbidity
if necessary because of the possibility of associated papillary cancer based on cytological examination

16. • 90% complete and spontaneous recovery to normal thyroid function.
• However, the thyroid glands of patients with subacute thyroiditis may exhibit irregular scarring between
islands of residual functioning parenchyma.
• Up to 10% become hypothyroid .
• Antibody positive PLSAT and especially PPT- ↑ Rates of permanent hypothyroidism.

21. Riedel Thyroiditis
• Rare and occurs primarily in middle-age women
• The etiologic mechanism is uncertain and any association with autoimmune thyroid disease is probably
coincidental.
• The morphologic similarities between the fibrosis of Riedel thyroiditis and IgG4-related sclerosing disease
suggest that these entities are closely related with thyroiditis representing an initial manifestation of a more
generalized process.

22. • Retroperitoneal, orbital, and mediastinal fibrosis, as well as rarer fibrotic syndromes, are associated with
Riedel thyroiditis.
• Symptoms-compression of adjacent structures, including the trachea, esophagus, and recurrent laryngeal
nerves.
• Systemic evidence of inflammation is uncommon.
• The thyroid gland is moderately enlarged, stony hard, and usually asymmetric.

23. • The consistency of the gland and the invasion of adjacent structures suggest carcinoma, but there is no
enlargement of regional lymph nodes.
• Temperature, pulse, and leukocyte count are normal.
• Severe hypothyroidism is unusual but does occur, as does loss of parathyroid function.
• The RAIU may be normal or low.

24. • Thyroid autoantibodies are much less common
• Tamoxifen, 10 to 20 mg/day (with or without corticosteroids) – suppress TGFβ.
• Surgery - tracheal and esophageal function.
• Treatment with thyroid hormone relieves the hypothyroidism but has no effect on the primary process.

25. • Atrophic thyroiditis - the gland is atrophied and consists of extensive fibrotic tissue, moderate lymphocytic
infiltration, and widespread loss of thyroid follicles, but the fibrosis is not as extensive as in Riedel
thyroiditis.
• The histopathologic changes in painless thyroiditis resemble Hashimoto thyroiditis.
• spectrum of disease arising from a common underlying autoimmune process-a distinct subset of patients
with Hashimoto thyroiditis has been delineated recently in whom there are high circulating levels of IgG4
and increased numbers of IgG4-positive plasma cells in the thyroid.
• IgG4-related thyroiditis is characterized pathologically by a greater degree of stromal fibrosis,
lymphoplasmacytic infiltration, and hypothyroidism.

26. • Treatment- In euthyroid patients with Hashimoto thyroiditis, no treatment is required because the goiter is usually
asymptomatic.
• Levothyroxine treatment may be indicated in patients when the goiter presses on adjacent structures or is unsightly, and it
is most effective in goiters of recent onset.
• The aim is to keep the TSH level in the lower half of the reference interval.
• In long-standing goiter, treatment with thyroid hormone is usually ineffective, possibly because of fibrosis. Rarely, the
goiter may be painful, and this symptom may respond to levothyroxine therapy.

27. • Glucocorticoids, such as prednisolone, are usually ineffective. Surgery may be justified if symptoms or unsightly
enlargement persists after a trial of levothyroxine therapy.
• Replacement doses of thyroid hormone should be given when hypothyroidism is present, appropriate to the degree of
hormone deficiency.
• There may be a spontaneous return to euthyroidism in up to 10% of patients after starting levothyroxine associated in
some cases with the disappearance of TSH receptor blocking antibodies.
• It has not been established that such remissions are durable and there is no need to routinely stop levothyroxine once it
has been started.
• Prednisolone treatment can reverse the hypothyroidism of IgG4-related thyroiditis, but the long-term outcome in such
cases is not yet known.

28. Miscellaneous
• 131I treatment for Graves disease
• Residual thyroid lobe in a patient with thyroid cancer of the contralateral lobe
• External beam therapy for conditions-Hodgkin or non-Hodgkin lymphoma, breast carcinoma, or other
lesions of the oropharynx.
• Anaplastic thyroid carcinoma may rarely be associated with a diffuse thyroiditis and elevation of thyroid
hormone levels.
• In general, only radioiodine-induced thyroiditis is associated with pain and glucocorticoid treatment may be
useful in symptomatic therapy

29. Postpartum thyroiditis
• Autoimmune inflammation
• 5% (range 4% to 10%) of women without preexisting thyroid disease and may also occur after early
pregnancy loss.
• Thirty-three to 50% of women with antithyroid antibodies in the first trimester will develop postpartum
thyroiditis with higher titers conferring a greater risk
Inaba H, Akamizu T. Postpartum Thyroiditis. 2018

30. • The classic form begins with transient thyrotoxicosis followed by transient hypothyroidism with a return to euthyroid state
by the end of the first postpartum year.
• It usually presents in one of three ways:
• transient hyperthyroidism (30%)
• transient hypothyroidism (44% to 48%)
• transient hyperthyroidism followed by hypothyroidism and recovery. (20%)
• it increases the risk for development of permanent hypothyroidism within 3 to 12 years in up to 40% of patients.
• acute onset of the thyrotoxic phase – 2 to 8 weeks after delivery and lasts for a few months- nontender thyroid
enlargement - euthyroid phase few months-- hypothyroid phase with symptomatic hypothyroidism which can
last for up to 1 year.

31. Differentiating postpartum thyroiditis from Graves disease
• Thyroid receptor antibodies are often positive in Graves disease but usually are negative in postpartum
thyroiditis.
• Radioiodine uptake is elevated or normal in Graves disease and low in postpartum thyroiditis.
• Elevated antimicrosomal and anti TG titers-PPT
• Ultrasound examination- diffuse hypoechogenicity which resolves with resolution of the thyroiditis.
• 123I or technetium scans are preferable to 131I scans in breastfeeding women.
• Treatment - control symptoms.

32. • Treatment - control symptoms
• In one prospective study of 605 asymptomatic pregnant and postpartum women, none of the women with
thyrotoxicosis and only 40% of women with hypothyroidism required treatment.
• If treatment is required, it can usually be tapered within 1 year.
• majority of studies - 10% and 20% of women with postpartum thyroiditis will require long-term treatment.
• A prospective study of 169 women - higher rate of 54% of women with persistent hypothyroidism after 1
year.

33. Women with the following highest risk for developing permanent hypothyroidism
1. highest levels of TSH
2. high TPO antibody titers
3. multiparous women
4. older women
5. history of miscarriage .

34. • levothyroxine and iodine treatment.
• TPOAb-positive women - selenium decreased both the incidence of postpartum thyroiditis and permanent
hypothyroidism.
• Selenium administration was also associated with a significant decrease in postpartum TPOAb titers.
• benefit are limited
• recurrent postpartum thyroiditis in a subsequent pregnancy is approximately 70%.
• Annual TSH screening to evaluate for permanent hypothyroidism.

35. Autoimmune thyroid disease
• AITD is the most common organ specific autoimmune disorder comprising of-
1. Graves' disease
2. Hashimoto's thyroiditis (goitrous)
3. atrophic thyroiditis,
4. postpartum thyroiditis
5. silent thyroiditis and
6. thyroid associated ophthalmopathy.

36. • These may occur sequentially and sometimes synchronously, in the same patient. These disorders share antibodies
against Tg Ab,TPO Ab and TSH-R Ab besides some minor antigen such as Na-I transporter.
• Middle age women and men - 2-4% of women and up to 1% of men .
• advancing age - 10% of population of age above 75 years is affected.
• Clinical features, autoantibody status, ultrasonographic features and FNAb findings are very useful in diagnosis of AITD

37. • Predisposition
• inherited predisposition to autoimmunity, with additional environmental and hormonal factor
• Genetic factors- monozygotic twins is 35-55% as compared to less than 5% in dizygotic twins.
• The predisposition to Graves' disease is genetic in 79% case while only 21% cases are due to non genetic factors.
• Thyroid antibodies have been found in nearly half of the relatives of AITD patients against only 8-27% in general
population.

38. • AITD is a component of some rare monogenic syndromes. Autoimmune hypothyroidism affects patient with type 1
polyendocrinopathy; immune dysregulation, 'polyendocrinopathy' and enteropathy [IPEX].
• Different alleles of MHC class I molecule - Graves' disease- HLA-A10, B8 and DQw2 is seen in India.
• Cytotoxic T lymphocyte antigen-4 (CTLA-4) -an immunomodulatory molecule expressed on the surface of activated T cell,
is its key negative regulator.
• CTLA-4 gene is a major candidate gene for common autoimmune disorders like Graves' disease, Type-1 diabetes and
Hashimoto's thyroiditis.

39. Environmental factors
• High dietary iodine intake - thyroglobulin immune reactivity.
• infective agents –unclear- rubella, Epstein Barr virus, yersinia, retrovirus.
• Stress disorders-Graves' disease -altering neuroendocrine interaction with immune system.
• Graves' ophthalmopathy- smokers.
• lithium, interferon-α and amiodarone exacerbate AITD.
• Female sex steroid.
• X chromosome -female susceptibility

40. Diagnosis of autoimmune thyroid disorders
• A firm, symmetrically enlarged thyroid gland in association with anti-thyroid antibodies and a high normal or elevated TSH level is virtually
diagnostic of Hashimoto's thyroiditis.
• hypothyroidism without goitre - atrophic thyroiditis.
• Graves' disease- thyrotoxicosis and diffuse goitre.
• Thyroid enlargement-diffuse hypoechogenecity

41. • Color flow Doppler (CFD) - distinct CFD pattern with marked increased in signals with patchy distribution.
• Estimation of thyroid autoantibodies and TSH, T3:T4 are useful in diagnosis of AITD.
• In Hashimoto's thyroiditis there is raised TSH level and raised antiTPO antibodies.
• In Graves' disease thyrotropin levels are suppressed.
• Routine measurement of TSHR antibodies titres are not performed for diagnosis of Graves' disease.
• Radioactive iodine uptake study helps differentiating Graves' disease and thyroiditis associated transient hyperthyroidism.

42. • Fine needle aspiration biopsy-useful in diagnosis of AITD.
In Hashimoto's thyroiditis- microscopic finding-
1. extensive infiltrate with lymphocytes, plasma cell and macrophages.
2. Germinal centre with giant cell is also seen.
3. Others features include –
obliteration of thyroid follicles by widespread apoptosis, some follicular cells are atrophic or damaged and many are
hyperplastic or metaplastic. These remaining thyroid follicular cells may be large and show oxyphilic changes in the
cytoplasm, the so-called oxyphilic cell / Hurthle cells/ Askanazy cells.
• Fibrosis is present in more long standing disease.

43. • Graves' disease –
1. hypertrophy and hyperplasia of thyroid follicles
2. colloid is scanty
3. cells are tall columnar, and are thrown in to papillary folds that extend into the lumina of the follicles.
4. Vascularity is increased
5. varying heterogeneous infiltration by lymphocytes and plasma cells and may form infrequent germinal centers.

44. Subacute thyroiditis-
1. disrupted follicles with micro abscesses form as some follicles are filled with polymorphonuclear leukocytes.
2. both follicular cells and colloid are destroyed focally.
3. A characteristic feature is the well developed follicular lesion that consists of a central core of colloid surrounded by the
multinucleated giant cells that arise from the fusion of macrophages.
4. Lymphoid germinal centers are absent with few plasma cells with normalization of histological changes once disease subsides.
Sporadic thyroiditis and postpartum thyroiditis fall into the spectrum of autoimmune thyroid disease with less remarkable lymphocytic
infiltration.
• Suppurative thyroiditis -abscess formation
• Riedel's thyroiditis - dense fibrosis.

45. • Classical Hashimoto thyroiditis
1. diffusely enlarged or nodular,
2. pale and firm , rubbery texture .
3. Diffuse lymphocytic infiltration with germinal center formation and obliteration of thyroid follicles, accompanied by a
variable degree of fibrosis .
4. Destruction of thyroid epithelial cells occurs as disease progresses from euthyroidism to hypothyroidism
5. some patients - follicular cell metaplasia and the formation of Hürthle cells.
6. Rarely, there are concurrent histologic changes of Graves disease, so-called hashitoxicosis.

46. • thyroid antigens-anti-TPO,anti-Tg and TSH receptor-blocking antibodies (TBII) - inadequate production of thyroid
hormone.
• 10-15% antibody-negative.
• Polyglandular Autoimmune Syndrome type 2 with autoimmune adrenal deficiency and type-1 DM.
• Hashimoto thyroiditis is also related to several other autoimmune diseases such as- pernicious anemia, adrenal
insufficiency, and celiac disease.

47. • After age six Hashimoto is the most common cause of hypothyroidism - iodine intake is adequate.
• 0.8 per 1000 per year in men and 3.5 per 1000 per year in women.
• Twin studies have shown an increased concordance of autoimmune thyroiditis in monozygotic twins as
compared with dizygotic twins.
• Danish studies-concordance rates of 55% in monozygotic twins, 3% in dizygotic twins- 79% of predisposition
is due to genetic factors, allotting 21% for environmental and sex hormone influences.

48. Pathophysiology
• lymphocyte infiltration and fibrosis.
• little evidence - Anti-TPO antibody in the pathogenesis of AITD.
• Anti-TPO antibodies can fix complement and in vitro have been shown to bind and kill thyrocytes.
• There has been no correlation noted in human studies between the severity of disease and the level of anti-
TPO antibody concentration in serum.
• positive serum anti-TPO antibody concentration is correlated with the active phase of the disease.
• Other theories implicated -
• immune complexes, containing thyroid directed antibodies, as culprits of thyroid destruction.

49. Histopathology
• diffuse, symmetric enlargement of the thyroid. The capsule is often intact with a prominent pyramidal lobe.
• When cut, the surface is similar to that of lymph nodes, with a pale brown to yellow color.
• Interlobular fibrosis may or may not be present.
• Atrophy may also occur and in some patients, the gland may become nodular or asymmetric. However, necrosis or
calcification does not occur and would suggest a different diagnosis.

50. History and Physical
• Initially-hyperthyroid symptom then hypothyroidism- insidious and variable and may affect almost any organ system in
the body.
• The classic skin characteristic- myxedema - increased glycosaminoglycan deposition.
• Skin can be scaly and dry, especially on the extensor surfaces, palms, and soles- epidermal thinning.
• Increased dermal mucopolysaccharides-water retention - palecolored skin.

51. • The rate of hair growth slows, and hair can be dry, coarse, dull, and brittle. Diffuse or partial alopecia is not
uncommon.
• Increase peripheral vascular resistance - 50% to 60% and reduce cardiac output by as much as 30% to 50%.
• Bradycardia may result from a loss of chronotropic action.
• most patients have a few symptoms directly attributable to the cardiovascular system.

52. • Fatigue, exertional dyspnea, and exercise intolerance-limited pulmonary and cardiac, decreased muscle strength or
increased muscle fatigue.
. Biochemical changes-
1. decreased muscle oxidation of pyruvate and palmitate,
2. increased utilization of glycogen stores, and
3. diminished fatty acid mobilization.
• Muscle weakness and myopathy
• The presentation may also be subclinical. Early symptoms- constipation, fatigue, dry skin, and weight gain.
• More advanced symptoms : cold intolerance, decreased sweating, nerve deafness, peripheral neuropathy, decreased energy,
depression, dementia, memory loss, muscle cramps, joint pain, hair loss, apnea, menorrhagia, and pressure symptoms-voice
hoarseness.

53. • Anemia is present in 30 to 40%.
• There can be decreased glomerular filtration rate (GFR), renal plasma flow, and renal free water clearance with resultant
hyponatremia.
• Creatine kinase is frequently elevated.
• Prolactin levels may be elevated.
• Elevated total cholesterol, LDL, and triglyceride levels can occur.
• A thyroid ultrasound assesses thyroid size, echotexture, and whether thyroid nodules are present; however, it is usually not
necessary for diagnosing the conditioning the majority.

54. Amiodarone Induced Thyrotoxicosis
• iodine-deficient regions.
• The incidence of AIT varies greatly (between 0.003% and 10%).
• AIT -M/F = 3/1.

55. There are two different forms of AIT-.
it is often not possible to clearly distinguish AIT1 and AIT2.
Type 1 AIT
• latent Graves’ disease, multinodular gland
• consequence of increased thyroid hormone biosynthesis due to iodine excess in patients with a preexisting thyroid disorder
• iodine deficient regions.
Trohman RG, Sharma PS, McAninch EA, Bianco AC. Amiodarone and the thyroid physiology, pathophysiology, diagnosis and management. Trends Cardiovasc Med. 2018 Sep 20;:S1050-1738(18)30195-6.

56. Type 2 AIT-
• Destructive process
• Intrinsic toxic effect of amiodarone.
• Type 2 AIT persists for one to three months until thyroid hormone stores are depleted.
• Type 2 AIT is more common than Type 1 AIT

57. • symptoms and signs of thyrotoxicosis are not apparent in all patients and may be obscured by an underlying cardiac
condition.
• Reappearance or exacerbation of an underlying cardiac disorder-suspected development of AIT.
• The development of angina may also occur.
• Similarly unexplained changes in warfarin sensitivity requiring a reduction in the dosage of this drug.
• AIT may develop early during amiodarone treatment after many months of treatment, and has even been reported to occur
several months after amiodarone withdrawal, since amiodarone and its metabolites have a long half-life due to
accumulation in several tissues especially fat.

58. Type 1 Type 2
Underlying thyroid disease Yes (Multinodular goiter, Grave’s) No
Time after starting amiodarone Short (median 3 months) Long (median 30 months)
24-hour iodine uptake Low-Normal (may rarely be high in
iodine deficient regions)
Low to Suppressed
Thyroid Ultrasound Diffuse or Nodular Goiter may be
present
Normal or small gland
Vascularity on Echo-color Doppler
ultrasound
Increased Absent
T4/T3 ratio Usually <4 Usually >4
TgAb / TPOAb/ TSI May be present Usually absent
Circulating interleukin-6 Normal to high Sometimes markedly elevated but
usually doesn’t differentiate from
AIT1

59. DIAGNOSIS
• suppressed serum TSH associated with an increase in serum FT3 and FT4 levels
• T3 levels may not be as elevated as expected and severe non-thyroidal illness may be present blocking the increase in T3.
• Type 2 AIT - increased T4/T3 ratio
• Thyroid antibodies may be present in Type 1 AIT depending upon the underlying thyroid disorder.
• High levels of thyroglobulin antibodies and TPO antibodies have also been reported in 8% of Type 2 AIT patients.
• Type 2 AIT - IL-6 may be markedly elevated but typically the IL-6 levels do not distinguish AIT2 from AIT1.

60. • Color flow Doppler ultrasonography
1. Intra-thyroidal vascular flow- increased in Type 1 AIT (pattern II-III)
2. Reduced or absent in Type 2 (pattern 0).
• In many patients with Type 1 AIT the 24-hr iodine uptake is low.
• In rare patients with Type 1 AIT, despite the very high iodine load, a normal or inappropriately elevated
24-hr iodine uptake may be observed, especially if the patients live in an iodine deficient area.
• Patients with Type 2 AIT typically have a radioactive iodine uptake < 1%.
• While the distinction between Type 1 and Type 2 may sometimes be clear, in many patients neither the
clinical findings nor the response to treatment clearly indicate whether the patient has Type 1 or Type 2
AIT.
• Some patients may have a mixed form of AIT.

61. • AIT may lead to increased morbidity and mortality- older patients with impaired left ventricular function.
• Prompt restoration and stable maintenance of euthyroidism should be achieved as rapidly as possible.
• Mild AIT may spontaneously resolve in about 20% of the cases.
•
• Type 1 AIT - methimazole (20-60 mg/day) or propylthiouracil (400-600 mg/day) to block the synthesis of
thyroid hormones.
•
• The response to methimazole or propylthiouracil is often modest due to the high iodine levels in patients
taking amiodarone.

62. • In selected patients, potassium perchlorate when available can also be used to increase sensitivity of the gland
to methimazole or propylthiouracil by blocking iodine uptake in the thyroid.
• KClO4 should be used for no more than 30 days at a daily dose < 1 g/day since this drug - aplastic anemia or
agranulocytosis.
• Once thyroid hormone levels are back to normal, definitive treatment of the hyperthyroidism should be
considered. If thyroid uptake is sufficient (>10%) radioactive iodine can be used.
• Thyroid surgery is a good alternative.

63. If thyrotoxicosis worsens after initial control a mixed form Type1-Type 2 should be considered and treatment for
Type 2 AIT should be started.
Type 2 AIT - prednisone 0.5-0.7 mg/kg body weight per day- three months.
If a worsening of the toxicosis occurs during the taper the prednisone dose should be increased.
Methimazole and propylthiouracil are generally not useful in Type 2 AIT.

64. • Because the distinction between AIT Type 1 and 2 is difficult and not always clear and because some patients
have mixed forms of AIT - therapies for AIT Type 1 and 2 are often combined.
• Persistent hyperthyroidism- surgery is the optimal choice.
• Propylthiouracil- inhibit T4 to T3 conversion.
• Beta blockers- preparation for surgery.

65. References
• Williams textbook of Endocrinology
• American thyroid association 2016 Guidelines
• Degroot Endocrinology

66. HAKARU HASHIMOTO