My Clinical Notes

• Thyroid hormones are synthesised in the thyroid gland by the iodination and coupling of two molecules of tyrosine, a process that is dependant on sufficient levels of iodide
• Fish and dietary salt are the main dietary sources of iodide
• Iodide is taken up actively under the control of TSH – uptake is blocked by thiocyanate and perchlorate
• Iodine is rapidly converted to iodine by the enzyme thyroperoxidase (TPO)
• Iodination of tyrosine residues in thyroglobulin is again catalysed by TPO to form mono-iodotyrosine (MIT) and di-iodotyrosine (DIT) – this step is inhibited by carbimazole and propylthiouracil
• Iodotyrosines are coupled to form T4 (DIT+DIT) and T3 (MIT+DIT) which are incorporated in thyroglobulin and stored in the colloid of the thyroid follicle. Generally more T4 is produced than T3
• In order for secretion of thyroid hormone, thyroglobulin is taken up by the follicular cells in a process involving endocytosis and phagocytosis and the T3 and T4 are then released by proteolytic enzymes into the bloodstream. This process is stimulated by TSH and inhibited by iodide
• The thyroid hormones immediately bind to plasma proteins and the MIT and DIT released are de-iodinated and the iodine is reused

 

• Most of the T3 and T4 is protein bound in the plasma;
  • 70% is bound to thyroxine-binding globulin
  • 10-15% is bound to transthyretin
  • 10-15% is bound to albumin and thyroxine-binding pre-albumin
• The free unbound fraction is the physiologically active form which also regulates TSH from the anterior pituitary
• It is free hormone levels that are measured in lab assays

 

Peripheral conversion of thyroid hormone

• 20% of T3 is produced by the thyroid, the rest is made by deionation of T4 by the peripheral tissues, mainly the kidney and liver
• Conversion is not affected by TSH
• T3 is produced by removal of the iodine atom from the outer β-ring.
• De-iodination of the inner α-ring, produces reverse T3 which is probably inactive
• T3 has greater avidity for the thyroid receptor than T4
• The conversion of T4 to T3 can be reduced by;
  • Systemic illness
  • Prolonged fasting
  • Drugs such as β-blockers and amiodarone (which contains iodine)
• The conversion of T4 to T3 can be increased by drugs that induce hepatic activity such as phenytoin
• The plasma T3 concentration is therefore a poor indicator of thyroid function as it is influenced by non-thyroidal factors. Its measurement is rarely indicated except in thyrotoxicosis

 

Action of thyroid hormones

• Thyroid hormones are essential from normal growth, mental development and sexual maturation
• They sensitise the cardiovascular and central nervous system to catecholamines, thereby influencing cardiac output and thyroid hormones

 

Control of TSH secretion

• TSH is released by the anterior pituitary under the control of TRH and the circulating concentrations of thyroid hormones
• Release of TSH follows a diurnal pattern, with high levels during sleep, which decrease abruptly upon wakening

 

Effects of TRH

• TRH is released by the hypothalamus into the portal capillary plexus
• Its action can be overridden by high free T4 concentrations therefore exogenous TRH has little affect on TSH secretion in hyperthyroidism
• The TRH receptor in the pituitary is a seven-transmembrane spanning family member coupled to G proteins

 

Effects of thyroid hormones in the secretion of TSH

• Thyroid hormones reduce TSH via negative feedback
• It is T3 that binds to receptors of the anterior pituitary
• In the anterior pituitary most of the T3 is derived from T4 therefore this gland is more sensitive to the changes in plasma T4 than T3

 

Thyroid function tests

 

Plasma thyroid-stimulating hormone

• Levels of TSH are high in primary hypothyroidism and low in secondary or pituitary hypothyroidism
• In hyperthyroidism TSH levels are low
• TSH assays are first-line for thyroid function assessment
• In normal individuals there is a log-linear relationshio between TSH and free T4, that is to say that exponential increases in TSH are accompanied by small incremental increases in free T4

 

Plasma total thyroxine or free thyroxine assays

• Plasma T4 is 99% protein bound, therefore total T4 assays reflect the protein bound fraction rather than the free fraction
• Total T4 reflects free T4 unless there are abnormalities of binding proteins
• In the euthyroid state, about a 1/3 of the biding sites on TBG are occupied by T4 the rest are unoccupied  irrespective of the concentration of binding protein
• In the hyperthyroid state, both total are free T4 are increased and the number of unoccupied binding sites on TBG are dcreased
• In hypothyroidism the opposite situation is true

 

• An increase in TBG concentration results in an increase in both bound T4 and unoccupied sites but no change in free T4 concentration. This can occur because of;
  • A high oestrogen concentration during pregnancy or in the newborn infant
  • Oestrogen therapy – COCP, HRT
  • Inherited TBG excess (rare)

 

• A decrease in plasma TGB concentration decreased both bound T4  and unoccupied binding sites but doesn’t alter the plasma free T4 concentration. This can occur because of;
  • Severe illness (usually temporarily)
  • Loss of low molecular weight proteins usually in urine e.g. nephrotic syndrome
  • Androgens or danazol treatment
  • Inherited TBG deficiency (rare)

 

• These changes may be misinterpreted if only total T4 was assayed and therefore free T4 measurement is preferred
• Some drugs such as salicylates and danazol bund to TBG and displace T4. The change in unoccupied site is variable and the levels of TGB are unchanged

 

Plasma total or free tri-iodothyronine

• As normal levels of plasma T3 are low, measurement on free or total T3  are not done routinely except occasionally
• In hyperthyroidism, the increase in T3 is greater and usually occurs earlier than that of T4
• Occasionally in hyperthyroidism the plasma T3 is elevated but not T4. This is called a T3 toxicosis
• If you are going to measure T3, measure free T3 as the total T3 may be altered by changes in the plasma concentration of TGB

 

Thyrotrophin-releasing hormone test

• The TRH test is used to confirm the diagnosis of secondary hypothyroidism or early primary hypothyroidism
• May be used in hyperthyroidism to differentiate between thyroid resistance syndrome or a TSH-secreting pituitary adenoma
• It is sometimes used as part of the pituitary stimulation test
• Allergic reactions may occur and therefore resuscitation facilities should be available and the test should be carried out by experienced staff
• Procedure;
• A basal blood sample is taken
• 200μg of TRH is injected IV over one minute
• further blood samples are taken 20 and 60 mins after then TRH injection and TSH is measured in all samples
• *note; certain drugs such as dopamine agonists and glucocorticoids reduce the response, whilst metaclopramide and oestrogens enhance it*

 

T3 Uptake test

• Measures the level of thyroid hormone-binding proteins in the blood
• Done by adding a known amount of radioactive T3 to a sample of the patients plasma and then assessing how much is bound

 

Interpretation

• In normal people the TSH increased at 20 mins to at least 2mU/L with a decline at 60 mins
• An exaggerated response at 20 mins and a slight fall at 60 mins is suggestive of primary hypothyroidism
• A normal or exaggerated but delayed response with TSH levels higher at 60 mins than at 20 mins suggests secondary hypothyroidism due to hypothalamic dysfunction
• A flat response of TSH of less than 5mU/L suggests hyperthyroidism, although this may occur in some euthyroid patients with multinodular goitre

 

 

Drug effects on thyroid function tests

 

Drug	T4	Free T4	T3	Free T3	Remarks
Amiodarone	Increase	Normal or ­	Normal	Normal	Blocks T4 to T3 conversion
Androgens	Decrease	Normal	Decrease	Normal	Reduced TGB
Carbamazepine	Decrease	Decrease	Normal	Normal	Increased T4 to T3 conversion
Carbimazole	Decrease	Decrease	Decrease	Decrease	Therapeutic
Lithium	Decrease	Decrease	Decrease	Decrease	May inhibit iodination
Oestrogens	Increase	Normal	Increase	Normal	Increase TGB
Phenytoin	Decrease	Decrease	Normal	Normal	Increased T4 to T3 conversion
Propranolol	Normal	Normal	Decrease	Decrease	Blocks T4 to T3 conversion
Propylthiuracil	Decrease	Decrease	Decrease	Decrease	Therapeutic
Salicylate	Decrease	Normal	Decrease	Normal	Reduced TBG binding
Some radiocontrast media	Increase	Normal	Decrease	Normal or¯	Blocks T4 to T3 conversion (transiently)

 

Interference of assays by immunoglobulins

• Anti-T4 or anti-T3 immunoglobulins such as heterophilic antibodies can cause spurious elevation of T4 or T3 (or free hormones) when assayed by immunoassay.
• Remember this when interpreting thyroid function test results

 

Disorders of the thyroid gland

 

Hypothyroidism

• Affects 6% of people over 60, usually women
• If the hormone deficiency is caused by a primary disorder of the thyroid gland, the patient may present with;
  • Weight gain
  • Myopathy
  • Menstrual disturbance e.g. menorrhagia
  • Constipation
  • Hair loss
  • Hoarse voice
  • Dry, thickened skin
  • In severe cases coma with severe hypothermia may develop

 

• The following laboratory changes may be associated with hypothyroidism, is particularly severe;
  • Plasma cholesterol concentration. In hypothyroidism, the clearance of plasma LDL-cholesterol is impaired and plasma cholesterol concentrations may be moderately high
  • Plasma creatine kinase activity is often raised due to possible myopathy
  • Hyponatraemia may be present when severe due to increased ADH release with excessive water rentention, occasionally precipitated by a constrictive pericardial effusion than some patients develop
  • Hyperthyroidism may be associated with hyperprolactinaemia
  • Reduced plasma sex hormone binding globulin
  • Macrocytic anaemia may occur with raised mean corpuscular volume
  • Sometimes liver and renal function tests may be abnormal

 

Causes of hypothyroidism

• Most common worldwide is iodine deficiency
• In areas of adequate iodine uptake hypothyroidism is mainly autoimmune – Hashimoto’s thyroiditis
• Most commonly seen in elderly women
• 90% have thyroid autoantibodies, anti-thyroid peroxidase, anti-thyroglobulin or TSH receptor blocking antibodies
• A positive TPO together with a mildly raised TSH predicts future thyroid failure
• Rare causes of hypothyroidism are goitrogens and dyshormonogenesis, a term which includes inherited deficiencies of any of the enzymes involved in thyroid hormone synthesis. The commonest form is the failure to convert iodine into tyrosine
• Secondary hypothyroidism is due to low concentrations of TSH from the anterior pituitary of low TRH. This is less common than primary disease
• In long standing secondary hypothyroidism, the thyroid gland may atrophy irreversibly
• The essential biochemical difference between primary and secondary hypothyroidism is in the plasma TSH concentrations which is high in primary disease and low in secondary disease

 

• Initially the plasma T4 or free T4 concentration may be within normal range (although low for the individual) therefore TSH levels are the most sensitive index of early hypothyroidism

 

Neonatal hypothyroidism

• Incidence is 1 in 3500, commoner than the other inborn errors of metabolism
• Immediately after birth the levels of TSH rise, probably in response to the stress of birth. They peak within the first hour and return to normal over the next week
• Levels of thyroxine peak within the first 24 to 48 hours after birth and then fall gradually
• Most labs screen using TSH alone, this should be done around one week after birth to allow levels to return to normal
• In premature babies TSH doenst rise after birth thus giving false negative results. Testing should be repeated at what should be 40 weeks gestation
• Thyroid function tests should be repeated in infants with a positive tests at birth and if positive they should be started on thyroid replacement therapy immediately
• Thyroid function should be reassessed after the withdrawl of treatment after one year because the neonatl hypothyroidism can be transient
• Hypothyroidism may be suspected clinically because of persistent jaundice or failure to thrive

 

Treatment of hypothyroidism

• Usually with T4 which can be titrated until the plasma TSH is within the reference range
• On rare occasions such as hypothyroid comas, T3 is given instead as its actions are more immediate
• The response to T4 therapy can be checked every 2-3 months until the patient is stable when 6-12 monthly checks can be useful
• Thyroxine should be used in caution in patients with IHD for fear of worsening angina  and low doses initially plus β-blockers may be indicated
• Thyroxine therapy may induce an Addisonian crisis in patients with adrenal insufficiency
• Over treatment with T4 can induce AF and osteoporosis, in such cases TSH is low
• If a patient is non-compliant, only taking the T4 near the time of the thyroid function test, levels of T4 and TSH will be high

 

Compensated hypothyroidism

• This is the state in which plasma TSH is raised but T4 levels still fall within the reference range
• In individuals over 60, the prevalence is around 10%
• Some patients may be asymptomatic whereas others may have clinical symptoms
• Thyroxine therapy may be indicated particularly in pregnancy, or when there are thyroid antibodies or the TSH is very high (>10mU/L)

 

Thyroid Hormone Resistance

• In this case the plasma total T3 and T4 levels are elevated and the TSH is normal or my be slightly raised
• Some patients appear euthyroid whilst others will have symptoms of hypothyroidism
• Defect may be inherited as an autosomal dominant disorder in some patients
• Thought to be due to a defect in T3 and/or T4 receptors and may be associated with end organ resistance states

 

Lab investigations of suspected hypothyroidism

• Take a careful history (including drugs) and examine, particularly checking for a goitre
• Plasma TSH and total of free T4 should be measured
• Slightly elevated TSH and normal free T4 suggested compensated hypothyroidism. It may be useful to measure autoantibodies and repeat thyroid function in 3-6 months as full blown hypothyroidism can develop
• Raised TSH and low T4 suggests primary hypothyroidism. The thyroid autoantibodies should be measured and if positive other autoimmune diseases should be excluded
• Low plasma TSH or T4 concentrations suggest hypothyroidism that is due to hypothalamic or pituitary dysfunction. A TRH test should be done and possibly pituitary function assessed
• Raised plasma TSH and raised or normal free T4 in the presence of hypothyroid symptoms indicated thyroid hormone resistance

 

Causes of hypothyroidism

• Primary
  • Iodine deficiency
  • Autoimmune thyroid disease;
    • Hashimoto’s disease
    • Subacute thyroiditis
    • Transient subacute thyroiditis
    • Multiple endocrine neoplasia (pluriglandular syndrome)
  • Following treatment of hyperthyroidism
    • Post-thyroidectomy
    • Post radio-iodine treatment
  • External irradiation to the neck
  • Surgery or trauma to the neck
  • Defects of thyroid hormone synthesis
  • Congenital absence of the thyroid gland
  • Infiltrative disease of the thyroid – sarcoid, haemochromatosis, fibrosis
  • Drugs; carbimazole, propylthiouracil, amiodarone, lithium, interferon α
• Secondary
  • Pituitary or hypothalamic disease
• Thyroid hormone resistance

 

Hyperthyroidism

 

• Causes sustained high plasma concentrations of T4 and T3
• There is often a generalised increase in metabolic rate as evidenced by heat intolerance, a fine tremor, tachycardia with AF, weight loss, tiredness, anxiety, sweating and diarrhoea

 

• The following biochemical changes can occur with hyperthyroidism
• Hypercalcaemia due to increased bone turnover
• Hypocholesterolaemia can occur due to increased LDL clearance
• Hypokalaemia can occur associated with hyperthyrotoxic periodic paralysis
• Plasma SHBG is increased
• Plasma creatine kinase may be increased with thyrotoxic myopathy

 

Causes of hyperthyroidism

• Autonomous secretion
  • Grave’s disease
  • Toxic multinodular goitre (Plummer’s disease) or a single functioning nodule
  • Subacute thyroiditis
  • Some metastatic thyroid carcinomas
• Excessive ingestion of thyroid hormones or iodine
  • Amiodarone
  • Thyrotoxicosis factitia (self-administration of thyroid hormones)
  • Administration of iodine to a subject with iodine-deficiency goitre
  • Jod-Basedow syndrome – hyperthyroidism caused by excessive intake of iodide
• Rare causes
  • TSH secretion by tumours, including pituitary tumours or those of trophoblastic origin
  • Struma ovarii (thyroid tissue in ovarian teratoma)
  • Excess hCG e.g. molar pregnancy or choriocarcinoma
  • Pituitary resistance to thyroid hormone

 

Graves’ disease

• Most common form of thyrotoxicosis – more common in females than males
• It is characterised by;
  • Exophthalmos
  • Pretibilal myxoedema
• It is an autoimmune disorder characterised by autoantibodies including anti-TPO and thyroid-stimulating immunoglobulin which can act as a TSH receptor agonist
• It is associated with other autoimmune diseases
• Nuclear medicine tests show a high radioactive uptake of iodine by the thyroid gland

 

Subacute thyroiditis

• Destructive thyroiditis resulting in the release of pre-formed thyroid hormones
• There are three subtypes;
  • Granulomatous (painful) - viral
  • Lymphocytic (silent) - autoimmune
  • Postpartum - autoimmune
• This condition is associated with extremely high levels of thyroid hormone and no radioactive iodine uptake by the thyroid gland
• The clinical course progresses through 6-8 weeks of thyrotoxicosis, 2-4 months of hypothyroidism and a return to euthyroidism in about 90% of patients

 

Toxic nodules

• Found more commonly in older age groups who may present with only limited symptoms e.g. cardiovascular symptoms
• May be detected by their uptake of radioactive iodine or technetium, with suppression of uptake of the rest of the thyroid tissue
• The secretion of TSH is suppressed by negative feedback

 

Treatment

• Various forms of treatment are available and selection depends upon the clinical presentation and the age of the patient;
• Î’-blockers such as propanolol which inhibit the peripheral conversion of T4 to T3 may be used initially
• Carbimazole inhibits the synthesis of T3 and T4
• Propylthiouracil also inhibits conversion of T4 to T3
• Often ‘block and replacement’ therapy is used – carbimazole blocks thyroid secretion and exogenous T4 maintains are replaces T4 concentrations *n.b. remember carbimazole has the side effect of inhibiting bone marrow function*
• Radioactive iodine can be used in resistant or relapsing cases
• Surgery is rarely indicated unless there is a large toxic goitre that is exerting pressure of drug therapy fails and radioactive iodine is contraindictated
• Thyroid function should be regularly checked as patients can become hypothyroid of relapse

 

Subclinical hyperthryoidism

• May occur with a low TSH but normal T4 and T3 concentrations
• May progress to full blown hyperthyroidism
• Can be associated with AF, decreased bone mineral density and other features of hyperthyroidism

 

Laboratory investigations of suspected hyperthyroidism

• A careful history (including drugs) should be taken and a full examination particularly looking for a goitre should be done. The plasma TSH, free T3 and free T4 should be measured
• Plasma free T3 and T4 will be high and TSH suppressed in clinically thyrotoxic patients
• In the face of a suppressed plasma TSH, a clearly elevated free T3 confirms the diagnosis of hyperthyroidism
• If the plasma free T4 is raised and the TSH is normal, this is suggestive of biochemical euthyroid hyperthyroxaemia
• Measurement of thyroid antibodies is useful particularly if the concentration TSI’s is raised which indicated Graves’ disease
• The rare TSH secreting pituitary tumours need pituitary assessment. Raised α-subunit concentrations are usually raised in such circumstances
• In difficult cases measure SHBG as it is lowered in hypothyroidism and raised in hyperthyroidism
• Radioiodine uptake studies can be used to determine some causes of hyperthyroidism
• The TRH test is sometimes useful in unclear cases

 

Euthyroid Goitre

• If plasma T4 concentrations fall, enlargement of the thyroid gland may be caused by TSH stimulation resulting in cellular hyperplasia
• Thyroxine synthesis may be impaired by drugs such as para-aminosalicyclic acid or possibly by partial deficiency of the enzymes involved in T4 synthesis
• Ultrasound scanning may be useful in the diagnosis of the goitre as can radiolabelled uptake studies

 

Sick Euthyroid

• Any severe illness may be associated with low plasma total or free T4 concentrations making interpretation  of thyroid function tests difficult
• Plasma TSH levels may be normal, slightly high or low
• The TSH response to TRH may also be impaired
• Free fatty acid levels may increase, this interferes with binding of thyroxine to TBG and therefore increases free T4
• There may be impaired conversion of T4 to T3 in the periphery
• Consequently the assessment of thyroid function is best deferred until the patient has recovered from their illness

 

Euthyroid hyperthyroxaemia

• This is defined as a condition where either the plasma total or free T4 concentration is abnormally raised without clinical evidence of thyroid disease
• These changes may be transient or persistent, with high, normal or low levels of T3
• Heterophilic antibodies to free T3 and/or T4 should be excluded as they interfere with some assays

 

Causes

• Physiological conditions resulting in raised plasma TGB concentration, for example pregnancy, concentrations of total T3 and T4 increase but there are usually normal levels of free T3 and T4

• TBG concentration is raised in newborns
• Hereditary causes;
  • Heriditary TGB excess is X-linked
  • Hereditary TBPA excess is X-linked
  • Familial dysalbuminaemia hyperthyroidism due to an abnormal form of albumin
• Drugs causing hyperthyroxaemia
  • Oestrogens raise TBG concentration as do 5-fluorouracil, heroin and methadone
  • Amiodarone blocks conversion of T4 to T3 resulting in an elevation of T4 and reverse T3 concentrations
  • Heparin, due to fatty acid release, inhibits free T4 binding to TBG
  • Propranolol inhibits extrathyroidal conversion of T4 to T3
• Some patients with certain illnesses for example hyperemesis gravidarum have low total and free T3 concentrations due to reduced peripheral conversion of T4 to T3 because 5-de-iodinase is inhhibted. This results in elevated levels of T4
• Some hepatic disorders such as acute hepatitis result in raised concentration of TBG and total and free T4
• In up to 10% of cases of acute psychosis, total and free T4 concentrations are raised. The mechanism is unclear but may be due to central activation of the hypothalamic-pituitary axis

 

Amiodarone and thyroid function

• Can evoke hypothyroidism as it inhibits the conversion of T4 to T3
• Also contains iodine so can evoke thyrotoxicosis by the Jod-Baselow phenomenon
• It may also elicit disruptive thyroiditis and thyrotoxicosis with raised Il-6 concentration
• It has a long half life (40-100 days) and thus takes a long time to clear from the body

 

Thyroid stimulating immunoglobulins

• There are two types of assay that measure antibodies which bind to the TSH receptor;
  • Those that measure the ability of the patients IgG to inhibit binding of TSH to soluablised TSH receptor
  • Bioassay measuring the ability of the patients IgG to stimulate cAMP in various tissues
• Problem with this is due to the fact that not all TSH receptor binding immunoglobulins are stimulatory. Some of the receptor binding antibodies are inhibitory and have been implicated in cases of Hashimoto thyroiditis.
• Assays that measure binding of TSH to solubilized receptor are often referred to as TRAb (thyroid receptor antibody), TBII (TSH-binding inhibitor immunoglobulin), or LATS (long-acting thyroid stimulator) assays. Assays that measure the ability of IgG to bind to TSH receptor on cells and stimulate adenylate cyclase production have generally been referred to as TSI (thyroid-stimulating immunoglobulin) assays
• The clinical utility of measuring TSI for the prediction of neonatal hyperthyroidism in the children of mothers with Graves’ disease has been well documented.
• This syndrome is caused by the transfer of maternal IgG across the placenta resulting in transient fetal hyperthyroidism.
• Generally, the titers of thyroid autoantibodies tend to drop during pregnancy, due to the presence of immunosuppressive trophoblastic factors; however, persistent elevation of TSI titers, especially during the third trimester, is associated with increased risk of neonatal hyperthyroidism.
• This form of hyperthyroidism tends to correct itself within 4 months of life. Measurement of TSI in the mother or the child can also be useful in distinguishing this transient autoimmune form of neonatal hyperthyroidism from other nonimmune forms of congenital hyperthyroidism.

 

Thyroglobulin as a tumour marker

• Produced by thyroid cancers particularly papillary and follicular cancers
• Used to determine effectiveness of treatment and reoccurrence

 

Thyroid gland in pregnancy

• Thyroid gland may enlarge by 50% during pregnancy as a result of increased thyrotrophin production
• But only total thyroxine levels increase, levels of free thyroid hormone don’t increase due to increased protein binding

 

Hyperthyroidism during pregnancy

• Rare due to the immunotolerant state characterised by pregnancy
• Treatment is tricky, underdosing with carbimazole may result in an increased incidence of miscarriage and premature labour. overdosing may result in excessive neonatal transplacental passage of antithyroid drug producing neonatal goitre and hypothyroidism
• The cannot be corrected by concurrent thyroxine administration since these hormones have only a limited ability to cross the placenta
• May be preferable to use propylthiouracil instead of carbimazole as it is less likely to cross the placenta or be excreted into the breast milk

 

Neonatal hyperthyroidism

• Due to transplacental passage of thyroid stimulating immunoglobulin
• May be seen in babies of Grave’s disease women, even if they appear to be in remission, as levels of this Ig can still be raised
• Condition is transient as subsides completely after 4-6 weeks without therapy

 

Postpartum thyroid dysfunction

• Affects around 6% of all women during the postpartum period
• Occurs in women who enter pregnancy with positive TPO levels
• There is a hyperthyroid state approximately 3 months postpartum and a hypothyroid state 4-6months postpartum
• Due to a reversal of the immunotolerant state of pregnancy
• As the hyperthyroid state is due to release of preformed hormone, it is treated by β-blockers
• Syndrome will reappear is subsequent pregnancies
• There may be later development of hypothyroidism in 30-50% of cases

 

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