Thyroid Disease

Last updated On August 2nd, 2020

Thyroid physiology

• Circulating thyroxine (levothyroxine, T4) and l-triiodothyronine (T3) are bound primarily to thyroxine-binding globulin (TBG) with <1% circulating as free (biologically active) hormone.
• Iodine is required for thyroid hormone production and fetal thyroid function is dependent on iodine from the mother.
• Non-thyroid medical illnesses and select drugs can affect thyroid function.

Thyroid function during pregnancy

• Estrogen has two effects on thyroid function in pregnancy:
1 It increases circulating TBG concentrations resulting in elevated levels of total T4 and T3
2 It increases TBG sialylation which reduces hepatic clearance ofT4 and T3. Despite these changes, circulating levels of free T4 and T3 remain unchanged.
• Less than 0.1% of the thyroid hormone crosses the placenta. As such, tests of fetal thyroid function (although rarely, if ever, indicated) are reliable and independent of maternal thyroid status.
• Thyroid hormone can be measured in fetal blood as early as 12 weeks’ gestation.

Maternal hyperthyroidism (thyrotoxicosis)

Incidence:

This is 0.05–0.2% of pregnancies.

Diagnosis:

A definitive diagnosis requires thyroid function testing.

Etiology

• Graves disease is the most common cause of maternal hyperthyroidism in pregnancy (95%). It results from the presence of circulating thyroid-stimulating antibodies. Eye signs (ophthalmopathy) are specific to Graves’s disease. As IgG antibodies cross the placenta, the fetus is at risk of thyroid dysfunction.
• Toxic multinodular goiter is characterized by hyperthyroidism and the presence of a large, palpable thyroid gland.
• Hyperemesis gravidarum is often associated with elevated human chorionic gonadotropin (hCG) levels; 50–70% of women will have biochemical studies suggestive of hyperthyroidism, but no symptoms or signs.
• Hyperthyroidism in the setting of gestational trophoblastic neoplasia is probably secondary to elevated levels of hCG.
• Metastatic follicular cell carcinoma of the thyroid (rare).
• Exogenous T3 or T3.
• De Quervain thyroiditis (rare) is acute and painful.

Complications

• Maternal complications.

Infertility, recurrent pregnancy loss, cardiac failure (10–20%), thyroid storm (<0.1%).

• Fetal complications.

Preterm delivery, intrauterine growth restriction (IUGR), increased perinatal mortality.

Management

• The goal during pregnancy is to control thyrotoxicosis while avoiding fetal and/or transient neonatal hypothyroidism.
• Antithyroid drugs are the treatment of choice during pregnancy. Propylthiouracil (PTU) is preferred because it blocks the release of hormone from the thyroid gland and – unlike carbimazole – also blocks peripheral conversion of T4 to T3. Carbimazole has also been associated with a rare congenital abnormality (aplasia cutis congenita). PTU treatment is initiated at 100–150 mg three times daily, but it takes 3–4 weeks before a clinical response is seen. Thyroid-stimulating hormone (TSH) levels should be checked every 4–6 weeks and treatment adjusted accordingly.
• Radioactive iodine to ablate the thyroid gland is absolutely contraindicated in pregnancy.
• Surgery is best avoided during pregnancy but, if indicated for failed medical therapy, is best performed in the second trimester.
• Regular fetal testing is recommended after 32 weeks to look for evidence of fetal thyroid dysfunction. Fetal tachycardia (>160 beats/min) is a sensitive index of fetal hyperthyroidism.

Maternal hypothyroidism

Incidence:

This is 0.6% of all pregnancies.

Diagnosis

Hyperthyroidism symptoms

1. Hair is soft and silky, loss of hair
2.Proximal myopathy
3.Warm skin, diaphoresis (sweating)
4.Normocytic anemia, mild neutropenia,
5.hypercalcemia,hypomagnesemia,
6.elevated liver function
7.tests, ± thyroidstimulating antibodies
8.Tremulousness, fine tremor
9.Pretibial myxedema
10.Emotional lability, anxiety, fatigue, heat intolerance
11.Ophthalmopathy (specific to Graves disease)
12.Goiter ± bruit,+ dysphagia
13.Tachycardia,palpitations,cardiac failure,arrhythmia
14.Weight loss, diarrhoea
15.Amenorrhea, oligomenorrhea,
16.Frequent urination

Hypothyroidism symptoms

1.Psychosis (‘myxedema madness’), coma, cold intolerance, intellectual limitation
2.Hair loss, coarse features (periorbital puffiness, expressionless face, large tongue)
3.Hoarse voice
4.Thyromegaly
5.Menorrhagia,
6.Infertility
7. General lethargy, decreased exercise capacity, muscle cramps
8.Pale, cool, thin, dry skin
9. Anemia, Increased LDH, Increased cholesterol, Increased CPK, ± antithyroid antibodies
10. Brittle nails
11. Cardiomegaly, pericardial effusion, cardiomyopathy
12. Modest weight, gain, constipation
13. Delayed tendon reflexes (slow relaxation phase)
• Thyroid function testing is required for a definitive diagnosis.
• Subclinical maternal hypothyroidism during pregnancy may be associated with long-term cognitive deficits in the offspring. However, routine TSH screening of all pregnant women is not as yet recommended.

Etiology

• Hashimoto thyroiditis (chronic lymphocytic thyroiditis) is characterized by hypothyroidism, a firm goiter, and the presence of circulating anti-thyroglobulin or anti-microsomal antibodies. In women with existing Hashimoto disease, pregnancy may result in a transient improvement of symptoms.
• Women previously treated for hyperthyroidism may manifest with hypothyroidism and require thyroid hormone replacement.
• Infectious (suppurative) thyroiditis is characterized by fever and a painful, swollen thyroid gland.
• Subacute thyroiditis is similar to suppurative thyroiditis with a painful, swollen thyroid with or without fever. It is usually the result of a viral infection, and is self-limiting.
• Iodine deficiency (rare).

Management

• Early diagnosis is essential to avoid antepartum complications (placental abruption, IUGR, stillbirth) and impaired neonatal and childhood development (cretinism).
• Levothyroxine (thyroxine) treatment should be initiated at 100–150 μg daily. TSH levels should be measured every 4–6 weeks, and the dose adjusted accordingly.
• Women on thyroxine before conception should have their TSH levels monitored every 4–6 weeks. Most women will need to increase their dose by 30–50% during pregnancy.

Postpartum Thyroiditis

• Incidence.

Four to ten percent of all postpartum women.

• Etiology.

Unknown, but maybe an autoimmune phenomenon.

• Clinical features.

characterized by a transient hyperthyroid state occurring 2–3 months postpartum (with dizziness, fatigue, weight loss, palpitations) or a transient hypothyroid state 4–8 months postpartum (with fatigue, weight gain, and depression).

• Treatment.

Therapy may be indicated to control symptoms, and can
usually be tapered within 1 year.