HYPOTHYROIDISM by Svetlana Shifrin-Douglas, MD (Endocrinologist in Red Bank, NJ www.endocrinologynj.com)

Hypothyroidism may be either subclinical or overt (symptomatic). Subclinical hypothyroidism is characterized by a serum TSH above the upper reference limit in combination with a normal free thyroxine (T4). An elevated TSH, usually above 10 mIU/L, in combination with a subnormal free T4 characterizes overt hypothyroidism. The prevalence of subclinical disease was 4.3% and of overt disease was 0.3%. Studies have shown that 5.9% of women and 2.3% of men over the age of 60 years have TSH values over 10 mIU/L, 39% of whom had subnormal T4 levels. The incidence of hypothyroidism in women was 3.5 per 1000 per year and in men it was 0.6 per 1000 per year.


Environmental iodine deficiency is the most common cause of hypothyroidism on a worldwide basis. In areas of iodine sufficiency, such as the United States, the most common cause of hypothyroidism is chronic autoimmune thyroiditis (Hashimoto’s thyroiditis). Hashimoto’s thyroiditis is 5–10 times more common in women than in men. Besides Hashimoto’s thyroiditis, autoimmune thyroid diseases (AITDs), include chronic autoimmune thyroiditis. Hypothyroidism may occur as a result of radioiodine or surgical treatment for hyperthyroidism, thyroid cancer, or benign nodular thyroid disease and after external beam radiation for non–thyroid-related head and neck malignancies, including lymphoma.

Central hypothyroidism occurs when there is insufficient production of bioactive TSH due to pituitary or hypothalamic tumors (including craniopharyngiomas), inflammatory (lymphocytic or granulomatous hypophysitis) or infiltrative diseases, hemorrhagic necrosis (Sheehan’s syndrome), or surgical and radiation treatment for pituitary or hypothalamic disease. In central hypothyroidism, serum TSH may be mildly elevated, but assessment of serum free T4 is usually low, differentiating it from subclinical primary hypothyroidism.


Besides clinical symptoms and blood tests for thyroid function (TSH, T3, T4 levels), determining the presence of elevated anti-thyroid antibody titers which include anti-thyroglobulin antibodies (TgAb), anti–microsomal/thyroid peroxidase antibodies (TPOAb), and TSH receptor antibodies (TSHRAb) is performed.

It is important to notice that many patients with chronic autoimmune thyroiditis are biochemically euthyroid. However, approximately 75% have elevated anti-thyroid antibody titers.


Dry skin, cold sensitivity, fatigue, muscle cramps, voice changes, and constipation are among the most common. Less commonly appreciated and typically associated with severe hypothyroidism are carpal tunnel syndrome, sleep apnea, pituitary hyperplasia that can occur with or without hyperprolactinemia and galactorrhea, and hyponatremia that can occur within several weeks of the onset of profound hypothyroidism.


There is general agreement that patients with primary hypothyroidism with TSH levels above 10 mIU/L should be treated. Treratment of patients with TSH levels of 4.5–10 mIU/L may benefit depending on specific patient symptoms and comorbidities and can be determine by thier physician


Treatment of hypothyroidism is best accomplished using synthetic L-thyroxine sodium (Synthroid, Thyroxine). Absorbtion of levothyroixine could depend on gastric acid secretion. The liquicap preparation (Tirosint) is the least affected by changes in pH. medication should be taken in the morning and on empty stomach - 60 minutes before breakfast on an empty stomach. It should not be taken with substances or other medications because that will interfere with its absorption and metabolism.

Dose adjustments are guided by serum TSH determinations in 4–8 weeks following initiation of therapy.

Once an adequate replacement dosage has been determined, a periodic follow-up evaluations with repeat TSH testing at 6-month and then 12-month intervals are appropriate.


Although most physicians can diagnose and treat hypothyroidism, consultation with an endocrinologist is recommended
in the following situations:

Children and infants

Patients in whom it is difficult to render and maintain a euthyroid state


Women planning conception

Cardiac disease

Presence of goiter, nodule, or other structural changes in the thyroid gland

Presence of other endocrine disease such as adrenal and pituitary disorders

Unusual constellation of thyroid function test results

Unusual causes of hypothyroidism as those induced by agents


Overt untreated hypothyroidism during pregnancy may adversely affect maternal and fetal outcomes. These adverse outcomes include increased incidences of spontaneous miscarriage, preterm delivery, preeclampsia, maternal hypertension, postpartum hemorrhage, low
birth weight and stillbirth, and impaired intellectual and psychomotor development of the fetus.

Women with positive TPO Antibodies may have an increased riskfor first trimester miscarriage, preterm delivery, and for offspring with impaired cognitive development.

Treatment with L-thyroxine before conception has been shown to reduce the miscarriage rate and to increase live birth rate in women with subclinical hypothyroidism undergoing assisted reproduction.

When a woman with hypothyroidism becomes pregnant, the dosage of L-thyroxine should be increased as soon as possible to ensure that serum TSH is 2.5 mIU/L, L-thyroxine treatment should be initiated. Serum TSH and total T4 measurements should be monitored every 4 weeks during the first half of pregnancy and at least once between 26 and 32 weeks gestation to ensure that the requirement for L-thyroxine has not changed. Some of us would continue to monitor thyroid indices after 32 weeks in order to confirm that thyroid indices are in the normal range. L-thyroxine dosages should be adjusted as indicated, aiming for TSH levels that are within the normal range for that phase of pregnancy.


Some patients with infertility and menstrual irregularities have underlying chronic thyroiditis in conjunction with subclinical or overt hypothyroidism. Expert endocrinologist can determine which patient will benefit from thyroid hormone replacement therapy. Thyroid hormone replacement therapy may normalize the menstrual cycle and restore normal fertility may normalize the menstrual cycle and restore normal fertility.


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