Dr. Geetha Philips MD, Dr. C.A. Latheef, Dr. N.N. Asokan, Dr. T.L.P. Prabhu, Dr. Anita Nambiar


Hypothyroidism results from reduced thyroid hormone actions at the

peripheral tissues. This reduction in thyroid hormone action is, in the

vast majority of cases, secondary to reduced thyroid hormone

synthesis and secretion by the thyroid gland. Occasionally, peripheral resistance to thyroid hormone is the culprit. The availability of sensitive biochemical tests and effective therapies has simplified the diagnosis and

management of this endocrine condition. Hypothyroidism may be transient or permanent, central, or primary. Central hypothyroidism can accompany disorders of the hypothalamic - pituitary axis, leading to reduced TSH secretion or reduced biological activity of TSH. Primary hypothyroidism refers to a defect in the thyroid gland resulting in reduced synthesis and secretion of thyroid hormones. Primary hypothyroidism

is responsible for the majority of hypothyroid cases. Chronic

autoimmune(Hashimoto’s) thyroiditis is the leading cause of primary hypothyroidism. Children and infants can present with hypothyroidism due to thyroid gland agenesis and dysenesis and defects in thyroid

hormone biosynthesis. Treatment of thyrotoxic women during pregnancy with antithyroid drug can result in hypothyroidism in the neonate. Subclinical hypothyroidism is the term used to define a state in which serum T4 and T3 levels are within normal limits, but there is underlying mild thyroid failure, as evidenced by a mild increase in serum TSH. Chronic autoimmune thyroiditis is the leading cause. Several epidemiologic studies have implicated subclinical hypothyroidism as a cardiovascular risk factor. The scope of thyroid hormone deficiency encompasses the different body systems and organs. The clinical presentation of a patient

who has hypothyroidism depends on the severity of the condition. Overt hypothyroidism is seen in about 1% of pregnant women . Subclinical hypothyroidism

is seen in another 2.5%. Most cases of hypothyroidism during pregnancy have the same etiology as in hypothyroidism in general. Women who have underlying thyroid disorders are more susceptible to becoming hypothyroid during pregnancy. Maternal

hypothyroidism, overt and subclinical, during pregnancy is associated with a number of complications including, spontaneous abortion, pre-eclampsia, miscarriage, still birth, preterm delivery and postpartum hemorrhage. Normal thyroid function in the

mother is neuropsychointellectual function. We meassure TSH, free T4 (FT4) and total T3 (TT3) in patients who are suspected of having thyroid dysfunction. In addition, we may order thyroid peroxidase (TPO) and thyroglobulin antibodies in a

subset of patients. Contrary to the situation in hyperthyroidism, radionuclide studies of the thyroid have much less of a role in hypothyroidism. In addition to its role in evaluating goiters and thyroid nodules, thyroid sonography can disclose the typical

heterogeneous parenchymal echogenicity that characterises Hashimoto’s thyroiditis. Patients who have primary hypothyroidism have elevated TSH and low FT4 and TT3. TPO antibodies are detectable in many patients who have Hashimoto’s thyroiditis. A repeatedly elevated TSH, between 4 and 15 mIU/mL, with normal

FT4 and TT3 is suggestive of subclinical hypothyroidism. This is a good indication for obtaining TPO antibbodies. Hypothyroidism can cause considerable morbidity. The treatment of hypothyroidism is, in principle, simple. Synthetic thyroxine is the preferred form of thyroid hormone replacement therapy. Hypothyroidism in the majority of patients is permanent and should be treated lifelong.