Indian Write-Ups

Primary Hypothyroidism

Primary (Thyroprivic): The disease called is “Primary” when direct involvement of thyroid causing destruction or damage causes hypothyroidism. Autoimmune thyroid disease (AITD), surgical or radioactive ablation of the gland, hereditary defects in hormone synthesis and drugs are causes that result in hypothyroidism, out of which AITD is the commonest. Goiter may be present during the early phase of autoimmunity, but the gland is usually atrophic at presentation.

Commonest cause of primary hypothyroidism in childhood to adulthood is AITD. Genetic predisposition to autoimmune disease is described. Activation of immune process takes place as in other autoimmune endocrine disorders. Both transient and permanent hypothyroidism can result. The different terminologies used to describe autoimmune hypothyroidism are Goitrous (Hashimoto’s) thyroiditis, lymphocytic thyroditis, Chronic fibrous thyroiditis and atropic autoimmune thyroiditis.

Autoimmune damage to functioning cells result in atrophy and hypothyroidism. Other factors that may have a role to play in autoimmunity are dietary iodide, drugs (amiodarone, contrast media), environmental pollution and stress. Association with other autoimmune disorders like IDDM, adrenal insufficiency, premature ovarian failure, rheumatoid arthritis and chronic active hepatitis are well described.

Postoperative hypothyroidism results from subtotal/total thyroidectomy for thyrotoxicosis or malignancy respectively. It is less frequent than post radioactive ablation and the incidence increases with duration of follow up. Almost all patients treated with radioactive iodine ablation develop hypothyroidism over a period of 10 to 15 years.

Postpartum thyroiditis and painless thyroiditis are variants of autoimmune thyroid disease. The immune reaction rapidly develops. Follicular cells are not destroyed, only damaged. An initial phase of thyrotoxicosis is followed by transient hypothyroidism lasting from two to eight weeks. Very often symptoms are too mild and the condition may go unrecognized. The hypothyroidism itself is because of the non-functioning of follicular cells damaged by the immune process. As soon as the cells recover, the function is regained and hypothyroidism remits.

Drugs: Amiodarone2 and lithium3 are known to produce hypothyroidism in adults. Amiodarone has iodine in the molecular structure & this can either produce an iodine induced hypothyroidism or can precipitate autoimmune process in susceptible individuals. The condition is usually self limiting and recovery occurs after stopping the drug. Rarely there is permanent hypothyroidism. Lithium causes hypothyroidism by inhibiting the transport of iodide by the thyroid and may also induce chronic autoimmune thyroiditis.

Thyroid hormones are necessary for normal functioning of each and every cell in the body and hence in the initial stages, patients have vague symptoms of general weakness, increased fatigue and lassitude. Very often they are attributed to increasing age, excessive work or even stresses and strains of life. Generally, the physical appearance at presentation will depend on the duration and severity of disease.

Hypothyroidism can be goitrous as in Iodine induced and synthetic defects or agoitrous as in autoimmune involvement.

There is a gradual onset of symptoms due to gradually progressive thyroid damage. Following the initial symptoms of weakness, fatigue, lassitude, weight gain and constipation, further symptoms develop. There is puffiness of face and intolerance to cold. The skin is scaly, pale, cool to touch; hair is coarse, dry, brittle and hair loss over lateral aspect of eyebrow is considered a classical (though late) clinical feature. There is bradycardia and decreased exercise tolerance. The cold skin and pallor are due to poor peripheral circulation resulting from increased peripheral vascular resistance. Nearly 10 to 20 percent of patients are hypertensive3 at presentation. Long standing hypothyroidism may cause pericardial effusion 5,6 rarely leading to cardiac tamponade.

Hoarseness of voice is another common complaint and is due to thickening of vocal cords resulting from deposition of hyaluronic acid as in the dermis. The tendon reflexes are delayed. Prolonged hypothyroidism can result in carpal tunnel syndrome and peripheral neuropathy. Rarely there is pseudohypertrophy of calf muscles and cerebellar ataxia.

Mental changes can sometimes be the presenting feature. There is slowness in speech and motor activities and there is decreased mutation. There is no interest in day to day activities and this is seen as laziness. Occasionally, severe depression or frank schizophrenia may lead to patient being seen in the psychiatric department. By this time other clinical features of hypothyroidism are usually present.

Females of reproductive age can present with irregular menstrual cycles (anovulatory) and infertility. Hence pregnancy is unlikely. If pregnancy does occur, there is increased risk of intrauterine fetal death, gestational hypertension and poor perinatal outcome7. Whether maternal hypothyroidism can result in fetal malformation and psycho-neurological changes is not clear. Rarely females can present with galactorhhoea due to long-standing hypothyroidism. This results from TRH induced stimulation of prolactin.

The clinical features are less classical in the elderly as compared to adults. Fatigue, weakness, cold intolerance, dry skin, constipation, mental deterioration and congestive cardiac failure gets attributed to aging or other pre-existing disorders8. Nearly 10 to 15 percent of elderly screened has been found to be hypothyroid and most have a positive antibody titer9,10.

Very rarely, myxoedema coma may be the first presentation.