Thyroid hormone deficiency may affect almost all body functions. The degree of severity ranges from mild and unrecognized states to striking myxedema. Hypothyroidism may be due to primary disease of the thyroid gland itself or lack of pituitary TSH. Florid hypothyroidism, i.e, myxedema and cretinism, is readily recognized on clinical grounds alone, but mild hypothyroidism often escapes detection without screening(i.e. serum TSH). Maternal hypothyroidism during pregnancy results in offspring with IQ scores that are an average 7 points lower than those of euthyroid mothers.

Goiter maybe noted when hypothyroidism is due to hashimoto’s thyroiditis, iodine deficiency, genetic thyroid enzyme defects, drug goitrogens (lithium, iodide, propylthiouracil or methimazole, phenylbutazone, sulfonamides, amiodarone, interferon-a, interferon-b, interleukin -2)food goitrogens in iodide-deficient areas(turnips, casava etc..), or, rarely, peripheral resistance to thyroid hormone or infiltrating diseases. A hypothyroid phase occurs in subacute(de Quervain’s) viral thyroiditis following initial hyperthyroidism.

Goiter is usually absent when hypothyroidism is due to deficient pituitary TSH  secretion, or destruction of the gland by surgery, external radiation.

Clinical findings

Most symptoms of Hypothroidism are non specific and develop gradually.They include cold intolerance, fatigue, somnolence, poor memory, constipation, menorrahagia, myalgias and hoarseness. Signs include slow tendon-reflex relaxation, bradycardia, facial and periorbital edema, dry skin, and nonpitting edema (myxedema). Mild weight gain may occur, but hypothyroidism does not cause marked obesity. Rare manifestations include hypoventilation, pericardial or pleural effusions, deafness and carpal tunnel syndrome.

Laboratory findings may include hyponatremia and elevated plasma levels of cholesterol, triglycerides and creatine kinase. The ECG may show low voltage and T-wave abnormalities.

Some clinically euthyroid patients have mildly elevated levels of serum TSH (5-10 milliinterntional units/L) without any other manifestations of hypothyroidism; serum FT4 levels are normal. Such patients are said to have “subclinical hypothyroidism”.

Diagnosis

Hypothyroidism is readily treatable an should be suspected in any patient with compatible symptoms, especially in the presense of a diffuse goiter or a history of RAI therapy or thyroid surgery.

1. In suspected primary Hypothyroidism, plasma TSH is the best initial diagnostic test, A normal value excludes primary hypothyroidism, and a markedly elevated value (> 20 mU/ml) confirms the diagnosis. Mild elevation of plasma TSH (<20mU/ml) maybe due to nonthyroidal illness but usually indicates mild (or subclinical) primary hypothyroidism, in which thyroid function is impaired but increased secretion of TSH maintain plasma free T₄ levels within the reference range. These patients may have nonspecific symptoms that are compatible with Hypothyroidism and a mild increase in serum cholesterol and low density lipoprotein (LDL) cholesterol. They develop more severe hypothyroidism at a rate of 2.5% per year.
2. If secondary hypothyroidism is suspected because of evidence of pituitary disease, plasma free T₄ should be measured. Plasma TSH levels are usually within the reference range in secondary Hypothyroidism and cannot be used alone to make this diagnosis. Patients with secondary hypothyroidism should be evaluated for other pituitary hormone deficits and for a mass lesion of the pituitary or hypothalamus.
3. In severe nonthyroidal illness, the diagnosis of hypothyroidism maybe difficult(Endocrinal Med Clin North Am 31:1159-1172, 2002). Plasma total T₄ and free T₄ measured by routine assays may be low.
   • Plasma TSH is the best initial diagnosis test. A normal TSH value is strong evidence that the patient is euthyroid, except when there is evidence of pituitary or hypothalamic disease or in patients treated with dopamine or high doses of glucocorticoids. Marked elevation of plasma TSH (>20 mU/ml) establishes the diagnosis of primary hypohyroidism.
   • Moderate elevation of plasma TSH (<20 mU/ml) may occur in euthyroid patients with nonthyroidal illness and are not specific for hypothyroidism. Plasma free T4 by analog immunoassay should be measured if TSH is moderately elevated, or if secondary hypothyroidism is suspected, and patients should be treated for hypothyroidism if plasma free T4is low. Thyroid function in these patients should be re-evaluated after recovery from illness.

Therapy/ Treatment

Please note that what we are detailing here is generic treatment, if diagnosed with this condition, CONSULT A DOCTOR and with LABORATORY REPORTS. You can mail us your reports and our doctors can advise you  but do consult your current doctor.

Now, continuing with the article, we would discuss the treatment. Levothyroxine is the drug of choice. The usual replacement dose is 100-125 mg PO qd, and most patients require doses between 75 and 100  mg qd. In elderly patients, the average replacement dose is somewhat lower. The need for lifelong treatment should be emphasized. T₄ should be taken 30 minutes before a meal, because dietary fibre may interfere with its absorption, and should not be taken with medications that effect its absorption.

Initiation of therapy: Young, otherwise healthy adults should be started on 100 mg qd. This regimen gradually corrects  hypothyroidism, as several weeks are required to reach steady-state plasma levels of T₄. In otherwise healthy elderly patients, the initial dose should be 50 mg qd. Patients with cardiac disease should be started on 25-50 mg qd and monitored carefully for exacerbation of cardiac symptoms.

Dose Adjustment and follow up

• In primary hypothyroidism, the goal of therapy is to maintain plasma TSH within the Normal range. Plasma TSH should be measured 2-3 months after initiation of therapy. The dose of T₄then should be adjusted in 12 to 25 mg increments at intervals of 6-8 weeks until plasma TSH is normal. Thereafter, annual TSH measurement is adequate to monitor therapy and to ensure compliance. TSH should also be measured in the first trimester of pregnancy, because the T₄ dose requirement increases at this time. Overtreatment, indicated by a subnormal RSH. Should be avoided because it increases the risk of osteoporosis and atrial fibrillation.
• In secondary hypothroidism, plasma RSH cannot be used to adjust therapy. The goal of therapy is to maintain the plasma free T₄ near the middle of the reference range. The dose T₄ should be adjusted at 6-8 week intervals until this goal is achieved. Thereafter, annual measurement of plasma free t4 is adequate to monitor therapy.
• Coronary artery disease may be exacerbated by treatment of hypothyroidism. The dose of T₄ should be increased slowly in patients with coronary artery disease, with careful attention to worsening angina, heart failure, or arrhythmias.

 Situations in which T₄ dose requirements change. Difficulty in controlling hypothyroidism is most often due to poor compliance with therapy. observed therapy may be necessary in some cases. Other causes of increasing T₄ requirements include

• malabsorption due to intestinal disease or drugs that interfere with T₄ absorption (e.g. calcium carbonate, ferrous sulphate, cholestyramine, sucrafate, aluminium hydroxide);
• drug interactions that increase T₄ clearance (e.g:- estrogen, rifampin, carbamazepine, phenytoin) or block conversion of T₄ to T₃ (amiodarone);
• pregnancy, in which T₄ requirement increases in the first trimester; and
• gradual failure of remaining endogenous thyroid function after RAI treatment of hyperthyroidism.

Mild (or subclinical) hypothyroidism should be treated with T₄ if any of the following are present

• lnonspecific symptoms compatible with hypothyroidism,
• a goiter,
• hypercholesterolemia that warrants treatment, or
• a plasma TSH that is greater than 10 mU/ml.

untreated patients should be monitored annually, and t4 should be started if symptoms develop or serum TSH  increases to greater than 10mU/ml

Urgent Therapy is rarely necessary for hyperthyroidism. Most patients with hypothyroidism and concomitant illness can be treated in the usual manner. However, hypothyroidism may impair survival in critical illness by contributing to hypoventiltion, hypotension, hyperthermia, bradycardia, or hyponatremia. Little evidence supports the contention that severe hypothyroidism alone causes coma or shock; most reports of alleged “myxedema coma” predate recognition that nonthyroidal illness itself lowers thyroid hormone levels.

References

“Current Medical Diagnosis & Treatment”, 45th edition