Indian Write-Ups
| Diagnosis | |
| Hypothyroidism - Padma S Menon Professor & Head, Endocrinology, SGS Medical College & KEM Hospital, Mumbai Source: Indian Journal Of Clinical Practice, Vol. 10, No. 7 |
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| Subclinical Hypothyroidism The combination of elevated serum thyrotropin and normal serum thyroxine is called compensated or subclinical hypothyroidism. Controversy exists regarding treatment of this condition. It is commonly seen in AITD. Females with TSH more than 10m U/L and/or positive thyroid microsomal antibodies and males regardless of antibody status are considered high risk for developing over hypothyroidism10. Secondary (Central) Hypothyroidism Central hypothyroidism results due to pituitary disorders including tumor and Sheehan’s Syndrome. This is generally associated with other hormonal deficiencies. Symptoms of tumor: like headache and visual disturbance may be the reason to seek medical advice. It has also been noticed that as age advances, the dose requirement may come down. Hence regular monitoring is required. It is not advisable to withhold therapy in elderly for fear of side effects, as quality of life improves with correction of even mild hypothyroidism. Clinical features are generally similar to those of primary hypothyroidism but are less pronounced. Major differences are: skin is pale and cool (but not coarse and dry). There is no change in voice; the blood pressure is low. The heart is small. There is no weight gain. Hypoglycemia can occur due to deficiency of both thyroid and adrenal hormones. Occasionally, hypopituitarism presenting with only thyroid axis involvement can present very similar primary disease. Laboratory Investigation of Hypothyroidism Primary The only test required for confirming the diagnosis of overt primary hypothyrodism is TSH by IRMA/ICMA, when classical clinical features are present. This is associated with low FT4 and low FT3. Laboratory investigations are dependent upon the stage of thyroid failure. The first suggestion of failing thyroid is shown by elevated TSH with normal total and free T4 and T3 (subclinical hypothyroidism). At this stage, the thyroid hormones are maintained by TSH drive. The hyperplasia of the still functioning cells maintains normal hormonal levels (hence called compensated). As the thyroid damage worsens, the TT4/FT4 starts declining. At this stage FT3/TT3 may still continue to be normal (increased T4 to T3 conversion mediated by TSH). However the complete damage of thyroid follicular cells finally results in low T4 low T3 and high TSH. By this time, the clinical features of hypothyroidism are usually classical. Other laboratory parameters show a hypochromic anemia and hypercholestrolemia. ECG shows bradycardia and low voltage. Echocardiography shows cardiac enlargement with/without pericardial effusion. Secondary Low TT4/FT4, low TT3/FT3 and normal or low TSH characterizes this. Other pituitary hormonal evaluation shows partial or panhypopituitarism. CT scan/MRI needs to be done to demonstrate the pituitary lesion. There is no hypercholestrolemia. The heart is usually small; there is no pericardial effusion. Differential Diagnosis It is not unusual for a hypothyroid patient to see a nephrologist first with suspected nephritic syndrome due to anasarca and vice versa. Normal TSH, TT4 and abnormal renal function tests including proteinurea, in nephritic syndrome can easily distinguish this. Ruling out hypothyroidism sometimes may be required in severely ill patients. The FT4 may be on the lower normal range. TSH is high in primary hypothyroidism, but normal or low in illness. However, a pituitary disease is difficult to rule out and may require further investigations (Other pituitary axis evaluation and CT scan) if suspected. In very young and very old, it is necessary to do thyroid function whenever suspected, as it is easily treatable disorder and clinical features may not always be classical. Management Thyroid hormone replacement should be instituted as soon as the diagnosis is established. The usual dose varies from 50 to 200 g/day. It is essential to treat with smallest dose that is required to have a normal TSH to avoid adverse effects of therapy on the bone and heart. Many (80 percent) of our patients required only 100 g/day. The TSH returns to normal 8 to 12 weeks and hence ideal time to monitor after initiation of therapy is three months. The commonest cause of poor response to treatment is noncompliance and this has to be kept in mind before increasing the dose of thyroxine. Proper education of patients and relatives regarding life long therapy is essential to ensure compliance. It has also been noticed that as age advances, the dose requirement may come down. Hence regular monitoring is required. It is not advisable to withhold therapy in elderly for fear of side effects, as quality of life improves with correction of even mild hypothyroidism. Post surgical or radioactive ablation induced hypothyroidism requires higher dose as compared to Graves’ treated with medical therapy. In the elderly, the therapy should be started with very small doses of thyroxine and can be as low as 0.025 g/day, with very gradual increases of 0.025 g/day every 15 or 30 days. The TSH should be maintained, nearer the higher normal values. If there is associated cardiac disease, the starting dose should be extremely low (0.0125 g/day) with increases of 0.0125 g/day, once a month. References |
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