Autonomous thyroid nodules. I. A clinical classification and the use of a diagnostic index.
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Biomedical subjects
Publications and source records attributed to G A Medeiros-Neto.
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Three consecutive cases of myxedema coma treated successfully with either nasogastric or intravenous route of administration of I-triiodothyronine, followed by oral thyroxine, are described. All were hypothermic, had biochemical evidence of advanced hypothyroidism (T4 less than 1.0 micrograms/dl, T3 less than 20 ng/dl and TSH greater than 150 microU/ml), severe hypoxemia, respiratory acidosis, hypercarbia and temporary depression of respiratory center responsiveness. In only one patient it was found significant hyponatremia (Na = 127 mEq/l). Two patients were successfully treated with the nasogastric route of administration of T3 (12.5 micrograms/6h) but in a female patient with intestinal atony (ileus) there was no absorption of the orally administered T3. Intravenously administered T3 promptly corrected the hypometabolic state in this patient. It was confirmed that T4 therapy, although promptly correcting low serum T4 concentration, failed to rise serum T3 levels due to lack of peripheral T4 5'-monodeiodination to T3 in these critically ill patients.
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Thyroid hormones exert potent effects in bone as evidenced by bone loss which accompany untreated thyrotoxicosis. Conventional thyroxine replacement therapy may be associated with some degree of biochemical or tissue hyperthyroidism, increasing the risk for late onset osteoporosis. This has led to recommendations for reductions in L-T4 dosages. More recently, however, other reports have indicated that L-T4 therapy does not have adverse effects on bone mass. The overall analysis of both past and recent published reports has indicated that the evidence that conventional thyroxine therapy has adverse effects on bone mass is hard to ignore, although the magnitude of these effects is likely to be relatively small and closely related to estrogen deficiency.