Primary hypothyroidism in an adult patient with protein-calorie malnutrition: A study of its mechanism and the effect of amino acid deficiency

Abstract

A man with diabetes mellitus, chronic hepatitis, chronic pancreatitis, and blind loop syndrome but without and previous thyroid disease developed three episodes of transient primary hypothyroidism associated with protein-calorie malnutrition (PCM). Clinical examinations suggested that this primary hypothyroidism was not caused by chronic thyroiditis, iodine deficiency, or iodine excess. Since the three times association of primary hypothyroidism with PCM suggested the possibility that the primary hypothyroidism was caused by PCM, we have tried to clarify its mechanism. For this purpose we have investigated the change of thyroid functions during protein-calorie repletion and the effect of amino acid deficiency. Total parenteral nutrition with full supplementation of amino acids resulted in a rapid increase in serum thyroxine (T 4), triiodothyronine (T 3), free T 4, and reverse T 3, and subsequently, a rapid decrease in TSH in several days after the nutrition was begun. When amino acid solution was changed to that depleted of phenylalanine and tyrosine after the restoration of thyroid functions, serum T 4 and T 3 showed a gradual decrease, but serum free T 4 and TSH remained within normal range. However, resupplementation of phenylalanine and tyrosine after 8 weeks of depletion gave a rapid increase in serum T 4, T 3, free T 4, and reverse T 3. These results suggested that the primary hypothyroidism was caused by an impaired T 4 production and that the deficiency of amino acids in PCM partly contributed to the impairment of T 4 production.