Tahara Y, Hirota M, Shima K, Kozu S, Ikegami H, Tanaka A, Kumahara Y, Amino N, Hayashizaki S, Miyai K
Department of Medicine, Osaka University Medical School, Japan.
Metabolism. 1988 Jan;37(1):9-14. doi: 10.1016/0026-0495(88)90022-4.
A man with diabetes mellitus, chronic hepatitis, chronic pancreatitis, and blind loop syndrome but without any 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 (T4), triiodothyronine (T3), free T4, and reverse T3, 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 T4 and T3 showed a gradual decrease, but serum free T4 and TSH remained within normal range. However, resupplementation of phenylalanine and tyrosine after 8 weeks of depletion gave a rapid increase in serum T4, T3, free T4, and reverse T3. These results suggested that the primary hypothyroidism was caused by an impaired T4 production and that the deficiency of amino acids in PCM partly contributed to the impairment of T4 production.
一名患有糖尿病、慢性肝炎、慢性胰腺炎和盲袢综合征但既往无甲状腺疾病的男性，出现了三次与蛋白质 - 热量营养不良（PCM）相关的短暂性原发性甲状腺功能减退发作。临床检查表明，这种原发性甲状腺功能减退并非由慢性甲状腺炎、碘缺乏或碘过量引起。由于原发性甲状腺功能减退与PCM三次相关，提示原发性甲状腺功能减退可能由PCM引起，我们试图阐明其机制。为此，我们研究了蛋白质 - 热量补充期间甲状腺功能的变化以及氨基酸缺乏的影响。完全补充氨基酸的全胃肠外营养导致血清甲状腺素（T4）、三碘甲状腺原氨酸（T3）、游离T4和反T3迅速升高，随后，在营养开始后的几天内TSH迅速下降。当甲状腺功能恢复后将氨基酸溶液换成缺乏苯丙氨酸和酪氨酸的溶液时，血清T4和T3逐渐下降，但血清游离T4和TSH仍在正常范围内。然而，在缺乏8周后重新补充苯丙氨酸和酪氨酸，血清T4、T3、游离T4和反T3迅速升高。这些结果表明，原发性甲状腺功能减退是由T4产生受损引起的，PCM中的氨基酸缺乏部分导致了T4产生的受损。
