IMPAIRED WATER EXCRETION CAPACITY IN PRIMARY MYXOEDEMA IMPROVED BY CORTICOSTEROIDS, CORTICOTROPHIN AND THYROID SUBSTITUTION

Abstract

In four out of twelve cases of primary myxoedema, water excretion after a water load was found to be impaired. In two cases the duration of myxoedema was less than a year. Thyroid substitution was given for more than a year in two of the cases before improvement of water excretion capacity was obtained. During thyroid substitution but before improvement of water excretion was obtained, cortisone in small doses improved water excretion. 17-ketosteroid excretion was low in all 4 patients and 17-ketogenic steroid excretion was normal, as was the response to corticotrophin (ACTH) except in the fourth patient, where the response to ACTH was subnormal even after 10 months of thyroid substitution and improved but was not completely normal after 16 months. In this case too improvement of water excretion by thyroid substitution was obtained, but only after 16 months of such therapy. Cortisone and ACTH corrected the faulty water excretion prior to correction by thyroid substitution as did prednisolone. but not aldosterone. Disagreement is expressed with the interpretation given by Crispell et al. (1954) of their findings in similar cases. The impaired water excretion is explained on the assumption of a sluggish release of ACTH in some cases of myxoedema in response to a water load. One of the patients recorded had a history of previous hepatitis and kidney infection, and definite but not serious liver damage. In this case liver function was definitely worse in the myxoedematous state, thyroid substitution slowly bringing about a considerable improvement. Plasma creatinine was increased in two patients when myxoedematous but normalized after long-lasting thyroid substitution. The improvement of hepatic function and renal glomerular filtration obtained during thyroid substitution is not considered to be the cause of the improved handling of a water load. In cases in which there is strong suspicion of impaired adrenocortical function, whether primary or secondary, intravenous ACTH infusion may cause an almost fatal shock. Intramuscular ACTH is well tolerated. Aldosterone treatment was tried in one of the patients suffering such shock.