Panel Discussion

Abstract

The role of the adrenal cortex in resistance to stress and strain has been reviewed. Certain experimental data indicating increased secretion of the adrenal cortical hormone in acute and chronic stress has been presented and discussed in terms of Sayers' homeostatic theory of the acute stress mechanism and in terms of Selye's "Adaptation Syndrome." In addition, studies made on a patient with acute rheumatic fever were discussed. Changes in uric acid metabolism compatible with those that might be seen in an alarm reaction were noted in this patient. [SEE THE TABLE I IN SOURCE PDF]. In the adrenogenital syndrome there is increased protein anabolism due to excessive androgen, in Cushing's syndrome inhibition of protein anabolism due to excessive gluconeogenetic hormones. The manifestations of the adrenogenital syndrome differ according to the patient's sex and the age of onset. Congenital adrenal hyperplasia causes pseudohermaphroditism in the female. This can be differentiated from various types of genetic intersexuality by the evidences of excessive androgen from infancy on and by a fairly uniform type of heterosexual development with a persistent urogenital sinus. In the male congenital adrenal hyperplasia causes macrogenitosomia precox which is sometimes accompanied by Addisonian-like symptoms. This can be differentiated from other types of male precocity by the excessive excretion of androgen and lack of maturation of the testes. In postnatal life androgenic adrenal tumors or hyperplasia cause virilization in both sexes unaccompanied by embryonic abnormalities. Occasionally gynecomastia occurs in males. Most of the symptoms of Cushing's syndrome are probably caused by excess of the gluconeogenetic hormones. However, there is also usually an increased secretion of androgen and in some cases evidences of increased electrolyte-controlling hormones.