Robert S. Ely

Blood Adrenocorticotrophin in Children with Congenital Adrenal Hyperplasia.

Summary The oxycellulose technic has been applied to the analysis of blood ACTH in children. ACTH was not present in detectable quantities in the blood of afebrile children without endocrine disease. ACTH was detected in the blood of untreated, but not of cortisone-treated, children with adrenogenital syndrome.

Studies of 17-hydroxycorticosteroids

Summary Plasma 17-hydroxycorticosteroidconcentrations were found to be elevated markedly in seven patients with salicylate intoxication and in guinea pigs given large doses of sodium salicylate intraperitoneally. Guinea pigs given sodium lactate or smaller amounts of sodium salicylate, intraperitoneally, were found to have levels of these steroids which were not significantly different from those of untreated animals.

Studies of 17-hydroxycorticosteroids in children

Summary 1. The blood levels of circulating 17-hydroxycorticosteroids in children with and without evident disease have been studied and are reported. 2. The data obtained do not justify an interpretation that the diseased groups differ significantly from the “well-control” group, with the exception of the group of children with congenital adrenal hyperplasia. 3. Serial values for 17-hydroxycorticosteroids in patients with rheumatic fever receiving hormone therapy are reported.

Species Differences in Circulating 17-Hydroxycorticosteroid Concentrations.∗

Summary 1. Quantitative determinations of 17-hydroxycorticosteroid concentrations in the peripheral blood of rabbits, rats, guinea pigs and human subjects were made. 2. Considerable species differences in these concentrations were noted. These differences appear to be quantitative as well as qualitative. 3. Of the species observed, the guinea pig appears to be the best experimental animal for studies of 17-hydroxycorticosteroids.

Comparison of eosinophil and circulating 17-hydroxycorticosteroid responses to epinephrine and ACTH.

Summary 1. A comparison of the responses of eosinophils and of circulating 17-hydroxycorticosteroid plasma concentrations; is presented. 2. In general, responses of eosinophils and 17-hydroxycorticosteroids to the injection of ACTH are adequate, with a reduction of the former and an elevation of the latter. 3. Certain exceptions to this generalization are noted. On the basis of these exceptions the question is raised whether the eosinopenic response to ACTH need be mediated by the mechanism previously accepted. 4. There is a strong suggestion that the eosinopenia in response to epinephrine is not mediated by an increased circulating concentration of 17-hydroxycorticosteroids secreted by the adrenal cortex.

Adrenocortical function in epilepsy: I. The role of cortisol (hydrocortisone) in the mechanism and management of seizures

CERTAIN CLINICAL and experimental observations indicate that adrenocortical hormones have an influence on various functions of the central nervous system. Mental disturbances, electroencephalographic abnormalities, intracranial hypertension, and convulsions reflect alterations in adrenocortical function and occur with either a lack or an excess of hormones produced by the adrenal cortex. Hartman, Beck, and Thornl*2 have called attention to the occurrence of mental disturbances in patients with Addison’s disease and pointed out that the administration of adrenocortical extract alleviated these symptoms. In patients with rheumatoid arthritis being treated with cortisone, changes in mood and mentation3r4 have been produced. These altered mental states can be reversed by discontinuing the medication. When ACTH, cortisone, or hydrocortisone is given therapeutically or experimentally, electroencephalographic abnormalities can occur.5-7 Hypoadrenocorticism, as it occurs in patients with Addison’s disease, has been associated with electroencephalograms that have abnormally slow frequencies. Several groups have reported such findings,s-lO and one grouplo demonstrated that adrenocortical extract restored normal brain wave patterns, whereas DCA failed to produce this effect. Increased intracranial pressure complicating steroid therapy has been noted by a number of observers,ll including the authors. The pathogenesis of this pressure is not clear, but it seems to be directly related to hormone therapy rather than to the underlying disease because the intracranial hypertension clears upon withdrawal of steroids. Convulsions, even status epilepticus, may occur in patients receiving cortisone12J3 and ACTH.14 ACTH has been shown to have little

Paper Electrophoresis of Duodenal Fluid from Patients with Cystic Fibrosis of Pancreas

Summary Duodenal fluids from patients with cystic fibrosis of the pancreas and from control subjects were studied by paper strip electrophoresis. Components with greater electrophoretic mobility than any in normal duodenal fluid occurred consistently in cystic fibrosis duodenal fluids. The most rapidly migrating of these fractions was identical in electrophoretic mobility to the albumin fraction of normal human serum.

Circulating 17-Hydroxyeorticosteroids in Ascorbic Acid-Deficient Guinea Pigs.

Summary 1. Quantitative determinations of plasma 17-hydroxycorticosteroids in guinea pigs with severe ascorbic acid deficiency were made. 2. Plasma concentrations of these steroids were found to be approximately 10 times those found in normal guinea pigs despite the virtual absence of adrenal ascorbic acid. 3. Scorbutic animals treated with ascorbic acid for 5 days prior to sacrifice had circulating 17-hydroxycorticosteroids in amounts not significantly higher than those of control animals.

Influence on circulating 17-hydroxycorticosteroid concentrations of compounds structurally related to salicylate.

Summary 1. Twenty-five compounds representing structural derivatives of benzoic acid were studied with regard to their effects on circulating 17-hydroxycorticosteroid (17-OHCS) concentrations in guinea pigs. 2. Benzoic acid had no effect on these concentrations. 3. Among the monohydroxybenzoic acids, the o- and m-substituted derivatives produced elevated plasma 17-OHCS concentrations. The latter compound exerted its effect earlier following administration than did salicylate. p-Hydroxybenzoate had no significant effect. 4. Among the mono-ether derivatives of benzoic acid only the o-substituted compounds produced significant elevations of plasma 17-OHCS concentrations. Significant elevations were produced by 3, 4, 5-trimethoxybenzoic acid. 5. Both o- and paminobenzoic acid produced steroid elevations of borderline significance. 6. The addition to the salicylate structure of a second hydroxyl group in the 3 or 6 position or of an ether group in the 3 position appeared to augment the effect on 17-OHCS concentrations. 7. Aspirin exerted the greatest effect on plasma 17-OHCS concentrations of any compound tested. 8. The salicylate metabolite, salicyluric acid, had no effect. 9. A comparison of the influence of these compounds on 17-OHCS concentrations with antirheumatic and anti-inflammatory properties and with effects on adrenal ascorbic acid concentrations, as reported by others, was attempted.

Studies of 17-hydroxycorticosteroids: IX. The influence of therapy on adrenal cortical function in patients with rheumatic fever

Summary 1. Data are presented concerning plasma 17-OHCS concentrations and the responses of these concentrations to ACTH in patients with rheumatic fever during the periods before and after hormone or salicylate therapy. 2. In all therapy groups, except the one treated with ACTH gel, the mean plasma 17-OHCS level was significantly lower during the post-therapy period than during the pre-therapy period, but not significantly lower than in untreated patients with active rheumatic fever of the same duration. 3. In all therapy groups, the 17-OHCS responses to intramuscular ACTH were normal during the pre-therapy period. During the post-therapy period the magnitude of this response was reduced significantly in the cortisone- and the salicylate-treated groups but not in the ACTH-treated groups. 4. The data presented are interpreted as indicating that a relative and temporary suppression of adrenal cortical responsiveness occurs following therapy with cortisone; this suppressive effect apparently persists for not more than one week. Within the range of size of dose and duration of therapy employed neither of these variables appeared to influence directly the adrenal hypofunction in the post-therapy period. 5. In the patients treated with salicylates, there appeared to be a decreased adrenal cortical responsiveness in the post-therapy period.