Corticotrophin Administration Research Articles

Managing Septic Shock in Patients With Cirrhosis: The Role of Adrenal Insufficency

Managing Septic Shock in Patients With Cirrhosis: The Role of Adrenal Insufficency

Cortisol metabolism in glucose-6-phosphate dehydrogenase deficiency

Ten subjects with glucose-6-phosphate dehydrogenase deficiency (G6PD Canton) and ten G6PD normal subjects matched for sex and age distribution were studied with respect to their plasma cortisol levels and 24-hr urinary total 17-oxogenic steroids excretion before and after maximal stimulation with B 1–24 corticotrophin (Synacthen depot). In five patients and five controls, the study included the metabolic clearance rate of cortisol which increased twofold after B 1–24 corticotrophin administration. No significant differences were found in these two groups of individuals. This indicates that in G6PD-deficient subjects, under basal conditions and with maximal stimulation, both cortisol production and metabolism proceed at a normal rate.

Plasma cortisol and response to corticotrophin in airways obstruction

In a small group of men with fairly severe fixed airways obstruction the mean basal plasma cortisol level was not reduced, and the mean increase in plasma cortisol after corticotrophin administration was normal.

Double isotope assay of aldosterone, corticosterone and cortisol in human peripheral plasma.

SUMMARY A double isotope derivative assay technique for the simultaneous estimation of aldosterone, corticosterone and cortisol in human peripheral plasma is described. With this method, concentrations of the corticosteroids in plasma from adrenalectomized subjects were not significantly different from zero. Further evidence of specificity for aldosterone was obtained by measuring the disappearance rate of a single intravenous injection of unlabelled aldosterone from peripheral plasma, by demonstrating a rapid rise in aldosterone concentration in normal subjects acutely depleted of sodium, and by a comparison of aldosterone levels in patients with primary aldosteronism before and after surgical treatment. A study has also been made of the variation of the ratio of cortisol to corticosterone in normal subjects and of the effect upon this ratio of corticotrophin administration and haemorrhage.

Oestrogens in congenital adrenal hyperplasia.

ABSTRACT Urinary oestrogen excretion was studied in 11 subjects with congenital adrenal hyperplasia, including 7 children and 3 castrates. Oestrogen excretion was significantly elevated in older children and adults, and could be decreased by adrenal suppression with steroids. In one adult castrate, oestrogen excretion was raised by corticotrophin administration but unaltered by 30 000 IU of human chorionic gonadotrophin. Isotope studies showed oestrone production rates up to 760 μg/day and oestradiol production rates up to 221 μg/day. There was a considerable discrepancy between these dynamic measurements and the levels of urinary oestrogen excretion. No peripheral conversion of dehydroepiandrosterone to oestrogen could be demonstrated, while androstenedione was aromatized to the extent of 0.7% in one adult castrate. The data suggest that de novo secretion of adrenal oestrogen occurs in some cases.

Depôt Fat Mobilization and Liver Lipogenesis and Ketogenesis in Ovine Pregnancy Toxaemia and the Effects of Corticotrophin Administration

SUMMARY The rates of 14C-1-acetate incorporation into lipids and of ‘ketone bodies’ have been measured in liver slices from normal pregnant ewes and ewes with experimental pregnancy toxaemia. Lipids were synthesized at a reduced rate in the liver slices from experimental toxaemia cases and ‘ketone bodies’ (mainly β-hydroxybutyrate) were formed at about 10 times the normal rate. The lipid contents of the liver and the rates of ketone body formation were directly related to the plasma non-esterified fatty acid (NEFA) concentrations and thus are dependent upon fat mobilization. The rates of lipogenesis by the liver, however, were related inversely to plasma NEFA and the significance of this is discussed. Although daily ACTH treatment during the 6-day fasting period prevented the development of symptoms of pregnancy toxaemia and partially reversed the 2 abnormalities in liver lipid metabolism, there was no effect on depot fat mobilization.

FREE 17-HYDROXYCORTICOSTEROID LEVEL AND EOSINOPHIL CELL COUNT DURING CORTICOTROPHIN TESTS.

ABSTRACT The effect of intravenous infusions for 5 hours of 20–25 IU corticotrophin on the free 17-OHCS content in the plasma and on the number of the eosinophil cells in the blood was studied in patients with normal adrenocortical function and in patients with allergic diseases receiving 40–60 mg cortisol daily in a dose which suppresses the function of the adrenal cortex, as well as in hypophysectomized and adrenalectomized patients. When the maximal content of free 17-OHCS during the corticotrophin infusion was above 25–30 μg/100 ml an inverse correlation with the number of eosinophils was found. When, however, the free 17-OHCS level reached in the plasma was in the normal range (< 25 μg/100 ml) or very low no correlation was found between the free 17-OHCS content in the plasma and the percentage changes in the number of eosinophils in the blood. In general the responses in the content of free 17-OHCS in the plasma and also in the number of the eosinophil cells in the blood, to intravenous corticotrophin administration is a good indicator of the adrenocortical function.

The measurement of urinary tetrahydroaldosterone by gas-liquid partition chromatography

A gas-chromatographic method for the analysis of tetrahydroaldosterone in urine has been devised. The mean basal excretion of 46.7 μg/24 h was determined in five normal subjects on normal sodium intake. This metabolite was observed to increase in response to sodium deprivation and to corticotrophin administration. Two other, more mobile components were also observed. One of these was found to be consistently increased by sodium restriction and was thought to represent an additional mineralocorticoid metabolite. The advantages of this method are those of efficiency, speed, accuracy and replicability.

Fractional determinations of urinary 17-ketosteroids in hyperemesis gravidarum.

ABSTRACT The fractional determination of 17-ketosteroids in the daily urine was performed in nine cases of hyperemesis gravidarum and in four control cases, in the first trimester of pregnancy both before and after corticotrophin administration. The excretion of total 17-KS is similar in the two groups. Only in the hyperemesis group does the excretion of total 17-KS increase significantly after corticotrophin administration. The fractional determination reveals no difference between the two groups of patients with regard to the values of the fractions U (unidentified 17-KS), A (androsterone) and Rest (11-oxygenated 17-KS). The excretion of dehydroepiandrosterone is significantly higher in the hyperemesis group than in the control group. The excretion of androstanolone seems to be lower in the hyperemesis group than in the control group, but the difference is not statistically significant. The differences in the correlation between dehydroepiandrosterone and androstanolone in the two groups is significant. The high excretion of dehydroepiandrosterone and low excretion of androstanolone in cases of hyperemesis gravidarum is a sign of adrenal dysfunction.

Triphosphopyridine nucleotide-linked dehydrogenases in the adrenal cortex in man: the effect of corticotrophin and the distribution of enzymes.

ABSTRACT Four TPN linked dehydrogenases – Isocitric Dehydrogenase, Glucose-6-phosphate Dehydrogenase, 6 Phosphogluconic Dehydrogenase and the Malic Enzyme – were studied in human adrenal cortex and found to be present almost exclusively in the soluble part of the cell sap. The effect of corticotrophin on these enzymes was studied by comparing the enzyme activities in the cortex of the adrenal glands removed before and after corticotrophin administration. Glucose-6-phosphate dehydrogenase showed marked increase in activity after corticotrophin administration. This increase was not parallel to the concomitant weight increase occurring in the adrenal gland. Glucose-6-phosphate dehydrogenase is uniformly distributed in the »normal« adrenal cortex. After corticotrophin administration however the increase takes place principally in the middle third of the cortex. These findings are discussed in relation to the current theories of the mechanism of corticotrophin action.

BEFUNDE AM GENITALTRAKTUS DER RATTE NACH CORTICOTROPIN-INJECTION UND IHRE DEUTUNG UNTER BERÜCKSICHTIGUNG DES ZELLBILDES DER ADENOHYPOPHYSE

ABSTRACT In normal adult female rats a single injection of 5 IU corticotrophin was followed by a retention of glucoproteid material in the anterior lobe of the hypophysis and by impairment of the luteinization. In spayed adult female rats the same corticotrophin administration caused stratification and mucification of the vaginal epithelium.

Effect of Corticotrophin on Guinea Pig Plasma Corticosteroids.

ConclusionThe plasma corticosteroid content of the guinea pig offers a suitable means for evaluating the potency of adrenocorticotrophic hormone, and also the menstrua which may be useful in extending the physiological or pharmacological effect of this hormone.Summary. The response of the guinea pig to exogenous adrenocorticotrophin was determined using plasma steroid concentration as criteria of response. Average steroid concentration for 50 untreated male guinea pigs was 43 ± 1.7. A graded response was obtained after corticotrophin administration which when plotted yielded a straight line with a slope adequate to determine differences between a 1 1/2 to 3-fold increment in dose. Comparison of corticotrophin administered subcutaneously in a gelatin menstruum with that administered in water showed a 2–3 time greater activity when gelatin is employed as a menstruum than when the hormone is dissolved in water. This is in accord with findings in the rat using the adrenal ascorbic acid depletion as a measure ...

Adrenal cortical response tested by intravenous and intramuscular injections of corticotrophin.

In 1948 Thorn and his associates introduced a test of adrenal cortical function using the eosinophil response following corticotrophin administration. The original Thorn test has since been modified, though the basic principle remains unchanged. The reliability of a corticotrophin test depends upon the validity of the criteria of adrenal function. The following criteria are used: 1. A decrease in circulating eosinophils, selected because of the rapidity and convenience of the measurement. 2. A rise in the urinary excretion of adrenal steroids, chosen because of the high degree of specificity of this response to adrenal cortical activation. The corticotrophin test is regarded as the most useful and informative test of adrenal function so far devised (Frawly, 1956). Forsham & Thorn (1955) describe diurnal variations of adrenal cortical activity as evidenced by changes in blood and urinary 17-hydroxy-corticoids. The diurnal changes in adrenal cortical activity are not

Effect of corticotrophin on chronic, severe primary thrombocytopenic purpura.

IDIOPATHIC thrombocytopenic purpura is one of the few disorders of obscure origin in which the effect of cortisone and corticotrophin (ACTH) therapy has not been extensively reported. 1 Results of administration of the hormones will be difficult to evaluate since spontaneous remissions are common. In some patients, however, the disease runs a chronic, unremitting course, so that the effect of agents of possible therapeutic value is of greater significance. During the past four years we have had the opportunity of observing the disease in a most severe and persistent form in a woman, and we wish to report the dramatic effect of corticotrophin administration. REPORT OF CASE The patient (A. M.) was a 41-year-old married school teacher who was well until 1945, when she noted the appearance of spontaneous bruising and small hemorrhages in the skin, along with bleeding of the gums and frequent nosebleeds. These symptoms continued without remission