In order to re‐assess the possible hormonal consequences of male sterilization, the peripheral plasma levels of lutropin (LH), follitropin (FSH), and dihydro‐testosterone sulphate (DHT‐S) were measured in a group of 20 healthy men at weekly intervals in the month before and at bimonthly intervals up to 2 years after vasectomy. In addition, the levels of 14 steroids of gonadal and/or adrenal origin were measured before, and then every second month (12 subjects) or every sixth month (8 subjects) following vasectomy No significant alterations were observed in the levels of any of the hormones studied The results are interpreted as indicating that in the first 2 years following vasectomy in men there is no consistent or progressive change in the peripheral plasma levels of gonadotrophins or in a variety of steroids of testicular and/or adrenocortical origin.
ABSTRACT Decapsulated testes of rats, guinea pigs and rabbits were incubated with or without labelled precursors and the steroids formed under various experimental conditions were analysed. Also a decapsulated human testis was incubated with labelled acetate. Cholesterol, testosterone and androstenedione were isolated in a radiochemically homogeneous form following the incubation of carbon-14-labelled sodium acetate with decapsulated testes of all 3 animal species. No other labelled steroid was detected following the incubation of rat testes. Guinea pig testes also converted labelled acetate to pregnenolone. Rabbit and human testes converted labelled acetate to cholesterol, pregnenolone, dehydroepiandrosterone, androstenediol, testosterone and androstenedione. When decapsulated testes of rats, guinea pigs and rabbits were incubated with carbon-14 labelled pregnenolone as a precursor, radiochemically homogeneous progesterone, 17-hydroxypregnenolone, dehydroepiandroster-one, androstenediol, androstenedione and testosterone were isolated in each experiment. Using radioimmunoassay techniques, preformed steroids together with steroids formed from endogenous precursors were analysed following the incubation of rat, guinea pig and rabbit testes in the absence and in the presence of human chorionic gonadotrophin (HCG). Marked (seasonal?) variations were observed between the results of experiments conducted at different times. Incubation of guinea pig testes in the absence as well as in the presence of HCG resulted in a major increase in pregnenolone levels. No such finding was encountered when rat and rabbit testes were incubated. The addition of HCG resulted in at least a 10-fold increase in testosterone formation by the testes of all three species. The addition of HCG to the incubation medium induced a marked rise in dihydrotestosterone levels in the rabbit testes but had no effect whatsoever on the levels of this steroid in guinea pig testes. It is concluded that considerable species differences exist in the steroid metabolism of decapsulated testes incubated in vitro .
Blood levels of dehydroepiandrosterone sulphate (DHEAS) were measured by radioimmunoassay (RIA) in patients with: a) polymyalgia rheumatica/giant cell arteritis (PMR:TA; N = 25), with and without cortisone derivative treatment (N = 10 and N = 15, respectively); and b) primary fibromyalgia (PF; N = 15). The mean DHEAS levels were found to be significantly reduced in PMR:TA, compared to those in PF (Geom. mean 820 vs. 2300 nmol/l, respectively; p < 0.001), and the reduction was more marked in patients on cortisone derivative treatment. The DHEAS levels found in PF were found to be normal and consistent with those previously reported in non-immune mediated rheumatological diseases such as osteoarthritis, and in healthy subjects, using the same method of analysis. The low levels found in patients with PM:TA are in accordance with those previously reported in immune-mediated diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis, suggesting that diminution of DHEAS is a constant endocrinologic feature in these categories of patients. The pathophysiological significance of these low DHEAS levels needs to be investigated.
To evaluate the levels of dehydroepiandrosterone sulphate (DHEAS) in the blood and tissues of patients with inflammatory bowel disease (IBD).DHEAS levels were measured by radioimmunoassay in blood from 112 patients with IBD: 46 with ulcerative colitis (UC) and 66 with Crohn's disease. The levels were compared with those in 80 healthy controls. In addition, DHEAS concentrations were measured in gut tissue from 40 patients (28 patients with IBD and 12 with other bowel disorders) who had undergone gut surgery. Correlation analyses were carried out between the blood and tissue levels of DHEAS.The mean levels of DHEAS in the blood were markedly lower in the two patient groups (1350 nmol/l in UC and 1850 nmol/l in Crohn's disease vs. 3300 nmol/l in controls; p < 0.001 and p < 0.01 respectively). A diminution below the confidence limits of the controls (< 2500 nmol/l) was found in 37 (79%) of the patients with UC and in 49 (74%) of those with Crohn's disease. The remainder had DHEAS levels within the normal range (> 2500 nmol/l). The overall mean DHEAS concentration in gut tissue was 226 nmol/kg. A significant correlation was found between levels in the blood and those in tissues (correlation coefficient = 0.469; p < 0.002).These data indicate that low blood DHEAS is a feature in a majority of patients with UC or Crohn's disease. The possibility that there is a functional relationship between low DHEAS levels and some of the pathophysiologic features of IBD needs to be investigated.
We have investigated the interrelationship of the levels of 10 steroids in peripheral venous, spermatic arterial and spermatic venous blood, and in tissue specimens from the epididymis, vas deferens and testis from 8 patients who underwent orchidectomy for pathological conditions of the reproductive organs. The steroids analyzed by radioimmunoassay were: pregnenolone (5‐P), dehydroepiandrosterone (DHEA), 17‐hydroxyprogesterone (17‐OH‐P), androstenedione (A), testosterone (T), dihydrotestosterone (DHT) and the sulpho‐conjugated forms (‐S) of 5‐P, DHEA, T and DHT. The quantitatively major steroids in peripheral venous blood were, in order of magnitude, DHEA‐S, 5‐P‐S, DHT‐S, T‐S and T. No difference was observed between the levels of any of the steroids measured in peripheral venous and spermatic arterial blood. With the exception of DHEA‐S and DHT‐S, the levels of all steroids in spermatic venous blood were substantially higher than in peripheral venous blood ( P < 0.001). No correlation was found between steroid levels in spermatic venous and peripheral venous blood. Steroid concentrations in tissue from the epididymis, vas deferens and testis were markedly higher than in peripheral venous blood ( P < 0.01 to P < 0.001), except for the levels of DHEA‐S which were about equal in the various blood and tissue specimens. Tissue to blood ratios varied from approximately 2.0 to 500 according to the steroid in question. The peripheral blood levels of 5‐P‐S, DHEA‐S and DHT‐S were substantially higher than respective unconjugated steroid levels ( P < 0.001); the ratios (sulphoconjugated to unconjugated) were approximately 17, 215 and 30, respectively. In contrast the respective ratios in the tissue specimens vaned from 0.3 to 5.0. These data indicate differences in the extent of tissue steroid accumulation and/or hnding. Furthermore, the varying relationship in different tissues between sulpho‐conjugated and unconjugated steroids suggests the existence of organ specific regulatory mechanisms for steroids in the human. The possibility that the various steroids, particularly the sulpho‐conjugated steroids studied, have specific tissue functions is discussed. It is suggested that the measurement of sulpho‐conjugated steroids may be useful for evaluation of certain disorders of the connective tissues.
To assess the relationship between blood and tissue steroid levels, cortisol and dehydroepiandrosterone sulphate (DHEAS) were measured by radioimmunoassay (RIA) in blood and joint tissues from a group of patients with RA (N = 29) ranging in age from 26 to 80 years (mean 63, SD: 13) and another group with secondary osteoarthritis (OA; N = 23), ranging in age from 47 to 86 years (mean 66, SD: 9), all of whom were scheduled for surgical correction of joint dysfunction. Seventeen of the RA patients were on steroid treatment at the time of the study. Assessing all the patients together, it was found that the tissue concentrations of DHEAS very closely paralleled the blood levels (r = 0.875; p < 0.001). The mean blood and tissue concentrations of DHEAS were found to be significantly reduced in RA, compared to those in OA (geometric means 540 vs. 2100 nmol/l blood, respectively, and 160 vs. 420 nmol/kg tissue, p < 0.001). Individual data indicated, however, that: (a) 3/29 patients with RA exhibited normal levels; (b) the reduction was more accentuated in those patients on steroid treatment; and (c) 5/23 patients with OA, who were treated for cardiovascular disorders, also had reduced DHEAS levels. Significant differences were not found between the mean cortisol levels in RA and those in OA, nor was there a correlation between the blood and tissue levels of this steroid. The possible influence of reduced DHEAS levels on immune-mediated diseases and/or pathophysiology is unknown, and needs to be investigated.
