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Biomedical subjects

J Fiet

Publications and source records attributed to J Fiet.

At least 109 records · Page 6Linked to original sources
PubMed1987

Detection of heterozygous carriers for 21-hydroxylase deficiency by plasma 21-deoxycortisol measurement.

Using a highly specific radioimmunoassay recently described, plasma 21-deoxycortisol levels were measured in 55 heterozygous carriers of 21-hydroxylase deficiency (as demonstrated by HLA typing). Mean baseline 21-deoxycortisol levels were above the normal range, but there was a 38% overlap with control values. In contrast to 17-hydroxyprogesterone levels, which in 71% of the subjects remained within the normal range one hour after ACTH stimulation, 21-deoxycortisol levels increased over stimulated control levels in all but two heterozygous carriers. No differences as to the levels were observed between heterozygous carriers for the classic and the late-onset forms. Plasma 21-deoxycortisol measurement appears to be a valid tool in the biological detection of heterozygosity for 21-hydroxylase deficiency and its implications in genetic counselling.

17-Hydroxycorticosteroids↗
PubMed1987

[Changes in several plasma and urinary components in marathon runners].

33 blood and urinary components were titrated in 11 men 5 days before a marathon race (42 km), just before the start of the race, 1/4 hour after the arrival, the following day and 5 days after the race. On arrival, or/and the following day, even still 5 days later, we observed an increase of: natremia, kaliemia, blood proteins, hematocrit, aldosteronemia, plasma renin activity, uricemia, creatininemia, blood cortisol, myoglobinemia, blood lactic acid, total enzymatic CK activity, enzymatic ASAT activity, urinary elimination of creatinin, urea and 3 methylhistidine. On the contrary, a decrease of plasma total CO2 and blood testosterone levels were observed. These biochemical modifications are the consequence of hydro-mineral losses, muscular necroses, alteration of energetic metabolism with increase of the protein catabolism.

Adult↗
PubMed1986

Pharmacology of an antiandrogen, anandron, used as an adjuvant therapy in the treatment of prostate cancer.

To improve the inhibition of prostate cancer growth obtained by surgical or chemical castration (estrogens or LHRH analogs), blockade of the action of residual androgens of adrenal origin has been proposed. Among antiandrogens acting through the androgen receptor (AR), the nonsteroid anandron (RU 23908) has several advantages over available compounds: megestrol acetate and cyproterone acetate, both steroids, bind substantially to other hormone receptors (progestin, gluco- and mineralocorticoid); and anandron binds only to AR. The nonsteroid flutamide is a prodrug converted to the active metabolite, hydroxyflutamide; anandron is well absorbed on oral administration of an active dose and intact compound disappears slowly from plasma. This may explain why, although in vitro anandron interacts very transiently with AR, in vivo a high level of untransformed anandron is present at the receptor site to induce its antiandrogenic activity. Animal experiments confirm that anandron can counteract the effect of adrenal androgens and inhibit the LHRH analog-induced initial increase in androgen ("flare-up"). Thus, in rats castrated either surgically or by buserelin or DES and supplemented with adrenal androgens (since endogenous adrenal secretion is very low in this species compared to man), anandron decreased prostate weight to control levels. The administration of buserelin to intact rats over 15 days resulted in a significant increase in prostate weight between Days 1 and 5. The addition of anandron to the buserelin inhibited this increase and, furthermore, led to a far greater decrease in prostate weight than that due to buserelin alone at 15 days, indicating a synergy of action.

Androgen Antagonists↗
PubMed1986

Gonadotropin responses to low dose pulsatile administration of GnRH in a case of anosmia with hypogonadotropic hypogonadism associated with gonadal dysgenesis 47 XXY.

A 25 year old man presented hypogonadotropic hypogonadism with complete anosmia (Kallman's syndrome). His chromosomic type was 47 XXY (Klinefelter's syndrome). Clinical findings were: height 183 cm, weight 62 kg, increased length of lower limbs, P2-A2 pilosity and micropenis. Only a left testis was present (1.5-1.5 cm). Bone age was 15. Testicular biopsy showed that the signs were more related to the gonadotropic deficit than to the gonadal dysgenesis; tubular hyalinization was not observed. Plasma levels of testosterone and oestradiol were very low. Plasma gonadotropin levels were below normal ranges and did not respond to an infusion test of GnRH. GnRH was administered iv every 90 min for 3 weeks by an auto syringe infusion pump and induced a pulsatile response of FSH and LH. Plasma levels of testosterone and oestradiol were unaffected. It may be concluded that the results of pulsatile injection of GnRH confirmed in this patient a unique association of Kallmann's syndrome with complete 47 XXY Klinefelter's syndrome.

Adult↗
PubMed1986

[Effect of marathons on neuromuscular excitability; comparison of electromyographic and biochemical findings].

The aim of this paper is to study the neuromuscular excitability of a group of marathon runners and to see how it can be modified right after the marathon. Spontaneously appearing multiplets in EMG signal under ischaemia served as a test of the neuromuscular hyperexcitability. The percentage of positive tests is much higher than in the control population; as a rule, the effect of the marathon is to diminish the neuromuscular hyperexcitability. The concentrations of Ca, Mg and P in the plasma as well as the globular concentration of Mg have been determined several times, both before and after the marathon; no correlation has been found with the neuromuscular hyperexcitability.

Adult↗
PubMed1985

Radioimmunoassay for 21-deoxycortisol: clinical applications.

A radioimmunoassay for 21-deoxycortisol is described. The immunogen, 21-deoxycortisol-3-(0-carboxymethyl) oxime-bovine serum albumin, was prepared, the antisera raised against it were studied and the reliability of the assay was checked. The antiserum selected cross-reacted with 11-deoxycortisol (0.08%), corticosterone (0.25%), cortisol (0.6%) and 17-hydroxyprogesterone (1.6%). 21-deoxycortisol was separated by celite partition chromatography and eluted in the 70/30 (v/v) isooctane/ethyl acetate fraction together with 11-deoxycortisol and corticosterone. The radioimmunoassay was used to measure 21-deoxycortisol in the plasma of normal subjects and patients with androgen excess. In normal subjects, men (0.19 ng/ml +/- 0.08) and women (0.18 ng/ml +/- 0.09) had similar basal levels (mean +/- SD). One hour after ACTH stimulation, these levels were increased by a factor of 3.5. In 7 patients treated for classical congenital adrenal hyperplasia associated with 21-hydroxylase deficiency, basal values varied between 9.1 and 39.9 ng/ml (measured at 8 a.m.). In 7 untreated women with late-onset congenital adrenal hyperplasia (with 21-hydroxylase deficiency), ACTH-stimulated levels were increased to between 9 and 25.5 ng/ml. In 14 heterozygous carriers of 21-hydroxylase deficiency, diagnosed by HLA genotyping, all ACTH-stimulated levels were well above the highest corresponding levels in normal subjects, whereas 17-hydroxyprogesterone levels remained within the normal range in 9 of the cases.

17-Hydroxycorticosteroids↗
PubMed1985

[Effects of nifedipine on carbohydrate metabolism in the non-insulin dependent diabetic].

The aim of this prospective, randomized, double-blind, placebo controlled study was to investigate the effect of nifedipine on carbohydrate metabolism in diabetic patients after a 3-day and a 3-month course of treatment. Sixteen non obese, well controlled non-insulin dependent diabetics, (HbA1 less than 10%), with moderate untreated hypertension were divided in two groups: nifedipine (group N, 8 patients) and placebo (group P, 8 patients). An oral glucose tolerance test (OGTT, 75 g glucose) and an arginine infusion were performed before, after a 3-day, and a 3-month course, either of nifedipine 30 mg/D or placebo. Blood samples obtained during OGTT were assayed for glucose and insulin, and during arginine infusion for insulin, glucagon and growth hormone. The differences between basal and peak values during tests were compared between both groups before and after treatment using Wilcoxon's rank sum test. Neither acute nor chronic administration of nifedipine or placebo modified the glucose tolerance. However, basal insulin levels were reduced by 3 month-administration of nifedipine (from 19 +/- 2 micromicrons/ml to 10 +/- 1 micromicrons/ml, p = 0,01). Otherwise the basal and peak hormonal values during tests were not significantly affected by nifedipine either at the start of after 3 months of treatment. These results suggest that nifedipine, when given in standard dosage for 3 months, has minor effects on carbohydrate metabolism in non-insulin dependent diabetic patients.

Adult↗
PubMed1985

[Value of the detection of myoglobin by immunoagglutination in myocardial infarction].

The abnormally elevated quantity of myoglobin present in the plasma of 11 patients suffering of myocardial infarction was demonstrated by a rapid immunoagglutination slide-test. The results of this qualitative test were compared to the myoglobin concentrations measured by radioimmunology. Although the immunoagglutination test is less sensitive than the myoglobin assay, it proved to be very specific. Its rapidity of use, its reliability shown on 121 plasma specimens collected during the myocardial infarction evolution in the patients under study, will enable the clinician to use advantageously the very rapid myoglobinemia taking place in the first hours of infarction. Indeed, we have shown in agreement with the literature that the rise of myoglobin during the first hours of infarction occurs at a much earlier stage than does the increase of creatine kinase activity which was equally assayed during this work.

Agglutination Tests↗
PubMed1985

[Radioimmunoassay of salivary l7 alpha-hydroxyprogesterone. Values obtained in healthy subjects and in patients treated for congenital hyperplasia of the adrenal glands].

The authors describe a method for the radioimmunoassay of 17 alpha-hydroxyprogesterone in the saliva. The limit of detection is 1.96 fmole/tube. Salivary 17 alpha-hydroxyprogesterone was measured in control subjects. Values found were of 296 +/- 115 pmol/l in the male, and 251 +/- 23 pmol/l in the female during the follicular phase and 401 +/- 94 pmol/l during the luteal phase, and 115 +/- 30 pmol/l in the prepubertal child. Concentrations were much higher in the newborn and decreased during the first days of life. Variations in salivary concentrations were compared with those in plasma 17 alpha-hydroxyprogesterone during the 24-hour period and with the Synacthene stimulation test. The excellent correlation (r = 0.0969) between salivary 17 alpha-hydroxyprogesterone and plasma 17 alpha-hydroxyprogesterone in 28 patients being treated for 21 hydroxylase deficiency makes it possible to suggest salivary assay in place of plasma assay in the therapeutic follow-up of such patients.

17-alpha-Hydroxyprogesterone↗
PubMed1984

[Cushing's syndrome: a diagnostic strategy].

Biologic and radiologic investigations in the diagnosis of Cushing syndrome are evaluated. A two-step diagnostic procedure is propounded. The combination of absence of overnight suppression of plasma cortisol by dexamethasone and elevation of urinary free cortisol and midnight plasma cortisol levels establishes the diagnosis of Cushing syndrome in most patients. The next step is to determine the precise cause of Cushing syndrome by baseline plasma ACTH assays, the high-dose dexamethasone test and the visualization of the adrenals by iodocholesterol scintigraphy and/or computed tomography.

17-Hydroxycorticosteroids↗
PubMed1984

[Plasma and saliva DST (dexamethasone suppression test) in depression. Clinical applications and kinetic approach].

Both plasmatic and salivary DST were simultaneously performed on a sample of 37 patients with a diagnosis of major depressive disorder (DMS III criteria): 22 primary depressions and 15 secondary depressions. Salivary DST showed a similar specificity but a decreased sensitivity in comparison with plasmatic DST. Essentially, the simultaneous use of both tests resulted in a better specificity for primary depression.

Adult↗
PubMed1983

Evidence for adrenal and/or ovarian dysfunction as a possible etiology of idiopathic hirsutism.

Thirty-one cases of idiopathic hirsutism, characterized biochemically in the basal state by increased levels of urinary 3 alpha-androstane-5 alpha, 17 beta-diol and normal levels of the main androgens, were studied. In order to determine a possible etiologic heterogeneity of idiopathic hirsutism, pituitary gonadotropin responses to synthetic luteinizing-releasing hormone (LRH) and adrenal steroid responses to adrenocorticotropic hormone (ACTH) stimulation were evaluated and the results were compared to those in six normal women. On the basis of the results obtained in each hirsute patient after LRH and ACTH tests, two groups were identified. The majority, 23 of 31 hirsute patients (group I), had results similar to those in the control group. In the other eight patients (group II), biologic abnormalities were disclosed and suggested a partial adrenal 11 beta-hydroxylase defect in two patients, an incomplete form of adrenal 3 beta-ol deficiency in one patient, an adrenal hyperreactivity without evident cause in two patients, and polycystic ovary syndrome in association with an adrenal hyperreactivity in three patients. As a group, the eight patients showed ACTH-stimulated increments in testosterone, delta 4-androstenedione, dehydroepiandrosterone, and 17-ketosteroids that were significantly greater (p less than 0.01) than the mean responses in the control group. The conclusion is that some women who previously were designated as having "idiopathic" hirsutism had an adrenal and/or ovarian component to their hyperandrogenism which could be shown only by appropriate dynamic tests.

17-Ketosteroids↗
PubMed1983

[Assay of plasma hCG. Our experience with the diagnosis of extra-uterine pregnancies. Apropos of 45 cases].

Two groups of patients who were admitted to hospital with a possible diagnosis of ectopic pregnancy were compared. The levels of HCG in the plasma were obtained as an emergency in the first group (45 cases). The levels were not obtained in the second group (34 cases). Only those cases in the first group where the assays had shown the presence of HCG underwent laparoscopy: 12 laparoscopies revealed 7 extra-uterine pregnancies. In the second group, on the other hand, all 34 patients had laparoscopy; only 8 extra-uterine pregnancies were discovered by this method. Because of this study we found that when HCG assays were carried out there was no false positive or negative. When we wanted to rule out an L.H. peak in a doubtful case the assay was repeated. The comparison between the two groups underlines the importance of carrying out the assay: it avoids useless laparoscopies but it also shortens the length of stay in hospital.

Chorionic Gonadotropin↗