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PubMed1985

[Effects of weakly androgenic anabolic steroids on growth in Turner's syndrome].

The effects of weakly androgenic steroids at minimal doses (norethandrolone 2.5 to 10 mg/day or methandienone 1 mg/day, administered 2 months every trimester) have been studied in 67 patients with Turner syndrome: 37 with 45 XO karyotype and 30 with mosaicism or partial X deletion. Mean bone age at the onset of treatment was 10 4/12 +/- 1 8/12 years, and the mean height retardation, adjusted to parents' height, was 3.7 +/- 1.2 standard deviations. Growth velocity was very significantly increased during the first 3 semesters of treatment. The ratio of bone age to height age, evaluated after 2 years of treatment, did not increase. The adult height reached by 37 treated patients was at the average 1.96 cm higher than that of a control group of 25 adult untreated Turner cases, this difference being not significant. The results varied greatly between individuals, without relation to the type of chromosomal abnormality or the kind and dose of steroid received. The psychological evolution of the treated patients was studied accordingly to their school and/or professional accomplishments. It was satisfactory in most of them. The anabolic treatment and/or the gain in growth velocity during treatment seemed to have positive psychological effect. No side-effects were noticed.

Body Height↗
PubMed1975

Effect of anabolic steroids on plasma antithrombin III. alpha2 macroglobulin and alpha1 antitrypsin levels.

The effect of seven different anabolic steroids (Ethyloestrenol, Methenolone acetate, Norethandrolone, Methylandrostenediol, Oxymetholone, Methandienone, and Stanozolol) on three alpha-globulin antiprotease inhibitors of thrombin and plasmin was studied in men with ischaemic heart disease. In distinct contrast to the oral contraceptives, five of the six 17-alpha-alkylated anabolic steroids studied produced increased plasma Antithrombin III levels and five produced decreased levels of plasma alpha2-macroglobulin. The effect on plasma alpha1-antitrypsin levels was less clear-cut but three of the steroids examined produced significantly elevated levels. The increased plasma fibrinolytic activity which the 17-alpha-alkylated anabolic steroids induce is therefore unlikely to be secondary to disseminated intravascular coagulation.

Adult↗
PubMedDate not supplied

[Treatment of pituitary nanism: is it necessary to treat adrenal androgen deficiency?].

In 17 hypopituitary prepubescent children (14 males and 3 females), aged 14.5 +/- 2.1 years, treated for more than 2 years with human growth hormone (hGH), with bone ages of 10.4 +/- 1.4 years and plasma dehydroepiandrosterone (DHA and/or DHA-S) levels lower than the normal values for bone age, low dose androgen therapy (norethandrolone 0.25 mg/kg/day 2 of 3 months) was added to the previous treatment. The speed of growth doubled during the first six months of associated treatment. For 15 patients so treated for one year,the height gain was 7.5 +/- 1.56 cm versus 4.47 +/- 1.2 cm the preceding year. During this first year of treatment, bone age, on an average, progressed less quickly than height. The combination of hGH and low grade androgenic steroid therapy allows for the acceleration of the growth in height without increasing the doses of hGH. A prolonged controlled trial of this therapy in hypopituitary prepubescent children with bone age of at least 8 years and known deficiency of androgenic secretion by the adrenal glands is suggested.

Adolescent↗
PubMed1982

Testosterone and synthetic and androgens improve the in vitro survival of human marrow progenitor cells in serum-free suspension cultures.

The direct effect of testosterone and its synthetic analogs on the maintenance of human erythroid progenitor cells (BFU-E) and GM-CFC was studied in suspension cultures. To avoid interference by serum components, the experiments were conducted in serum-free media containing insulin, transferrin, selenium, BSA, and alpha-thioglycerol. When added at concentrations between 10(-7)M and 10(-9)M, testosterone improved survival of BFU-E and GM-CFC. Of the nine analogs tested, eight improved BFU-E maintenance in vitro: nandrolone norethandrolone, and oxymetholone were most active, whereas etiocholanolone had only marginal effects. The influence of these compounds on GM-CFC was less pronounced, with testosterone showing the highest activity. It is concluded that testosterone and some of the synthetic analogs tested exert their hemopoietic effect, at least partly, by affecting the maintenance of erythroid and granulocytic stem cells, directly by increasing their survival or proliferation or indirectly by increasing the input from multipotent stem cell pool, or by both mechanisms.

Cell Count↗
PubMed2006

Rapid test by liquid chromatography/tandem mass spectrometry to evaluate equine urine reactivity towards 17beta-OH steroids.

Bacteria frequently found in equine urine samples may cause degradation of 17beta-OH steroids. A simple liquid chromatography/tandem mass spectrometry (LC/MS/MS) method has been developed to evaluate the microbiological contamination of equine urine as a marker of poor storage conditions. Norethandrolone was used as the internal standard, and the linearity, sensitivity, precision and accuracy of the method were evaluated. 17beta-OH oxidation was demonstrated for testosterone, nandrolone, trenbolone and boldenone, but did not occur in alpha-epimers such as alpha-boldenone and epitestosterone, demonstrating the stereoselectivity of the reaction. A rapid test was performed by spiking one of the four 17beta-OH steroids in samples of diluted equine urine. The steroids were transformed into their respective ketones in the presence of bacterial activity. The test allows direct injection of diluted samples into the LC/MS system, without the need for prior extraction. Results show that the best method of storage is freezing at -18 degrees C. Urine specimens should be analyzed as soon as possible after thawing. This allows bacterial degradation of equine urine to be arrested temporarily, so that the urine can be used for qualitative or quantitative analysis of 17beta-OH steroids.

Animals↗
PubMed1986

Destruction of cytochrome P-450 and formation of green pigments by contraceptive steroids in rat hepatocyte suspensions.

The contraceptive steroid norethindrone caused a rapid time and dose-dependent loss of cytochrome P-450 from rat hepatocytes in suspension cultures. Up to 30% of this cytochrome was lost in the first 5 min of incubation; longer incubations resulted in little further loss even though not all the steroid was metabolised and the cells remained viable. Such cultures were used to investigate the formation of N-alkylated porphyrins (green pigments) which could be extracted from cell incubation mixtures following exposure to norethindrone and separation by HPLC or TLC. The number of N-alkylated porphyrins formed was dependent both on the time of incubation and the concentration of steroid. After 1 min, 1 major green pigment (GP1) was resolved using either high (0.3 mM) or low (0.03 mM) norethindrone concentrations. With longer incubation times (60 min), at high steroid concentrations, only one additional polar adduct (GP2) was formed. At lower steroid levels, 3 more polar components (GP2, 3 and 4) were seen. As judged by HPLC or TLC, GP1 corresponds to the pigment formed in microsomal preparations incubated with norethindrone in vitro, while GP2, 3 and 4 correspond to the pigments extracted from the livers of rats administered this steroid in vivo. Pretreatment of rats with either phenobarbitone or 3-methylcholanthrene induced cytochrome P-450s. Relative to controls, phenobarbitone pretreatment also resulted in a greater accumulation of green pigments in hepatocytes incubated with norethindrone, the more polar forms of green pigments (GP3 and 4), showing a disproportionate increase in concentration. The mixed function oxidase inhibitor SKF 525-A or high concentrations of steroid not containing an ethynyl function, e.g. norethandrolone, when added to cell cultures containing norethindrone, preferentially inhibited the formation of GP3 and 4. When purified green pigments were added to cell incubation mixtures in the absence of norethindrone, preferentially inhibited the formation of GP3 and 4. When purified green pigments were added to cell incubation mixtures in the absence of norethindrone, no interconversion of one form to another could be demonstrated. The results suggest that the more polar norethindrone-protoporphyrin IX adducts (GP2, 3 and 4) arise as a result of metabolic modification of norethindrone rather than the protoporphyrin IX moiety, either prior to or after activation of the ethynyl function. The formation of several green pigment components in hepatocyte suspensions was not unique to norethindrone but occurred with a number of other 17-ethynyl-substituted steroids.

Animals↗
PubMed1976

Interactions of various 19-nor steroids with human placental microsomal cytochrome P-450 (P-450hpm).

Each of seven 19-nor steroids exhibited the capacity to facilitate the binding of carbon monoxide (CO) to human placental microsomal cytochrome P-450 although quantitative differences were shown to exist. In every case the facilitation was antagonized by androstenedione. 19-Norandrostenedione produced the most pronounced effect followed by 19-nortestosterone, nandrolone decanoate, norethandrolone, norgestrel, norethynodrel and norethindrone in that order. All steroids investigated produced typical type I binding spectra when added to placental microsomes. Scatched plots also indicated binding of each steroid to two sites--a high-affinity, low-capacity binding site and a low-affinity, high-capacity binding site. Correlations between affinity for either site and capacity to facilitate binding of CO to the cytochrome were not observed nor were there good correlations between maximal absorbance differences (approximately390-420 nm) producible and facilitation capacity. It was therefore concluded that no definitive relationships existed between facilitation capacity and qualitative or quantitative aspects of the steroid-binding spectra. The capacity to facilitate CO binding appeared to reside in the absence of a chemical group substituted at the 10 position on molecules of androgenic steroids since all investigated steroids possessing 10-methyl or other 10-substituted groups either had no effect on the CO-binding spectrum or caused a displacement of CO from ferrous heme. In contrast, all steroids studied that lacked a substitution at C-10 (19-nor steroids) produced a facilitating effect on heme-ligand binding.

Androstenedione↗
PubMed1980

Cytotoxic effects of norethindrone-4 beta,5 beta-epoxide to Walker cells in culture and to rat liver in vivo.

1. Norethindrone-4 beta,5 beta-epoxide was toxic to Walker cells in culture. The concentration required to produce a 50% reduction in the increase in cell numbers 72 h after exposure (ID50) was 0.05 mM. In this assay, the parent contraceptive steroid, norethindrone, was at least four times less toxic than the epoxide. 2. Norethandrolone-4 beta,5 beta-epoxide and norethynodrel-5 beta,10 beta-epoxide were as toxic as norethindrone epoxide to the Walker cells. 3. The cytotoxicity of norethindrome epoxide was dependent on the time of exposure of the cells to this compound if excess unreacted epoxide was removed by washing the cells with cysteine. The results are consistant with norethindrone epoxide causing cell death by reacting with sulphydryl groups of cellular proteins. 4. No metabolites toxic to Walker cells could be detected when the cells were incubated with norethindrone, rat liver microsomes and a NADPH generating system. 5. Cells treated with an ID50 of norethindrone epoxide for 1 h showed marked cytoplasmic vacuolation 3 hr after exposure. This vacuolation was much less marked in cells treated with an ID50 of norethindrone or in the controls. Neither group showed any nuclear abnormalities. 6. Norethindrone epoxide when given to rats in large doses (50 mg/kg) by lateral tail vein injection also caused cytoplasmic vacuolar degeneration of the liver hepatocytes, especially in the perilobular areas 3 days after dosing. When this compound was administered at a similar dose level via the hepatic portal vein massive haemorrhagic necrosis of the liver resulted. No damage to either lungs or kidneys was evident, irrespective of the route of administration.

Animals↗
PubMed1992

Steroids and "the pill": early steroid research at Searle.

The announcement from the Mayo Clinic in 1949 of the dramatic effectiveness of cortisone in the treatment of rheumatoid arthritis stimulated tremendous interest in steroid chemistry, endocrinology, and related areas of medicine. Shortly thereafter, G. D. Searle & Co. initiated a major effort in steroid research, the objective of which was to discover better steroid drugs than those available at that time or steroids that could be used for conditions for which no compounds were previously available. This effort was remarkably successful and resulted in the introduction of several important pioneering drugs. These included norethandrolone, marketed in 1956 as Nilevar, the first anabolic agent with a favorable separation between protein building and virilization, and spironolactone, introduced in 1959 as Aldactone, the first steroid antialdosterone antihypertensive agent. Of special importance was the research that culminated in the discovery of Enovid. This substance, a combination of the progestin norethynodrel and the estrogen mestranol was first approved in 1957 for the treatment of a variety of disorders associated with the menstrual cycle. The era of oral contraception began in May 1960, when Enovid was approved by the Food and Drug Administration for ovulation inhibition, and was immediately thereafter introduced for such use.

Contraceptives, Oral, Hormonal↗
PubMed2006

[Nosologic discussion between Fanconi disease and congenital dyskeratosis: 1 case of congenital bone marrow aplasia].

UNLABELLED: Based on a case report of aplastic anemia associated with malformation, we discuss the diagnostic criteria and the nosologic problem between the 2 principal aplastic anemia accompanied with malformation: Fanconi disease and dyskeratosis congenita. CASE REPORT: A 19-year-old girl, issued from a third degree consanguineous marriage, was admitted because of anemic and hemorrhagic syndrome. Physical examination showed several malformations: microphtalmia, brownish spots, generalized hyperpigmentation and ungueal dystrophy without mucosal leucoplasia. Statural and ponderal retardation were noted. On the hemogram there was a pancytopenia and on biopsy, the bone marrow was desertic. The caryotype performed on peripheral blood lymphocytes after sensibilisation with mitomycin C revealed chromosomal instability aspects. Based on these clinical and biological features, the diagnosis of hereditary aplastic anaemia was retained. The patient was given norethandrolone. She died 3 months later by septic shock. DISCUSSION: Coexistence of aplastic anemia with a malformative syndrome suggests most probably an hereditary form of aplastic anemia. Fanconi anemia is the most frequent. It associates characteristic anomalies of the face, with microphtalmia, brownish spots, statural and ponderal retardation, and thumb anomalies. Ungueal dystrophy, mucosal leucoplasia are almost pathognomonic of congenital dyskeratosis. When the malformative syndrome is not characteristic, the cytogenetic study may also fail to make the differential diagnosis, as was the situation in our case.

Adult↗
PubMed1998

Metabolites in feces can be important markers for the abuse of anabolic steroids in cattle.

In Belgium, to control the abuse of anabolic steroids in cattle, urine samples have been gradually replaced by feces samples, because the latter can be obtained more easily from living animals. Urine and feces samples were collected from heifers after administration of boldenone, norethandrolone or ethylestrenol. Metabolites present in feces or urine were determined by GC-MS. Large qualitative and quantitative differences in the metabolic profiles were observed. In feces, in contrast to urine, the parent compounds or their major metabolites were detectable only shortly after administration. On the other hand, metabolites resulting from the reduction of the 3-oxo group and the unsaturated carbon-carbon bonds, present on the A-ring, allow for long-term detection in feces. A-ring reduced metabolites have been identified in samples found positive for norgestrel, boldenone, methylboldenone and methyltestosterone, respectively. These results are in agreement with concomitant in vivo experiments.

Anabolic Agents↗
PubMed1961

Serum haptoglobin in liver disease.

Serum haptoglobin levels have been measured in 115 cases of widely differing liver disease. Although low levels were found in some cases of cirrhosis and a number of patients with obstructive jaundice had increased levels, 70% of the values fell within the normal range. The estimation was of no help in distinguishing between intra- and extrahepatic obstructive jaundice. A characteristic pattern was observed in infective hepatitis, and a falling serum haptoglobin in the presence of increasing jaundice is diagnostic of the latter condition. The cause of these changes is uncertain. Low levels could not be accounted for by increased red cell breakdown and there was no correlation with the serum albumin level. Prednisolone therapy produced a rise in serum haptoglobin level in cirrhosis, which was accompanied by an improvement in liver function. Temporary rises in level were observed in intrahepatic obstructive jaundice and were probably due to a non-specific effect of prednisolone. In the latter condition norethandrolone therapy was often associated with high levels.

Female↗
PubMed1967

Cortisol metabolism in cirrhosis.

The production and peripheral metabolism of cortisol have been studied in 10 cirrhotics and 11 controls after i.v. tracers of cortisol-(14)C. The findings were as follows: (a) Total urinary excretion of radioactivity was normal (81% of the dose) but a decreased fraction was present as glucosiduronates: 18-47% of the dose (average 34%) compared to a normal average of 54%. (b) There was a distinctively abnormal pattern of cortisol metabolites, not previously observed in other illnesses: tetrahydrocortisone was decreased to 14% of the enzyme hydrolysate (normal 26%); cortolones were increased to 34% (normal 19%), owing entirely to an increase in cortolone (20alpha) formation, since beta-cortolone (20beta) was not significantly increased; Reichstein's substances U and epi-U were increased, averaging 2.6% for the former and 4.7% for the latter; tetrahydrocortisol, allotetrahydrocortisol and cortols were normal. This pattern was independent of the degree of decreased glucosiduronate formation and also independent of the presence or absence of a portacaval shunt. (c) Cortisol production, determined by isotope dilution, was normal in each of six cirrhotic patients. From these data, taken in conjunction with our previously reported findings concerning the influence of norethandrolone on cortisol metabolism, the following conclusions were drawn: (a) Cirrhotic patients have decreased A-ring reduction of cortisone to tetrahydrocortisone and correspondingly increased 20-ketone reduction of cortisone to Reichstein's substances U and epi-U and then to the cortolones. (b) Intrahepatic cholestasis, a regular pathophysiological feature of cirrhosis, may be responsible for the observed abnormal cortisol metabolite pattern in this disease. (c) The slowed metabolic turnover rate of cortisol in cirrhosis may be due to decreased transport and/or binding of cortisol to its intracellular metabolic sites rather than to abnormalities of any specific metabolizing enzymes.

Adult↗
PubMed1975

Plasma fibrinolytic activity following oral anabolic steroid therapy.

Six anabolic steroids were assessed for their ability to enhance plasma fibrinolytic activity in males with ischaemic heart disease. Five 17alpha-alkylated steroids (Ethyloestrenol, Norethandrolone, Methandienone, Methylandrostenediol and Oxymetholone) were examined and all produced a significant increase in plasma plasminogen activator as measured by the euglobulin lysis time. The only non-17alpha-alkylated steroid studied (Methenolone acetate) failed to enhance fibrinolysis. The 17alpha-alkylated steroids studied all deserve more detailed evaluation of their long term effects on plasma fibrinolytic activity.

Adult↗
PubMed1991

[Compared action of norethindrone and various steroids on Müller ducts of the female chick embryo].

Treatment of female chick embryo with norethindrone (NET), a potent progesterone-like steroid, caused caudal agenesia and cephalic regression of Mullerian ducts as the normal regression induced by anti-Mullerian-hormone in the male embryo. The comparative study of five other progesterone-like steroids shows that only lynestrenol which is metabolized into NET at least in man, possesses the same properties as NET. The four others, i.e. medroxyprogesterone, medrogestone, norgestrienone and 17 alpha hydroxyprogesterone are only able to induce agenesia, an unspecific property, which was observed with many steroidal hormones, as norethandrolone here studied.

Animals↗