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Biomedical subjects

F Bidlingmaier

Publications and source records attributed to F Bidlingmaier.

At least 109 records · Page 6Linked to original sources
PubMed1980

Antibodies against testosterone: valuable tools for the investigation of the hypothalamo-pituitary-gonadal system in the rabbit fetus.

16 female rabbits were actively immunized against testosterone (T). 9 of them conceived and gave birth to 89 neonates. In all neonatal plasma samples antibodies against T were detected. In the males the plasma T levels were elevated 1,000-fold. The testes of these animals were examined by means of morphometrical and biochemical methods. The results indicate increased stimulation of Leydig cells in fetuses exposed to antibodies against T, and suggest that even in the fetus a negative feedback is acting between testes and hypothalamo-pituitary system, which is interrupted by the antibodies which bind and inactivate T.

Animals↗
PubMed1980

Plasma levels of aldosterone, corticosterone, 11-deoxycorticosterone, progesterone, 17-hydroxyprogesterone, cortisol, and cortisone during infancy and childhood.

Plasma aldosterone (A), corticosterone (B), deoxycorticosterone (DOC), progesterone (P), 17-hydroxyprogesterone (17-OHP), cortisol (F), and cortisone (E) were measured simultaneously by specific radioimmunoassays in small plasma samples obtained from 174 normal infants and children between 2 hr and 15 yr of age. The significantly elevated neonatal mean levels (ng/ml) of 2.5 (A), 4.1 (DOC), 53.0 (P), and 6.6 (17-OHP) dropped significantly during infancy reaching prepubertal levels between 3 months and 3 yr of age, with a transient, significant DOC increase between 1--7 yr. The glucocorticoids F andB declined significantly from means of 68 and 4.4 to 11.4 and 0.28 ng/ml, respectively, during the first weeks of life, then increased significantly reaching adult levels between 1--3 yr of age. Mean E fell progressively from 74 ng/ml after birth to 10 ng/ml during 1--5 yr (P less than 0.0001), then slightly increased to adult levels. After age 7 yr, P and 17-OHP, in contrast to the other steroids, rose significantly in both boys and girls relative to pubertal development. The observed changes are thought to be due to (1) adaptation of the adrenal neocortex to extrauterine life after disruption of the fetoplacental unit, (2) a physiologic lack of corticosteroid binding globulin (CBG) during infancy due to maturation of hepatic CBG biosynthesis, (3) the functional immaturity of the infant kidney compensated by an increased activity of the renin-angiotensin-aldosterone system, and (4) gradually increasing gonadal secretion of progestins during puberty.

Adolescent↗
PubMed1980

17-ketosteroid reductase deficiency -- plasma steroids and incubation studies with testicular tissue.

The patient, diagnosed as a case of testicular feminisation in infancy, was examined at the age of 15 years because of severe symptoms of virilising puberty with poor breast development. Plasma steroid analyses revealed a 10-fold elevated androstenedione concentration (A: 1562 ng/100 ml). Testosterone (T: 266 ng/100 ml) was in the male pubertal range. Thus the A/T-ratio was far above normal. The oestrone/oestradiol ratio was also elevated (Oe1/Oe2: 10.2/2.2 ng/100 ml). A, T, Oe1 and Oe2 could not be suppressed by dexamethasone, but reacted promptly to fluoxymesterone (A: 781 ng/100 ml). hCG caused a further increase of the A/T-radio (2220/246 ng/100 ml); ACTH did not alter the A-concentration. These findings together with simular investigations after gonadectomy suggest that the failure to convert A to T and Oe1 to Oe2 is essentially located in the testes. In vitro incubations of testicular tissue showed reduced 17-ketosteroid reductase activity in tissue slices and in the subcellular fractions microsomes and cytosole. This form of male pseudohermaphroditism can easily be detected already in infancy, if steroid analyses and stimulation tests are performed. In case of female sex assignment patients should be submitted to early orchidectomy in order to avoid virilisation in puberty.

17-Hydroxysteroid Dehydrogenases↗
PubMed1980

Treatment of anorchia with oral testosterone undecanoate: pharmacodynamics and clinical effectiveness.

The pharmacodynamics of plasma testosterone (T) and androstenedione (A) levels were studied in ten hypogonadal boys after oral administration of testosterone undecanoate (TU). Plasma T and A levels were measured by specific radioimmunoassays. Six hours after a single dose of 120 mg TU, there was a significant increase (P < 0.005) in plasma T and A with a median T peak level of 940 ng/100 ml. Furthermore, twelve agonadal boys treated with a mean dose of 60 mg TU/day were examined over a period of 18-24 months. During this therapy, plasma T and A levels were significantly higher than before (P < 0.005), whereas plasma levels of LH and FSH did not decrease significantly. With the exception of one anorchic boy, all patients showed signs of sexual maturation, such as growth of pubic and axillary hair, and steady development of bone age during oral TU treatment.

Administration, Oral↗
PubMed1979

Simultaneous determination of seven unconjugated steroids in maternal venous and umbilical arterial and venous serum in elective and emergency cesarean section at term.

In order to assess specific gluco- and mineralocorticoid functions in both mother and fetoplacental unit in relation to the presence or absence of labor, serum levels of unconjugated aldosterone (A), corticosterone (B), deoxycorticosterone (DOC), progesterone (P), 17-hydroxyprogesterone (17-OHP), cortisol (F), and cortisone (E) were determined simultaneously. These levels were determined by specific radioimmunoassays in two groups of 24 paired maternal venous and umbilical arterial and venous samples obtained at term delivery by either elective (Group I, N = 8) or emergency (Group II, N = 8) cesarean section. In Group II, after spontaneous labor, mean maternal serum levels of all steroids investigated exceeded those found in Group I (not in labor). These increases were most pronounced (p less than 0.005) in F (74%) and DOC (106%) levels demonstrating stimulation of both the glucocorticoid (cortisol)--and the mineralocorticoid (aldosterone)--producing pathways of the maternal adrenals by spontaneous labor. Arteriovenous differences in umbilical steroid levels revealed in both groups the placental origin of P, 17-OHP, and E (p less than 0.05 to 0.005), with greater (more negative) mean AV differences after labor (Group II). The negative AV difference of DOC, B, A, and F found in Group I, however, decreased after labor and became even positive in the cases of B and F, reflecting the close relationship between spontaneous labor and the fetal adrenal's active production not only of the glucocorticoids B and F, but also, to a lesser extent, of the mineralocorticoids DOC and aldosterone.

Adrenal Cortex Hormones↗
PubMed1979

[High-dose methotrexate therapy in osteogenic sarcoma: plasma pharmakokinetics to predict toxicity (author's transl)].

In 22 patients with osteogenic sarcoma, treated with 103 high-dose methotrexate infusions (6-8.5 g/m2 in 4-6 h) plasma methotrexate levels were measured with a specific and rapid radioimmunoassay. Nontoxic infusions were associated with methotrexate concentrations below 8.0 X 10(-6) mol/l at 24 h, 8.0 X 10(-7) mol/l at 48 h and 4.25 X 10(-7)/mol/1 at 72 h. All patients with 48 h methotrexate levels above 1 X 10-6 mol/l manifested severe toxicity with myelosuppression and stomatitis due to delayed methotrexate excretion. Rise of serum creatinine was not reliable to predict oxicity. Determination of 48- and 72-h methotrexate concentrations proved to be a valuable method for identifying patients at high risk for toxic side effects. Additional citrovorum factor may thus be given in time.

Adolescent↗
PubMed1979

Hereditary deficiency of triosephosphate isomerase in four unrelated families.

Triosephosphate isomerase deficiencies in erythrocytes and leucocytes were discovered in three unrelated families by a heterozygote screening of 3000 blood samples. In addition, a family found by Schroter et al. [not published] was studied. In these four families, only heterozygote carriers were found. In the family described by Freycon et al. with hetero- and homozygote carriers of triosephosphate isomerase deficiency, the heterozygotes were reinvestigated. There was 51% of normal enzyme activity in three of the families. In the other two families the enzyme activity was 64% and 71% of normal. Two of the eleven heterozygotes, both children, were diseased, but it seems unlikely that the disorders resulted from the deficiencies. The activities of thirteen enzymes, the Km of triosephosphate isomerase for glyceraldehyde phosphate and the concentrations of metabolites were normal. Antibody titration showed normal specific activities in four families and 50% of normal in one family. No electrophoretic variant was detected. From the proved heredity, a heterozygous frequency of at least 1/1000 is indicated. A maximal frequency of 5/1000 is estimated by using further instances of triosephosphate isomerase deficiency where heredity has not yet been investigated. An explanation for the small number of known cases is that this enzyme is not routinely assayed.

Carbohydrate Epimerases↗
PubMed1979

Comparison of two tests for heterozygosity in congenital adrenal hyperplasia (CAH).

The increase of plasma cortisol (F), androstenedione (A), 17 alpha-hydroxy-progesterone (17-OH-P) and testosterone (T) was measured after iv administration of ACTH in heterozygotes for CAH and in controls under two different conditions: Test 1: ACTH stimulation was performed without any particular preparation. Test 2: 1.5 mg of dexamethasone (dex.) was given the evening before the ACTH stimulation. Plasma F, A, 17-OH-P and T were measured by specific radioimmunoassays (RIA). Following ACTH stimulation, the increase of 17-OH-P was significantly higher in CAH-heterozygotes than in controls in both tests (P less than 0.0005). Heterozygotes were characterized by a 17-OH-P increase after ACTH stimulation exceeding the + 2 SD limit of the 17-OH-P increase found in controls. The detection of female heterozygotes was considerably improved by the administration of dex. before testing (test 2). In males, however, a better identification of heterozygotes was obtained without previous administration of dex. (test 1). By these tests, 100% of female (test 2) and 79% of male (test 1) CAH heterozygotes could be correctly identified. There were no significant differences in the levels of F, A and T between heterozygotes and controls except for decreased T levels in test 1 (2P less than 0.01) in most male heterozygotes after ACTH stimulation.

Adrenal Cortex Function Tests↗
PubMed1979

Plasma testosterone in male puberty. II. hCG stimulation test in boys with hypospadia.

Plasma testosterone was determined by radioimmunoassay in 36 prepubertal boys with hypospadia prior to and 3 days after stimulation with 5000 IU of human chorionic gonadotrophin (hCG). As a control group, 30 boys of comparable age, predominantly with unilateral cryptorchidism, were studied. The increase in plasma testosterone levels after hCG was (median and range) 204 (83-393) ng/100 ml in the control group, whereas in the hypospadiac group a median increase of only 90 (33-272) ng/100 ml was found. The difference between the median testosterone levels after hCG stimulation in the two groups investigated is statistically highly significant (P less than 0.0001). After hCG stimulation, 13 out of the 36 boys with hypospadia did not reach the lowest stimulated testosterone level (87 ng/100 ml) found in the control group. It is concluded that a substantial portion of the aetiologically obscure cases of hypospadia are caused by an endocrine testicular insufficiency.

Child↗
PubMed1978

Longitudinal studies of plasma aldosterone, corticosterone, deoxycorticosterone, progesterone, 17-hydroxyprogesterone, cortisol, and cortisone determined simultaneously in mother and child at birth and during the early neonatal period. I. Spontaneous delivery.

In order to obtain the still lacking reference data of individual plasma steroids in the immediate postnatal period needed for the assessment of adrenocortical function in various neonatal maladaptation syndromes, aldosterone (A), corticosterone, deoxycorticosterone (DOC), progesterone (P), 17-hydroxyprogesterone (17-OHP), cortisol, and cortisone were simultaneously followed in the same human newborn in a single 250-500 microliters peripheral plasma sample obtained at constant times during the first week of life using a mechanized Sephadex LH-20 multicolumn chromatography and standardized RIAs. Mean concentrations in 12 spontaneously delivered full term newborns of either sex and in paired umbilical (UV) and peripheral maternal (MV) venous plasma are given in the table. Besides significant maternoumbilical gradients in each steroid, DOC, P, 17-OHP, and cortisone, originating predominantly from the fetoplacental unit, disappear rapidly with steadily increasing half-lives. A, corticosterone, and cortisol, however, remain elevated in comparison with later infancy, with the exception of a marked "glucocorticoid dip" in cortisol and corticosterone levels between 2 and 12 h after birth.

17-alpha-Hydroxyprogesterone↗
PubMed1977

Plasma gonadotropins and estrogens in girls with idiopathic precocious puberty.

Luteinizing hormone (LH), follicle-stimulating hormone (FSH) estrone, and estradiol were measured radioimmunologically in more than 60 plasma specimens of 34 girls suffering from idiopathic precocious puberty. Although the median values of both gonadotropins in the plasma of the patients (LH = 1.0 ng/ml; FSH = 1.6 ng/ml) were higher than those from healthy prepubertal girls (LH = 0.6 ng/ml; FSH = 0.5 ng/ml), only 23 out of 64 LH levels and 30 out of 64 FSH levels exceeded the upper normal limit for age. While the median value of plasma estrone (13 pg/ml) was found to lie within the normal range for prepubertal girls (7-29 pg/ml) and only 13 out of 75 estrone values were pathologically elevated, the median value of plasma estradiol (22 pg/ml) was nearly 3 times higher than the normal median for prepuberty (8 pg/ml). Of 75 estradiol levels, 35 were above normal for age. Grouping the values according to the stage of sexual development revealed considerably lower gonadotropin and estrogen levels in the patients than in normally maturing girls of the same developmental stage. However, patients who were examined repeatedly at short intervals over a 1-month period showed an almost cyclic sequence of their estradiol levels similar to the pattern observed in healthy pubertal girls.

Age Factors↗
PubMed1976

Mean 24-hour growth hormone and testosterone concentrations in relation to pubertal growth spurt in boys with normal or delayed puberty.

The mean growth hormone concentration during 24-hour period in 7 boys of short familial stature and a growth rate of 3.2-5.4 cm/year was between 1.0 and 4.6 ng/ml serum. In 7 boys with pubertal growth spurt and familial tallness (growth rate 7.2-11.0 cm/year) it varied from 0.97 to 4.4 ng/ml and in 6 boys with constitutional delay of puberty (a growth rate of 4.2-5.2 cm/year prior to puberty) from 1.3 to 4.3 ng/ml. No correlation was found between the 24-hour mean growth hormone concentration and the mean 24-hour testosterone concentration in serum or the growth rate, but a correlation was found between testosterone and the growth rate. It is concluded that the growth spurt in puberty is not due to a change in growth hormone concentration but rather to the increase of androgen production in puberty.

Adolescent↗
PubMed1976

Effect of p-chlorophenylalanine (PCPA) on pituitary hormones and testosterone in the human.

L-p-Chlorophenylalanine (L-PCPA) was given in a dosage of 1.5 g daily, to 6 healthy male subjects over a period of 12 days. No effect on plasma luteinizing hormone (LH), follicle stimulating hormone (FSH), growth hormone (GH), thyroid stimulating hormone (TSH), testosterone and other steroid hormones could be observed. These results are discussed in respect to the sexually stimulating effect of PCPA.

Adult↗