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Biomedical subjects

H Dörr

Publications and source records attributed to H Dörr.

16 recordsLinked to original sources
PubMed2005

Are antisperm antibodies indeed sperm-specific?

Antisperm antibodies (ASA) are present in a high percentage of infertile patients. The development of ASA in the male depends on the sequestration of antigens on germ cells, the testis being an immune privileged region. In this study, we investigated the specificity of ASA binding to sperm antigens by exposing a number of organ preparations to ASA. In none of the organ homogenates was a significant difference between the results of the Western blot with ASA-containing fluids, neither serum nor seminal plasma, and those without ASA observed. We conclude from our results that the ASA tested in our study obviously are sperm-specific. ASA as an autoimmune are thus restricted to spermatozoa. The antigens are suitable for trials in immune therapy, they may also serve for the development of antigen-specific diagnosis and treatment in infertility. They also indicate cognate antigens of possible immune contraceptive agents.

Antibody Specificity↗
PubMed2000

Effects of subchronic paroxetine administration on night-time endocrinological profiles in healthy male volunteers.

To evaluate the subchronic effects of paroxetine, a selective serotonin reuptake inhibitor, on nocturnal endocrinological profiles, eight healthy male volunteers with no personal or family history of a psychiatric or neurological disease were administered paroxetine (30 mg/day) or placebo in a double-blind cross-over design. Drugs were given as a single dose at 10:00 h for a period of 4 weeks each. Between days 21 and 28 of each treatment period, sleep EEG was registered for four consecutive nights from 23:00 to 07:00 h. During the last night, hormonal profiles for prolactin, growth hormone (GH), cortisol, corticotropin (ACTH), luteinizing hormone (LH), testosterone and melatonin were determined, and area-under-the-curve values were calculated. None of the endocrinological parameters revealed any statistically significant changes. A trend could be found for an increased cortisol production under paroxetine (P = 0.069). ACTH, LH, and melatonin showed slight and non-significant decreases. Prolactin release was only marginally elevated (+7%). The mean sleep onset GH release (as measured for a time period of 180 min after sleep onset) was decreased by about 30% under paroxetine. However, statistical significance could not be reached. For hGH, there was a delayed mean GH-peak under paroxetine. Nocturnal testosterone secretion remained almost unaltered. The lack of significant endocrinological alterations might be partially explained by both adaptational phenomena under subchronic treatment conditions and the extended time span between the single morning dose and the registration period, respectively.

Adrenocorticotropic Hormone↗
PubMed1985

Effect of a single bolus of etomidate upon eight major corticosteroid hormones and plasma ACTH.

In a prospective controlled trial we investigated the effect of an induction dose of etomidate (0.26 mg/kg i.v.) on plasma ACTH, progesterone, 17 alpha OH-progesterone, 11-deoxycortisol, cortisol, cortisone, corticosterone, 11-deoxycorticosterone, and aldosterone in seven males undergoing general anaesthesia. Seven other male patients receiving thiopentone at induction (5.0 mg/kg i.v.) served as controls. Plasma ACTH concentrations rose higher in the etomidate group (346 +/- 124 vs. 117 +/- 74 pg/ml, mean +/- SEM), but the difference was not significant. After etomidate we found a clear suppression of plasma cortisol (P less than 0.01), cortisone (P less than 0.01), corticosterone (P less than 0.01), and aldosterone (P less than 0.05) compared to corticosteroid levels after induction with thiopentone. Plasma 11-deoxycortisol and 11-deoxycorticosterone concentrations were grossly elevated 210 min after etomidate (91 +/- 28 nmol/l and 7.04 +/- 0.47 nmol/l, respectively, P less than 0.01) demonstrating inhibition of 11 beta-hydroxylation of both glucocorticoid and mineralocorticoid intermediates. In contrast, no significant difference in plasma progesterone and 17 alpha-OH-progesterone levels was found between the two groups indicating that the cholesterol-side-chain cleavage enzyme is less sensitive to etomidate than 11 beta-hydroxylase. Our results suggest that after induction of anaesthesia with a single bolus of etomidate, inhibition of other enzymes in the corticosteroid-synthetic pathway (e.g. cholesterol-side-chain cleavage enzyme) is of little clinical relevance.

17-alpha-Hydroxyprogesterone↗
PubMed1984

[Growth hormone secretion and plasma renin activity in children following administration of clonidine].

Growth hormone and plasma renin activity were measured following oral clonidine. 50 out of 61 (82%) children without pituitary dysfunction receiving 75 micrograms Clonidine per sqm bodysurface area reached maximal levels of more than 6 ng GH/ml, and only 44 (72%) of more than 8 ng/ml. Following 25 micrograms Clonidine only 50% of children without pituitary dysfunction reached GH-levels of more than 6 ng/ml, and only 40% of more than 8 ng/ml. In 72% of children the growth hormone level determined in a single specimen taken 60 min after they fell asleep was higher than 6 ng/ml. Only 2 out of 33 children without pituitary dysfunction did not present sufficient amounts of growth hormone following clonidine or sleep to exclude growth hormone deficiency to screen for growth hormone deficiency. It is recommended to use 75 micrograms of Clonidine/m2 as a provocative test, and additionally to determine growth hormone after onset of sleep. Plasma renin activity prior to clonidine was 3.13 ng/ml/h, and 2.03 ng/ml/h 30 min after drugintake. Systolic blood pressure decreased from 118 mm Hg initially to 104 mm Hg (mean) within 30 min after clonidine was given orally.

Adolescent↗