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Biomedical subjects

H Vierhapper

Publications and source records attributed to H Vierhapper.

At least 91 records · Page 5Linked to original sources
PubMed1997

Routine measurement of plasma calcitonin in nodular thyroid diseases.

In a prospective study, plasma concentrations of human calcitonin (hCT) were determined in 1062 consecutive patients with thyroid nodular disease. Basal plasma hCT was above the normal range (>6 pg/mL) in 55 patients and was elevated up to more than 100 pg/mL (range, 127-5459) in 3 of these 55 patients. A pentagastrin-induced rise in hCT up to more than 100 pg/mL was observed in only 1 of 38 patients with a basal concentration of hCT between 5-10 pg/mL, but was found in 10 of 31 patients with basal hCT ranging from 10-100 pg/mL. Histologically, 7 of the 14 patients with either basal or stimulated plasma concentrations of hCT above 100 pg/mL presented C cell hyperplasia, which in one case showed histological transition into a small (diameter, 3 mm) medullary thyroid carcinoma (MTC). Including this patient, MTC was found in 6 of the 12 patients. We conclude that the routine determination of hCT in all patients with thyroid nodular disease should be supplemented by pentagastrin-stimulation when the basal hCT concentration exceeds 10 pg/mL. Patients with basal and/or stimulated plasma CT concentrations of more than 100 pg/mL should be operated on because they run a substantial risk to suffer either MTC or C cell hyperplasia, a potentially precancerous condition. This will increase the chance of a timely diagnosis of MTC and provide the chance of curative surgery.

Calcitonin↗
PubMed1997

Determination of testosterone production rates in men and women using stable isotope/dilution and mass spectrometry.

Production rates of testosterone were determined in healthy men and women during the follicular phase of their menstrual cycle using the stable isotope dilution technique and analysis by gas chromatography/mass spectrometry. In an initial series of experiments, 0.07 mg/h (men) or 0.01 mg/h (women) 1,2-d-testosterone was infused for 36 h. After an equilibration period of 12 h, blood samples were obtained at 20-min intervals throughout 24 h. In men, no diurnal rhythmicity of testosterone production was observed, whereas in women, testosterone production rates were largest from 0400-1200 h. In a second series of experiments, the infused dose of 1,2-d-testosterone was reduced to 0.015 mg/h (men) and 0.0001 mg/h (women), respectively. Blood samples were obtained at 20-min intervals during the last 12 h (0800-2000 h) of the observation period. In accordance with results obtained by others using radioactive tracers, estimated production rates were 147 +/- 31 microg/h (3.7 +/- 2.2 mg/day in men) and 1.8 +/- 0.6 microg/h (0.04 +/- 0.01 [corrected] mg/day in women). To reduce both the duration of the experiment and the number of samples to be processed, we subsequently demonstrated that similar production rates may be obtained when the equilibration period before blood sampling is reduced to 6 h and the period of blood sampling is reduced to 4 h. This protocol is suitable for clinical use in a routine setting to obtain analytically correct estimates of testosterone production in vivo.

Deuterium↗
PubMed1997

Thromboxane A2 does not mediate angiotensin II-dependent nonischemic peripheral vasoconstriction in healthy men: a pilot study.

It has been suggested that angiotensin II-dependent hemodynamic effects are in part mediated by thromboxane A2 (TXA2). The present study investigates in 6 healthy normotensive men whether prostaglandin H2-TXA2 receptor blockade with 100 mg of linotroban (5(2-(phenylsulfonylamino)ethyl)-thienyloxy-acetic acid) p.o. influences angiotensin II-dependent peripheral regional vasoconstriction. Moreover, the regional balance of thromboxane B2 (TXB2), a stable metabolite of TXA2, across the leg vascular bed was assessed at baseline conditions as well as during exogenous infusion (0.2 microgram/min) of angiotensin II. Net transfemoral TXB2 balance was calculated from the respective arteriovenous plasma concentration differences and the corresponding regional plasma flow, the latter being determined by indocyanine-green dye, using appropriate catheterization techniques. Angiotensin II (0.2 microgram/min) induced a 66% increase in leg vascular resistance (p < 0.01) without affecting systemic hemodynamics. These regional hemodynamic effects of angiotensin II were not influenced by prostaglandin H2-TXA2 receptor blockade. Baseline TXB2 balance across the femoral vascular bed was equilibrated at slight extraction rates or around zero and remained unchanged during angiotensin II infusion. These results suggest that, in healthy man, angiotensin II-dependent, nonischemic peripheral vasoconstriction is not mediated by TXA2. Possible benefits of prostaglandin H2-TXA2 receptor blockade in pathological conditions with tissue malperfusion or ischemia are discussed.

Adult↗
PubMed1997

[Therapeutic possibilities in metastatic pheochromocytoma].

Malignant pheochromocytomas are rare. Although 5-year survival is less than 50%, the prognosis varies. Some patients, even those with extensive metastases, have been followed up for many years. If the tumor tissue's uptake is adequate (> 5 Gy/100 mCi) the therapeutic use of 131I-meta-iodobenzylguanidin (131I-MIBG) is at present the therapy of first choice. The use of cytostatic chemotherapy should be limited to patients with rapidly progressive disease.

3-Iodobenzylguanidine↗
PubMed1996

Effect of endothelin-1 in man--impact on basal and stimulated concentrations of luteinizing hormone, follicle-stimulating hormone, thyrotropin, growth hormone, corticotropin, and prolactin with and without pretreatment with nifedipine.

In healthy men, intravenous (IV) endothelin-1 suppresses the growth hormone (GH)-releasing hormone (GHRH)-stimulated increase in GH and prolactin (PRL) and augments corticotropin (ACTH)-releasing factor (CRF)-stimulated secretion of ACTH. Since some actions of endothelin-1 on pituitary function in vitro are antagonized by calcium channel antagonists, we have studied the effect of pretreatment with oral nifedipine (10 mg, given before infusion of endothelin-1 or vehicle) on basal and stimulated concentrations of pituitary hormones in a group of healthy men (N = 6). The augmentative effect of endothelin-1 on CRF-induced ACTH secretion (P < .05) was counteracted by pretreatment with nifedipine. Pretreatment with nifedipine further inhibited (P < .01) the GHRH-induced increase in plasma concentrations of GH (P < .05), which, in keeping with previous data, had already been reduced by IV endothelin-1 alone (P < .05). Thus, both endothelin-1 and nifedipine influence pituitary hormone secretion in healthy man. However, nifedipine does not ubiquitously counteract the effects of endothelin-1 since it enhances some of its actions on the pituitary and diminishes others. Endothelin-1 may therefore influence pituitary function by mechanisms other than activation of calcium channels alone.

Adrenocorticotropic Hormone↗
PubMed1996

CYP11B1 mutations causing congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency.

Accurate knowledge of the molecular basis of congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency is a prerequisite for genetic counseling, prenatal diagnosis, and treatment. Analysis of nine patients suffering from severe manifestations of this disorder led to the identification of seven novel mutations in their CYP11B1 genes. A Caucasian patient was homozygous for the missense mutation R448H, previously found only in Jews of Moroccan origin. An Iranian patient was found to be homozygous for a different mutation in the same codon, R448C. Of four unrelated patients, two were homozygous for a nonsense mutation (W247X), whereas two others were compound heterozygotes for W247X in combination with either R448H or E371G. Two other patients were homozygous for either the missense mutation A331V or an in-frame CTG insertion adjacent to codon 464 (InsCTG464). One patient was a compound heterozygote for two mutations in exon 2, a 28-bp deletion (delta 28bpEx2) and the missense mutation V129M. All of the missense mutations and the CTG insertion caused a complete loss of steroid 11 beta-hydroxylating activity when expressed in cultured cells. These data support previous suggestions of mutational hot spots in CYP11B1 and confirm that severe clinical manifestations are associated with complete loss of enzymatic activity.

Adrenal Hyperplasia, Congenital↗
PubMed1995

Kinetics of plasma cyclic GMP and atrial natriuretic peptide after intravenous, intramuscular and subcutaneous injection of 50 micrograms hANP in man.

Plasma kinetics of immunoreactive natriuretic peptide (IR-ANP) and cyclic guanosine monophosphate (cGMP) were studied after intravenous (i.v.), intramuscular (i.m.) and subcutaneous (s.c.) application of 50 micrograms human ANP (hANP) in six healthy, male volunteers. The study was single blind. Mean base-line IR-ANP value (N = 54) was 10.8 +/- 1.8 pmol/l. Five min after injection peak IR-ANP concentrations were reached i.v.: 149.5 +/- 94, i.m.: 25.6 +/- 10.8 and s.c.: 18.3 +/- 3.3 pmol/l while cGMP levels reached maximum values at 15 min or 30 min after application: i.v.: 30.6 +/- 12.1, i.m.: 19.2 +/- 8.5 and s.c.: 17.3 +/- 12.3 nmol/l with a mean base-line value of 13.2 +/- 2.1 nmol/l. The calculated corresponding areas under the IR-ANP curves (AUC) achieved about 22% bioavailability for i.m. and s.c. in comparison with the i.v. application. cGMP bioavailability was about 32%. No statistical difference was calculated between i.m. and s.c. application of 50 micrograms hANP. Changes in IR-ANP levels after i.m. and s.c. administration were not accompanied with effects on urine and electrolyte excretion while there was only a tendency in urine volume and sodium increase after i.v. administration. In conclusion after i.m. or s.c. application of hANP only a minor fraction (approximately 1/5) of IR-ANP is available in circulation in comparison with i.v. application with little or no biological effects.

Adult↗
PubMed1995

Activated naive CD4+ peripheral blood T cells in autoimmune thyroid disease.

To better understand the clinical significance of changes in lymphocytes in thyroid disease this study analyzed the proportion of CD19+, CD3+, CD4+ and CD8+ cells among circulating lymphocytes in Graves' disease (GD, n = 34) and autoimmune hypothyroidism (AH, n = 28) vs healthy subjects (n = 15). In addition, the expression of CD25 and CD45 isoforms on CD4+ T cells as well as their modulation by methimazole in patients with GD was measured using three color flow cytometry. It was observed that, irrespective of age, both patients with GD (17.6 +/- 7.0% +/- SD) and those with AH (19.0 +/- 9.5%) had an increased percentage of the CD25+CD45RA+ (naive) subpopulation of helper cells vs healthy subjects (7.9 +/- 2.3%, p < 0.0001). In patients with AH peripheral memory cells and hence overall CD25+ cells were more frequent among helper cells (56.7 +/- 12.2%) than in healthy subjects (40.8 +/- 14.0%, p < 0.001). Patients with GD (46.2 +/- 13.4%) did not differ from normal subjects in this respect. Treatment of GD with MMI reduced the percentage of CD25+CD45RA+ cells among CD4+ cells toward values seen in healthy subjects. In addition, we confirm previous reports that CD8+ cells toward values seen in healthy subjects. In addition, we confirm previous reports that CD8+ cells are significantly reduced in AH (23.9 +/- 4.9%) and untreated Graves' disease (23.2 +/- 6.6%) vs healthy subjects (32.2 +/- 5.9%, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effect of endothelin-1 in man: impact on basal and adrenocorticotropin-stimulated concentrations of aldosterone.

The effect of exogenous endothelin-1 [2 pmol (5 ng)/kg.min for 15 min, followed by 1 pmol (2.5 ng)/kg.min for 105 min] on basal and ACTH (250 micrograms, i.v.)-stimulated plasma concentrations of aldosterone, cortisol, testosterone, corticosterone, and 18-hydroxycorticosterone was investigated in a group of healthy male volunteers (n = 6). Plasma concentrations of aldosterone remained unchanged during a placebo experiment (i.e. in the absence of both exogenous ACTH and of endothelin-1). In the absence of exogenous ACTH, the i.v. administration of endothelin-1 did not influence plasma concentrations of aldosterone. The i.v. administration of 0.25 mg ACTH induced a rise in plasma concentrations of aldosterone from a basal value of 152.6 +/- 38.8 to 362.6 +/- 77.7 pmol/L. This ACTH-induced rise was markedly augmented (P < 0.01) by the concomitant administration of endothelin-1, when peak plasma concentrations of aldosterone of 632.5 +/- 230.2 pmol/L were observed. Basal and ACTH-stimulated concentrations of cortisol, corticosterone, and 18-hydroxycorticosterone were unchanged by the concomitant infusion of endothelin-1. Thus, exogenous endothelin-1 influences adrenal function in healthy men by selectively augmenting the ACTH-induced secretion of aldosterone.

Adrenocorticotropic Hormone↗
PubMed1995

[Diagnosis of endocrine-induced forms of hypertension].

High blood pressure is due to endocrine disorders in only a small fraction of hypertensive patients. However, the recognition of these conditions offers the potential chance to cure hypertension and hence to avoid secondary cardiovascular complications. It is therefore of pivotal importance for the group of patients in question.

Diagnosis, Differential↗
PubMed1994

Evidence for phosphoramidon-sensitive cleavage of big endothelin-1 involved in endothelin-stimulated hepatic glucose production.

Endothelin-1 (ET-1) is known to stimulate glycogenolysis in perfused rat livers and isolated rat hepatocytes. To determine the potential action of endothelin's precursor, big endothelin-1 (big ET-1), isolated rat livers were perfused with big ET-1 in a non-recirculating system. Thereby, big ET-1 (10 nM) induced a maximally three-fold increase (P < 0.01 vs. basal values) in hepatic glucose production at 60 min, which was almost completely abolished by concomitant infusion of 50 microM phosphoramidon, a sensitive inhibitor of the enzymatic cleavage of big ET-1 to ET-1. The corresponding incremental release of glucose by big ET-1 was 20.9-fold higher in the absence of phosphoramidon than in its presence (P < 0.01). In contrast, phosphoramidon did not inhibit hepatic glucose production induced by ET-1 (1 nM), glucagon (1 nM), and phenylephrine (5 microM). Glycogenolytic responses to 1 nM ET-1 (P < 0.01), but not to 1 nM glucagon (n.s.) were blocked by indomethacin (100 microM), indicating that prostaglandin release by non-parenchymal cells is at least in part involved in the hepatic ET-1 action. In conclusion, big ET-1 induces hepatic glucose release, which is suggested to depend on intrahepatic conversion of big ET-1 to ET-1 by a phosphoramidon-sensitive pathway.

Animals↗