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Biomedical subjects

K Sinterhauf

Publications and source records attributed to K Sinterhauf.

At least 19 recordsLinked to original sources
PubMed1999

Prevalence of risk factors of coronary heart disease in Turks living in Germany: The Giessen Study.

Turkish people represent the majority of immigrants in Germany. Even though a high proportion of Turks has been living in Germany since about 20 years, little is known about risk factors of coronary heart disease (CHD) in this population. In this study a sample of 325 male and 155 female Turks are investigated, who voluntarily underwent a health check-up in Germany. Data about the presence of CHD, risk factors and blood parameters were collected. Mean residence time was 21 and 17 years (males/females). A low percentage of female participants was observed compared to the general Turkish population in Germany. Age adjusted prevalence of CHD reached 9.5% in males and 6.7% in females, respectively. Dyslipoproteinemia (DLP) showed the highest prevalence of all risk factors investigated in both genders. Total cholesterol (TC) levels were comparable to those of other western countries and remarkably higher than reported for the population in Turkey. Besides this, low high density lipoprotein-cholesterol (HDL-C) and apolipoprotein A-I (ApoA-I) levels could be found in the majority of the sample. The highest odds ratios for CHD were estimated for stress and hypertension in males and obesity in females. It is concluded that Turkish immigrants in Germany showed an assimilation of lipid pattern to western populations. However, reasons for low HDL-C levels remain unclear. Changes in the lipid metabolism chiefly seem to contribute to the risk factor pattern of Turkish immigrants in Germany.

Adolescent↗
PubMed1980

Urinary kallikrein in normotensive subjects and in patients with essential hypertension.

Basal 24 hour urinary kallikrein excretion of 20 patients with uncomplicated essential hypertension did not differ significantly from that of 18 normotensive age-matched control subjects. 4 of the 20 hypertensive patients, however, had low kallikrein excretion. Furosemide (40 mg i.v.) caused an increase of urinary kallikrein excretion in the normotensive subjects and in most of the patients with essential hypertension. The stimulating effect of furosemide was less pronounced or even absent in 7 hypertensives. No circadian rhythm of urinary kallikrein excretion was observed. There were weak correlations between 24 hour kallikrein excretion and urinary volume (r=0.59; p < 0.05), and potassium excretion (r=0.51; p < 0.05) in the normotensives. In the hypertensives correlations were found between 24 hour kallikrein excretion and potassium excretion (r=0.51; p < 0.05), aldosterone excretion (r=0.57; p < 0.01), and creatinine clearance (r=0.59; p < 0.01). Our findings do not support the concept that the renal kallikrein-kinin system might play a primary role in the pathogenesis of essential hypertension.

Adult↗
PubMed1980

[Plasma levels and renal excretion of [3H]-codeine phosphate in humans receiving tablets or depot capsules (author's transl)].

In two studies (a) a single 50 mg [3H]-codeine phosphate depot capsule (a special sustained-release form) and (b) two dosages of 25 mg [3H]-codeine phosphate tablets with a time lag of 4 h for the second administration were given to the same 4 healthy volunteers. In both studies plasma level and renal excretion of the radioactivity and plasma level of the specifically extracted unchanged drug were measured. The renal exretion was nearly complete within 48 h in both studies. The relative bioavailability of the [3H]-codeine phosphate released from the capsule and from the two tablets was shown to be the same comparing the areas under the plasma level curves. Assuming that the effective codeine plasma level is about 20 ng/ml a cough preventing period of at least 8 h after administration of a codeine depot capsule can be concluded from the given results.

Adult↗
PubMed1980

[Effect of bromopride on gastric acid secretion (author's transl)].

It has been shown that bromopride (Viaben) stimulates esophageal and gastric motility but no information exists regarding its effect on gastric acid secretion. The current study investigates the effect of bromopride on the basal and cephalic phase of gastric acid secretion and on serum gastrin levels. Studies were performed in 10 healthy volunteers using a standard aspiration technique. Following the collection of basal acid secretion all subjects received an i.v. injection of 10 mg bromopride or placebo in randomised order. 1 h after drug injection sham feeding was performed while gastric acid was continuously collected and repeated blood samples were drawn for serum gastrin determination. Neither basal secretion nor the cephalic phase of gastric acid secretion were altered by bromopride. Though secretion tended to be less following drug injection, none of these differences reached statistical significance. In addition serum gastrin levels remained unchanged following drug injection. The results of this study suggest that bromopride does not alter gastric acid secretion.

Adult↗
PubMed1980

[Experience with CT and adrenal venography in the diagnosis of adrenal disease with endocrine activity (author's transl)].

Report of the result of CT and venography in 12 patients with suspected adrenal disease, venography being combined with selective blood sampling for hormone analysis. In one patient CT showed a 1.6 cm big pheochromocytome in the left adrenal gland, not demonstrated by venography, but proven by analysis of the blood sample. Both methods showed hyperplasia of both adrenals in one patient with Cushing Syndrome with elevated Cortisol levels found in the analysis of the blood smples. Of 3 patients with hyperaldosteronism, venography was able to demonstrate 2 Conn adenomas, not seen on CT; whereas CT showed the third 2 X 1.5 cm big Conn adenoma hidden in an enlarged adrenal gland. Hormone analysis was helpful in 2 of these cases, while in the third it was misleading. The authors believe that both methods should be employed to localise over adrenal disease with endocrine activity.

Adrenal Gland Diseases↗
PubMed1979

[The influence of primidone on thyroid function (author's transl)].

The influence of primidone on thyroxine level, T3 index, FT4 index, triiodothyronine level, T3 (RIA)/T4 (RIA) quotient as well as on the TSH basal and stimulated values was investigated in 30 children on long-term treatment. The values obtained were compared statistically with those of a normal group. During primidone treatment a drop in T4 level and in FT4 index as well as an increase in T3 (RIA)/T4 (RIA) quotient was observed. On the other hand the triiodothyronine level and the T3 index were not influenced. The TSH basal and stimulated values were not statistically different from the control group. Thus the primidone-treated children are euthyroid according to the TRH test. Primidone probably stimulates hepatocellular thyroxine breakdown.

Child↗
PubMed1979

Urinary kallikrein in normotensive subjects and in patients with essential hypertension.

1. Excretion of urinary kallikrein was normal in 13 out of 15 patients with uncomplicated essential hypertension. 2. Frusemide increased urinary kallikrein excretion in normotensive subjects and in patients with essential hypertension. The stimulating effect of frusemide on urinary kallikrein was significantly diminished in patients with essential hypertension. 3. No correlations of urinary kallikrein with sodium, potassium, and aldosterone excretion were found. 4. The results do not support the idea that urinary kallikrein plays a primary role in the pathogenesis of essential hypertension.

Adult↗
PubMed1979

[Enflurane anaesthesia and plasma cortisol (author's transl)].

The influence of enflurane on adrenocortical function was investigated by determining the concentration of plasma cortisol by a radioimmunoassay during general anaesthesia and abdominal operations. Thirty minutes after the start of anaesthesia with enflurane 0.8--2.0%, N2O:O2 (2:1) and pancuronium, the plasma cortisol decreased slightly in the preoperative period; it increased markedly and continuously during the intra- and postoperative period. There was no correlation between plasma concentrations of enflurane, determined by gas chromatography, and cortisol.

Adrenal Cortex↗
PubMed1979

[Plasmacortisol and parturition under epidural anaesthesia (author's transl)].

Plasma cortisol was determined by a radioimmuno assay during labour, at and after delivery in 16 primigravidas und epidural anaesthesia and was compared with 13 primigravidas, who delivered under pentazocine or pethidine and pudendal block. Cortisol levels decreased after effective epidural anaesthesia during the first stage of labor and for delivery. They increased in the control patients for delivery and was significantly higher than in the patients under epidural anaesthesia. Two and 20 hours post partum cortisol concentrations decreased in both groups. Cortisol levels in the fetuses and newborns was markedly lower than those of mothers. At delivery, the cortisol concentration of the newborns of both groups was the same. The changes of cortisol concentrations in this study support the conclusion that epidural anaesthesia during labor and delivery reduces stress for the mother, but not for the fetus.

Anesthesia, Epidural↗
PubMed1978

Testosterone metabolism in patients with advanced carcinoma of the prostate: a comparative in vivo study of the effects of oestrogen and antiprolactin.

In the light of the high incidence of cardiovascular side effects with oestrogen therapy in patients with prostatic cancer, other medications altering androgen metabolism are under investigation. The influence of the anti-prolactin bromocriptin (CB157) on plasma kinetics of testosterone and on endogenous hormones was studied and compared with the effect of ethinyl oestradiol in 25 patients with prostatic carcinoma. Bromocriptine significantly suppressed both prolactin and testosterone, inhibited the transfer of androgen from the inner pool into the deep compartment and favoured its degradation. Ethinyl oestradiol decreased testosterone, LH and FSH, and prolonged the biological half-life of testosterone. The effects of bromocriptine on androgen metabolism might be of therapeutic value in patients with prostatic carcinoma.

Bromocriptine↗
PubMed1978

Prostatic carcinoma: plasma kinetics and intraprostatic metabolism of testosterone in low-dose estrogen-treated patients in vivo.

Plasma kinetics, in vivo uptake, and intraprostatic metabolism of 3H testosterone was investigated in 9 patients with advanced carcinoma of the prostate. The metabolic effect of low-dose ethinyl estradiol was studied (estrogen suppressed testosterone, luteinizing hormone, and follicle-stimulating hormone). The production rate of testosterone was lowered, the elimination of androgen from plasma delayed. The uptake of testosterone and metabolites by the prostatic carcinoma was suppressed. Estrogen did not alter significantly the intraprostatic androgen turnover.

Aged↗
PubMed1978

Bromocriptine and prostatic carcinoma: plasma kinetics, production and tissue uptake of 3H-testosterone in vivo.

The influence of the anti-prolactin bromocriptine on plasma kinetics, production rate and tissue uptake of testosterone was investigated in 15 patients with newly diagnosed stages C and D prostatic carcinoma. Bromocriptine was given for 5 days in a daily dose of 15 mg. orally. The studies were performed with the single injection technique using the 2-compartment model. Plasma testosterone, serum prolactin, and luteinizing and follicle-stimulating hormones were determined initially. Blood samples were drawn up to 5 hours after the injection of 3H-testosterone. For tissue studies a transrectal needle biopsy was done 3 hours post-injection. Bromocriptine suppressed prolactin and the endogenous testosterone level. Furthermore, it favored the elimination of 3H-testosterone, lowered the production rate of testosterone and hampered the in vivo uptake of the 3H-label into prostatic carcinoma tissue. Finally, the grading of the tumor lesions affected only the pre-bromocriptine uptake of radioactive androgens and not the uptake in response to bromocriptine. The potential clinical impliications of these observations are discussed.

Aged↗
PubMed1977

Low renin hypertension.

Low renin hypertension probably does not represent a clinical entity. In many patients with low renin hypertension blood pressure is normalized by treatment with diuretics only; in these patients a (genetic?) sensitivity to salt might play a predominant role in the pathogenesis of hypertension and renin suppression. In another group of patients renin suppression appears to be secondary to the hypertensive process. This is indicated by the observation that prevalence of low renin hypertension increases with age and that it is more frequent in advanced stages of hypertension. Also a diminished sympathetic tone might play a part in the renin unresponsiveness. Finally, although no positive evidence was found, the possibility cannot be excluded that, at least in some cases, a mineralocorticoid other than aldosterone is involved. Neither in normotensive subjects nor in hypertensive patients, both with normal and with low plasma renin was a correlation between plasma renin concentration and plasma aldosterone concentration following stimulation by upright posture found. More detailed studies will be necessary to clarify the relationship between the renin-angiotensin system and aldosterone secretion during upright posture, in particular in patients with low renin hypertension.

Adrenal Cortex↗