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Biomedical subjects

W Röllinghoff

Publications and source records attributed to W Röllinghoff.

17 recordsLinked to original sources
PubMed1983

Absence of in vivo and in vitro interactions of an aluminum hydroxide, magnesium hydroxide containing antacid with cimetidine in patients with peptic ulcer.

In view of contradictory reports on the bioavailability of cimetidine in the presence of concomitantly administered antacids we studied the areas under the plasma concentration time curves (AUC) of cimetidine, the maximal concentrations (cmax) and the time, at which cmax was reached (tmax) in eight patients (five patients with duodenal ulcer, three patients with gastric ulcer) with and without the administration of an aluminum hydroxide magnesium hydroxide containing antacid (Maaloxan). No significant effects of the antacid on AUC, cmax and tmax of cimetidine were found. In vitro studies also showed no adsorption of cimetidine to aluminum hydroxide, magnesium hydroxide or the antacid.

Adult↗
PubMed1982

Inhibition of drug metabolism by cimetidine in man: dependence on pretreatment microsomal liver function.

The effect of cimetidine on hepatic microsomal drug metabolism was studied in six patients with normal liver and eleven patients with chronic liver disease using the aminopyrine breath test. Before administration of cimetidine, the elimination rate constant of 14CO2 from breath (Kb) was 28.3 +/- SD 1.3%/h in patients with normal liver and 13.5 +/- 7.7%/h in patients with liver disease (P less than 0.001). After 7 days of cimetidine therapy (1 g/day) Kb decreased to 23.3 +/- 5.2%/h (19.0 +/- 13.8% decrease; P less than 0.05) and 7.4 +/- 5.8%/h (50.5 +/- 14.4% decrease; P less than 0.001), respectively. Plasma levels of cimetidine were not significantly different (1.05 +/- 0.14% micrograms/ml v. 0.88 +/- 0.41; P greater than 0.05). The findings indicate that therapeutic doses of cimetidine lead to an inhibition of drug metabolism which is more pronounced in patients with impaired liver function than in liver normals. Therefore, patients with chronic liver disease may be at increased risk with respect to interactions between cimetidine and other drugs which are demethylated by the liver.

Aged↗
PubMed1981

Nicotinic acid test in the diagnosis of Gilbert's syndrome: correlation with bilirubin clearance.

A provocation test with nicotinic acid (50 mg intravenously) was performed in 13 patients with Gilbert's syndrome and seven healthy volunteers to investigate the diagnostic value of several test parameters and to correlate them with the bilirubin clearance. The maximal increment of unconjugated serum bilirubin, the retention at four hours, and the area under the bilirubin concentration time curve. (AUC) were measured. Significant differences between patients and controls were found with regard to the AUC (7.95 +/- SD, 3.29 mmol/min/l vs. 3.08 +/- 0.57; P less than 0.001), the increment of unconjugated bilirubin (24.1 +/- 7.1 mumol/l vs. 10.2 +/- 3.2; P less than 0.001) and the retention (77.7 +/- 8.9% vs. 45.8 +/- 27.4%; P less than 0.02). Of those, the AUC discriminated best between patients and controls. Five patients with Gilbert's syndrome had normal serum bilirubin concentrations (less than 17.1 mumol/l = 1 mg%) at the time of the study, but abnormal AUC and bilirubin increment. A significant correlation was found between the bilirubin clearance and the retention (r = -0.96; P less than 0.001) as well as the AUC (r = -0.82; P less than 0.05) but not with the bilirubin increment. This simple test may be used to assess the disturbance of bilirubin clearance in Gilbert's syndrome.

Adult↗
PubMed1977

[Lysozyme levels in chronic inflammatory bowel diseases (author's transl)].

Lysozyme concentrations in serum and urine were determined in 101 patients with Crohn's disease and 26 patients with ulcerative colitis. Lysozyme was assayed according to the lysoplate method of Osserman against a standard of humam lysozyme. The mean serum lysozyme concentrations (+/- S.E.M.) for each group were as follows: controls 8.4 +/- 1.8 (n equals 38), Crohn's disease 8.2+/-2.6 (n equals 101), ulcerative colitis 8.7+/-3.0 (n equals 26). No significant differences were found in serum lysozyme levels of the various groups of patients (2p is greater 0.05). There existed no correlation (r equals 0.12, n equals 129, p is greater than 0.05) with the activity of the disease. Serum lysozyme levels were significantly higher in patients affected by Crohn's disease of the small and the large bowel than in patients with involvement of the small intestine only and operated patients (2p is less than 0.05). The discriminative value of these findings with respect to the clinical course of such patients is limited because no significant differences are found between the levels of patients with Crohn's disease and controls. Neither in case of Crohn's disease nor ulcerative colitis were the mean urine lysozyme concentrations increased. These findings show that the determination of serum and urine lysozyme levels is unsuitable in respect of the differential diagnosis of inflammatory bowel disease as well as of the assessment of activity and extent of the disease.

Adolescent↗
PubMed1977

[Immunological diagnosis of filariosis in persons returning from tropical countries and in European and indigenous inhabitants of endemic areas (author's transl)].

Serum samples from persons who lived in areas where onchocerciasis occurred or who had filariasis were examined with the complement fixation test and the indirect hemagglutination test for the presence of antibodies against crude extracts from Dirofilaria immitis, Onchocerca volvulus, Dipetalonema viteae, and Ascaris suum. The results could be interpreted as follows: 1. The indirect hemagglutination test was more sensitive than the complement fixation test for the demonstration of antibodies in sera from European and indigenous inhabitants of endemic areas. 2. There were no differences between the responses to the four crude worm extracts among the groups of 21 patients with Loa loa, 12 patients with Onchocerca volvulus, 11 patients with Dipetalonema perstans, and 22 patients with clinical filariasis in whom no microfilaria had been found. It was concluded that the examination with crude extracts cannot give any information about the antigens that had caused the stimulation of antibodies.

Adolescent↗
PubMed1976

[Primary amyloidosis presenting as intrahepatic cholestasis (author's transl)].

In a 37-year-old female patient with marked signs of cholestasis and excessive hyperbilirubinaemia without any recognisable cause, the unexpected diagnosis of massive amyloidosis of the peri-collagenous and perireticular type was made after hepatic needle biopsy. There were also amyloid deposits in the rectal mucosa and in the bone marrow. Fifteen months after the onset of disease symptoms the patient died from the consequences of spontaneous intrahepatic haemorrhage. At the post-mortem investigation generalised amyloidosis with massive involvement of nearly all organs was found. Primary amyloidosis should be considered in the differential diagnosis of any aetiologically unexplained cholestasis.

Adult↗