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Biomedical subjects

G Bodemar

Publications and source records attributed to G Bodemar.

At least 73 records · Page 4Linked to original sources
PubMed1982

Pharmacokinetics of cimetidine and its sulphoxide metabolite during haemodialysis.

A single intravenous dose of cimetidine 200mg was administered to 6 patients with severe chronic renal failure one hour prior to haemodialysis. The plasma concentrations of cimetidine and its sulphoxide metabolite at the start of haemodialysis were 2.74 +/- 0.12 and 0.76 +/- 0.08 microgram/ml, and after dialysis for 4h 1.08 +/- 0.10 and 0.51 +/- 0.08 microgram/ml, respectively (mean +/- SE). The average haemodialysis clearance (ClHDa) of cimetidine during dialysis was 46-92 ml/min at a dialysate flow rate of 320 ml/min and blood flow rates in the 6 patients between 160-240 ml/min. The mean ClHDa of the sulphoxide metabolite was 44% higher than that of cimetidine, and ranged between 49-148 ml/min. During haemodialysis the mean plasma elimination half-life (t 1/2) of cimetidine was 3.24h (range 2.08-5.08) and of the sulphoxide metabolite 9.49h (range 4.70-14.39). There was a significant relationship between the elimination rate constant (beta) and ClHDa of the sulphoxide metabolite (p less than 0.01), but no such relationship was found between beta and ClHDa of cimetidine. The mean total amount of cimetidine eliminated during dialysis was 27.3mg (range 17.9-31.8), which was 9.0-15.9% of the given dose. Between 12.2-21.2mg (mean 15.3) of the sulphoxide metabolite was eliminated in the dialysate. Major adjustment of the dose of cimetidine on days of dialysis is not necessary.

Adult↗
PubMed1982

The pharmacokinetics of cimetidine and its sulphoxide metabolite in patients with normal and impaired renal function.

1 The pharmacokinetics of cimetidine and its sulphoxide metabolite was studied after a single intravenous dose of 200 mg cimetidine in nine patients with normal renal function and ten patients with severe renal failure on regular haemodialysis and during continuous oral cimetidine treatment in ten patients with normal renal function and 31 patients with different degrees of renal failure. 2 In normal renal function a mean of 47.3% of the single intravenous dose was excreted as unchanged drug and 12.8% as cimetidine sulphoxide. The mean plasma elimination half-life (T1/2) of cimetidine was 2.0 h and of cimetidine sulphoxide 1.7 h. 3 In severe renal failure a mean of 2.2% of the single intravenous dose was excreted as unchanged drug and 0.5% as cimetidine sulphoxide. The mean plasma T1/2 of cimetidine was 3.9 h. The plasma concentrations of the sulphoxide metabolite increased successively with time after dosing and no elimination phase was observed still 9 h after dose. The mean non-renal clearance of cimetidine was 210 ml/min and lower than in normal renal function, suggesting decreased metabolism of cimetidine in uraemia. 4 During continuous oral cimetidine treatment in patients with normal renal function and in patients g and no elimination phase was observed still 9 h after dose. The mean non-renal clearance of cimetidine was 210 ml/min and lower than in normal renal function, suggesting decreased metabolism of cimetidine in uraemia. 4 During continuous oral cimetidine treatment in patients with normal renal function and in patients g and no elimination phase was observed still 9 h after dose. The mean non-renal clearance of cimetidine was 210 ml/min and lower than in normal renal function, suggesting decreased metabolism of cimetidine in uraemia. 4 During continuous oral cimetidine treatment in patients with normal renal function and in patients with different degrees of renal failure given reduced doses of cimetidine the plasma concentrations of the sulphoxide metabolite were higher with decreasing renal function. The mean plasma T1/2 of cimetidine was 3.1 h in mild renal dysfunction (creatinine clearance 50-75 ml/min) and 4.5 h in severe renal failure (creatinine clearance 5-15 ml/min) and of cimetidine sulphoxide 5.3 and 14.4 h respectively. 5 Toxicity studies of cimetidine sulphoxide may be needed to assess if high plasma concentrations of the sulphoxide metabolite in severe renal failure are of clinical significance.

Administration, Oral↗
PubMed1982

Cimetidine, but not oxmetidine, penetrates into the cerebrospinal fluid after a single intravenous dose.

1 Thirty-six patients with various neurological diseases or symptoms received single intravenous doses of either cimetidine 400 mg (n = 19) or oxmetidine 200 mg (n = 17), 15 or 60 min before a diagnostic lumbar puncture. 2 In the 15 min CSF samples concentrations of cimetidine were detectable but not measurable in 5 and non-detectable in 3 patients. 3 In the 60 min CSF samples the concentrations of cimetidine were detectable in all 11 patients and were measurable in 8 of these patients with a mean +/- s.e. mean of 0.12 +/- 0.01 microgram/ml. These CSF concentrations were correlated to simultaneously measured plasma concentrations (P less than 0.01). The mean ratio CSF/plasma concentration was 0.03. 4 No detectable concentrations of oxmetidine were found either in the 15 min (n = 9) or in the 60 min (n = 8) liquor samples. 5 Cimetidine penetrates the blood-drain barrier slowly and not freely after a single dose. Our data suggest that the new histamine H2-receptor antagonist oxmetidine does not cross this barrier.

Adult↗
PubMed1981

Antacid/anticholinergic, cimetidine, and placebo in treatment of active peptic ulcers.

Seventy-two patients with duodenal (54) or prepyloric (18) ulcers have taken part in a 12-week double-blind trial. Twenty-four patients received cimetidine, 1 g/day; 24 patients received 10 ml of an antacid suspension (buffering 85 mmol acid) 1 and 3 h after every meal and at bedtime and 0.6 mg L-hyoscyamine in sustained-release tablets twice a day; and 24 patients received placebo. The healing rate after 3 weeks' treatment was 67% (p less than 0.005 compared with placebo) with cimetidine, 50% (p less than 0.01) with antacid/anticholinergic, and 13% with placebo. After 6 weeks' treatment 83% were healed with cimetidine (p less than 0.005 compared with placebo), 96% with antacid/anticholinergic (p less than 0.005), and 33% with placebo. A further 6 weeks' treatment gave healing rates of 96% for cimetidine, of 100% for antacid/anticholinergic, and of 50% for placebo. Compared with placebo, cimetidine but not antacid/anticholinergic caused a faster relief of night-time ulcer pain (p less than 0.05). There was a significant correlation between healed ulcers and complete relief of ulcer symptoms (p less than 0.05). In the placebo group the ulcers of nonsmokers healed to a higher extent than those of smokers (p less than 0.05). During 1 year of follow-up there was no difference between the two actively treated groups in number or severity of symptomatic relapses. Time to relapse was, however, significantly shorter after treatment with cimetidine than after antacid/anticholinergic (p less than 0.05). Recurrences occurred more often (p less than 0.05) after slow healing (6-12 weeks) than after fast healing (3 weeks).

Aluminum Hydroxide↗
PubMed1980

The effects of cimetidine (Tagamet) on renal function in patients with renal failure.

Cimetidine has been administered during 7 days to 28 patients with different degrees of renal failure. Thirteen of these patients had a further week's treatment at least one month later. The daily dose of cimetidine was reduced in relation to pretrial values of creatinine clearance. There was a clear rise in serum creatinine all through the trial (22.3 +/- 2.6% at day 7) (p < 0.001). Maximal decreases in creatinine clearance occurred on day 2 (21.8 +/- 2.2%) and day 3 (23 +/- 2.0%) (p < 0.001), but were still present on days 6 (16.4 +/- 2.9%) and 7 (17.3 +/- 2.8%) (p < 0.001). There was a small rise in serum uric acid all through the trial (p < 0.05). Three days after finished treatment there were no significant differences in serum creatinine, creatinine clearance and serum uric acid when compared to pretrial values. The pattern of changes in serum creatinine and creatinine clearance was the same in both mild and severe renal failure. Glomerular filtration rate determined by |52Cr¿ EDTA clearance before, on day 3 of treatment and 3 days after treatment did not show any differences. No change was seen in serum beta 2-microglobulin during the trial. The decrease in creatinine clearance during treatment with cimetidine is probably not caused by a reduction of glomerular filtration rate, but could be explained by competition by cimetidine for tubular secretion of creatinine. Treatment with cimetidine of patients with renal failure may invalidate measurements of serum creatinine and creatinine clearance as standard routine tests for glomerular filtration rate.

Adult↗
PubMed1979

Oral absorption of cimetidine and its clearance in patients with renal failure.

The plasma concentration curve after a single oral dose of cimetidine 200 mg was followed in 27 patients with varying degrees of chronic renal failure (creatinine clearance 1--52 ml/min) and in 46 patients with normal serum creatinine. Compared to the latter patients, the plasma concentration was higher and the elimination rate was slower in all uraemic subjects, including a group with moderate renal impairment. The preliminary recommendations of dosage for patients with a creatinine clearance below 5 ml/min, and for patients on regular haemodialysis, is cimetidine 200 mg every 12 h, 5-15 ml/min 200 mg every 12 to 8 h, 15-30 ml/min 200 mg every 8 h and 30-52 ml/min 200 mg every 6 h.

Adult↗
PubMed1979

The effect of cimetidine, a new histamine H2-receptor antagonist, on renal function.

Serum creatinine, endogenous creatinine clearance, (51Cr)EDTA plasma clearance and the concentration of beta2-microglobulin in serum and urine were determined in 19 patients before and during treatment with cimetidine for peptic ulcer disease. The mean concentrations of creatinine and beta2-microglobulin in serum increased significantly within normal limits after 2 and 6 weeks' treatment. However, creatinine clearance and (51Cr)EDTA plasma clearance were unchanged during the treatment. Thus, the observed increases in serum creatinine and beta2-microglobulin could not be explained by a diminished glomerular filtration rate. Inhibited tubular secretion of creatinine may explain the observed increase in serum creatinine during cimetidine treatment. Another hypothetical possibility is that a small increase in tubular reabsorption of both creatinine and beta2-microglobulin would account for the observed increases in creatinine and beta2-microglobulin in serum. It is concluded that, although statistically significant, the increases in serum creatinine and beta2-microglobulin are small and therefore of little relevance for the patient's treatment with cimetidine.

Adult↗
PubMed1979

The absorption of cimetidine before and during maintenance treatment with cimetidine and the influence of a meal on the absorption of cimetidine--studies in patients with peptic ulcer disease.

1 The absorption of a single oral dose of cimetidine taken on a fasting stomach or together with a meal was studied in 28 patients before and during 12 weeks treatment with cimetidine. 2 No significant changes in bioavailability were seen during treatment measured as the area under the blood concentration curve (AUC). 3 AUC after a single dose of 400 mg cimetidine was 2.05 times the area after a 200 mg dose. 4 There was a good correlation between AUC and the dose of cimetidine given corrected for body weight (r=0.89). 5 There was no difference in bioavailability if 200 mg cimetidine was taken on a fasting stomach or together with a beef steak meal. 6. During fasting conditions there was a peak in blood concentration at about one hour followed by a second unexplained peak during the third to fifth hour after dose administration. 7 With food the initial rise in blood concentrations was slower and there was only one peak occurring about 2 h after dose administration.

Adult↗
PubMed1978

Maintenance treatment of recurrent peptic ulcer by cimetidine.

68 patients with chronic peptic ulcer took part in a double-blind trial in which 32 received the histamine H2-receptor antagonist cimetidine, (400 mg twice daily) and 36 received a placebo, for a year. 6 of those on cimetidine had an endoscopically proven recurrent ulcer within a mean of 7 months, while 30 of those on placebo had one after a mean of 4 months (P less than 0.0005). 1 patient on cimetidine had two recurrences compared with 12 patients on placebo (P less than 0.0005). No patient in the cimetidine group had complications compared to 4 patients in the placebo group, 2 of whom had melaena and haematemesis and 2 melaena alone (P less than 0.05). 15 patients on placebo and 1 on cimetidine were referred for surgery during the trial because of symptoms from their recurrent ulcers. Day and night ulcer pain and antacid consumption were significantly less, and general wellbeing better, in cimetidine group. The only probable side-effect of cimetidine was reversible drug-induced liver damage of hypersensitivity type in 1 patient.

Adult↗
PubMed1978

Food-stimulated acid secretion measured by intragastric titration with bicarbonate in patients with duodenal and gastric ulcer disease and in controls.

Gastric acid secretion stimulated by a normally eaten beefsteak meal was measured for 4 h in 16 patients with duodenal ulcer disease (DU), in 9 patients with gastric ulcer disease (GU), and in 14 controls by intragastric titration with bicarbonate to a constant pH 5.5. Reproducibility of the method investigated in 6 DU and in 5 controls gave similar acid secretory values (var. coeff. = 7.5%). DU produced acid on a higher level and with longer duration after food than controls and GU (p less than 0.001). Apart from the second half of the first hour after food, when the acid secretion was higher in controls than in GU (p less than 0.025), there was no significant difference in acid output after food between GU and controls. Maximum gastrin values and 'total gastrin output' after food were significantly higher in GU than in controls, but these differences were not significant between GU and DU and between DU and controls. Fasting gastrin and gastrin levels after food were not correlated to basal acid output or acid output after pentagastrin or food in any of the groups. The maximal acid output after food was higher than the peak acid output after pentagastrin in controls, DU and GU. The relation between food- and pentagastrin-stimulated acid output was not statistically significantly different between the three groups. Instead, acid secretion after food was well correlated to acid secretion after pentagastrin in controls, DU and GU (r = 0.85).

Adult↗
PubMed1977

Influence of food on the effect of propantheline and L-hyoscyamine on salivation.

The absorption of a quartenary (propantheline, 30 mg) and a tetiary (1-hyoscyamine, 0.8 mg) anticholinergic compound was studied in 8 healthy volunteers by measuring the effects on salivation. Both compounds were administered as rapidly disintegrating tablets, 1-hyoscyamine also in a slow-release formulation (Egazil Durules). The three preparations and placebo were administered under fasting conditions and with a standardized light meal using a randomized cross-over design. Salivation measurement were performed with a citric acid stimulation method every hour for 10 hours. In the fasting patient, all three anticholinergic test preparations decreased the salivation significantly. When taken with food, the effect of propantheline was almost abolished, while the effects of the 1-hyoscyamine preparations were uninfluenced. It was concluded that the clinical effects of proprantheline might be extremely varying depending how the drug is taken in relation to meals. In contrast the clinical effects of 1-hyoscyamine seem to be independent of food intake.

Adolescent↗
PubMed1976

Cimetidine in the treatment of active duodenal and prepyloric ulcers.

44 patients with endoscopically confirmed duodenal (36) or prepyloric (8) ulcers have received in a double-blind trial either the histamine H2-receptor antagonist cimetidine (30 patients) or placebo (14 patients) for six weeks. At three weeks 67% of patients treated with cimetidine and 17% of those receiving placebo had endoscopically healed ulcers (chi2 = 8.49; P less than 0.005). At six weeks all except 3 patients receiving cimetidine (90%) had healed ulcers compared with 36% receiving placebo (chi2 = 11.11; P less than 0.001). Those receiving cimetidine had less daytime and nocturnal pain than patients on placebo. The differences were statistically significant for daytime pain during four of six weeks. The cimetidine-treated patients consumed significantly less antacids than placebo-treated patients and these patients' overall assessments of their wellbeing were significantly better. All patients on cimetidine had a significant reduction (P less than 0.0005) of their basal and pentagastrin-stimulated acid secretion, but no reduction in acid secretion was measured in the group who received placebo.

Adult↗