Postprandial VLDL-triacylglycerol secretion is not suppressed in obese type 2 diabetic men.

AIMS/HYPOTHESIS: Type 2 diabetes is characterised by insulin resistance and increased post-absorptive secretion of VLDL-triacylglycerol (VLDL-TAG). Whether postprandial suppression of endogenous VLDL-TAG secretion is abnormal--a finding that would link hyperlipidaemia and type 2 diabetes--remains unclear. METHODS: Eight type 2 diabetic men and eight healthy men were studied before and after a fat-free test meal (40% of resting energy expenditure). VLDL-TAG kinetics were assessed using a primed-constant infusion of ex vivo labelled [1-(14)C]triolein VLDL-TAG using non-steady-state calculations. RESULTS: Type 2 diabetic men had a higher basal VLDL-TAG secretion rate and concentration than healthy men (mean ± SD secretion rate 137 ± 61 vs 78 ± 30 µmol/min, respectively [p = 0.03]; median concentration 1.03 [range 0.58-1.75] vs 0.33 [0.13-1.14] mmol/l, respectively [p < 0.01]). Postprandially, the VLDL-TAG secretion rate decreased in healthy men (p < 0.01), but remained unchanged in diabetic men (p = 0.47). The VLDL-TAG concentration increased in diabetic men and decreased in healthy men postprandially (p < 0.05). The difference in VLDL-TAG secretion rate between the two groups approached significance (p = 0.06) and the relative change in VLDL-TAG secretion rate was significantly different (p = 0.01) between the two groups. Basal VLDL-TAG clearance was significantly lower in diabetic men (diabetic men 133 [49-390] ml/min; healthy controls 215 [137-933] ml/min [p < 0.05]). After meal ingestion, clearance decreased in healthy men (p = 0.03), but was unchanged in diabetic men (p = 0.58). CONCLUSIONS/INTERPRETATION: Obese type 2 diabetic men have impaired postprandial suppression of VLDL-TAG secretion compared with lean healthy men, contributing to their postprandial lipaemia and hypertriacylglycerolaemia.

[Effect of 1-year long-term treatment with sucralfate on symptomatic recurrence of duodenal ulcer]. / Effekt af ét års langtidsbehandling med sukralfat på symptomatisk recidiv af duodenalt ulcus.

One hundred and two patients, who obtained relief from their duodenal ulcer symptoms with sucralfate (Antepsin R) in a dosage of 2 g b.i.d. for four weeks, were randomized to maintenance therapy with sucralfate 2 g at bedtime or a placebo for one year or until possible recurrence of symptoms. Ninety-four patients completed the study, 46 on sucralfate and 48 on the placebo. Eighteen of the sucralfate-treated patients (39%) experienced relapse of symptoms, as did 36 (75%) of the placebo treated patients. This difference was significant (p = 0.0008). In the sucralfate group most of the symptoms recurred within three months after randomisation, whereas the relapse rate seemed constant in the placebo group. It is concluded that 2 g sucralfate at bedtime is effective in preventing recurrence of duodenal ulcer symptoms.

Comparison of the iodide permeability test, the surface microhardness test, and mineral dissolution of bovine enamel following acid challenge.

The relationship among the iodide permeability (Ip) test, the surface microhardness (SMH) test, and enamel demineralization chemically analyzed as mineral loss was investigated using bovine enamel blocks. Demineralization periods of 0 (control) and 5, 15, 30, and 45 min using 0.05 mol/l lactate (pH 4.75) were chosen to approximate the acid challenge occurring during the intraoral enamel demineralization test. Mineral loss (Ca and PO4) was found to be directly proportional to dissolution time (r = 0.95). Changes (delta) in Ip and SMH each increased linearly over time (r = 0.58 and 0.64, respectively) and were similarly related to mineral loss (r = 0.60 and 0.65, respectively). The correlation between delta Ip and delta SMH was 0.55. When longer demineralization periods (60, 120, and 240 min) were included, the correlation between delta Ip and delta SMH was 0.68. We conclude that both the Ip test and the SMH test can be used as measures of the early stages of enamel dissolution.

Recurrence of duodenal ulcer pain after treatment with cimetidine for four and eight weeks.

This double-blind controlled trial compares the relapse rate in 19 duodenal ulcer patients who received cimetidine for eight weeks with that in 19 patients who received cimetidine for four weeks and inactive tablets for four weeks. Only patients who became symptom-free during the initial four weeks' treatment with cimetidine were included. The median period of remission after withdrawal of cimetidine was 50 days in patients treated with cimetidine for eight weeks and 76 days in patients treated with cimetidine for four weeks (P greater than 0.10). Six months after withdrawal of cimetidine 15 relapses had occurred in both groups. It is concluded that patients who become symptom-free during four weeks' cimetidine treatment do not benefit by continuation of treatment for another four weeks.

Prophylactic effect of cimetidine in gastric ulcer patients.

Nineteen patients entered a double-blind randomized trial of the prophylactic effect of cimetidine in gastric ulcer disease. The diagnosis of gastric ulcer had been established endoscopically prior to the trial, but at the time of entry the patients were symptom-free and their ulcers had healed. The patients received either cimetidine, 400 mg twice daily or inactive tablets. Ten cimetidine-treated patients completed 12 months' treatment without suffering a recurrence of symptoms, whereas 5 of 9 placebo-treated patients suffered a symptomatic relapse after 7 to 18 weeks (P less than 0.025). In 4 of the 5 patients an ulcer was found at gastroscopy. It is concluded that maintenance treatment with cimetidine helps to prevent symptomatic relapses in gastric ulcer patients.

Prophylactic effect of cimetidine in duodenal ulcer disease.

Fifty-seven symptom-free patients with duodenal ulcer entered a double-blind trial to assess the prophylactic effect of cimetidine. Patients were randomly allocated to receive cimetidine 400 mg twice daily (29 patients) or placebo (28 patients). The trial was designed to imitate daily clinical practice, so duodenal ulcer disease was diagnosed by means of x-ray examination. Three patients from each group withdrew from the trial. All remaining patients continued to receive treatment for 12 months or until symptoms recurred. Three out of 26 patients suffered relapses during cimetidine treatment, compared with 20 out of 25 receiving placebo. No side effects were attributable to cimetidine. Long-term cimetidine treatment had no curative effect as relapses occurred soon after treatment was stopped. The estimated chance (cumulative remission rate +/- 2 SE) of remaining symptom-free 13 weeks after one year's cimetidine treatment had been completed was 47 +/- 21%. Maintenance treatment with cimetidine is a suitable alternative to elective in surgery in patients with duodenal ulcer subjects frequent relapses. Further study is needed to establish the optimal duration and safety of prolonged cimetidine treatment.

Cimetidine in patients with gastric ulcer: a multicentre controlled trial.

Forty-five adult outpatients with endoscopically confirmed gastric ulceration completed a double-blind trial of either cimetidine (1 g/day) or placebo. After six weeks 18 of the 23 patients receiving cimetidine showed complete ulcer healing compared with only six of the 22 patients receiving placebo. The cimetidine group also had fewer days with pain than the placebo group but the difference was not statistically significant. Cimetidine therefore seems to promote healing of gastric ulcers without severe side effects, although its effect on pain is less pronounced than in patients with duodenal ulcers.

Evaluation of single-drug versus multiple-drug chemotherapy in the treatment of advanced breast cancer.

Fifty-one postmenopausal patients with advanced breast cancer were randomized to receive either cyclophosphamide given continuously or cyclophosphamide given continuously with methotrexate, 5-fluorouracil, vincristine, and prednisone given intermittently. The results with the multiple-drug therapy were significantly better than with the single-drug therapy, both with regard to percentage (63% versus 25%) and median duration (400 versus 210 days) of objective response. Toxicity was moderately increased with the combination as compared to the single-drug treatment.

A pragmatic trial of cimetidine in duodenal ulcer patients.

Fifty-eight outpatients with a clinical and radiological diagnosis of duodenal ulcer completed a double-blind randomized trial of the effect of cimetidine on ulcer symptoms. Patients normally treated in general practice were included in the trial. The patients in the treatment group received cimetidine 1 g daily and the controls received inactive tablets. The treatment period was four weeks. During the last nine days 18 (60%) of 30 cimetidine-treated patients were symptom-free against 5 (18%) of 28 controls (P less than 0.005). The antacid consumption, the number of days with pain and the number of hours with pain also differed significantly in the two groups. Apart from a transient rash in one patient no important clinical side-effects were noted. The serum creatinine rose slightly in the cimetidine-treated patients.

Gastroscopic evaluation of the effect of a new anti-rheumatic compound, ketoprofen (19.583 R.P.), on the human gastric mucosa. A double-blind cross-over trial against acetylsalicylic acid.

The tolerance of the gastric mucosa to a new anti-inflammatory product, ketoprofen (19.583 R.P., Orudis, Profenid N.D.) was compared to the tolerance of acetylsalicylic acid in a double-blind cross-over trial using selected healthy volunteers. The effect of the medication on the gastric mucosa was examined by the use of a gastrocamera technique. The volunteers received during 2 one-week periods either acetylsalicylic acid 3 g daily or ketoprofen 100 mg daily. The sequential diagram shows that the upper barrier was crossed (preference for ketoprofen) when 10 volunteers had been analysed.