[Torsades de pointes during sultopride poisoning]. / Torsades de pointes lors d'une intoxication par sultopride.

A case of sultopride poisoning (ingested dose 16 g) in a 35-year-old, 65 Kg man is described. On admission myoclonus, mydriasis, vomiting and cardio-respiratory arrest were observed. Torsades de pointes were treated with potassium chloride infusion and pace maker stimulation. Plasma sultopride concentration was 25 mg/l and urinary concentration 12 g/l. A prolongation of Q-T interval may announce severe arrhythmias in sultopride poisoning.

Gastric emptying and gastrointestinal absorption of alcohol ingested with a meal.

We have measured, by an intubation method, gastric evacuation and gastrointestinal absorption of alcohol ingested with a meal in seven healthy nonalcoholic subjects. A homogenized meal containing [14C]PEG and ethanol (1 g/kg body wt) was given intragastrically while saline containing [57CO]vitamin B12 was perfused into the duodenum. Of the ingested alcohol, 39.4 +/- 4.1% was absorbed through the stomach wall during the first postprandial hour and 73.2 +/- 4.2% during the total postcibal period, whereas only 24 +/- 3% was absorbed during the same time in the duodenum. Thus alcohol ingested with a meal is mainly and rapidly absorbed in the stomach; the contribution of the small intestine below the angle of Treitz to alcohol absorption is negligible.

[Serum pepsinogen: its value as index of basal and stimulated gastric acid secretion (author's transl)]. / Le pepsinogène sérique, index de la sécrétion gastrique acide basale et stimulée. Intérêt de son dosage.

Group I pepsinogen serum levels (PG I) and gastric acid outputs were determined before ("basal") and after pentagastrin or insulin stimulation in 13 patients with active duodenal ulcer and in 4 patients with hyperselective vagotomy. There was a statistically significant correlation between basal PG I serum level and basal acid output (r = 0,88, p less than 0,01) and between PG I serum level 45 min after stimulation and peak acid output (r = 0,68, p less than 0,01). However, the scattering of individual values was such that serum PG I cannot be used as an index of gastric acid secretion in clinical practice.

Intestinal clearance of alpha 1-antitrypsin. A sensitive method for the detection of protein-losing enteropathy.

Gastrointestinal loss of plasma is usually measured with radiolabeled macromolecules. These methods are expensive and cumbersome. The use of alpha 1-antitrypsin as an endogenous marker and the determination of alpha 1-antitrypsin fecal clearance enable the diagnosis of protein-losing enteropathy. alpha 1-Antitrypsin is measured in feces and blood by radial immunodiffusion, and the results are expressed as clearance. There is a significant correlation between alpha 1-antitrypsin fecal clearance and 51Cr-plasma protein clearance (r = 0.96, p less than 0.001). The sensibility of alpha 1-antitrypsin test compared to [51Cr] is 93.3%, the specificity is 90%. The positive predictive value is 97.7%, the negative predictive value 75%. We found no alpha 1-antitrypsin in gastric juice of pH below 3. In vitro studies confirmed the destruction of alpha 1-antitrypsin in gastric juice of pH below 3. There is a slight decrease of alpha 1-antitrypsin concentration when stools are incubated at 37 degrees C. In duodenal juice there is a small lessening of alpha 1-antitrypsin concentration after an incubation at 37 degrees C for 1 h. In conclusion, the fecal clearance of alpha 1-antitrypsin seems to be an inexpensive and quite reliable test of protein-losing enteropathy.

Colonic inhibition of gastric secretion in man.

The effect of colonic infusion of various solutions on submaximal pentagastrin-stimulated gastric secretion was determined in healthy volunteers. Hypertonic (823 mOsm/kg) glucose, mannitol, and saline, and also isotonic glucose significantly induced a marked and sustained inhibition of gastric acid secretion of 74%, 66%, 79%, and 54%, respectively. A similar degree of inhibition was obtained for pepsin secretion with hypertonic glucose and mannitol. Isotonic triglycerides and isotonic saline solutions had no significant effect on gastric acid secretion. Hypertonic glucose, mannitol, and saline infusions significantly increased plasma concentrations of enteroglucagon, whereas other solutions had no effect. No correlation, however, was found between the percentage rise of enteroglucagon and the percentage inhibition of gastric secretion obtained from any of the three hypertonic solutions. The physiological significance of these findings remains to be established.

Diagnosis of protein-losing enteropathy by gastrointestinal clearance of alpha1-antitrypsin.

Alpha1-antitrypsin was assessed, in 10 patients with protein-losing enteropathy and 13 control subjects, as an endogenous marker of plasma-protein loss into the gastrointestinal tract. Both faecal alpha1-A.T. concentrations and faecal alpha1-A.T. clearance were significantly higher in patients than in controls. Wtih clearance there was no overlap between the groups. Over 10 days the normal gastrointestinal clearance of alpha1-A.T. was 3.07 +/- 2.25 (S.D.) ml/day. Measurement of alpha1-A.T. clearance is easy and requires no radioisotopes.

Evidence for excessive absorption of oxalate by the colon in enteric hyperoxaluria.

This work was designed to investigate the site of oxalate hyperabsorption in malabsorption syndromes. 1) Urinary oxalate excretion was measured in 27 patients with ileal resection (IR) and steatorrhea. Mean urinary oxalate excretion was high in 13 patients with IR and intact colon and in 9 subjects with IR and right hemicolectomy (90.2 +/- 11.9 and 108 +/- 18.6 mg per 24 hours; mean +/- S.E.M.), whereas it was normal in 5 patients with IR and ileostomy (21.9 +/- 4.4 mg per 24 hours). Steatorrhea was similar in the three groups. 2) On one patient of the last group in whom the colon had not been removed initially but excluded closure of the ileostomy resulted in the development of frank hyperoxaluria. 3) Intracolonic perfusion of calcium (1.93 g per day) abolished or greatly reduced the hyperoxaluria in 3 patients. These results indicate that the colon is the major site of oxalate hyperabsorption, and the right colon is not necessary for the development of hyperoxaluria in malabsorption syndromes.