Confirmation of the PEG tube placement by ultrasonic probe obviating the need for reinsertion of the gastroscope.
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Biomedical subjects
Publications and source records attributed to N S Mann.
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Enterokinase is a glycoprotein and is now designated enteropeptidase (E.C.3.4.4.8.). It is present in the duodenal and jejunal mucosa. Pancreatic proteolytic enzymes are secreted as proenzymes. Enterokinase converts trypsinogen to trypsin in the duodenal lumen. Duodenopancreatic reflux of duodenal enterokinase may be important in the pathogenesis of experimental and clinical acute pancreatitis. Congenital enterokinase deficiency is a distinct clinical entity characterized by diarrhea, failure to thrive, hypoproteinemia, and edema. Acquired enterokinase deficiency may occur in some diffuse small bowel diseases. Steatorrhea of celiac spruce may be due partly to the fact that deficiency of secretin and cholecystokinin may interfere with the action of enterokinase. The interrelationship between secretin, cholecystokinin, enterokinase, and bile salts is not completely understood.
The frequent association of celiac sprue (CS) and insulin-dependent diabetes mellitus (DM) which may be the result of interplay between genetic, hormonal, and immunologic factors has obvious therapeutic implications. A gluten-free diet may improve the diarrhea in some patients with DM where the reason for diarrhea is underlying celiac sprue; the diet may also improve control of DM by normalizing the serum hormonal profile.
A small ulcer produced in vitro by monopolar electrocoagulation on endoscopically obtained human antral biopsies and incubated in Trowel T-8 medium at 37 degrees C for 8 h has many histologic features of chronic gastric ulcer in man. Zinc sulfate and acetylcysteine in low concentrations had a significant healing effect in this ulcer model. Since the beneficial effect of zinc sulfate and acetylcysteine was counteracted by N-ethylmaleimide, a known blocker of sulfhydryl compounds, the beneficial effect of these two compounds probably was mediated through sulfhydryl compounds. Using special stain, N-(4-aminophenyl)maleimide, the sulfhydryl groups were localized in the epithelial cells of the surface layer and gastric glands.
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We evaluated the frequency with which Barrett's esophagus (BE) occurs in patients with symptomatic reflux esophagitis, and compared the clinical endoscopic and manometric features of patients with Barrett's esophagus with those of patients who had non-Barrett's esophagitis (NBE). The effect of 6 months' medical treatment on BE patients was reevaluated by repeating manometry, endoscopy, and biopsy. Esophageal manometry was performed by perfusion technique and endoscopic biopsies were obtained. There were 180 patients; 20 (11%) were found to have BE. The vast majority of BE patients were caucasians. BE patients had symptoms of gastroesophageal reflux for a longer time than did NBE patients. Mean lower esophageal sphincter pressure in BE patients was lower than that in NBE patients. On medical treatment, the severity of esophagitis as judged by endoscopic criteria in BE patients was reduced, but there was no increase in lower esophageal sphincter pressure and no regression of the columnar epithelium.
We report a 56-year-old man with sclerosing cholangitis and oxalate urolithiasis. These complications occurred five years after proctocolectomy and ileostomy were performed for ulcerative colitis. Two years before, at the time of proctocolectomy, there was no clinical or biochemical evidence of liver abnormality. The occurrence and progression of sclerosing cholangitis five years after proctocolectomy is unusual. Also unusual is the occurrence of oxalate urolithiasis; more common in ulcerative colitis, especially after ileostomy, are uric acid stones.
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Total parenteral nutrition can maintain good nutritional status in selected patients. However, it can be accompanied by serious complications. It is generally agreed that enteral alimentation is more economical and safer. Gut should be used for nutritional replenishment whenever feasible. However, large-bore nasogastric feeding tubes can cause problems. Even fine-bore nasogastric tubes can cause aspiration pneumonia in obtunded and debilitated patients. In some patients it is clearly desirable to have the tip of the feeding tube in the distal duodenum or proximal jejunum. Previously described methods for placement of nasoenteral tubes may be unsatisfactory. We describe a safe, simple, and reliable method for endoscopic insertion of fine-bore nasoenteral feeding tube. We have used this method on 15 patients without complication.
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