Corrosive oesophageal strictures following acid ingestion: Clinical profile and results of endoscopic dilatation

There are several reports on oesophageal strictures caused by alkali ingestion, but information on oesophageal strictures due to acid ingestion is scarce. Endoscopic dilatation, which has been found to be quite safe and effective in the treatment of benign oesophageal strictures of other aetiology, has also not been evaluated adequately in the treatment of these strictures. Over a period of 2 years, of 47 patients treated at this centre of benign oesophageal strictures, 17 (36.2%) patients had strictures following ingestion of corrosive agents. Thirteen patients had ingested acids and only four gave a history of alkali ingestion. The age range of these 13 patients was 14-50 years (mean = 25.5 years, s.d. = 2.6). The amount of acid ingested varied from 10 to 100 ml (median = 50 ml). The interval between acid ingestion and presentation to hospital ranged from 1 to 60 months (median = 2 months). Ten patients had multiple strictures, and the most common site of involvement was the upper third followed by the lower third of the oesophagus. Only five of these 13 patients had evidence of gastric involvement in the form of antral stricture (four) and hour glass deformity (one). Strictures were dilated using Eder-Puestow metal olives passed over a guide wire. The total number of sittings required to achieve adequate dilatation in this group ranged from 1 to 30 (median = 14). Most patients were managed successfully with dilatation (good response 63.6%, satisfactory response 18.2%). On follow-up, recurrence of dysphagia was seen in a high number of patients (66%), but this could be managed easily with repeat dilatation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Corrosive ingestion in adults

Ingestion of a corrosive substance can produce severe injury to the gastrointestinal tract and can even result in death. The degree and extent of damage depends on several factors like the type of substance, the morphologic form of the agent, the quantity, and the intent. In the acute stage, perforation and necrosis may occur. Long-term complications include stricture formation in the esophagus, antral stenosis and the development of esophageal carcinoma. Endoscopy should be attempted and can be safely performed in most cases to assess the extent of damage. Procedure-related perforation is rare. Stricture formation is more common in patients with second and third degree burns. Corticosteroids may help prevent stricture formation. Esophageal carcinoma may develop beginning 30 to 40 years after the time of injury.     

Gastro-oesophageal reflux disease in Sudan: a clinical endoscopic and histopathological study.

This study was conducted to assess the frequency of gastroesophageal reflux disease (GERD) and Barrett's esophagus among Sudanese patients with clinical symptoms of heartburn. One hundred and five patients were included in the study; forty seven patients had evidence of reflux oesophagitis, 61.7% of whom had grade B oesophagitis according to the modified Los Angeles classification and 10.6% had Barrett's oesophagus. 78.7% of the biopsies from the esophageal cardia revealed presenced of inflammation (Carditis). Dysplasia was documented in 21.3% of these biopsies. Helicobacter pylori was detected 59.6% of gastrooesophageal reflux disease patients and 56.8% of patients with carditis. However, 80% of patients with Barrett oesophagus were positive for Helicobacter pylori. It was concluded that gastro-oesophageal reflux disease affects all age groups with males being affected more than females and Helicobacter pylori infection did not play a major role in gastro-oesophageal reflux disease orits complications.     

Corrosive oesophagitis in Nigeria: clinical spectrums and implications

Ingested corrosive agents produce oropharyngeal and gastro-oesophageal injuries ranging from minor burns to severe necrosis, depending on the agent, amount, concentration and duration of exposure. A 10-year (1990-1999) study of 23 corrosive oesophagitis patients depicting the clinical spectrums and implications was done. There were 17 (74%) males and 6 (26%) females, with an average age of 16 years: 35% were in the first decade of life and 39% in the second, with an average occurrence of three new cases a year. The main corrosive agents were alkali (NaOH) 48% and sulphuric acid 39%. The factors that predisposed to corrosive ingestion included: accidental 43%; suicidal 35%; homicidal 13% and 'therapy' 9%. Of the accidental cases 60% were seen in children; 75% of suicide attempts were in the second decade of life. Eleven (48%) patients developed complications, namely laryngeal stenosis 4% and oesophageal strictures 44%. The hospital stay ranged from 2-4 weeks. Awareness of the dangers of corrosive ingestion should be extensively publicized. Government regulations permitting the sales and procurement of corrosive substances should be strictly enforced and, if not yet in place, should be enacted without further delay.     

Corrosive acid gastric stricture: a plea for conservative surgery

Acid ingestion is known to cause a corrosive stricture of the stomach. Subsequent metaplasia in the gastric mucosa has been noted and cases of malignant change shown to have occurred. Gastrectomy has, therefore, been advocated. A less radical approach of gastrojejunostomy with regular endoscopic follow-up is here recommended.     

Annular pancreas: a clinical, endoscopic, and immunohistochemical study.

A patient with annular pancreas presenting with severe upper abdominal pain is discussed. Endoscopic retrograde cholangiopancreatography (ERCP) was diagnostic, with successful injection of major and minor papillae showing pancreas divisum, an annular duct emptying at the major papilla and changes of severe chronic pancreatitis in all duct systems. Pylorus preserving pancreatoduodenectomy gave complete pain relief. The annulus was shown immunohistochemically to be entirely of ventral gland origin. Chronic pancreatitis was histologically less severe in the dorsal gland. Antegrade dye injection with x-ray showed dorsal to ventral connection in the resected specimen.     

Effect of endoscopic sphincterotomy on bile acid pool size and bile lipid composition in man

The effect of endoscopic sphincterotomy on bile acid pool size and lipid composition was studied in 3 patients with an intact gallbladder and in 7 patients who had previous cholecystectomy. Measurements were made at two time intervals after endoscopic sphincterotomy, early (3-9 days) and late (6-9 months). Patients with an intact gallbladder showed a marked reduction in their total bile acid pool during follow-up examinations (95.3 +/- SD 14.0 vs. 18.6 +/- 8.1 mumol/kg), whereas in the cholecystectomized patients the pool size showed no significant change (29.4 +/- 13.4 vs. 26.6 +/- 11.4 mumol/kg). The reduction in bile acid pool size caused by sphincterotomy in patients with an intact gallbladder did not increase the degree of cholesterol saturation in hepatic bile.     

Diabetes mellitus and neuropathy following Vacor ingestion in man.

Two patients ingested Vacor, a rodenticide containing the active ingredient N-3 pyridylmethyl-N'-p-nitrophenyl urea. Both patients developed ketosis-prone diabetes mellitus and severe autonomic neuropathy. Niacinamide therapy given nine hours after Vacor ingestion in one patient and 14 hours after ingestion in the other was not successful in preventing these sequelae. Physicians need to be aware of the toxicity of Vacor, and the potential therapeutic benefit of early niacinamide therapy.     

Elevation of plasma glucose and glucagon after tryptophan ingestion in man

To evaluate the effect of tryptophan on blood sugar in man, we have orally administered 10 g of this amino acid to 14 normal subjects and determined their plasma levels of glucose, insulin, glucagon, and growth hormone for 4 hr after the load. Seven of the subjects also received a placebo. Tryptophan intake was followed by a slight but significant elevation of glycemia (maximum increment: 11% above basal values at 180 min, p = 0.02). This elevation of plasma glucose was accompanied by a clear rise of glucagon levels (peak: 60% at 140 min, p = 0.0007) and by increased concentrations of circulating insulin and growth hormone. Placebo administration did not significantly modify blood glucose or any of the hormones measured. In contrast to the reported hypoglycemic effect of tryptophan in rats, our data indicate that this amino acid increases plasma glucose in man. Given that tryptophan appears to possess the capability of eliciting glucagon secretion, its effect on blood glucose can be reasonably attributed to an enhanced glycogenolysis and/or gluconeogenesis provoked by its release of this hormone.     

Treatment of duodenitis with cimetidine: a clinical, endoscopic, and histologic study

We studied the effectiveness of cimetidine in the treatment of endoscopically diagnosed duodenitis. Sixty-nine patients with the solitary endoscopic finding of duodenitis (6% of 1,200 patients who underwent fiberoptic endoscopy of the upper gastrointestinal tract in our unit over 3 years) were studied retrospectively: a good clinical response was apparent in 45 of 69 patients treated with cimetidine (65%), and a fair response in another four (6%). In a controlled, randomized prospective study, we evaluated the effectiveness of cimetidine in duodenitis. Statistically significant improvement for the clinical and endoscopic scores was found in 10 patients treated with cimetidine (p less than 0.01). Improvement in the histologic score did not reach statistical significance. No such improvement was demonstrated in seven placebo-treated patients. We believe that duodenitis is a "peptic syndrome," has a good response to cimetidine treatment, and behaves much like duodenal ulcer disease.     

Daytime ingestion of alcohol alters nighttime jejunal motility in man

We studied the effects of acute ingestion of intoxicating doses of alcohol on jejunal motility in six male volunteers ages 24–45 who had two 24-hr ambulatory manometries, one week apart, that each included three standardized meals with either red wine (0.6 g of alcohol/kg) or dealcoholized wine. Breath alcohol was measured at regular intervals for 3 hr following alcohol. The results show that the MMC cycle was significantly (P<0.01) shorter during the night than during the day in the “nonalcohol” group but not in the “alcohol” group and that the amplitude of contractions was higher during the night than in day in the alcohol group (P<0.01). All meals interrupted the MMC and induced a fed pattern. After the 300-kcal liquid meal, the duration of the fed pattern was shorter (P<0.01), with a lower motility index (P<0.01) and fewer contractions (P<0.01), than following the two 600-kcal meals. The number of clustered contractions occurring in the postprandial period was lower in the alcohol group than in the nonalcohol group. After the three alcohol doses, a breath alcohol peak was reached in 20–60 min, and in all subjects, breath alcohol fell below 22 µg/100 ml after the third hour. This study showed that alcohol had only minor effects on postprandial contractile activity but abolished the circadian variation of the MMC normally seen in healthy subjects. The fact that breath alcohol was low by the time of onset of sleep, suggests that the effects on the MMC may be mediated through central rather than local mechanisms.     

Insulin mediators in man: effects of glucose ingestion and insulin resistance

Summary Insulin mediators (inositol phosphoglycans) have been shown to mimic insulin action in vitro and in intact mammals, but it is not known which mediator is involved in insulin action under physiological conditions, nor is it known whether insulin resistance alters the mediator profile under such conditions. We therefore investigated the effects of glucose ingestion on changes in the bioactivity of serum inositol phosphoglycan-like substances (IPG) in healthy men and insulin resistant (obese, non-insulin-dependent diabetic) men. Two classes of mediators were partially purified from serum before and after glucose ingestion. The first was eluted from an anion exchange resin with HCl pH 2.0, and bioactivity was determined by activation of pyruvate dehydrogenase in vitro. The second was eluted with HCl pH 1.3, and bioactivity was determined by inhibition of cyclic AMP-dependent protein kinase. In healthy men, the bioactivity of the pH 1.3 IPG was not altered by glucose ingestion, whereas bioactivity of the pH 2.0 IPG increased to approximately 120 % of the pre-glucose ingestion value at 60–240 min post-glucose ingestion (p < 0.05 vs pre-glucose). There was no change in either IPG after glucose ingestion in the insulin-resistant group. These data suggest that the pH 2.0 IPG plays an important role in mediating insulin's effect on peripheral glucose utilization in man under physiological conditions. The data further show, for the first time, a defective change in the bioactivity of an insulin mediator isolated from insulin-resistant humans after hyperinsulinaemia, suggesting that inadequate generation/release of IPGs is associated with insulin resistance. [Diabetologia (1997) 40: 557–563] Received: 4 October 1996 and in revised form: 2 January 1997     

Effect of chenodeoxycholic acid on liver structure and function in man: a stereological and biochemical study

Chenodeoxycholic acid (CDCA) is an effective treatment for dissolving gallstones but experimental studies have suggested that it might be hepatotoxic. The present study is concerned with a group of patients undergoing medical therapy for gallstones for periods of 30 days up to 14 months with CDCA (15 mg/kg/day). Routine functional tests, determination of some liver microsomal enzymes and stereological studies of the liver tissue have been performed and the data have been compared with those obtained before treatment. No significant changes were observed in the functional tests throughout the study. Also the microsomal mixed function oxidase system seemed unaffected by CDCA therapy. The histological features of the liver biopsies were not appreciably different from those observed prior to treatment. Although there were large interindividual variations, the volume density of parenchymal steatosis and of the lipocytes remained comparable in the ssme individual. The ultrastructural features noted in untreated subjects such as curled mitochondrial cristae, slight intracellular bile retention, increased surface density of the rough endoplasmic reticulum were still evident after 14 months of treatment. No additional changes were noted. These results show that no evidence of hepatotoxicity seems to develop in man under therapy with CDCA at the dose considered. But the structural abnormalities observed before treatment appear to persist even in subjects under long-term therapy.