Biomedical subjects
Publications and source records attributed to J C Soule.
Ectopic subdiaphragmatic development of a bronchogenic cyst is rare. We report the case of a 28-year-old woman with a symptomatic bronchogenic cyst of the right hemidiaphragm simulating a hydatic cyst of the liver on ultrasonography and CT scan. Diagnosis of a diaphragmatic lesion was made during laparotomy, and complete resection was successful. Final diagnosis was done on pathology.
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No reliable identification of quiescent Crohn's disease (CD) patients with a high risk of relapse is available. The aim of this study was to develop a prognostic index to identify those patients. Untreated adult patients with quiescent disease (not induced by surgery) included in three phase III clinical trials were analysed retrospectively with respect to time to relapse. Nineteen factors related to biology, disease history, and topography were investigated. A relapse was defined as either a CD Activity Index (CDAI) > or = 200, a CDAI > or = 150 but over the baseline value by more than 100, or acute complications requiring surgery. The inclusion criteria were fulfilled by 178 patients. The median follow up was 23 months. The Cox model retained the following bad prognostic factors: age < or = 25 years, interval since first symptoms > 5 years, interval since previous relapse < or = 6 months, and colonic involvement (p < 0.001). Bootstrapping confirmed the variable selection. Patients were classified into three groups with an increasing risk of relapse (p < 0.001). The worst risk group was composed of patients presenting at least three of the four bad prognostic factors. These results make possible the design of clinical trials in quiescent CD patients with a high risk of relapse.
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We report a case of scurvy. This case is interesting by the unilateral character of the ecchymotic leg's purpura. Ascorbic acid assays do not yet enable subclinical vitamin C deficiency to be reliably detected. Hence the importance of knowing the situation which expose to this deficiency.
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A randomized clinical trial was conducted to determine whether colonoscopy is useful in deciding how long to maintain steroid treatment in attacks of Crohn's disease involving the colon. One hundred forty-seven patients with acute attacks of colonic or ileocolonic Crohn's disease were treated by oral prednisolone, 1 mg.kg-1.day-1; 136 achieved clinical remission, but 96 of them still had active endoscopic lesions and were randomized either to immediate start of steroid tapering (group A; n = 46) or to continued prednisolone treatment at the same dosage for 5 more weeks before steroid tapering was begun (group B; n = 50). In the remaining 40 patients (already in endoscopic remission, group C), steroid tapering was begun immediately. After prednisolone discontinuation, patients were followed up for 18 months or until clinical relapse. Prolongation of prednisolone therapy significantly improved the endoscopic scores in group B (30% of endoscopic remission). The frequency of successful steroid weaning was almost identical in groups A and B (82% and 80%, respectively), as was the actuarially calculated relapse clinical rate after steroid withdrawal (P = 0.22). No factor predictive of clinical relapse could be found. The clinical course of patients in group C was similar to that of those in groups A and B. Overall, only 22% of the 147 patients were still in clinical remission and off steroids 18 months after prednisolone discontinuation, outlining the need for maintenance therapy. In conclusion, for patients who have achieved clinical remission, adjustment of steroid treatment duration on the basis of endoscopy results is of no benefit, and the endoscopic aspect has no prognostic value; thus, it appears unnecessary to repeat colonoscopy in such patients before steroid tapering is begun.
The 24-hour intragastric pH of 12 patients with an acute duodenal ulcer was recorded with the aim of comparing the effects of two different times of administration of 300 mg ranitidine: post evening meal, or bedtime. This double-blind crossover trial involved 3 centres. Twenty-four-hour gastric pH was measured under standard conditions (meals, time schedule) at the middle of each 14-day treatment period. The analysis was performed on the percentage of times spent at pH levels below 1.5, 2, 3 and 4 for different periods and for the total 24 hours. During the whole day and night combined, as well as during the afternoon (12.00 hours-19.00 hours), there was no difference between the 2 regimens regardless of the pH profile studied. During the morning (07.30 hours-12.00 hours), the time spent below pH 1.5 and 2 was less when the drug was taken at bedtime (P less than 0.05). In contrast, during the whole night (19.00 hours-07.30 hours) the percentage of time spent below pH 1.5, 2 and 3 was significantly less when the drug was taken at post evening meal (P less than 0.05). These results show that in patients with acute duodenal ulcer, 300 mg ranitidine administered at the end of the evening meal provides better control of nocturnal acidity than administration at bedtime and hence is suggested for optimization of therapeutic efficacy.
The effect on steatorrhoea of a pH-sensitive enteric-coated pancreatic preparation (Eurobiol 25,000) was compared with a conventional pancreatic enzyme preparation (Eurobiol) in six adult patients with exocrine pancreatic insufficiency. In addition, the fate of orally ingested pancreatic enzymes in the upper digestive tract was evaluated by measuring gastric and duodenal pH, amount of enzymes in the stomach, duodenal enzyme output, and fat absorption at the angle of Treitz for the 4 hours following a standard meal. When compared with placebo, Eurobiol and Eurobiol 25,000 reduced daily faecal fat excretion by 24% (not significant) and 43% (P less than 0.05), respectively. With the conventional preparation, enzyme output and fat absorption at the duodeno-jejunal flexure were significantly improved (P less than 0.05). Marked inter-individual differences in duodenal enzyme recovery (lipase 3% to 80%; chymotrypsin 26% to 100%) and, consequently, in the reduction of steatorrhoea (0% to 67%) were observed, with the gastric emptying rate emerging as a key determinant factor. With the enteric-coated preparation, enzyme output and fat absorption at the duodenojejunal flexure were not significantly improved. Discrepancy between the marked reduction of faecal fat excretion and the low duodenal enzyme recovery could indicate that enzyme delivery from microtablets occurs further down in the small bowel. Efficacy of enteric-coated preparations could be enhanced by adding unprotected enzymes, especially in patients with rapid gastric emptying.
In a double-blind, randomized, comparative trial of the prokinetic drug cisapride and the H2-blocker cimetidine, mucosal healing and changes in symptoms of gastroesophageal reflux were evaluated in patients with erosive reflux esophagitis. The patients were treated with either cisapride, 10 mg four times a day (N = 36) or cimetidine, 400 mg four times a day (N = 37) for six weeks, or for 12 weeks if mucosal healing was not obtained by week 6. Upon entry, two thirds of the patients in each group had grade I (Savary-Miller) esophagitis, and the remainder grade II or III. At the end of treatment, endoscopy showed mucosal healing in 56% (38-72%; 95% confidence interval) of cisapride and 57% (39-73%; 95% confidence interval) of cimetidine patients. After six weeks, both drugs significantly (P less than 0.01) decreased the intensity and frequency of heartburn, regurgitation, and the postural syndrome. No significant intergroup differences were found regarding endoscopic parameters or the improvement of heartburn and regurgitation. Concomitant antacid use was also comparable. Adverse effects were reported by four cisapride and nine cimetidine patients. These results indicate that the effects of cisapride compare well with those of cimetidine in terms of both esophageal mucosal healing and symptom relief.
One hundred forty-two patients with active colonic or ileocolonic Crohn's disease were included in a multicenter prospective study. Data collection included 28 clinical, biological, and endoscopic items; the latter were recorded according to a standardized colonoscopic protocol; a previously validated endoscopic index of severity was calculated. Oral prednisolone (1 mg/kg body wt per day) was started and maintained until clinical remission and for at least 3 and at most 7 wk. A second clinical biological and endoscopic evaluation was then performed. At initial colonoscopy, mucosal lesions were, by decreasing order of frequency, superficial ulcerations, deep ulcerations, mucosal edema, erythema, pseudopolyps, aphthoid ulcers, ulcerated stenosis, and nonulcerated stenosis (93%, 74%, 48%, 44%, 41%, 35%, 10%, 8%, and 2% of cases, respectively). No correlation was found between the clinical activity index and any of the endoscopical data (lesion frequency and surface, endoscopic severity index). Ninety-two percent of patients underwent clinical remission within 7 wk of treatment. None of the 28 clinical biological and endoscopical items collected just before treatment could predict clinical response to steroids. Only 38 of the 131 patients in clinical remission were also in endoscopic remission. In conclusion, (a) the description and severity of colonoscopic lesions in active Crohn's disease have been quantified; (b) no correlation exists between clinical severity and nature, surface, or severity of endoscopic lesions; (c) Oral prednisolone (1 mg/kg body wt per day) induces a clinical remission in 92% of patients within 7 wk; (d) resistance to steroids cannot be predicted from the data collected before treatment onset; and (e) only 29% of patients in clinical remission also achieve endoscopic remission.
The purpose of the present study was to compare omeprazole 20 mg once daily and ranitidine 150 mg twice daily in healing duodenal ulcers unhealed by previous treatment with cimetidine greater than or equal to 0.8 g or ranitidine greater than or equal to 0.3 g daily for at least six weeks. In a double blind multicentre trial, 151 patients were randomly assigned to either omeprazole or ranitidine. Clinical assessments and endoscopies were carried out at two and four weeks. Patients characteristics were similar in both groups. Statistical analysis (chi 2 test) did not show any significant difference in healing rate (p greater than 0.20) irrespective of the method of calculation. On an 'intent-to-treat' analysis (n = 151), healing was: omeprazole 46.6%, ranitidine 43.3% at day 15 and omeprazole 70.7%, ranitidine 68.4% at day 29; and among the patients who completed treatment, healing was: omeprazole 48.3%, ranitidine 46.3% at day 15 (n = 125; 95% confidence interval of the difference--17 to 21) and omeprazole 79.6%, ranitidine 75.4% at day 29 (n = 115; 95% confidence interval of the difference--13 to 21). After a further four weeks treatment with omeprazole, healing occurred in 16/20 (80%) who still had active disease at day 29. Patients on omeprazole and on ranitidine experienced similar decrease in day time and night time epigastric pain and in heartburn. Multivariate analysis (logistic regression) did not indicate any influence on age, sex, smoking and alcohol habits, previous drug administered, duodenitis and duodenal erosions on the healing rate. In this model, healing rate was not significantly influenced by previous treatment duration (p = 0.09 at day 15 and p greater than 0.2 at day 29) but was significantly influenced by ulcer size (p = 0.04 at day 15 and p = 0.02 at day 29). Forty one patients complained of adverse events: 19 on omeprazole (four trial withdrawals), 22 on ranitidine (three trial withdrawals).
Combined treatment with cimetidine 1 g daily and cisapride 40 mg daily in patients with endoscopically diagnosed severe reflux oesophagitis was compared with single drug therapy (cimetidine and placebo). At the end of the six to 12 weeks treatment, 11 (46%) of the 24 patients under single drug therapy were endoscopically healed and three were improved. In contrast, 16 (70%) of the 23 patients under combined therapy were healed and all of the remainder were improved (p = 0.025). The severity of diurnal and nocturnal heartburn, decreased significantly more (p less than 0.05) on cimetidine + cisapride than on cimetidine + placebo. The combined treatment was well tolerated. These results suggest that combined therapy with cisapride and cimetidine may be useful in patients with severe reflux oesophagitis.
The inhibitory effect of omeprazole, a benzimidazole derivative, on gastric acid secretion was investigated in seven patients with Zollinger-Ellison syndrome resistant to treatment with large doses of histamine H2-receptor antagonists administered alone or in combination with pirenzepine. In two patients with an acute form of the syndrome, rapid control of acid overproduction was achieved with 180-mg intravenous and 120-mg oral daily doses, respectively. The other five patients, who were free of complication, initially received a standard regimen of omeprazole 60 mg orally once a day; dosage was subsequently adjusted until the basal acid output, measured 1 hr before the next dose of the drug, was less than 10 mmol/hr. The initial daily dose proved to be adequate in three patients and had to be increased to 80 mg and 60 mg bid, respectively in the remaining two patients. In all patients omeprazole therapy resulted in clinical recovery and rapid healing of mucosal lesions. The seven patients have now been followed up for 4-24 months (average 15 months). The adequacy of the daily dosage was periodically reassessed by measuring basal acid output in the hour preceding the morning dose. In one patient initially treated with 180 mg/day, dosage could be reduced to 60 mg/day. In three others, who were initially controlled with 60 mg/day, dosage had to be increased during follow-up. Despite adequate control of gastric acid secretion, one patient underwent total gastrectomy and tumor resection and another died of extensive liver metastases. The five patients still receiving omeprazole remain free of symptoms and mucosal lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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Urinary recovery and plasma time curve of PABA were determined in 15 control subjects and 65 patients during a six hour period after ingestion of a meal containing 1 g BT-PABA (2.333 mmol PABA). In controls, the plasma PABA time curve registered a peak at two hours followed by a rapid decrease to reach its lowest value at six hours. In patients with chronic pancreatitis (n=32), the peak was lower and was followed by a slow decrease; furthermore, it was delayed in those with severe pancreatic insufficiency. The best discrimination between controls and patients with chronic pancreatitis was obtained by using the maximal value of plasma PABA (MPPABA) at two or three hours. In 56 subjects a hyperbolic relationship between MPPABA and duodenal lipase output stimulated by a meal was mathematically demonstrated and it was calculated that the lower limit of normal MPPABA (mean -2 SD) corresponded to a lipase output equal to 20.6% of the mean value of normal subjects (lower limit of normal lipase output = 40%). By comparison, steatorrhoea occurred when lipase output was less than 10%. Consequently, MPPABA was low not only in all patients with steatorrhoea but also in some who had pancreatic deficiency but normal daily faecal fat. With lipase output as the reference, 12 subjects who had normal MPPABA were proved to have falsely abnormal urinary results. Urinary PABA excretion after oral administration of 2.333 mmol free PABA was also determined in 27 subjects. The PABA excretion index (PEI) was calculated: PEI = PABA urinary excretion after BT-PABA/PABA urinary excretion after free PABA. Seven patients with normal MPPABA but low urinary excretion after BT-PABA had a normal PABA excretion index. It was also observed that, in five patients with intestinal disease, free PABA absorption was not impaired. In conclusion, BTPABA test with MPPABA determination used as an index of exocrine function is (1) less sensitive than Lundh's test, but more sensitive than steatorrhoea; (2) more specific than the test with urinary recovery determination alone, and as specific as PABA excretion index, which requires a double test.
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