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Biomedical subjects

M J Collen

Publications and source records attributed to M J Collen.

At least 19 recordsLinked to original sources
PubMed1996

Do non-steroidal anti-inflammatory drugs cause duodenal ulcer? Evaluation of basal acid output and ulcer complications.

Non-steroidal anti-inflammatory drug (NSAID) use and basal acid outputs determined by nasogastric suction were evaluated prospectively in 184 patients with endoscopically documented duodenal ulcer. The mean basal acid output and percentage of gastric acid hypersecretion for duodenal ulcer patients who used NSAID were compared with duodenal ulcer patients who did not use NSAID to determine whether patients using NSAID who develop duodenal ulcer have basal acid outputs in the normal range or in the duodenal ulcer range. Results were compared with 65 normal subjects and 105 patients with nonulcer dyspepsia. There were no significant differences with regard to the percentage of male gender, mean age, mean basal acid output, percentage of gastric acid hypersecretion and percentage of cigarette smoking history between duodenal ulcer patients who used NSAID and duodenal ulcer patients who did not. However, significant differences were observed between duodenal ulcer patients who used NSAID and duodenal ulcer patients who did not use NSAID with regard to the percentage of bleeding duodenal ulcer (59 compared with 23%; p = 0.0008) and the percentage of patients with giant duodenal ulcer (41 compared with 5%; P = 0.00001). These results suggest that NSAID use does not cause duodenal ulcer but does make pre-existing duodenal ulcer worse by causing duodenal ulcer complications.

Adolescent↗
PubMed1996

Omeprazole versus ranitidine or ranitidine/metoclopramide in poorly responsive symptomatic gastroesophageal reflux disease.

OBJECTIVES: To evaluate complete symptom resolution, mucosal healing, and tolerability of omeprazole, ranitidine, or ranitidine/metoclopramide in patients with poorly responsive, symptomatic gastroesophageal reflux disease (GERD). METHODS: Adults with persistent symptomatic GERD after ranitidine treatment were stratified by esophagitis grade and randomized to omeprazole 20 mg once daily, ranitidine HCI 150 mg twice daily, or ranitidine HCI 150 mg twice daily plus metoclopramide HCI 10 mg four times daily. Endoscopies were conducted at baseline and at wk 4 and 8. Patients assessed overall symptom improvement at wk 4 and 8 and evaluated daytime and nighttime heartburn, dysphagia, and acid regurgitation daily. RESULTS: After 1 wk, 13% of patients receiving omeprazole (N = 100) had complete resolution of all GERD symptoms versus 1% and 3% of patients receiving ranitidine (N = 97) or ranitidine/metoclopramide (N = 93), respectively (p < 0.001). More patients receiving omeprazole had complete symptom resolution at wk 4 (33%) and at the end of the study (64%; both p < 0.001) than patients receiving ranitidine (8% and 28%, respectively) or ranitidine/metoclopramide (7% and 29%, respectively). Regardless of baseline esophagitis grade, more patients receiving omeprazole had complete symptom resolution. At wk 8, more than 91% of patients with grade 0 or 1 esophagitis at baseline were still healed irrespective of treatment. At wk 8, 80% of patients with esophagitis grade 2 or higher at entry were healed with omeprazole (p < 0.001 vs ranitidine [40%] and ranitidine/metoclopramide [46%]). Thirty-four percent of patients reported an adverse event. Significantly more patients receiving combination treatment reported an adverse event than patients treated with single agents. CONCLUSIONS: In patients with persistent GERD symptoms after ranitidine, omeprazole (20 mg daily for up to 8 wk) provides faster and more complete resolution of common GERD symptoms than continued ranitidine (300 mg daily) alone or in combination with metoclopramide (40 mg daily). Omeprazole provides significantly higher rates of endoscopic healing than ranitidine alone or with metoclopramide. Omeprazole and ranitidine are generally well tolerated. The addition of metoclopramide to ranitidine significantly increases adverse events.

Dopamine Antagonists↗
PubMed1995

Ranitidine therapy in patients with idiopathic gastric acid hypersecretion. A prospective study.

One hundred twenty-four patients with idiopathic gastric acid hypersecretion (basal acid output greater than 10.0 meq/hr) were prospectively evaluated and treated with ranitidine twice a day. Fifty-four patients (44%) required standard doses of ranitidine 300 mg/day for adequate treatment, and the other 70 patients (56%) required increased doses of ranitidine (mean 994 mg/day, range 600-3000 mg/day). Mean basal acid outputs for these two groups were 14.0 and 16.6 meq/hr, respectively, which were not significantly different. Nevertheless, there was a significant correlation between basal acid output and daily ranitidine dose required for therapy (r = 0.18, P = 0.05). The duration of ranitidine therapy consisted of: < 1 year (N = 46), 1 year (N = 16), 2 years (N = 19), 3 years (N = 22), 4 years (N = 15), 5 years (N = 6). Only five patients required progressive increases in ranitidine during the time of treatment, which consisted of an average of 0.5 dose adjustments per year. No side effects occurred with any of these high doses of ranitidine. These results indicate that, as in Zollinger-Ellison syndrome, ranitidine is effective therapy for patients with idiopathic gastric acid hypersecretion; however, markedly increased doses as large as 3000 mg/day may be required.

Adolescent↗
PubMed1995

Gastroesophageal reflux disease in the elderly: more severe disease that requires aggressive therapy.

OBJECTIVE: To evaluate gastroesophageal reflux disease in the elderly (people > or = 60 yr). METHODS: Basal gastric acid secretion was prospectively determined in 228 consecutive patients with symptomatic gastroesophageal reflux disease who had upper gastrointestinal endoscopy and were diagnosed with either pyrosis alone (n = 98), erosive esophagitis (n = 87), or Barrett's esophagus (n = 43). RESULTS: Patients > or = 60 yr (n = 66) had significantly more esophageal mucosal disease (erosive esophagitis, Barrett's esophagus) than patients < 60 yr (n = 162)--81% versus 47% (p = 0.000002, Fisher's exact test). Furthermore, 87% of patients > or = 70 yr had esophageal mucosal disease. For each decade from < 30 yr to > or = 70 yr, there was a significant increase in esophageal mucosal disease (p = 0.002; chi 2 test, 23.96); however, there were no significant differences in severity of pyrosis symptoms or in mean basal acid output for each decade. When 146 of the 228 patients with gastroesophageal reflux disease were given enough ranitidine (mean, 630 mg/d; range, 300-3000 mg/d) for the relief of all pyrosis symptoms and healing of all esophageal mucosal disease, there were no significant differences in ranitidine therapy between each decade. CONCLUSIONS: Elderly patients with pyrosis symptoms severe enough to require upper gastrointestinal endoscopy have gastroesophageal reflux disease with more esophageal mucosal disease (erosive esophagitis, Barrett's esophagus) than patients < 60 yr, and like younger patients, may require markedly increased doses of ranitidine as large as 2400 mg/d for effective therapy.

Adult↗
PubMed1995

Clinical outcome of post-ERCP pancreatitis: relationship to history of previous pancreatitis.

OBJECTIVE: The aim of this prospective study was to evaluate the relationship between clinical outcome of post-ERCP pancreatitis and history of previous pancreatitis. METHODS: Fifty patients (3.5%) developed procedure-related pancreatitis during the study period. Twenty-one patients had a history of previous pancreatitis (group I), and 29 patients had no history of previous pancreatitis (group II). There were no significant differences between the two groups with regard to age, gender, pancreatic duct injection, acinarization, or type of ERCP procedure. Grading of clinical severity was based on length of hospitalization, presence of pancreatic complications, and need for intervention: mild 28%, moderate 54%, and severe 18%. Four patients (8.0%) had pancreatic complications, but only one patient required surgery. There were no associated mortalities. RESULTS: Patients in group I had a shorter median hospital stay and were less likely to develop severe pancreatitis than patients in group II: 4.0 versus 7.0 days, p = 0.001 and 4.8 versus 27.6%, p = 0.038, respectively. CONCLUSIONS: Intralobular and/or periductal fibrosis secondary to prior pancreatitis may limit the degree of ERCP-induced pancreatic acinar damage.

Adolescent↗
PubMed1995

Colocare self-test versus Hemoccult II Sensa for fecal occult blood testing.

OBJECTIVES: To compare the efficacy of ColoCARE Self-Test pads against Hemooccult II SENSA, a traditional guaiac-based card test, in the screening for colorectal neoplasia. METHODS: Prospective crossover analysis of 102 high-risk patients for screening of colorectal neoplasia with fecal occult blood testing, using ColoCARE Self-Test pads and Hemoccult II SENSA cards. RESULTS: Sixty-eight of the 102 patients (67%) had colorectal lesions diagnosed at colonoscopy. Of this group, 55 patients (81%) had either a polyp or cancer diagnosed at colonoscopy, with 13 of these 55 patients having polyps > or = 1 cm. ColoCARE detected 21% of all lesions, compared with 72% for Hemoccult II SENSA. ColoCARE detected only 16% of cases involving either a cancer or a polyp, and 24% of cases involving either a cancer or polyp > or = 1 cm in size. This compares with 75% and 95%, respectively, for Hemoccult II SENSA. Significantly more patients preferred ColoCARE (84%) to Hemoccult II SENSA (5%) (p < 0.00001), and patients found it easier to use ColoCARE (p < 0.01). However, 33% of patients did not feel comfortable interpreting the ColoCARE results, and 29% found it difficult to interpret the color change. CONCLUSION: These results indicate that patients may prefer the simplicity and convenience of ColoCARE; however, the test is not sensitive for the detection of colorectal neoplasia. Furthermore, patients do not feel comfortable interpreting ColoCARE results and prefer to have fecal occult blood testing interpreted by medical personnel.

Adult↗
PubMed1994

Giant duodenal ulcer. Evaluation of basal acid output, nonsteroidal antiinflammatory drug use, and ulcer complications.

Patients with giant duodenal ulcer (> 2 cm) have more ulcer complications (ie, bleeding) than patients with duodenal ulcer in the standard range (0.5-1.5 cm). To evaluate possible differences between patients with giant duodenal ulcer and those with duodenal ulcer in the standard range, we determined basal acid outputs by nasogastric suction, percentage of patients with daily nonsteroidal antiinflammatory drug (NSAID) use, and percentage of ulcer complications in 184 patients with endoscopically documented active duodenal ulcer. Seventeen patients had giant duodenal ulcer, and 167 patients had duodenal ulcer in the standard range. The mean basal acid outputs for the 17 patients with giant duodenal ulcer was 7.9 meq/hr (range 0.0-27.8 meq/hr) and for the 167 patients with duodenal ulcer in the standard range was 9.0 meq/hr (range 0.0-49.1 meq/hr), which were not significantly different. There was a significant difference in the percentages of ulcer complications between the 17 patients with giant duodenal ulcer and the 167 patients with duodenal ulcer in the standard range: 65% compared to 25% (P = 0.001), and in the percentages of patients with regular daily NSAID use, during the one month preceding the upper gastrointestinal endoscopy: 53% compared to 8% (P = 0.00001). However, a significant association between NSAID use and duodenal ulcer complication was not apparent. These results suggest that the development of giant duodenal ulcer and the significant increase in complications associated with giant duodenal ulcer are not attributable to increased basal acid output, however, they may be attributable to increased NSAID use.

Adolescent↗
PubMed1994

Idiopathic gastric acid hypersecretion. Comparison with Zollinger-Ellison syndrome.

Many patients with acid-peptic disease have idiopathic gastric acid hypersecretion defined as a basal acid output > 10.0 meq/hr; however, a significant proportion have basal acid outputs > 15.0 meq/hr, which is within the range found in Zollinger-Ellison syndrome. Although idiopathic gastric acid hypersecretion is more common than Zollinger-Ellison syndrome, it is important that these two disorders be differentiated because of differences in treatment and natural history. In the present study, we compared 124 patients with idiopathic gastric acid hypersecretion and 137 patients with Zollinger-Ellison syndrome. There were no significant differences with regard to age at diagnosis, history of upper gastrointestinal hemorrhage, nausea, vomiting, and family history of duodenal ulcer and other acid-peptic disease. However, significant differences were observed between patients with idiopathic gastric acid hypersecretion and patients with Zollinger-Ellison syndrome with regard to percentage of males: 77% compared to 64% (P = 0.008), mean serum gastrin: 60 pg/ml compared to 3679 pg/ml (normal < 100 pg/ml) (P < 0.001), mean basal acid output: 15.4 meq/hr compared to 47.0 meq/hr (P < 0.001), mean age at onset of symptoms: 33 years compared to 41 years (P < 0.001), mean duration of symptoms before diagnosis: 11 years compared to five years (P < 0.001), percentage with abdominal pain: 67% compared to 82% (P = 0.00004), percentage with diarrhea: 12% compared to 75% (P < 0.000001), percentage with pyrosis: 58% compared to 40% (P = 0.003), percentage with duodenal ulcer: 53% compared to 74% (P < 0.000001), and percentage with esophagitis: 31% compared to 42% (P = 0.0004).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Basal acid output and gastric acid hypersecretion in gastroesophageal reflux disease. Correlation with ranitidine therapy.

The purpose of this study was to evaluate possible differences in basal gastric acid secretion with regard to severity of gastroesophageal reflux disease. Basal acid output was determined by nasogastric suction in 228 patients with gastroesophageal reflux disease who received upper gastrointestinal endoscopy and were diagnosed with either pyrosis alone (N = 98), erosive esophagitis with or without pyrosis (N = 87), or Barrett's esophagus (N = 43). Mean basal acid output for the 228 patients with gastroesophageal reflux disease was 6.5 +/- 5.6 meq/hr, which was significantly different from 65 normal subjects with a mean basal acid output of 3.0 +/- 2.7 meq/hr (P < 0.0001). Compared to normal subjects, mean basal acid outputs significantly differed for patients with pyrosis (P < 0.05), esophagitis (P < 0.01), and Barrett's esophagus (P < 0.01). There was also a significant difference in mean basal acid output between the patients with pyrosis and Barrett's esophagus (P < 0.01). Nineteen of the 98 patients with pyrosis (19%), 24 of the 87 patients with esophagitis (28%), and 15 of the 43 patients with Barrett's esophagus (35%) had gastric acid hypersecretion (basal acid output greater than 10.0 meq/hr). One hundred forty-six patients with gastroesophageal reflux disease were treated with ranitidine in doses that resulted in complete healing of esophagitis and disappearance of pyrosis. Ninety-three patients responded to ranitidine 300 mg/day; however, 53 patients required increased dose of ranitidine (mean 1205 mg/day, range 600-3000 mg/day).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Endoscopic sphincterotomy-induced pancreatitis: increased risk associated with nondilated bile ducts and sphincter of Oddi dysfunction.

OBJECTIVE: to evaluate the relationship between common bile duct diameter and the risk of sphincterotomy-induced pancreatitis. METHODS: Two hundred and ten consecutive patients were prospectively investigated. Patients were divided into three groups according to the indication for sphincterotomy: Group I had common bile duct stones (n = 108), group II had sphincter of Oddi dysfunction (n = 48), and group III had sphincterotomy for other indications (n = 54) (i.e., stent, dilation). RESULTS: There were 62 males and 148 females with a mean age of 60 yr (range 15-93 yr). Eleven of the 210 patients (5.2%) developed pancreatitis. Other sphincterotomy-induced complications were bleeding (n = 2), cholangitis (n = 2), retroperitoneal duodenal perforation (n = 1), and bile duct leakage (n = 1). The percentages of pancreatitis in groups I (3.7%), II (12.5%), and III (1.9%) were significantly different (p = 0.03). Patients with nondilated common bile ducts (< or = 10 mm) had more pancreatitis than patients with dilated common bile ducts (8.8% vs. 2.8%), but the difference was not significant (p = 0.07). However, when group III was excluded from the analysis, there was a significant difference in the percentage of pancreatitis between the patients with nondilated bile ducts and those patients with dilated bile ducts (13.1% vs. 2.2%, respectively; p < 0.01). Analysis for trend did not show a significant inverse relationship between bile duct diameter and the rate of sphincterotomy-induced pancreatitis. However, for all complications combined, the inverse relationship between bile duct diameter and rate of sphincterotomy-induced complications was significant: < or = 5 mm (23.1%), > 5-10 mm (13.8%), > 10-15 mm (3.2%), > 15 mm (2.4%) (p = 0.002). CONCLUSIONS: Endoscopic sphincterotomy is more hazardous in patients with nondilated bile ducts and sphincter of Oddi dysfunction. Further studies are needed to determine whether pancreatic stenting reduces the risk of sphincterotomy-induced pancreatitis in those clinical settings.

Common Bile Duct↗
PubMed1994

Age does not affect basal gastric acid secretion in normal subjects or in patients with acid-peptic disease.

OBJECTIVES: To determine whether basal acid output was affected by patient age. METHODS: Basal acid output determined by nasogastric suction was prospectively evaluated in normal subjects (n = 65) and patients with gastroesophageal reflux disease (n = 228), gastric ulcer (n = 81), duodenal ulcer (n = 184), and nonulcer dyspepsia (n = 105). RESULTS: There was no correlation between basal acid output and age for the normal subjects and the patients with gastroesophageal reflux disease, gastric ulcer, duodenal ulcer, and nonulcer dyspepsia. However, there was a significant inverse correlation between age and basal acid output for the 33 male patients with gastric ulcer (r = -0.41, p < 0.05) and the 130 male patients with duodenal ulcer (r = -0.18, p = 0.05). Furthermore, mean basal acid outputs were significantly higher for male patients than for female patients with gastroesophageal reflux disease (p < 0.001), gastric ulcer (p < 0.05), and duodenal ulcer (p < 0.001). Mean basal acid output for the 184 patients with duodenal ulcer was significantly higher than the mean basal acid output for the 228 patients with gastroesophageal reflux disease (p < 0.001), and both were significantly higher than mean basal acid outputs for the normal subjects and the patients with gastric ulcer and nonulcer dyspepsia (p < 0.0005). CONCLUSIONS: Basal acid output can vary with gender and acid-peptic disease process; however, basal acid output does not vary with regard to age of subject.

Adult↗
PubMed1993

Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion.

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output > 10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence of Helicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis). Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P < 0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found among Helicobacter pylori-positive compared to Helicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr were Helicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence of Helicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.

Adult↗
PubMed1993

Gastric ulcers differ from duodenal ulcers. Evaluation of basal acid output.

Patients with pyloric channel and prepyloric gastric ulcers are often considered to have an ulcer diathesis similar to patients with duodenal ulcers, while patients with more proximal gastric ulcers (ie, fundus, body, antrum) are excluded. To evaluate possible differences in basal acid outputs with regard to gastric ulcer location, basal acid outputs were determined by nasogastric suction in 80 patients with endoscopically documented benign active gastric ulcers. The results were compared to 65 normal subjects and 155 patients with endoscopically documented duodenal ulcers. There were no significant differences in basal acid outputs among the 80 patients with gastric ulcers with regard to location (ie, fundus-body, antrum, prepyloric, channel), and no significant differences compared to the 65 normal subjects. However, basal acid output for the 155 patients with duodenal ulcers was significantly different from the 80 patients with gastric ulcers (P < 0.05) and the 65 normal subjects (P < 0.05). Basal acid outputs tended to be higher and there was more gastric acid hypersecretion when gastric ulcers were located near the pylorus. However, irrespective of gastric ulcer location, basal acid outputs were higher in patients with duodenal ulcers. Seventy-one of the 80 patients with gastric ulcers were treated for eight weeks with standard doses of antisecretory medications, and endoscopic healing or nonhealing was documented. In 60 patients their gastric ulcers completely healed, while 11 patients had nonhealed gastric ulcers. There were no significant differences between the two groups with regard to gender, mean age, or basal acid output.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Bleeding duodenal ulcer. Role of gastric acid hypersecretion.

Basal gastric acid output was analyzed prospectively in 110 patients with endoscopically documented duodenal ulcer disease to determine the frequency of gastric acid hypersecretion in patients with bleeding versus nonbleeding ulcers. Thirty-eight patients with stigmata of an actively or recently bleeding duodenal ulcer had a mean basal output of 12.6 +/- 8.9 meq/hr. In comparison, 72 patients with nonbleeding duodenal ulcers (and no history of prior bleeding) had a significantly lower mean basal acid output of 8.7 +/- 7.5 meq/hr (P < 0.05). Twenty-four of the 38 patients (63%) with bleeding and 28 of the 72 (39%) with nonbleeding duodenal ulcers had gastric acid hypersecretion, defined as a basal acid output of greater than 10.0 meq/hr. There was a statistically significant association between bleeding duodenal ulcer and acid hypersecretion (P = 0.01). All 110 patients were treated with standard doses of H2-receptor antagonists for eight weeks. In that time, 87 patients healed and 23 patients (14 with prior bleeding and nine with nonbleeding duodenal ulcers) remained unhealed. Significantly more patients who had bled had nonhealing duodenal ulcers (P = 0.004). Irrespective of bleeding history, all 23 patients with nonhealing duodenal ulcers at eight weeks had basal acid outputs of greater than 10.0 meq/hr (range 10.1-49.1 meq/hr). These 23 patients with nonhealing duodenal ulcers were treated with increased doses of ranitidine (mean 690 mg/day, range 600-1200 mg/day) for up to eight additional weeks. All were observed to have complete endoscopic healing documented within that period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Dieulafoy-like lesion of the rectum presenting with exsanguinating hemorrhage: successful endoscopic sclerotherapy.

The classic Dieulafoy lesion is a minute gastric mucosal defect that bleeds massively from an exposed artery. Similar lesions have been identified in the small intestine, colon, and rectum. In this report, we describe a patient who presented with an exsanguinating hemorrhage from a small rectal ulcer with a visible vessel. Control of the bleeding was achieved with endoscopic sclerotherapy using absolute alcohol and 1.5% sodium tetradocyl sulfate, with eventual complete healing of the site.

Adult↗