Endosonography of an abdominal bronchogenic cyst.
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Aged↗
Biomedical subjects
J M Scheiman
Publications and source records attributed to J M Scheiman.
Massive secretory diarrhea and pseudo-obstruction as the initial presentation of Crohn's disease.
We report large-volume secretory diarrhea and intestinal pseudo-obstruction in a man whom ultimately proved to have Crohn's disease that responded to sulfasalazine and steroids with resolution of all his symptoms. Although this is an unusual presentation, Crohn's disease should be included in the differential diagnosis in patients whose initial symptoms are intestinal pseudo-obstruction and secretory diarrhea.
Anti-Inflammatory Agents↗
One-week therapy for Helicobacter pylori. A randomized trial of two treatment regimens.
In clinical practice, eradication of Helicobacter pylori infection may be difficult due to medication side effects and the need for 2 weeks of therapy. Because therapies of shorter duration may improve patient compliance and reduce treatment side effects, we compared the efficacy and tolerability of two anti-H. pylori treatments of 1 week's duration. Patients with H. pylori infection were randomized to treatment with either (a) short-course triple therapy, composed-of bismuth subsalicylate (Pepto-Bismol, Procter & Gamble, Cincinnati, OH, U.S.A.) two tablets four times daily, amoxicillin 1 g (two 500-mg tablets) twice daily, and metronidazole 500 mg four times daily on days 5-7 or (b) omeprazole 40 mg twice a day with amoxicillin 1 g twice a day for 1 week. At least 4 weeks posttreatment, efficacy was evaluated with either histological evaluation of antral biopsies for H. pylori or 14C urea breath testing. Patients who failed initial therapy were allowed to cross over to the alternative treatment regimen after a minimum "wash-out" period of 5 weeks. Patients completed a diary during therapy to monitor both compliance and side effects. Thirty-four patients completed the study, 10 receiving both treatment regimens. Treatment with the shortcourse triple therapy eradicated H. pylori in 78.3% of treatments compared with 38% with the high-dose omeprazole/ amoxicillin combination (p < 0.05). Patients were highly compliant with both treatments, and mild side effects, such as transient loose stools or abdominal pain, were common in both groups. This is the first report from North America confirming the success of the short-course triple therapy for the eradication of H. pylori. The high-dose omeprazole/ amoxicillin regimen's eradication rate was markedly inferior to that achieved by the short-course triple therapy regimen and should not be used. Comparative studies of the short-course triple therapy regimen with other 7-day anti-H. pylori treatment regimen therapies are indicated.
Amoxicillin↗
Prolonged effect of omeprazole on the 14C-urea breath test.
OBJECTIVES: We investigated omeprazole's effect on 14C-urea breath testing. We also determined the duration of omeprazole's effect on the breath test. Finally, we studied whether effects on breath testing were dose dependent. METHODS: Fifty-seven employees and outpatients were screened for Helicobactor infection. Those positive for serology, CLO, or histology were asked to undergo baseline breath testing. Those with a positive breath test took omeprazole 20 mg/day for 14 days followed by repeat breath testing, 1, 3, and 5 days after therapy. Subjects with persistently positive breath tests despite omeprazole 20 mg/day were asked to take omeprazole 20 mg b.i.d. for 14 days. Repeat breath tests were performed as above. RESULTS: Thirteen of 57 had HP infection. Ten of 13 underwent a baseline breath test. Eight of 10 with baseline breath test experienced a significant decrease in expired 14CO2 after omeprazole 20 mg/day. Five of 13 with active HP infection developed a negative breath test after omeprazole. All subjects had a positive breath test within 5 days of stopping omeprazole 20 mg/day. Five of eight with persistently positive breath tests despite omeprazole 20 mg/day took omeprazole 40 mg/day. Four of five developed a significant decrease in 14CO2 excretion after omeprazole. All subjects had a positive breath test within 5 days of stopping omeprazole 40 mg/day. CONCLUSIONS: Recent treatment with omeprazole 20 mg/day led to a false-negative breath tests in 38.5%. This effect appeared to be dose dependent and lasted up to 5 days after cessation of omeprazole.
Anti-Bacterial Agents↗
Localization of neuroendocrine tumors utilizing linear-array endoscopic ultrasonography.
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Duodenal Neoplasms↗
Diagnosis of colonic pneumatosis cystoides intestinalis by endosonography.
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Colonic Diseases↗
Acid secretion during indomethacin therapy. Effect of misoprostol.
Secretin is an important physiologic regulator of gastric acid and pancreatic bicarbonate secretion. Endogenous prostaglandins play an important intermediary role, because indomethacin pretreatment prevents the physiological actions of secretin. Misoprostol is a prostaglandin E1 (PGE1) analog used for the prevention of nonsteroidal antiinflammatory drug (NSAID)-induced ulceration. This study sought to determine whether cotherapy with misoprostol reverses the NSAID-induced blockade of secretin's inhibition of human gastric acid secretion. Seven healthy volunteers were studied. Gastric acid secretion was measured during the basal, pentagastin-stimulated and intravenous secretin--inhibited states. The studies were then repeated after 3 days of oral indomethacin (50 mg p.o. t.i.d. for 10 doses) with and without concomitant misoprostol (200 micrograms q.i.d. for 13 doses). Exogenous secretin reduced pentagastrin-stimulated acid secretion by 35%, and this inhibition was reduced to 9% during indomethacin treatment (p < 0.05). Cotherapy with misoprostol during indomethacin treatment did not restore secretin's inhibition of gastric acid secretion; paradoxically, during secretin administration, acid secretion increased. When subjects received misoprostol treatment only, secretin failed to inhibit gastric acid secretion. We conclude that during indomethacin treatment, cotherapy with misoprostol cannot restore the inhibitory action of secretin to inhibit gastric acid secretion. These results suggest that PGE1 is an unlikely intermediate in secretin's physiological action. Although misoprostol can prevent NSAID-induced ulcers, it does not ameliorate all physiological perturbations induced by cyclooxygenase inhibition.
Adult↗
Long-term follow-up of Helicobacter pylori treatment in non-ulcer dyspepsia patients.
BACKGROUND/AIMS: It remains controversial whether Helicobacter pylori infection causes symptoms in non-ulcer dyspepsia. One hundred non-ulcer dyspepsia patients were screened for H. pylori infection between November 1989 and February 1994. Forty patients entered a trial where both infected and uninfected patients were treated with H. pylori therapy, with the uninfected group serving as controls. METHODS: Non-ulcer dyspepsia was defined as unexplained epigastric discomfort lasting for at least 4 wk. From November 1989 until February 1992, all patients, regardless of H. pylori status, were treated with bismuth subsalicylate tablets (524 mg q.i.d.) for 4 wk and metronidazole (250 mg q.i.d.) for the first 2 of the 4 wk. From March 1992 until February 1994, only infected patients were treated in an attempt to obtain equal numbers in each group. H. pylori infection was diagnosed histologically at the index endoscopy and 1 month after completion of therapy. Symptoms were scored on a 0-5 scale for both frequency and severity. RESULTS: Of 100 patients screened, 33 were infected with H. pylori (mean age, 42; 10 men, 23 women), and 67 were uninfected (mean age, 38; 16 men, 51 women). Thirty-six uninfected patients were not offered treatment during the latter part of the trial. Of the remaining 31 uninfected patients, 10 dropped out; of the 33 infected patients, 14 dropped out. Twenty-one uninfected patients and 19 H. pylori-infected patients completed treatment; in 13 of 19 patients (68%), H. pylori was eradicated. Symptoms improved in eight of 13 (61%) H. pylori-eradicated patients and in four of six (66%) H. pylori-persistent patients, compared with 14 of 21 (66%) uninfected patients. Long-term follow-up (mean, 34 months) showed similar symptom outcome in the two treatment groups. CONCLUSIONS: Thirty-three percent of our non-ulcer dyspepsia patients were infected with H. pylori, a number similar to the percentage of infected age-matched controls in the U.S. Treatment with bismuth subsalicylate and metronidazole resulted in symptomatic improvement in 61-66% of non-ulcer dyspepsia patients regardless of initial or post-treatment H. pylori status. Long-term symptom follow-up in both the control and infected groups gave similar results. H. pylori infection is not related to the symptoms of non-ulcer dyspepsia.
Adult↗
Effect of naproxen on gastroesophageal reflux and esophageal function: a randomized, double-blind, placebo-controlled study.
OBJECTIVES: Gastrointestinal symptoms, particularly pyrosis, complicate nonsteroidal anti-inflammatory drug (NSAID) use. NSAIDs cause esophageal injury, and H2 blockers are often prescribed for, and successfully control, NSAID-related symptoms. To determine whether NSAIDs can induce gastroesophageal reflux, we studied the effect of a commonly used NSAID, naproxen, on reflux parameters and esophageal function. METHODS: Nine healthy volunteers (five males, four females, age 23-34 yr) were studied. After basal measurements were taken, the subjects randomly received naproxen 500 mg p.o. b.i.d. or placebo for 1 wk. On day 6, the subjects underwent esophageal manometry with a water-perfused system and Dent sleeve. Body pressures, contraction velocity, and duration of contraction were recorded in the distal 7 cm of the esophagus. The lower esophageal sphincter pressure (LESP) and number of transient relaxations (TLESRs) were monitored. This was followed by 24-h pH monitoring. The subjects then crossed over to the other drug after a minimum 14-day wash-out period. RESULTS: No subject experienced any GI symptoms during the study. One subject developed reflux-induced symptoms a few months after completing the study and was excluded from the analysis. The total fraction of time (pH < 4) was 4.9 +/- 1.0% in the basal state, 5.5 +/- 1.4% on placebo, and 5.4 +/- 1.5% on naproxen. These differences were not significant. The number of reflux episodes and the esophageal clearance time were not affected by naproxen. The LESP in the basal state was 32.1 +/- 5.6 mm Hg, 32.3 +/- 4.2 mm Hg on placebo, and 29.9 +/- 3.3 mm Hg on naproxen (p = NS). The number of TLESRs per 30 minutes in the basal state was 3.5 +/- 0.9, 4.6 +/- 1.2 on placebo, and 5.8 +/- 1.0 on naproxen (p = NS). The speed and duration of contractions were not affected by naproxen. The excluded subject had marked basal reflux (total fraction of time pH < 4 = 10.7%), low LESP (8 mm Hg), and a marked increase in reflux on naproxen (total fraction of time pH < 4 = 53%). CONCLUSIONS: Naproxen did not induce reflux in normal subjects, although reflux did increase in some subjects. Naproxen had no significant effect on motility parameters. Our data suggest that NSAIDs do not impair the anti-reflux barrier or induce reflux. Pyrosis experienced during NSAID use may not arise from the esophagus or may reflect altered esophageal sensitivity. A single subject with decreased LESP and asymptomatic increased acid exposure in the basal state had a marked increase in reflux on naproxen. This person subsequently developed symptomatic gastroesophageal reflux. The effect of NSAIDs on individuals with a propensity to reflux deserves further study.
Adult↗
Omeprazole ameliorates aspirin-induced gastroduodenal injury.
Aspirin and nonsteroidal antiinflammatory drugs (NSAIDs) damage the gastroduodenal epithelium by two mechanisms: direct toxic effects and effects related to the depletion of endogenous prostaglandins. The prostaglandin-depleted mucosa has increased susceptibility to luminal aggressive factors, yet the role of acid in the pathogenesis of the NSAID ulcer is controversial. In humans, standard doses of H2-receptor antagonists prevent only duodenal injury and provide no protection for the gastric mucosa. It is not known whether more potent suppression of acid can prevent NSAID damage. Twenty healthy volunteers were randomized to a double-blind, placebo-controlled, crossover study to determine if omeprazole, 40 mg/day prevents gastroduodenal injury due to two weeks of aspirin administration (650 mg four times a day). The severity of mucosal injury was quantitated by endoscopy and stratified by a scale from 0 (normal) to 4 (ulcer). Fourteen of the 20 subjects had less gastric injury during cotherapy with omeprazole. All six with no difference received aspirin plus omeprazole in the first treatment period. Omeprazole significantly decreased aspirin-induced gastric mucosal injury (P < 0.001, Wilcoxon signed-rank test). Omeprazole protected 85% of subjects from extensive gastric erosions (often associated with evidence of intraluminal bleeding) or ulceration, whereas 70% of the subjects developed aspirin-induced grades 3 and 4 gastric injury on placebo (P < 0.01 by chi 2). No subject taking omeprazole developed duodenal injury of any grade, while 50% taking placebo developed erosions and 15% had ulcer (P < 0.001). Medication side effects were mild in the majority of subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Duodenal acidification and secretin, but not intraduodenal fat, inhibit human gastric acid secretion via prostaglandins.
BACKGROUND/AIMS: Acid and fat in the duodenum inhibit gastric acid secretion and increase plasma secretin. The role of prostaglandins and secretin in the inhibition of gastric acid secretion by duodenal infusion of hydrochloric acid and fat in healthy human volunteers was studied. METHODS: Gastric acid secretion was submaximally stimulated with intravenous pentagastrin followed by duodenal infusion of 0.1N hydrochloric acid, oleic acid, or intravenous secretin. To inhibit endogenous prostaglandins, the protocol was then repeated after indomethacin treatment. RESULTS: Duodenal fat infusion inhibited acid secretion 80% +/- 5% and was unaffected by indomethacin treatment. Intraduodenal acidification inhibited acid secretion by 43% +/- 8% and was reduced by indomethacin treatment to 15% +/- 4% (P < 0.01). Similarly, intravenous secretin inhibited acid secretion by 34% +/- 3%, which was decreased to 13% +/- 6% by indomethacin treatment (P < 0.01). The increase in plasma secretin levels after intraduodenal hydrochloric acid treatment was significantly greater than that observed with intravenous secretin or introduodenal oleic acid treatment; all were within the physiological range. Acid in the duodenum releases secretin, which inhibits gastric acid secretion at least in part via prostaglandins. In contrast, fat in the duodenum strongly inhibits gastric acid secretion via a nonprostaglandin pathway. CONCLUSIONS: Secretin is the predominant mediator for the inhibition of human gastric acid secretion induced by the presence of acid, but not fat, in the duodenum.
Adolescent↗
Role of endoscopic ultrasonography in the localization of insulinomas and gastrinomas.
BACKGROUND: We have previously found selective venous sampling to be the most sensitive method to localize otherwise occult functioning endocrine tumors. However, recently we have used endoscopic ultrasonography (EUS) as the initial and in some cases the only localization study in the preoperative evaluation of proven insulinomas and of selected cases of gastrinoma. METHODS: All patients referred between April 1993 and April 1994 with a subsequently confirmed diagnosis of organic hyperinsulinism or Zollinger-Ellison syndrome (ZES) underwent EUS. Ten patients with insulinomas and six with gastrinomas were studied. Only one patient with ZES had multiple endocrine neoplasia type I. Patients with negative EUS findings had additional localization procedures including angiography and arterial stimulation tests. All but one patient underwent surgical exploration. RESULTS: Solitary insulinomas were found in all 10 patients. EUS correctly identified and localized the insulinoma in seven (70%) of 10 patients but failed to identify two pedunculated insulinomas that were easily found at exploration. Because of an incomplete examination, a single insulinoma was not detected within the parenchyma. The EUS examination correctly excluded the pancreatic gastrinomas in five patients. The sixth patient, who had multiple endocrine neoplasia type I, had two 0.5 cm tumors in the head. CONCLUSIONS: EUS is a sensitive and cost-effective technique for localization of insulinomas and may be the only study needed. In patients with ZES a negative pancreatic result suggests the likelihood of a duodenal or other extrapancreatic tumor.
Adult↗
Giant splenomegaly and refractory hypercalcemia due to extrapulmonary sarcoidosis. Successful treatment by splenectomy.
Sarcoidosis is a granulomatous disease of unknown origin with a variable clinical presentation. The presenting complaint is usually referable to the lung. We describe an unusual presentation of sarcoidosis in a young black man who received medical attention for evaluation of pancytopenia, giant splenomegaly, and marked, refractory hypercalcemia. After extensive evaluation, including exploratory laparotomy, he was found to have sarcoidosis, with extensive involvement of his spleen, liver, and abdominal lymph nodes. Pulmonary involvement was notably absent, with no suggestive findings radiographically on gallium citrate Ga 67 scanning or on bronchoscopy with transbronchial biopsy. This patient underwent splenectomy and, following removal of the massive splenic granuloma burden, the hypercalcemia resolved completely with no other therapy.
Adult↗
Liver biopsy in fever of unknown origin. A reappraisal.
We assessed the value of liver biopsy in the diagnosis of fever of unknown origin (FUO) in hospital-based patients by a retrospective analysis of all cases (24 cases) seen at the University of Michigan Medical Center over a 5-year period. Based on the findings of a liver biopsy performed in the course of the evaluation of FUO, patients were divided into two groups: a diagnostic group, in which an abnormal liver biopsy was helpful in determining the cause of the FUO, and a nondiagnostic group, which included those who had either normal biopsy results or abnormal biopsy results that did not lead to a final diagnosis. Four patients (16.7%) had diagnostic liver biopsy results (histoplasmosis in three and tuberculosis in one). Physical findings, such as hepatomegaly, and laboratory data, including routine liver chemistries, were not predictive of a diagnostic liver biopsy. Therefore, despite advances in diagnostic technology since this subject was last reviewed, liver biopsy continues to be useful in the diagnosis of FUO. Furthermore, in endemic or borderline endemic areas, histoplasmosis should be considered in the differential diagnosis of FUO, and liver biopsy can be helpful to confirm this diagnosis.
Adolescent↗
Role of prostaglandin E2 in cholinergic-mediated glycoprotein synthesis in canine antrum.
We studied the mechanism of cholinergic stimulation of mucin synthesis in canine antral explants, including the role of PGE2 as an intermediate messenger. Isolated antral mucosa was incubated with 10(-5) M carbachol (Cb), 10(-5) M indomethacin (IND), 10(-5) M pirenzepine (PZ), 10(-5) M Cb + 10(-5) M PZ, 10(-5) M Cb + 10(-5) M IND, and 10(-5) M IND + PGE2 (10(-8), 10(-7) and 10(-6) M) in the presence or absence of [3H]glucosamine. After 24 hr, total glycoprotein synthesis was quantitated by Sepharose-4B chromatography and by 10% TCA/1% PTA precipitation with lipid extraction. PGE2 released into the media was measured by radioimmunoassay (RIA). Cb significantly increased total glycoprotein synthesis and produced a significant increase in PGE2 release. The increase in glycoprotein synthesis and the release of PGE2 was blocked by the addition of muscarinic antagonist PZ. The addition of IND significantly inhibited glycoprotein synthesis and almost entirely suppressed PGE2 secretion. IND also inhibited the effect of Cb on glycoprotein synthesis and PGE2 release. Moreover, PGE2 (10(-6) and 10(-7) M) significantly increased the glycoprotein synthesis in the canine stomach. This suggests the coordinate participation of PGE2-releasing cell population in modulation of glycoprotein synthesis in gastric mucosa.
Animals↗
Effect of sucralfate on components of mucosal barrier produced by cultured canine epithelial cells in vitro.
The mucous gel maintains a neutral microclimate at the epithelial cell surface, which may play a role in both the prevention of gastroduodenal injury and the provision of an environment essential for epithelial restitution and regeneration after injury. Enhancement of the components of the mucous barrier by sucralfate may explain its therapeutic efficacy for upper gastrointestinal tract protection, repair, and healing. We studied the effect of sucralfate and its major soluble component, sucrose octasulfate (SOS), on the synthesis and release of gastric mucin and surface active phospholipid, utilizing an isolated canine gastric mucous cells in culture. We correlated these results with the effect of the agents on mucin synthesis and secretion utilizing explants of canine fundus in vitro. Sucralfate and SOS significantly stimulated phospholipid secretion by isolated canine mucous cells in culture (123% and 112% of control, respectively). Indomethacin pretreatment significantly inhibited the effect of sucralfate, but not SOS, on the stimulation of phospholipid release. Administration of either sucralfate or SOS to the isolated canine mucous cells had no effect upon mucin synthesis or secretion using a sensitive immunoassay. Sucralfate and SOS did not stimulate mucin release in the canine explants; sucralfate significantly stimulated the synthesis of mucin, but only to 108% of that observed in untreated explants. No increase in PGE2 release was observed after sucralfate or SOS exposure to the isolated canine mucous cells. Our results suggest sucralfate affects the mucous barrier largely in a qualitative manner. No increase in mucin secretion or major effect on synthesis was noted, although a significant increase in surface active phospholipid release was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Induction of cytochrome P450IA genes (CYP1A) by omeprazole in the human alimentary tract.
Cytochrome P450 enzymes are capable of converting procarcinogens into either active mutagens or inactive metabolites. Because the distribution of these enzymes may be important for tissue susceptibility to procarcinogens, the expression and induction of CYP1A genes in the human alimentary tract were investigated. Endoscopic biopsy specimens were obtained from buccal mucosa, esophagus, gastric body, antrum, duodenum, and colon of 6 healthy volunteers before and 1 week after taking 20 mg of omeprazole daily. Tissue specimens were analyzed for the presence of CYP1A1 and 1A2 transcripts using hybridization methods and the polymerase chain reaction. P450-dependent enzymatic activity was assessed by deethylation of ethoxyresorufin. CYP1A1 messenger RNA (mRNA) and ethoxyresorufin activity were present constitutively in the duodenum of each volunteer. Omeprazole (20 mg/day for 1 week) induced CYP1A1 mRNA and enzymatic activity in 5 of 6 volunteers. The one individual who did not initially respond had a marked increase in both mRNA and enzymatic activity after receiving 60 mg of omeprazole daily for 1 week. After treatment with omeprazole, two individuals had low levels of CYP1A1 mRNA in several other alimentary tissues as well as low levels of CYP1A2 mRNA in the duodenum. The expression and induction by a pharmaceutical agent of CYP1A genes may have implications for intestinal metabolism of ingested xenobiotics including procarcinogens.
Adult↗