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Biomedical subjects

G H Elta

Publications and source records attributed to G H Elta.

At least 19 recordsLinked to original sources
PubMed1995

Single-day, divided-dose oral sodium phosphate laxative versus intestinal lavage as preparation for colonoscopy: efficacy and patient tolerance.

Polyethylene glycol-electrolyte lavage solutions are widely used to prepare the colon for colonoscopy. Unfortunately, some patients find this preparation difficult to complete. Recent studies of a sodium phosphate-based laxative have shown both good patient tolerance and good bowel preparation. In these studies, the laxative has generally been prescribed in two doses, with the second dose taken early the morning of colonoscopy. Because the morning dose is inconvenient for many patients, we compared giving a common polyethylene glycol-based electrolyte lavage solution the day before colonoscopy with our method of giving both doses of sodium phosphate-based laxative the day before colonoscopy: one dose at 4 PM and the second dose at 8 PM. We judged efficacy by an assessment of residual liquid and fecal matter in the colon and judged tolerance by the results of a symptom questionnaire completed by each patient immediately before the procedure. Our results in more than 200 patients showed similar efficacy ratings and similar symptom scores for both preparations, but patients rated the sodium phosphate-based preparation as easier to tolerate. In conclusion, in selected patients this new dosing method for sodium phosphate is preferable to large-volume, whole-gut lavage solutions.

Administration, Oral↗
PubMed1992

Absorption of flurbiprofen in the fed and fasted states.

The oral absorption of flurbiprofen, an antiinflammatory nonsteroidal compound, was compared in the fasted vs the fed state. When ingested as an aqueous solution of the sodium salt, absorption kinetics followed a monoexponential pattern in half of the subjects and a bimodal pattern with a lag time before the onset of the second phase of absorption in the other half of the subjects. When ingested in the free acid form as a tablet either with water (fasted state) or with water 15 min after 330 ml of apple juice (fed state), flurbiprofen absorption was always bimodal, and the lag time before the onset of the second phase was shown to be dependent on the gastric emptying time (r = 0.623, P less than 0.01). The gastric emptying times were significantly longer when the drug was administered in the fed state (average GET = 57 min in the fasted state and 102 min in the fed state; P less than 0.01). These results suggest that gastric emptying effects are one important way in which absorption of drugs can be affected by meal intake.

Administration, Oral↗
PubMed1991

Injection sclerotherapy-induced esophageal strictures. Risk factors and prognosis.

Injection sclerotherapy (IS) has become an effective modality for the treatment of bleeding esophageal varices. Despite improvements in equipment, sclerosant solutions and operator technique, injection sclerotherapy-induced esophageal strictures (ISES) remain a significant cause of patient morbidity. To analyze the risk factors and prognosis of ISES, the records of 117 patients who underwent IS over a 6-year period at a single teaching institute were reviewed. The predictive value of multiple risk factors including the patient's age, Child's risk classification, previous bleeding episodes, etiology of varices, cumulative amount of sclerosant used, and the number of IS treatments were determined using ANOVA. A P value of less than 0.05 was considered significant. In all cases, a free-hand injection technique, flexible endoscopes and sodium morrhuate were used. During a mean follow-up period of 228 days (1-1,469 days), 41 patients (35%) died and 24 patients (20.5%) developed symptomatic strictures. The cumulative amount of sclerosant used (81.4 +/- 9.5 ml) and the number of IS treatments (6.5 +/- 0.7) required in the stricture group was significantly greater than in the nonstricture group (49.1 +/- 2.7 and 4.0 +/- 0.3, respectively). The risk of stricture formation did not correlate with the volume of sclerosant injected per treatment, cause of varices, number of previous bleeds, or Child's hepatic risk class. A mean of 3.6 +/- 4.5 dilations was required for treatment of established strictures and 18 patients (75%) required r 4 dilations. One esophageal perforation occurred following dilation. Mortality correlated with hepatic risk class as 30/41 (73%) of deaths occurred in Child's C patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Esophageal Stenosis↗
PubMed1990

Gastroduodenal mucosal damage with salsalate versus aspirin: results of experimental models and endoscopic studies in humans.

Animal models have identified multiple mechanisms of aspirin toxicity. Aspirin inhibits cyclooxygenase in the gastroduodenal mucosa leading to a decrease in endogenous prostaglandins. Prostaglandin mediated mucus and bicarbonate secretion, epithelial hydrophobicity, blood flow, and cellular proliferation are all decreased. Salicylates may cause direct cellular toxicity via inhibition of energy metabolism and membrane transport properties. Salicylate preparations have been designed to decrease gastroduodenal absorption. Endoscopic studies in humans have confirmed that buffering of aspirin does not ameliorate damage, but enteric coating does. Salicylsalicylic acid (salsalate) is an effective antirheumatic drug that bypasses gastric absorption and also avoids cyclooxygenase inhibition. In a randomized, single-blind, endoscopic comparison of salsalate versus enteric-coated aspirin, significantly less gastroduodenal damage was observed in volunteers after salsalate administration compared to enteric-coated aspirin. An endoscopic study in rheumatoid arthritics also confirmed the ability of salsalate to spare gastroduodenal mucosa when compared to naproxen administration. Salsalate may cause less gastroduodenal damage than enteric-coated aspirin based on the results of animal models and endoscopic studies in humans.

Animals↗
PubMed1990

Comparison of coffee intake and coffee-induced symptoms in patients with duodenal ulcer, nonulcer dyspepsia, and normal controls.

Coffee and decaffeinated coffee stimulate acid secretion. In addition, many patients experience dyspepsia after coffee ingestion. Therefore, coffee is often prohibited by physicians in patients with peptic diseases. However, the association between peptic disease and symptoms remains unclear. This study compares coffee intake and the induction of symptoms by coffee in patients with duodenal ulcer disease, nonulcer dyspepsia, and normal controls. We have studied the coffee drinking habits of 58 duodenal ulcer patients, 55 nonulcer dyspepsia patients, and 55 normal controls. The use of coffee on a daily basis was not significantly different between duodenal ulcer patients (64%) and controls (56%), or between nonulcer dyspepsia patients (55%) and controls. There was also no difference between the three groups in the use of decaffeinated coffee, the number of cups per day, the method of preparation, the length of time of coffee use, or any change in coffee intake in the previous year. The intake of tea, caffeinated carbonated beverages, and aspirin or nonsteroidal anti-inflammatory drugs was also similar in the three groups. The duodenal ulcer patients were more likely to be cigarette smokers (45%) than either the controls (16%) or the nonulcer dyspepsia patients (24%). Daily alcohol intake was not significantly different in the three groups. The prevalence of coffee induction of dyspeptic symptoms was similar in duodenal ulcer patients (29%) and controls (22%), but was much more common in nonulcer dyspepsia patients (53%) than in controls (22%), p = 0.0036. In conclusion, there was no difference in coffee intake between patients with duodenal ulcer, nonulcer dyspepsia, or normal controls. However, patients with nonulcer dyspepsia, but not duodenal ulcer, were more likely to experience dyspeptic symptoms after coffee ingestion.

Caffeine↗
PubMed1990

Persistent immune deficiency in patients with alcoholic hepatitis.

T-lymphocyte subset numbers, recall-antigen skin test responses and mitogen-induced lymphocyte proliferation assays were investigated in 12 patients with severe alcoholic hepatitis (AH). Serial studies of these parameters were obtained at intervals of 1 or 2 wk. Patients with AH had lower peripheral blood lymphocyte counts with corresponding decreases in T-cell subset numbers that were persistent in the serial evaluations. T8 cells were disproportionately decreased, with a significant resultant increase in the T4:T8 ratios. Compared with controls, AH patients had significantly smaller cutaneous responses to Candida albicans antigen (p less than 0.05) and mumps antigen (p less than 0.005). Fifty-eight percent of patients were anergic when tested with a battery of four antigens. Patients with AH had increased concanavalin A-, but not phytohemagglutinin-induced lymphocyte proliferative responses. These serial analyses confirm previous observations of cell-mediated immune dysfunction in patients with severe AH. Moreover, there is a persistence of these abnormalities for at least 6 wk after withdrawal from alcohol.

Hepatitis, Alcoholic↗
PubMed1989

Salicylsalicylic acid causes less gastroduodenal mucosal damage than enteric-coated aspirin. An endoscopic comparison.

The gastroduodenal mucosal damage caused by aspirin and nonsteroidal antiinflammatory drugs is a common clinical problem. We compared two medications designed to diminish mucosal damage: enteric-coated aspirin and salicylsalicylic acid (salsalate). Ten healthy volunteers were randomized to receive either 1.5 g salsalate twice a day or 650 mg enteric-coated aspirin four times a day for six days and were then crossed over to the other drug after a one-week medication-free period. Endoscopic inspection of gastroduodenal mucosa was performed at entry and again after six days of drug therapy for each medicine. Mean serum salicylate concentrations taken before the morning drug dose were 11.2 mg/dl for enteric-coated aspirin and 18.1 mg/dl for salsalate. Only one of 10 subjects receiving salsalate developed mild (grade 1) mucosal damage while six of 10 receiving enteric-coated aspirin developed moderate to severe damage (grade 2-3) (P = 0.01). Symptoms were mild in both groups. We conclude that salsalate causes less gastroduodenal mucosal damage than enteric-coated aspirin.

Adolescent↗
PubMed1989

Campylobacter pylori is not associated with gastroparesis.

There is a high incidence of Campylobacter pylori in the gastric mucosa of patients with duodenal ulcer, gastric ulcer, and nonulcer dyspepsia. Factors that lead to development of this infection are unknown. We hypothesized that delayed solid-phase gastric emptying, a condition characterized by antral stasis, might predispose to Campylobacter pylori infection. We prospectively studied 51 patients with symptoms of gastroparesis using a solid-phase gastric emptying study and upper endoscopy. Patients were excluded if they had predominant symptoms of epigastric pain or an abnormal endoscopy. Three biopsies were obtained from the antrum and stained with H&E. When any inflammation was present, a Warthin-Starry stain was also performed. These were blindly examined for chronic inflammation, activity, and presence of Campylobacter pylori. Campylobacter pylori was not more common in patients with gastroparesis, documented by delayed gastric emptying, than in patients with a normal emptying study. On the contrary, there was a significantly lower incidence of Campylobacter pylori in those with delayed emptying compared to those with normal emptying (5% vs 31%, P less than 0.05). Gastritis activity correlated closely with Campylobacter presence. Inactive chronic gastritis with Campylobacter was equally common in those with delayed or normal gastric emptying. Diabetics were no more likely to harbor Campylobacter pylori than nondiabetics (16% vs 25%). The 5% incidence of Campylobacter in the gastroparesis group is less than, but approaches, that previously reported in asymptomatic controls. The 31% incidence of Campylobacter in the group with symptoms of gastroparesis but normal gastric emptying approaches that reported for nonulcer dyspepsia. Our data suggest that gastroparesis does not predispose to Campylobacter pylori infection or histologic chronic gastritis.

Adult↗
PubMed1989

Effect of iron on the guaiac reaction.

Most studies show that oral ingestion of iron does not cause a positive stool guaiac reaction. However, all in vitro studies show that iron does cause a positive guaiac reaction and some in vivo studies have shown a positive stool guaiac reaction in response to oral iron. This study examines this unresolved question. Twenty-five normal volunteers were given 900 mg of ferrous sulfate a day. Two Hemoccult II and two HemoQuant tests were obtained before and during iron therapy. All Hemoccult II tests were negative before and after oral iron. Four HemoQuant tests were slightly elevated before oral iron and one was slightly elevated after oral iron. Ferrous sulfate, 300 mg, was dissolved in 1 L of water. The solution was acidic (pH = 3.9) and produced a positive Hemoccult II test. When the solution was titrated with sodium hydroxide to a pH of greater than or equal to 6.0, iron precipitated out and the mixture no longer produced a positive Hemoccult II reaction. Our data show that ferric iron (Fe3+) in solution will give a positive guaiac reaction directly and ferrous iron (Fe2+) will give a positive guaiac reaction after hydrogen peroxide is added because it oxidizes Fe2+ to Fe3+. Iron solutions are acidic and when titrated toward a neutral pH, the iron is precipitated out and the solution is then guaiac-negative. Thus, our in vivo data confirm most previous in vivo studies; furthermore, the discrepancy between in vivo and in vitro studies can be explained as a pH-dependent phenomenon of in vitro iron solutions. Oral iron should not cause a positive guaiac reaction, and the HemoQuant results show no increase in occult blood loss in subjects on oral iron therapy.

Administration, Oral↗
PubMed1989

Treatment of Campylobacter pylori does not alter gastric acid secretion.

The effect of treatment of Campylobacter pylori-associated gastritis on acid secretion was studied to examine further the strong association between C. pylori and peptic diseases. Twelve symptomatic patients with non-ulcer dyspepsia and C. pylori-associated histologic gastritis had basal and pentagastrin-stimulated gastric acid analysis before and after a 14-day course of amoxicillin 250 mg qid and bismuth subsalicylate 524 mg qid. Endoscopy, antral biopsies, and symptom questionnaires were obtained at entry and at the conclusion of the study. C. pylori was identified by Warthin-Starry stain. Biopsy specimens were also graded for the severity of chronic inflammation and the presence of neutrophils in the epithelium. The treatment regimen cleared C. pylori in 10 of 12 patients. Dyspeptic symptoms improved in 10 of 12 patients, two of whom did not clear the organism, and were unchanged in the remaining two patients, both of whom cleared the bacteria. Neutrophil infiltration in the antral biopsies resolved in 10 patients, including nine with C. pylori clearance and one with persistence of the organism. The severity of the underlying chronic inflammation improved in only one of the 10 organism-free patients and one of the two persistently infected individuals. Pretreatment gastric acid analysis demonstrated hypochlorhydria in three of 12 patients, mild hyperchlorhydria in three of 12 patients, mild hyperchlorhydria in two of 12, and normal acid secretion in the remaining seven patients. Posttreatment acid studies revealed that four of 12 patients were hypochlorhydric, one of 12 had hyperchlorhydria, and seven of 12 were normochlorhydric. After treatment, there was no significant change in basal or maximal acid secretion in the 10 patients who cleared the organism. The two patients who failed to clear C. pylori had insignificant increases in acid secretion after treatment. Our data show no consistent pretreatment pattern of acid secretion in patients with C. pylori-associated gastritis. In addition, gastric acid output did not show a consistent change after treatment for C. pylori. This suggests that the association between C. pylori infection and peptic diseases does not occur via altered acid secretion.

Amoxicillin↗
PubMed1989

Campylobacter pylori in patients with dyspeptic symptoms and endoscopic evidence of erosion(s).

The relationship between Campylobacter pylori (CP), histologic gastritis, and dyspeptic symptoms is becoming gradually clearer, but there is still a lack of knowledge of the natural history of treated or untreated gastritis. We examined serial biopsies from the gastric fundus, body, and antrum, and from the duodenum in 16 dyspeptic patients. Patients with concomitant peptic ulcers, alcoholism, or nonsteroidal anti-inflammatory drug use were excluded. CP was present in the biopsies of 50% of patients at presentation. When CP was present, the antrum was always infected, and often had the highest density of organisms. In the duodenum, CP was found only in areas of gastric metaplasia. The presence of CP was highly correlated with gastritis activity (neutrophilic infiltrate). A 4-yr follow-up study of symptoms, endoscopic appearance, and histologic findings including the presence of CP was performed in 10 of the original 16 patients. After 4 yr, both the severity and frequency of epigastric pain remained the same in seven patients, worsened in one, and improved in two. All patients who had CP at initial presentation retained the organism (5/10), whereas none of the previously noninfected patients acquired the infection (5/10). Both CP-positive and -negative patients were treated for 3 wk with 524 mg bismuth subsalicylate qid, and for the first 2 of 3 wk with 250 mg metronidazole qid. One patient who was CP positive was lost to follow-up. In three of the remaining four patients on this regimen, the organism was eradicated. Of the nine patients who completed the treatment program, two had no change in symptoms and seven improved. CP was present in three of seven with improved symptoms and in one of two with no change in symptoms. After treatment, the only change in histology was the disappearance of activity in the CP-positive patients who lost the organism. In conclusion, CP was present in 50% of dyspeptic patients with endoscopic evidence of at least one erosion. Both the symptoms and CP persisted for 4 yr. Dyspeptic symptoms improved after bismuth subsalicylate/metronidazole therapy, regardless of the presence or absence of CP, although the regimen did succeed in eradicating the organism in three of the four CP-positive patients who completed the study.

Adolescent↗