Search PubMed⌕ Search

Biomedical subjects

D Y Graham

Publications and source records attributed to D Y Graham.

At least 433 records · Page 24Linked to original sources
PubMed1990

Gastritis in the elderly.

The elderly have an increased prevalence of gastritis and the complications associated with it. The two major classes of acute and chronic gastritis, type A and B, are discussed as they relate to clinical findings, histologic features, and pathogenesis. An age-related increase in the frequency of Helicobacter pylori (formerly Campylobacter pylori) infection in the elderly parallels the known age-related increase in the prevalence of gastritis. The close association between gastritis in the elderly and hypochlorhydria and gastric carcinoma is also explored.

Achlorhydria↗
PubMed1990

Ablation of exaggerated meal-stimulated gastrin release in duodenal ulcer patients after clearance of Helicobacter (Campylobacter) pylori infection.

An exaggerated increase in meal-stimulated gastrin is a common finding in patients with duodenal ulcer. Duodenal ulcer patients also exhibit an increase in the number of parietal cells, which results in an increase in maximum acid output. There are also data to suggest that acid hypersecretion may not predate the ulcer disease, but is acquired, possibly due to the trophic effects of the exaggerated gastrin release on parietal cells. We investigated meal-stimulated gastrin release in nine Helicobacter pylori-infected individuals; eight patients with chronic duodenal ulcer and one H. pylori-infected healthy control, both before and after therapy designed to eradicate H. pylori infection. We also simultaneously measured intragastric pH in six duodenal ulcer patients. Eradication of the H. pylori infection reversed the exaggerated meal-stimulated gastrin release (gastrin secretion fell from 141 + 16 pg/ml/h before treatment to 98 +/- 7 pg/ml/h after, p less than 0.01) without affecting intragastric pH. Whereas exaggerated meal-stimulated gastrin release may be an important pathogenetic feature of duodenal ulcer disease, we conclude that it is secondary to the H. pylori infection. This study provides further insight into the role of H. pylori in the pathogenesis of duodenal ulcer disease. We postulate that reversal of the abnormalities in gastrin secretion will be associated with a gradual return of gastric secretion to normal.

Bismuth↗
PubMed1990

Prevalence of Helicobacter (formerly Campylobacter) pylori infection in Saudia Arabia, and comparison of those with and without upper gastrointestinal symptoms.

A causative role is now accepted for Helicobacter (formerly Campylobacter) pylori in type B gastritis, and evidence is accumulating that H. pylori infection plays a major contributory role in duodenal ulcer, gastric ulcer, and epidemic gastric cancer. The prevalence of H. pylori in any population remains unknown. We compared the prevalence of H. pylori infection in the Riyadh region of Saudia Arabia, using a specific and sensitive ELISA for IgG antibody against the high molecular weight cell-associated antigen of H. pylori (urease). Subjects were interviewed, demographic data were collected, and a serum sample was obtained. Subjects completed a questionnaire that included questions about level of education, smoking, medications used, presence and frequency of symptoms referable to the upper gastrointestinal tract, and family history of ulcer disease. We studied 557 individuals (ranging in age from 5 to 91 yr). The prevalence of H. pylori infection increased rapidly with age: from 40% of those ages 5-10 yr, to more than 70% of those 20 or older. H. pylori infection occurred with significantly more frequency in adults with less than 12 yr of schooling, compared with adults who had attended college. The high rate of acquisition of H. pylori infection in Saudia Arabia emphasizes that studies of H. pylori-disease associations must consider the baseline prevalence of H. pylori infection in that population.

Adolescent↗
PubMed1989

Influence of media supplements on growth and survival of Campylobacter pylori.

Experiments were designed to determine the role of heme and the importance of other factors in the growth of Campylobacter pylori. Campylobacter pylori strains were tested for their ability to synthesize porphyrin, for their ability to grow and be maintained on basal medium and basal medium supplemented with blood or blood products, and for the influence of bovine serum albumin and catalase on viability. Results indicated that Campylobacter pylori does not require heme as a source of porphyrin. Growth of Campylobacter pylori could not be sustained on media containing starch or hemoglobin, but was sustained on media containing erythrocytes, serum, bovine serum albumin or catalase. The ability to grow on media containing bovine serum albumin and catalase suggests that protection from toxic fatty acids and the prevention of toxic product formation may be important factors in the growth and survival of Campylobacter pylori in vitro. Both bovine serum albumin and catalase combined provide the minimum requirements which allow the spectrum of Campylobacter pylori present in a single culture to grow on blood-free media.

Bacteriological Techniques↗
PubMed1989

Suppression of nocturnal acid secretion with famotidine accelerates gastric ulcer healing.

Although nocturnal acid secretion has been emphasized in the pathophysiology and treatment of duodenal ulcer, its importance in gastric ulcer disease has been questioned. To explore this area, this multicenter U.S. trial compared the effect of a once-daily nighttime dose of H2-receptor antagonist with placebo on the healing of gastric ulcer and relief of associated symptoms. One hundred fifty-seven patients with endoscopically verified benign gastric ulcers were randomized in a double-blind fashion to either famotidine (40 mg at bedtime) or placebo. Antacid tablets were allowed as needed. The healing rates for famotidine were 45%, 66%, and 78% at weeks 4, 6, and 8, respectively. In comparison, placebo healing rates were 39%, 44%, and 64%. These differences were statistically significant in favor of famotidine at weeks 6 (p less than or equal to 0.01) and 8 (p less than or equal to 0.05), as well as in a life-table analysis (p less than or equal to 0.05). Nocturnal famotidine was also significantly better than placebo with respect to time to complete relief of pain and to the percentage of patients with complete relief of pain. No concomitant factor (including ulcer size, ulcer location, smoking history, or regular alcohol use) affected healing rates in this study. Famotidine was well-tolerated and no serious clinical or laboratory adverse effects were judged to be related to this dosing regimen of famotidine. In conclusion, suppression of nocturnal acid secretion with famotidine (40 mg at bedtime) was more effective than placebo in promoting the healing of acute benign gastric ulcer and its associated symptoms. The results of this study suggest that suppression of nocturnal acid secretion alone is as effective as "around the clock" acid suppression in the healing of benign gastric ulcer.

Clinical Trials as Topic↗
PubMed1989

A sensitive and specific serologic test for detection of Campylobacter pylori infection.

Campylobacter pylori has been associated with gastritis, duodenal ulcer, gastric ulcer, and nonulcer dyspepsia. Evidence that C. pylori may be the causative agent or at least a major contributory factor in peptic ulcer disease has generated intense interest in the development of reliable methods for detecting C. pylori infections. We have developed a specific and sensitive enzyme-linked immunosorbent assay (ELISA) that detects serum immunoglobulin G antibodies directed against high molecular weight cell-associated proteins (HM-CAP) of C. pylori. In a blinded fashion we tested sera from 300 individuals and found that all of 147 HM-CAP ELISA-negative individuals were also negative for C. pylori, as documented by a negative urea breath test; also, 151 of 153 C. pylori-positive (by urea breath test) individuals were HM-CAP ELISA-positive. Campylobacter pylori was cultured from the two ELISA-negative but infected patients and these isolates did possess HM-CAP antigens, showing that these two individuals had failed to seroconvert. Thus, the specificity and positive predictive value of the HM-CAP ELISA were each 100%; the sensitivity of the assay was 98.7%, and the negative predictive value was 98.6%. The HM-CAP ELISA and the urea breath test both proved valuable for detecting C. pylori infection, the urea breath test being a more direct method whereas the ELISA is less expensive and easier to perform. Furthermore, the results of a serologic test such as the HM-CAP ELISA would not be influenced by recent ingestion of bismuth compounds or antimicrobial therapy, which might suppress C. pylori and cause a transient false-negative result in the urea breath test.

Adult↗
PubMed1989

Campylobacter pylori and peptic ulcer disease.

Campylobacter pylori is now known to be the most common and important cause of gastritis, and C. pylori infections have been associated with duodenal ulcer, gastric ulcer, nonulcer dyspepsia, and gastric cancer. Although it has been only possible to culture C. pylori for about 5 yr, there are already sufficient data available to allow us to develop the basic framework that relates C. pylori gastritis to the causation of peptic ulcer disease. We review the data and propose mechanisms that implicate C. pylori as an important factor in the pathogenesis of peptic ulcer disease and consider the therapeutic implications. What we now know about C. pylori begins to unravel some of the mysteries surrounding peptic ulcer disease.

Campylobacter Infections↗
PubMed1989

Prevention of gastroduodenal injury induced by chronic nonsteroidal antiinflammatory drug therapy.

The fact that nonsteroidal antiinflammatory drugs (NSAIDs) damage the gastroduodenal mucosa is now accepted as NSAID use has been associated with a disproportionately high frequency of upper gastrointestinal bleeding and perforation of gastric and duodenal ulcers. More than 10% of patients receiving NSAIDs chronically will have a gastric ulcer on any given day, a point prevalence of ulcer disease 5-10 times higher than in patients who are not taking NSAIDs. Endoscopic studies comparing the effect of acute administration of NSAIDs on the gastroduodenal mucosa in normal volunteers have failed to predict which NSAIDs would be safest when administered chronically. All of the newer NSAIDs appear to be similar in their propensity to cause chronic mucosal damage, including peptic ulceration. Recent studies have suggested that in those starting NSAID therapy, prophylactic cotreatment with H2-receptor antagonists or sucralfate has minimal or no effect on preventing the development of NSAID-induced gastric ulcers, although duodenal ulcers may be reduced. Nonsteroidal antiinflammatory drug-induced gastric ulcers are also not prevented by drug formulations that prevent or markedly reduce the amount of active NSAID in the stomach. Cotreatment with the synthetic prostaglandin misoprostol was associated with a marked reduction in gastric ulcer development in patients with osteoarthritis receiving NSAIDs chronically, suggesting that prevention of prostaglandin generation in the gastric mucosa may play a pivotal role in NSAID-induced gastric ulcers.

Acute Disease↗
PubMed1989

Dyspepsia in NSAID users: the size of the problem.

Gastroduodenal intolerance is one of the major factors limiting the use of aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) in patients with rheumatic diseases. We previously demonstrated that dyspepsia was not a marker for ulcer in NSAID users. We have now evaluated dyspeptic symptoms in 245 arthritic patients (receiving 13 different NSAIDs) from the practices of two rheumatologists. Fifty-seven patients (23%) gave a history of previous peptic ulcers. Heartburn, indigestion, or sour stomach at least once within the past year was present in 62.5%; 36.7% had experienced these symptoms within the previous 2 months and 28.6% within the previous week. Only 39 patients (15.9%) had experienced dyspepsia more than once daily within the previous month, and 8 (3.3%) had dyspepsia greater than 5 times/day. Thirty-four of the 39 patients with daily dyspepsia claimed to obtain relief with cimetidine or antacids (34 patients) or food (2 patients), whereas 3 had not discovered anything that provided relief. Women smokers were more likely than nonsmokers to experience dyspepsia (p less than 0.001). Neither men smokers nor those with a history of previous ulcer were more likely to have dyspepsia than nonsmokers or those without a history of ulcer (p greater than 0.5). We were not able to find a statistical association between any NSAID, or combination of NSAIDs, and the frequency of dyspepsia.

Adolescent↗
PubMed1989

Serum antibody responses to the N-acetylneuraminyllactose-binding hemagglutinin of Campylobacter pylori.

We recently reported that Campylobacter pylori possesses a surface-associated fibrillar hemagglutinin which has an affinity for N-acetylneuraminyllactose; this hemagglutinin may function as a colonization factor for attachment to the gastric epithelium. In the present study we examined serum samples obtained from 65 C. pylori-infected individuals with gastric ulcers, duodenal ulcers, or both and from 121 asymptomatic volunteers, including 62 who were infected with C. pylori, for immunoglobulin G (IgG) specific for the C. pylori neuramin-lactose-binding hemagglutinin (NLBH). The NLBH purified from a single isolate was used as the antigen in an enzyme-linked immunosorbent assay. A positive result was obtained with serum from 81.5% (53 of 65) of the individuals with ulcers, 67.7% (42 of 62) of the C. pylori-infected volunteers, and 1.7% (1 of 59) of the C. pylori-negative volunteers. This result confirms that NLBH is produced in vivo. There are several possible explanations for the fact that only 75% of 127 C. pylori-infected individuals were positive for anti-NLBH IgG in serum. We favor the hypothesis that there are probably several antigenically distinct C. pylori NLBHs, i.e., NLBHs which would stimulate antibody that was undetectable by the antigen used in the enzyme-linked immunosorbent assay described here.

Antibodies, Bacterial↗
PubMed1989

Receptor-mediated adherence of Campylobacter pylori to mouse Y-1 adrenal cell monolayers.

An in vitro adherence assay was developed to study the adherence of Campylobacter pylori to mammalian cells. Strains of C. pylori were isolated from individuals with gastritis. These strains possessed the fibrillar N-acetylneuraminyllactose(neuraminlactose)-binding hemagglutinin (NLBH) and were found to adhere to monolayers of mouse Y-1 adrenal cells. Adherence was rapid, prevented by pretreatment of the Y-1 cells with Clostridium perfringens neuraminidase, and blocked by the neuraminlactose-containing protein fetuin. Electron microscopy by the immunogold technique and with anti-NLBH antibody showed that NLBH was present at the sites of interaction between C. pylori and the Y-1 cells. These results indicate that the Y-1 monolayer is a valid model for receptor-specific adherence of C. pylori.

Adrenal Glands↗
PubMed1989

Campylobacter pylori as a pathogenetic factor in duodenal ulcer: the case for.

This debate addresses whether Campylobacter pylori contributes to the development and maintenance of chronic peptic ulcer disease. C. pylori may be both an aggressive factor and may also impair mucosal defence. C. pylori causes the inevitably ulcer-associated gastritis and duodenitis and eradication of the C. pylori infection is associated with resolution of the inflammation and virtual elimination of the problem of duodenal ulcer relapse. A model is suggested that requires two separate factors to combine to cause chronic duodenal ulcer disease with other environmental factors (e.g. smoking) modifying the interaction between C. pylori and genetic susceptibility. Both genetic susceptibility and C. pylori infection are required to produce duodenal ulcer disease; neither alone is sufficient. C. pylori is the most important factor in the pathogenesis of duodenal ulcer disease because it is the only pathogenetic factor that can be easily reversed by medical therapy.

Campylobacter Infections↗
PubMed1989

Pleural effusion: comparison of clinical judgment and Light's criteria in determining the cause.

Pleural fluid analysis is often the initial diagnostic test used to determine the cause of a pleural effusion. We prospectively studied 33 consecutive patients with pleural effusions to determine whether the fluid arose from a transudative or an exudative process. Clinical judgment by an internist before thoracentesis and both serum and pleural fluid protein and lactic dehydrogenase levels (commonly referred to as "Light's criteria") were compared to the patient's final diagnosis. The internist correctly classified 15 of 17 exudative processes and all 16 transudative processes; the presence of any one of Light's three criteria correctly classified 15 of 17 exudative processes, whereas the absence of all three criteria correctly classified 14 of 16 transudative processes. Clinical judgment and Light's criteria are comparable in their ability to predict whether an exudative or transudative process was responsible for the effusion. Both methods are associated with errors, though of different kinds; these errors occurred infrequently. Recognizing the limitations of these methods will permit the most accurate effusion categorization.

Aged↗