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Biomedical subjects

D Y Graham

Publications and source records attributed to D Y Graham.

At least 469 records · Page 26Linked to original sources
PubMed1988

Diagnosis and course of nephrogenic ascites.

Nephrogenic ascites is a complex diagnostic problem with poorly understood pathophysiology. Morbidity and eventual mortality from this ongoing problem are significant. The diagnosis of nephrogenic ascites must be established by exclusion. We report the cases of nine patients investigated between 1978 and 1985. Laparoscopy, which was utilized in all nine patients, led to a specific diagnosis in two. We believe that a vigorous diagnostic evaluation, including laparoscopy, is essential in patients with chronic renal failure who develop persistent ascites.

Adult↗
PubMed1988

Gastroduodenal complications of chronic NSAID therapy.

The fact that nonsteroidal anti-inflammatory drugs (NSAIDs) damage the gastroduodenal mucosa is no longer contested. Endoscopic studies in normal volunteers after NSAID administration have failed to predict which NSAIDs would be safest when administered chronically. NSAID use has been associated with a disproportionately high frequency of upper gastrointestinal bleeding and perforation of ulcers. All of the newer NSAIDs appear to be similar in their propensity to cause mucosal damage, including peptic ulceration. On any given day, more than 10% of patients receiving NSAIDs chronically will have a gastric ulcer, a point prevalence of ulcer disease at least 5 to 10 times higher than in patients who are not taking NSAIDs. The dose-response relationship between anti-inflammatory activity and untoward events, coupled with increased use of newer more potent NSAIDs, explains, in part, the increased incidence of NSAID-associated ulcer complication of bleeding and perforation. The possible association of the increase in prevalence of Campylobacter pylori gastritis with aging and the apparent increase in NSAID-associated complications in the elderly is discussed. The current status of nonsteroidal drug therapy can be summarized as follows: 1) new NSAIDs are not safer than the old NSAIDs, as far as major gastrointestinal side effects are concerned, 2) NSAIDs should be avoided when analgesia is the main goal, 3) if NSAIDs are required, the lowest possible dose that achieves pain relief should be used, 4) newer NSAIDs available only in relatively high anti-inflammatory activity dosages should be restricted to those patients in whom high levels of anti-inflammatory activity are desired.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1988

Epidemiology of Campylobacter pylori infection: ethnic considerations.

A proper perspective of the association of Campylobacter pylori with various diseases can be achieved only when the incidence of C. pylori infection in the normal population is known. We used the 13C urea breath test (a simple, specific, noninvasive, safe, and reproducible method to assess the presence of active C. pylori infection) to compare the frequency of C. pylori infection in healthy young adults from three areas of the world. We studied 26 women and 32 men (ages 20 to 29): 29 from the United States, 10 from China, 6 from Mexico, and 13 from India. All foreign nationals had been in the United States 5 years or less. The frequency of C. pylori infection was 21%, 67%, 33% and 46%, for those from the U.S., China, Mexico and India, respectively. Although, we found no difference in the frequency of C. pylori infection among ethnic groups from North America (U.S. citizens compared with citizens of Mexico), all individuals studied were of middle to upper class socioeconomic status. Subsequent studies will investigate whether the prevalence of C. pylori infection is different in economically disadvantaged populations. Our results suggest that there may be major differences in the age-related frequency of C. pylori infection in individuals from different parts of the world.

Adult↗
PubMed1988

Gastric adaptation. Studies in humans during continuous aspirin administration.

To study the process of gastric mucosal adaptation to aspirin administration, 14 normal men underwent a study with continued administration of aspirin. Endoscopic assessment, biopsies, and gastric wash collections for acid, mucus, and deoxyribonucleic acid recovery were performed weekly; aspirin was continued until the endoscopy showed minimal damage. Six subjects took 650 mg of aspirin b.i.d., and 8 took 650 mg q.i.d.; adaptation and resolution took longer with the higher dose (median 4.5 wk vs. 1 wk, p less than 0.01). Despite improvement in mucosal appearance, gastric microbleeding remained elevated throughout aspirin administration. In contrast, deoxyribonucleic acid recovery (a marker for cellular exfoliation and regeneration) increased significantly just before the time of resolution, when, on average, it more than doubled. As no other biochemical or histologic changes could be associated with the resolution of damages, we conclude that gastric adaptation to chronic injury may involve increased cellular regeneration.

Adaptation, Physiological↗
PubMed1988

Iatrogenic Campylobacter pylori infection is a cause of epidemic achlorhydria.

On a number of occasions, there have been descriptions of epidemic achlorhydria in subjects undergoing repeated gastric secretory studies, typically as part of research protocols. We observed a case in a 37-yr-old healthy man undergoing weekly gastric analyses, along with endoscopy and gastric biopsy, as part of a research protocol studying gastric adaptation to aspirin. In the middle of the 2nd wk of aspirin administration, he developed severe nausea and epigastric discomfort. Aspirin administration was discontinued, but, as per protocol, gastric analyses, endoscopies, and biopsies were continued. Compared to the week preceding the acute illness, biochemical analyses showed a transient 7.4-fold increase in basal gastric acid, 3.6-fold increase in pepsin secretion, 8.8-fold increase in DNA loss, 5.6-fold increase in mucus secretion, and 12-fold increase in gastric bleeding. Basal acid secretion was zero, and pepsin secretion was one-third of control during the 2nd wk of the infection. Endoscopy at the time of symptoms showed erosions in the gastric body and antrum, as well as numerous mucosal hemorrhages and an acute ulcer in the antrum. Endoscopy 7 days later revealed that the gastric mucosa had almost completely recovered, with only a shallow erosion seen at the site of the previous ulcer. Gastric biopsies were normal before and during the first 2 wk of aspirin ingestion. Gastric biopsies taken at the time of the acute illness (associated with increased basal acid secretion) showed marked acute inflammation of the antrum with many Campylobacter pylori bacilli. At that time, neither acute inflammation nor C. pylori were found in biopsies from the body of the stomach. Biopsies obtained 1 wk later (zero basal acid) showed acute inflammation of both the gastric body and antrum. One week later, biopsies from the gastric body showed mild focal acute inflammation, moderate chronic inflammation, and an occasional lymphoid follicle; the gastric antrum showed chronic inflammation. Antral biopsies obtained 2 yr later showed persistent chronic gastritis with prominent lymphoid follicles and scattered foci of acute inflammatory cells; C. pylori bacilli were still present, but were less apparent. We believe that the syndrome of acute (epidemic) gastritis is often iatrogenic C. pylori infection. Our case shows that increased basal acid and pepsin secretion occur before onset of basal acid hypochlorhydria in the acute phase of C. pylori infection.

Achlorhydria↗
PubMed1987

Campylobacter pylori detected noninvasively by the 13C-urea breath test.

The high endogenous urease activity of Campylobacter pylori was exploited in a non-invasive test for the presence of this organism in the stomach. When 13C-urea was administered orally after a test meal, urea-derived 13CO2 appeared in the respiratory CO2 of infected individuals at a constant rate for greater than 100 min. The test was validated in 26 individuals who underwent both the 13C-urea breath test and endoscopic biopsy of the antral mucosa for culture and histological examination. Each positive breath test proved to be correlated with a positive culture or Warthin-Starry silver stain of a mucosal biopsy specimen, or both.

Adult↗
PubMed1987

Minimal infective dose of rotavirus.

We studied the minimal infective dose of the gastroenteritis virus, rotavirus. Increasingly lower doses [10(4), 10(3), 10(1), 1, 10(-2) plaque forming units (PFU)] of the OSU strain of porcine rotavirus were administered to highly susceptible (colostrum deprived, cesarean derived) newborn miniature swine piglets. In vitro studies showed that virus infectivity was inactivated in piglet gastric juice, both by low pH and by pH- and concentration-dependent factor(s). These factors remain unidentified, but to prevent intragastric viral inactivation, sodium bicarbonate was administered prior to oral virus inoculation of piglets with virulent (non-tissue culture passaged) virus. The lowest dose of virus to induce clinical illness or to demonstrate viral replication by recovery of significantly more infectious virus than was administered, or both, was 1 PFU. These results should help establish standards for virus contamination of water and recommendations for evaluating disinfection procedures for rotaviruses.

Animals↗
PubMed1987

Mycobacteria and inflammatory bowel disease. Results of culture.

We have been able to isolate mycobacteria from intestinal specimens obtained by surgical resection or endoscopic biopsy from patients with Crohn's disease, ulcerative colitis, and noninflammatory bowel diseases. Nineteen slow-growing (Runyon groups I and III) and 17 rapid-growing (Runyon group IV) mycobacterial isolates were obtained. Slow-growing mycobacteria were recovered from approximately one-third of intestinal biopsy specimens from Crohn's disease, one-quarter of ulcerative colitis biopsies, and 40% of biopsies from noninflammatory bowel disease patients. Isolates were most commonly members of the Mycobacterium avium-complex. One isolate (from an ulcerative colitis patient) was biochemically similar to the Mycobacterium strain previously associated with Crohn's disease, and one from a Crohn's disease patient was Mycobacterium kansasii. The rapid-growing organisms were members of the Mycobacterium fortuitum-complex. In addition to conventional mycobacteria, spheroplasts (cell wall-defective forms) were isolated from 12 patients with Crohn's disease (most often from surgically resected colon) and 3 patients with ulcerative colitis; none were isolated from non-inflammatory bowel disease patients. We have been unable to identify a consistent relationship between the presence, or the species, of Mycobacterium and Crohn's disease. Our results do not support the proposed role of a specific mycobacterium in the pathogenesis of Crohn's disease. The cause of Crohn's disease remains unclear.

Colitis, Ulcerative↗
PubMed1987

Gastroscopic localization of a microencapsulated KCl preparation in the human stomach.

A slow release polymer-coated preparation of potassium chloride granules (Micro-K Extencaps) was initially thought not to be associated with gastric mucosal damage. Recent studies have shown that acute gastric ulcers occur with approximately the same frequency as in patients taking wax matrix KCl formulations. The development of acute gastric ulcers was not consistent with the proposed dispersion characteristics of the microencapsulated KCl preparation. The authors therefore endoscopically evaluated the dispersion characteristics of microencapsulated KCl in a double-blind, placebo-controlled study. Subjects received four capsules of Micro-K or matching placebo and endoscopy was performed 30, 60, or 120 min after each drug ingestion. The material was identified with the Olympus HM (high magnification) endoscope and then quantitatively aspirated using the 3.5-mm biopsy channel of the Pentax 34JA endoscope. Microencapsulated KCl particles dispersed poorly and were found adhering to the mucosa and to one another, as a semisolid mass, most frequently in the gastric antrum. In contrast, the placebo (ethyl cellulose) was widely dispersed throughout the stomach. The authors concluded that gastric emptying must be considered in three phases: liquids, solids, and solids which adhere to the mucosa. No unique dispersion characteristics of Micro-K Extencaps were identified, and adherence of the KCl to the gastric mucosa may explain its ability to cause occasional acute gastric ulceration.

Adult↗
PubMed1987

Nonpathogenic nematodes in gastrointestinal aspirates obtained during endoscopy.

The gastroenterologist must be alert to diagnosing parasitic diseases when collecting intestinal fluid samples or cytologies during endoscopy. Between 1979 and 1982, we identified nematodes in 10 endoscopic specimens. None were Strongyloides stercoralis. We emphasize the importance and technical aspects of distinguishing nonpathogenic nematodes from Strongyloides.

Colonoscopy↗
PubMed1987

Source of upper gastrointestinal bleeding in patients with esophageal varices seen at endoscopy.

Many claim that upper gastrointestinal hemorrhage in patients with varices is frequently not of variceal origin. Such teaching is contrary to our experience. We therefore reviewed the records of 127 consecutive patients with 165 episodes of acute upper gastrointestinal bleeding who were found to have esophageal varices by endoscopy. Varices were the only potential site of the index bleed in 101 of the 127 patients (79.5%). In addition to varices, other potential sites of bleeding were gastric ulcer in 9 (7%), Mallory-Weiss tear in 4 (3.1%), duodenal ulcer in 3 (2.3%), and multiple gastroduodenal erosions in 10 (7.8%). We used the characteristics of the clinical presentation (e.g., varix seen bleeding) and the known natural course of the variceal bleeding to attempt to define the site of bleeding in the group with more than one potential site. In 15 we could make a judgment as to the likely source: In 9 it was variceal and in 6 nonvariceal. When varices are seen at endoscopy in a patient with a major hemorrhage, they are responsible for the bleeding in greater than 80% of cases.

Esophageal and Gastric Varices↗
PubMed1987

Clinical impact of stool cultures for Campylobacter in adults with acute or chronic diarrhea.

Campylobacter jejuni has emerged as a frequent cause of diarrhea. During a 12-month period at the Houston Veterans Administration Medical Center, we isolated C jejuni from 3.4% of the 290 stool cultures from patients with diarrhea. This compared to an isolation rate of 4.1% for Salmonella and 3.1% for Shigella. During the same period, 17 additional cases of Campylobacter-associated diarrhea were identified in adults at the two other Baylor College of Medicine teaching hospitals. We correlated the clinical history, treatment, and outcome of these 27 cases of Campylobacter-associated diarrhea (22 cases of acute diarrhea and five of chronic diarrhea). In most patients with acute disease, the diarrhea was resolving by the time the results of the cultures were available. The duration of illness was the same whether treated with antibiotics to which Campylobacter was susceptible (effective therapy) or antibiotics to which it was not susceptible (ineffective therapy); the mean duration of diarrhea after submitting the culture was 5.2 days for those with ineffective therapy versus 5.6 days for those receiving effective therapy. Thus, antibiotic therapy did not appear to shorten the duration of acute diarrhea due to Campylobacter. Five patients had chronic diarrhea; all had an unrelated underlying disease, and antibiotic treatment did not change the clinical course despite bacteriologic cure. This study raises questions as to the value of antibiotic therapy for campylobacteriosis, and in this light, we discuss the value of routine culturing for Campylobacter.

Acute Disease↗
PubMed1987

Investigation of association of mycobacteria with inflammatory bowel disease by nucleic acid hybridization.

We used DNA-DNA hybridization to characterize a mycobacterial isolate, strain Linda, that was obtained from a patient with Crohn's disease and that has been reported to cause ileitis in experimental animals. We also investigated the association of this mycobacterium with Crohn's disease. Our results identified Mycobacterium strain Linda as a strain of Mycobacterium paratuberculosis, the etiologic agent of Johne's disease, a disease of ruminants that has some superficial resemblance to Crohn's disease. Sequences that hybridized with strain Linda DNA probes were detected in DNA extracted from human intestinal tissues from patients with Crohn's disease, ulcerative colitis, and noninflammatory bowel disease. These hybridizing DNA sequences were more prevalent in the muscle layers than in the intestinal mucosa, making it unlikely that they represented DNA from bacterial contaminants in the intestinal lumen. Measurement of the melting temperatures of the DNA-DNA hybrids formed between strain Linda probes and tissue DNAs indicated that the related sequences detected were of mycobacterial origin but were not identical to each other or to strain Linda DNA. These results do not support the proposed specific relationship between Mycobacterium strain Linda and Crohn's disease. The possible etiologic role of mycobacteria in Crohn's disease is discussed.

Colitis, Ulcerative↗
PubMed1987

Detection of antibody to group B adult diarrhea rotaviruses in humans.

Group B rotaviruses have been responsible for annual epidemics of severe diarrhea affecting both adults and children in China. We developed a specific and sensitive enzyme-linked immunosorbent blocking assay to detect antibody to group B rotaviruses that will be useful to assess the role of group B rotavirus infections as a cause of human gastroenteritis. We tested 219 human sera and 18 immunoglobulin pools collected from eight countries for antibodies to both group A and group B rotaviruses. Overall, a low proportion (10 of 237 or 4.2%) of sera contained antibody to group B rotaviruses. Antibody to group B rotavirus was detected in only 1 of 155 serum samples from healthy or hospitalized individuals in the United States, including patients with the chronic inflammatory bowel diseases Crohn's disease and ulcerative colitis. No antibody was detected in 15 serum samples from Australia and from an outbreak of gastroenteritis on a cruise ship or in nine immunoglobulin pools from Japan and the United Kingdom. Antibody to group B rotaviruses was detected in 8 convalescent-(but not acute-)phase serum samples from Chinese patients with group B gastroenteritis, in five immunoglobulin pools from China, in 1 of 6 serum samples from Chinese students in the United States, and in 1 each of 10 serum samples from Kenya, 20 from Thailand, and 15 from Canada. In contrast, most of these samples (226 of 237 or 95.4%) had antibody to group A rotaviruses. These results indicate that human infection with group B rotavirus has not been widespread in areas outside China. Seroconversion observed between the acute-and convalescent-phase serum samples from China also suggests that infections with this virus are primary infections. Continued surveillance for this new group of rotaviruses should determine whether the many susceptible people become infected of whether other factors influence the severe pathogenicity of human infections with these viruses in China.

Adolescent↗
PubMed1987

Effect of red pepper and black pepper on the stomach.

Spices have long been implicated as a cause of gastric mucosal injury. We assessed the effects of red and black pepper on the gastric mucosa using double-blind intragastric administration of test meals containing red pepper (0.1-1.5 g) or black pepper (1.5 g) to healthy human volunteers; aspirin (655 mg) and distilled water were used as positive and negative controls, respectively. Serial gastric washes were performed after test meal administration and gastric contents were analyzed for DNA, pepsin, blood, sodium, potassium, parietal cell secretion, and nonparietal cell secretion. Both red pepper and black pepper caused significant increases in parietal secretion, pepsin secretion, and potassium loss. Gastric cell exfoliation (as reflected in DNA loss into gastric contents) was increased after red or black pepper administration; the increase after red pepper administration was dose dependent. Mucosal microbleeding was seen after spice administration and one subject had grossly visible gastric bleeding after both red pepper and black pepper administration. There were no significant differences from control between the test meals, in nonparietal volume, fractional recovery of the gastric secretions, or sodium secretion. Finally, no spice was significantly different from aspirin in any parameter studied; indeed, aspirin was comparable to the higher doses of pepper. The long-term result of daily pepper ingestion is unknown. Whether spices are detrimental, beneficial (e.g., inducing an adaptive cytoprotective response), or have no significant long-term effect on the gastric mucosa is unknown and deserves further study.

Adult↗