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Biomedical subjects

W M Weinstein

Publications and source records attributed to W M Weinstein.

At least 37 records · Page 2Linked to original sources
PubMed1996

Metaplastic columnar cells in Barrett's esophagus: a common and neglected cell type.

Goblet cells are considered by most to be a prerequisite for the diagnosis of Barrett's esophagus. Columnar cells that are alcian blue (AB) positive (as are goblet cells) are commonly observed in the surface epithelium of Barrett's esophagus, but their distribution in relation to goblet cells has not previously been defined. The authors analyzed the prevalence and distribution of these cell types in the surface but not pit epithelium (where they may sometimes be present in normal gastric mucosa). The distribution of the AB-positive columnar cells was mapped out in the entire mucosa of nine esophagectomy specimens, resected for Barrett's-associated high-grade dysplasia or carcinoma, and compared with other cell types, especially goblet cells. AB-positive goblet and columnar cells were present in 87.1% +/- 5.6% and 85.7% +/- 5.9%, respectively, of the evaluated sections of Barrett's mucosa, whereas gastric-type, AB-negative cells were observed in 46.3% +/- 8.7% of the sections. In 53% of the sections, the surface epithelium contained more than 25% AB-positive cells, and in more than three quarters of these sections, AB-positive columnar cells were the dominant AB-positive cell type. No difference in the distribution of the AB-positive epithelial cells was noticed between the proximal and distal halves of the Barrett's mucosae. In the cardia region, seven of nine cases showed a few scattered AB-positive columnar cells, and five of nine cases showed a few scattered goblet cells. No AB-positive cells were found in fundic gland mucosa. These findings indicate that the metaplastic AB-positive columnar cells are more prevalent than goblet cells. They may be analogous to incomplete metaplastic cells of the stomach, and, therefore, their role in the development of neoplasia needs further study.

Aged↗
PubMed1996

Duodenal bicarbonate secretion: eradication of Helicobacter pylori and duodenal structure and function in humans.

BACKGROUND & AIMS: Eradication of Helicobacter pylori expedites duodenal ulcer healing and prevents recurrences. Most patients with duodenal ulcers have impaired proximal duodenal mucosal bicarbonate secretion (DMBS). In patients with inactive, healed duodenal ulcers and normal subjects, the effect of H. pylori infection on DMBS and proximal duodenal secretory function and structure were examined. METHODS: DMBS was quantitated before and after eradication of H. pylori. Mucosal structure (duodenal bulb histopathology) and function (DMBS at rest and stimulated, effect of active vs. healed ulcer and of age) were determined in patients with duodenal ulcers and normal subjects. RESULTS: In patients with duodenal ulcers, H. pylori eradication normalized proximal DMBS. Histological examination of duodenal biopsy samples was comparable in patients with duodenal ulcers and normal subjects without apparent relationship between inflammation and DMBS. Significantly impaired DMBS occurred in response to all agonists tested (luminal acid, prostaglandin E2, and cephalic-vagal stimulation) in patients with duodenal ulcers, suggesting a generalized secretory defect. Neither the presence of active (vs.inactive) ulcer nor age significantly affected bicarbonate secretion. CONCLUSIONS: In patients with duodenal ulcers, eradication of H. pylori normalized proximal DMBS and may thereby reduce ulcer recurrences. Altered DMBS in patients with duodenal ulcers was unrelated to histopathologic abnormalities. Impaired bicarbonate secretion in patients with duodenal ulcers could be caused by a cellular and/or physiological regulatory transport defect possibly related to H. pylori.

Adult↗
PubMed1995

Interobserver agreement and predictive value of endoscopic findings for H. pylori and gastritis in normal volunteers.

BACKGROUND: Endoscopic findings such as erythema are frequently labeled as gastritis. We sought to determine interobserver agreement for specific endoscopic features and assess the diagnostic value of features with good agreement for Helicobacter pylori and histologic gastritis. METHODS: Fifty-two healthy subjects without ulcers, erosions, or hemorrhages had a full endoscopy recorded on video tape. Biopsy specimens were examined for H. pylori and gastritis. Two endoscopists independently reviewed the tapes for predefined features (erythema, area gastricae, clefts, and nodularity) in the gastric body and antrum. Diagnostic value of endoscopic features with acceptable agreement (kappa > 0.40) was then determined for H. pylori and gastritis. RESULTS: Kappa was greater than 0.40 only for prominent body area gastricae (0.49), body nodularity (0.65), and antral nodularity (0.68). For antral nodularity, sensitivity was 32%, specificity was 96%, and positive predictive value was 90% for H. pylori. when both antral nodularity and body area gastricae were both present, sensitivity was only 18% but specificity and positive predictive value were 100%. CIRCULATION: Interobserver agreement is poor for some features such as erythema labeled as gastritis. Antral nodularity is a fairly reproducible finding and is very specific, though not sensitive, for H. pylori gastritis.

Adult↗
PubMed1995

Patchiness of mucosal inflammation in treated ulcerative colitis: a prospective study.

Conventional wisdom dictates that ulcerative colitis affects contiguous areas of the colon and is most severe in the rectum, and that the finding of rectal sparing or patchy involvement should raise suspicions of Crohn's disease. We and others have noted occasional rectal sparing and patchy involvement in patients with ulcerative colitis. Therefore, we prospectively studied the prevalence of patchiness, including rectal sparing, in treated cases of ulcerative colitis. Consecutive patients with longstanding ulcerative colitis were studied. The left colon was divided into three zones for scoring degree of activity, and biopsy specimens from each zone were graded for histologic activity by a blinded observer. Patchiness by endoscopy or histology was defined as (1) frank rectal sparing (normal appearance endoscopically; absence of inflammation of the lamina propria and crypts histologically); (2) areas of greater inflammation proximally than distally; or (3) discrete areas of patchiness endoscopically within any one zone. Of 39 patients evaluated, 17 (44%) had endoscopic evidence of patchiness, including 5 (13%) with rectal sparing. Thirteen (33%) had histologic evidence of patchiness, including 6 (15%) with rectal sparing. Both endoscopic and histologic patchiness were seen in 9 patients (23%). The patchy and nonpatchy groups did not differ in regard to the use of rectal therapy. In patients with treated ulcerative colitis, the finding of rectal sparing or patchiness should not necessarily indicate a change in the diagnosis to Crohn's disease.

Adult↗
PubMed1995

Interaction of NSAIDs and Helicobacter pylori on gastrointestinal injury and prostaglandin production: a controlled double-blind trial.

BACKGROUND: H. pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are major causes of gastroduodenal injury in man. We assessed the effect of daily NSAID ingestion on gastric histology and the interaction of H. pylori infection and NSAID ingestion on gross and histological injury and prostaglandin production. METHODS: Fifty-two healthy volunteers with normal baseline endoscopy were randomly assigned to receive identical-appearing naproxen 500 mg b.d., etodolac 400 mg b.d., or placebo b.d. for 4 weeks. The number and size of all erosions and ulcers were recorded by endoscopy at weeks 1 and 4. Biopsies taken at baseline, week 1 and week 4 were assessed for H. pylori, histology and gastric prostaglandin E2 production. RESULTS: No significant changes occurred with treatment in any histological feature in the three study groups or in H. pylori positive or negative subsets. Antral inflammation scores (scale, 0-6) for the NSAID group were: week 0--1.2 +/- 0.3; week 1--1.1 +/- 0.3; week 4--1.3 +/- 0.3; findings of 'chemical gastritis' were not seen. No significant difference in gross gastroduodenal injury (number or total surface area of ulcers or erosions) was seen between H. pylori positive and negative subjects in the three groups at week 1 or 4. Baseline prostaglandin E2 production was significantly higher in H. pylori positive subjects (2398 +/- 400 vs. 1064 +/- 255 pg/mg protein) and decreased significantly with 1 week of naproxen in H. pylori positive and negative subjects. CONCLUSIONS: NSAID ingestion does not cause diffuse histological injury. Any diffuse histological injury in the gastric mucosa is related to the presence of H. pylori, and this H. pylori-associated gastritis is not altered by NSAID ingestion. Furthermore, the development of gross gastroduodenal damage with 4 weeks of NSAID use is not influenced by underlying H. pylori infection.

Adolescent↗
PubMed1995

Pathologist-gastroenterologist interaction. The changing role of the pathologist.

The importance of interaction between clinicians and pathologists is examined in the setting of gastroenterology and gastrointestinal disease, and the importance of communication is emphasized. The endoscopist must provide the pathologist with information about the patient, including results of the gross examination, biopsy location, relevant clinical history, bowel preparation, and current medications. The pathologist must provide a reproducible and useful report that answers the clinical questions posed by the endoscopist. This consultation between the gastroenterologist and pathologist provides the framework for proper patient care.

Gastroenterology↗
PubMed1995

Physicians' perceptions of dysplasia and approaches to surveillance colonoscopy in ulcerative colitis.

OBJECTIVE: Colonoscopic biopsy surveillance to detect dysplasia, defined as a neoplastic change of the epithelium without invasion into the lamina propria, in patients with ulcerative colitis has become a widespread practice. We undertook a survey study to determine physicians' perceptions of, and approaches to, dysplasia surveillance colonoscopy in ulcerative colitis. METHODS: Members of two regional gastroenterology associations in the United States, including both academic and private practice-based gastroenterologists, and a group of senior gastroenterology trainees were surveyed by means of a written questionnaire. The questionnaires were distributed at three separate meetings of practicing gastroenterologists or trainees: 1) a Gastrointestinal pathology course for second-year gastroenterology fellows from training programs around the United States (February 1993, Los Angeles, CA); 2) a meeting of the Southern California Gastroenterology Society (March 1993, Los Angeles, CA); and 3) a meeting of the Pacific Northwest Gastroenterology Society (June 1993, Seattle, Washington). The percentages of all responses were tallied and analyzed for the group as a whole as well as by subgroup analysis. Understanding of the definition of dysplasia and specific practice techniques and approaches were the main outcomes sought. RESULTS: Only 19% of respondents correctly identified the definition of dysplasia. More respondents (48%) correctly defined high grade dysplasia specifically compared with only 16% who correctly defined low grade dysplasia. The majority of respondents (69%) recommended colectomy when high grade dysplasia was diagnosed, yet nearly one-third of respondents pursued continued surveillance in this setting. Almost uniformly, respondents pursued continued surveillance and not colectomy when low grade dysplasia was diagnosed. Nearly one-half of the respondents thought that there was only < 20% chance of finding invasive cancer in patients with preoperative diagnoses of high grade dysplasia. On average, respondents performed surveillance colonoscopy every 1-2 yr and took an average of three biopsies per site, at approximately eight sites in the colon, and most respondents confidently relied on their local pathologist at making the diagnosis. There were, however, wide variations in the practice of dysplasia surveillance. CONCLUSIONS: The majority of respondents did not know the definition of dysplasia, and most viewed it as a preneoplastic lesion. Furthermore, there was a lack of appreciation that the difference between low grade and high grade dysplasia is one of degree or severity of neoplastic change and for the likelihood of finding invasive cancer at surgery if there is only a diagnosis of dysplasia preoperatively. Dysplasia surveillance colonoscopy in ulcerative colitis is not a well standardized, clearly understood screening tool, and continued education of the gastroenterology community regarding its outcomes and pitfalls is needed.

Colectomy↗
PubMed1994

Are we telling patients the truth about surveillance colonoscopy in ulcerative colitis?

The recommended approach to the increased risk of colorectal carcinoma in ulcerative colitis has been colonoscopic surveillance rather than prophylactic colectomy. This strategy is based on the assumption that dysplastic lesions can be detected before invasive cancer has developed. We have analysed published reports on dysplasia surveillance to find out whether this assumption is valid. Ten prospective studies (1225 patients) satisfied our criteria. Of 40 patients with dysplasia-associated mass or lesion (DALM) detected, 17 (43%) already had cancer at immediate colectomy. The risks of cancer at immediate colectomy were 42% (10 of 24 patients) for high-grade and 19% (3 of 16) for low-grade dysplasia. Of 47 patients found to have high-grade dysplasia after the initial colonoscopy, 15 (32%) had cancer. 16-29% of patients with untreated low-grade dysplasia progressed to DALM, high-grade dysplasia, or cancer. Of patients with indefinite results, 28% progressed to high-grade dysplasia and 9% to cancer, so continued surveillance is essential. The risk of progression to dysplasia was only 2.4% for patients whose initial result was negative, so surveillance could perhaps be less frequent for these patients. Immediate colectomy is essential for all patients diagnosed with high-grade or low-grade dysplasia. A diagnosis of dysplasia does not preclude the presence of invasive cancer. We believe that patients should be informed about the limitations of colonoscopic surveillance so that they can take part rationally in decision-making about their management.

Colitis, Ulcerative↗
PubMed1994

Effects of vitamin/mineral supplementation on the prevalence of histological dysplasia and early cancer of the esophagus and stomach: results from the General Population Trial in Linxian, China.

A randomized nutrition intervention trial was conducted among 29,584 adult residents of Linxian, China, to examine the effects of vitamin/mineral supplementation on the occurrence of esophageal/gastric cardia cancer in this high-risk population. A fractional factorial study design allowed evaluations of four different combinations of nutrients: (A) retinol and zinc; (B) riboflavin and niacin; (C) vitamin C and molybdenum; and (D) beta-carotene, vitamin E, and selenium. During the 5.25-year intervention, significant reductions in total mortality, total cancer mortality, and stomach cancer mortality occurred among those receiving beta-carotene, vitamin E, and selenium. At the end of intervention, an endoscopic survey was carried out in a sample of subjects to see if the nutritional supplements had affected the prevalence of clinically silent precancerous lesions and early invasive cancers of the esophagus or stomach. Endoscopy was performed on 391 individuals from two study villages. The prevalences of esophageal and gastric dysplasia and cancer were compared by nutrient factor. Cancer or dysplasia was diagnosed in 15% of the participants. No statistically significant reductions in the prevalence of esophageal or gastric dysplasia or cancer were seen for any of the four vitamin/mineral combinations. The greatest reduction in risk (odds ratio, 0.38; P = 0.09) was seen for the effect of retinol and zinc on the prevalence of gastric cancer. Although no significant protective effects were seen in this endoscopic survey, there was a suggestion that supplementation with retinol and zinc may protect against the development of gastric neoplasia in this high-risk population. Additional studies with larger numbers of endpoints will be needed to further evaluate this possibility.

Adenocarcinoma↗
PubMed1994

Effects of vitamin/mineral supplementation on the prevalence of histological dysplasia and early cancer of the esophagus and stomach: results from the Dysplasia Trial in Linxian, China.

Linxian, China has some of the highest rates of esophageal/gastric cardia cancer in the world, and epidemiological evidence suggests that chronically low intake of micronutrients may contribute to these high cancer rates. To examine whether supplementation with multiple vitamins and minerals can affect the occurrence of esophageal/gastric cardia cancer in this population, a two-arm randomized nutrition intervention trial was conducted among 3318 Linxian residents with cytological evidence of esophageal dysplasia. During the 6-year intervention, esophageal/gastric cardia cancer mortality was 8% lower among those receiving the active supplements. After 30 and 72 months of intervention, endoscopic surveys were carried out to see if the nutritional supplements had affected the prevalence of clinically silent precancerous lesions and early invasive cancers of the esophagus and stomach. In the first survey, in 1987, 833 subjects were endoscoped; in the second survey, in 1991, 396 subjects were examined. The histological diagnoses from each survey were compared by treatment group. Cancer or dysplasia was diagnosed in 28% of the subjects endoscoped in 1987 and 24% of those examined in 1991. The odds ratio for subjects in the treatment group (versus those in the placebo group) having esophageal or gastric dysplasia or cancer was 0.84 (95% confidence interval, 0.61-1.15) in 1987 and 0.86 (0.54-1.38) in 1991. Although modest protective effects on worst overall diagnosis were seen in the supplemented group in both surveys, none of the results was statistically significant, and the findings must be considered inconclusive.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1993

Squamous dysplasia and early esophageal cancer in the Linxian region of China: distinctive endoscopic lesions.

BACKGROUND: Linxian, China, has one of the highest rates of esophageal cancer in the world. To design a logical biopsy strategy for large-scale endoscopic surveys in Linxian, the aim of this study was to determine whether squamous dysplasia and early squamous cancer are associated with visible lesions that can be targeted for biopsy. METHODS: Sixty-three Linxian patients with balloon cytological evidence of squamous dysplasia or early cancer of the esophagus had biopsy specimens taken every 4 cm and additional specimens taken from all visually abnormal areas. The appearance of the 398 biopsy sites was described, and abnormal-appearing areas were photographed. The endoscopic descriptions were then compared with the biopsy diagnoses. RESULTS: Twenty-five of 31 (81%) moderately dysplastic or worse specimens (including all nine specimens of invasive cancer) came from visually abnormal sites classified as friability, focal red area, erosion, plaque, or nodule. Fifteen of 16 (94%) patients with moderate dysplasia or worse biopsy diagnoses would have been identified if only these visible target lesions had been sampled. CONCLUSIONS: For surveillance in this high-risk population, random biopsy specimens may be unnecessary; sampling the target lesions described appears sufficient to detect nearly all invasive cancer and most dysplasia. Awareness of these lesion appearances may also aid in earlier detection of squamous cancers of the esophagus in lower-risk populations such as those in Europe and North America.

Biopsy↗
PubMed1993

Helicobacter pylori-associated gastric pathology.

H. pylori is the most common cause of nonerosive nonspecific gastritis; however, its main importance has been as a marker in research studies of eradication in relation to duodenal ulcer relapse. In developed countries, the most common histologic pattern appears to be that of a mild superficial chronic active gastritis. When H. pylori is present in the antrum it is virtually always present in the body as well, although inflammation in body mucosa is usually milder than that in the antrum. The organisms do not overlie areas of intestinal metaplasia; thus, H. pylori is commonly absent in individuals with diffuse intestinal metaplasia as seen in severe atrophic gastritis. Studies of H. pylori gastritis have been of enormous value in research studies; however, in the clinical management of the individual patient there is only limited value to documenting the presence, character, and severity of H. pylori gastritis.

Gastric Mucosa↗
PubMed1992

Nonsteroidal antiinflammatory drug-associated gastric ulcers do not require Helicobacter pylori for their development.

Nonsteroidal antiinflammatory drugs (NSAIDs) have been linked with a high incidence of ulcer complications. Histologic gastritis is present in most patients with standard peptic ulcers, and this gastritis is generally related to Helicobacter pylori (HP). We questioned whether gastric ulcers associated with nonsteroidal antiinflammatory drugs (NSAIDs) develop via a novel mechanism, distinct from the usual HP-gastritis-ulcer diathesis. Two groups of patients with newly discovered gastric ulcers were assessed: 1) daily NSAID use > 1 month (n = 19), 2) no NSAID use (n = 36). Biopsy specimens from the rim of the ulcer and adjacent normal mucosa were coded, randomized, and evaluated for histologic features and HP. HP prevalence was significantly lower in the NSAID group (10/19 (53%) vs. 30/36 (83%), p = 0.01). In biopsies from the ulcer rim, inflammatory cell density and epithelial abnormalities were significantly less in the NSAID group than in the no-NSAID group. Biopsies from adjacent mucosa exhibited the same trends, but the differences did not reach statistical significance (inflammation, p = 0.06; epithelium, p = 0.05). HP-positive patients had similar inflammation and epithelium scores, whether or not they took NSAIDs. However, HP-negative NSAID patients had significantly lower scores than HP-positive NSAID users (inflammation, 0.6 +/- 0.2 vs. 2.4 +/- 0.4; epithelium, 1.1 +/- 0.6 vs. 3.5 +/- 0.7). Patients with NSAID-associated gastric ulcers have a lower prevalence of HP and less histologic gastritis than patients with non-NSAID gastric ulcers. The gastritis is related to the underlying HP and not to NSAID ingestion. NSAID-associated gastric ulcers may represent a major subset of peptic ulcers that do not require HP for their development.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

Partial regression of childhood Barrett's esophagus after fundoplication.

A 12-yr-old boy presented with Barrett's esophagus, the nature and extent of which were thoroughly documented with multiple endoscopic biopsies. He had an excellent symptomatic response to antireflux surgery. Radiologic studies, esophageal manometry, and intraesophageal pH studies were performed before surgery and at intervals thereafter, and documented the success of antireflux surgery. Within 2 yr of surgery, there was endoscopic and histologic evidence of squamous regression of columnar mucosa, and this process of regression to squamous epithelium continued over a further 3 yr. This case suggests that partial squamous regression of Barrett's esophagus may occur in children. Studies dealing with regression are reviewed and proposals are made for a standardized approach to its documentation.

Barrett Esophagus↗
PubMed1991

Nonsteroidal anti-inflammatory drugs and peptic ulcer disease.

Evidence has accumulated that nonsteroidal anti-inflammatory drugs (NSAIDs) cause clinically important gastroduodenal ulcers. The pathogenesis, which involves the impairment of mucosal resistance to injury in an acid-peptic environment, is multifactorial and controversial. Ulcers caused by NSAIDs can occur either in mucosa inflamed because of infection with Helicobacter pylori or in histologically normal mucosa. The use of these drugs has been linked to an unexpectedly high incidence of ulcer complications, and a history of peptic ulcer disease is common in such cases. Nonsteroidal anti-inflammatory drugs thus appear both to exacerbate an underlying peptic diathesis and to cause de novo ulcers. The association between the use of these drugs and ulcer complications is supported by ulcer prevalence data from cross-sectional studies, and by data from case-controlled and cohort studies, and from randomized, experimental trials. Drug-induced gastric ulcers have been prevented by misoprostol, but not by H2 blocker therapy. Several therapies have been reported to promote ulcer healing despite continued use of NSAIDs, but adequate controlled trials have not been done. Small gastric and duodenal ulcers readily heal, whereas larger gastric ulcers require vigorous and prolonged therapy. The relative efficacies of various therapies in preventing ulcers, healing ulcers, or preventing complications remain to be established.

Anti-Inflammatory Agents, Non-Steroidal↗