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Biomedical subjects

R M Genta

Publications and source records attributed to R M Genta.

At least 109 records · Page 6Linked to original sources
PubMed1995

Geographical pathology of Helicobacter pylori infection: is there more than one gastritis?

Helicobacter pylori is the aetiological agent of chronic gastritis and a major causative factor in duodenal and gastric peptic ulcer disease; a strong association also exists with gastric cancer and primary gastric lymphoma. The prevalence of infection in adults ranges from less than 15% in developed countries to virtually 100% in less developed areas. If H. pylori infection alone was responsible for the development of gastritis, peptic ulcer disease, gastric carcinoma and primary gastric lymphoma, one would expect the frequency of all these conditions to parallel closely the prevalence of H. pylori infection. This is clearly not the case: therefore, genetic, environmental and cultural factors must act in concert with H. pylori to induce different outcomes of the infection. This paper outlines the geographic approach to the study of disease and discusses the possible application of this methodology to the inquiry into the relationship between H. pylori, atrophic gastritis and gastric cancer. Preliminary results of a study showing great variation in the prevalence of intestinal metaplasia in duodenal ulcer patients from different geographic origin are presented and briefly discussed.

Adult↗
PubMed1995

Confirmation of successful therapy of Helicobacter pylori infection: number and site of biopsies or a rapid urease test.

BACKGROUND: Although a number of tests have been described to detect the presence of Helicobacter pylori in biopsy specimens, studies of positive and negative value have largely been performed on untreated patients; testing the reliability of posttherapy has not been done. METHODS: We examined the value of the number and site of biopsies performed and the method used for specimen evaluation posttherapy. For postantimicrobial therapy of 141 patients with previously confirmed H. pylori infection, three biopsies were taken, two from the antrum and one from the corpus. Individual slides were coded, randomized, and interpreted blindly by two pathologists. Furthermore, in 143 patients, a biopsy specimen was taken from the antrum and was immediately inserted into the gel of the rapid urease test, and the results were compared with those obtained from histopathology obtained at the same time. RESULTS: In 71 patients, H. pylori therapy was unsuccessful; in 61 (86%), all three sites were positive. The highest yield with a single large cup biopsy specimen was 94%; the lowest was 91%. Two antral biopsies were negative in 4% [95% confidence interval (CI) = 1-12%]. The combination of a biopsy from the angulus incisura and one from the greater curvature of the corpus correctly identified all treatment failures (95% CI = 95-100%). The rapid urease test was false-negative in 5% (95% CI = 1-13%); there were no false-positives. CONCLUSION: Use of either the rapid urease test or two antral biopsies for evaluation of success of antimicrobial therapy for H. pylori infection will result in a false declaration of cure in at least 5% of cases. Three large cup gastric mucosal biopsies for histology are recommended for evaluation of the success of anti-H. pylori therapy.

Bacteriological Techniques↗
PubMed1995

Evaluation of a new urease reagent strip for detection of Helicobacter pylori in gastric biopsy specimens.

OBJECTIVES: Determine sensitivity and specificity of a new urease reagent strip (URS) test for detection of Helicobacter pylori in gastric biopsy specimens. METHODS: Six paired biopsy specimens were obtained from the greater curvature of the distal antrum, the lesser curvature near the incisura, and the corpus along the greater curvature during 66 procedures on 59 patients with endoscopic findings of gastric antral mucosal erythema or erosions, or gastric or duodenal ulcers. One biopsy from each site was tested with the URS. The second was evaluated with histology. A final antral biopsy was evaluated with a urea/gel test. RESULTS: Twenty-eight of the 66 cases were histologically positive, with H. pylori observed in at least one of the three biopsy sites. The URS test correctly identified all 28. Of 193 individual biopsy specimens, 78 were positive for H. pylori. The URS correctly identified 77. Sensitivity was 0.99, specificity 0.95, positive predictive value 0.93, negative predictive value 0.99, and kappa 0.92. Average time to positive was 20 min. Twenty-seven antral biopsies were histologically positive for H. pylori. The URS test correctly identified all 27, whereas the urea/gel test correctly identified 21. For antral sites, URS sensitivity was 1.00 and specificity 0.95 versus urea/gel test sensitivity of 0.75 and specificity of 1.00. CONCLUSIONS: In this sample, the URS test is as accurate as histology in diagnosing H. pylori infections, and it provides results in less time and at a lower cost than histology.

Bacteriological Techniques↗
PubMed1995

Treatment of Helicobacter pylori infection with omeprazole-amoxicillin combination therapy versus ranitidine/sodium bicarbonate-amoxicillin.

OBJECTIVES: Simpler, effective therapies to treat Helicobacter pylori infection are greatly needed. Omeprazole co-therapy apparently enhances effectiveness of some antimicrobials. Our objective in this study was to determine whether the apparent additional benefit provided by omeprazole to amoxicillin therapy could be equaled by a high dose of ranitidine plus sodium bicarbonate. METHODS: In a prospective randomized trial, we tested 1 g amoxicillin b.i.d. with either omeprazole 20 mg b.i.d., or high dose ranitidine (900 and 1800 mg) plus sodium bicarbonate tablets 650 t.i.d. (with meals) for 14 day. RESULTS: Fifty-two patients with documented H. pylori infection and peptic ulcer completed therapy. The cure rate with omeprazole and amoxicillin was poor (46%), with the 95% confidence interval (CI) = 25-67%. Ranitidine plus sodium bicarbonate was also poor (39% cure) with the 95% CI = 21.5-59% (p > 0.57). Average compliance was more than 92% for all three groups. Side effects were experienced in only two patients (stomatitis and mild diarrhea). CONCLUSION: Neither the omeprazole nor ranitidine plus bicarbonate plus amoxicillin therapies used here can be recommended for treatment of H. pylori infection.

Amoxicillin↗
PubMed1995

Variability with omeprazole-amoxicillin combinations for treatment of Helicobacter pylori infection.

OBJECTIVE: Although omeprazole co-therapy enhances the effectiveness of some antimicrobials for the treatment of Helicobacter pylori infection, results have not been uniform. A meta-analysis suggested that 20 mg of omeprazole b.i.d. and 2 g or more of amoxicillin would yield a > 80% success rate (Gastroenterology 1994; 106: 142A). Our objective in this study was to test that hypothesis. METHODS: Volunteers with H. pylori infection were studied. Anti-H. pylori therapy was administered with meals for 14 days (omeprazole 20 mg b.i.d. plus amoxicillin 1 g t.i.d., or omeprazole 20 mg b.i.d. plus amoxicillin 0.5 g t.i.d.). Endoscopy was performed 4-6 wk after antimicrobial therapy ended, and the presence or absence of H. pylori was determined with biopsy specimens by Genta stain. RESULTS: Fifty-nine volunteers completed the study; 30 were studied twice. The overall success for initial treatment with either combination of amoxicillin and omeprazole was 18 of 59 [30.5%; 95% confidence interval (CI) = 19-44%]. The success rate with 500 mg amoxicillin t.i.d. was 7 of 29 (24%; 95% CI = 10-43%). With 1 g t.i.d. amoxicillin, the cure rate was higher (36.6%) (11 of 30; 95% CI = 20-56%), or intention-to-treat result was 11 of 31 (35.4%), which includes the early dropout. Compliance was > 95% for both therapies. Side effects were experienced by eight patients, two receiving 1.5 g amoxicillin and six receiving 3 g amoxicillin (p > 0.2). German trials suggest that better results might be achieved when amoxicillin is given as suspension while fasting. Thirty treatment failures were re-treated with 1 g amoxicillin suspension t.i.d., given fasting, and omeprazole 20 mg b.i.d. The cure rate was 16.6% (95% CI = 6-35%). CONCLUSION: Amoxicillin/omeprazole combinations for treatment of H. pylori infection do not yield consistent results. The reason is unknown, but the reported high rate of success with 40 mg of omeprazole and 750 mg t.i.d. suggests that almost complete inhibition of acid secretion is necessary to obtain consistent results with this combination.

Adult↗
PubMed1995

Azithromycin triple therapy for Helicobacter pylori infection: azithromycin, tetracycline, and bismuth.

BACKGROUND: Azithromycin is new acid-stable macrolide that achieves 10- to 40-fold higher tissue levels than erythromycin after oral dosing. Important to note, the tissue half-life of azithromycin is measured in days instead of hours. METHOD: We evaluated two new triple therapies for Helicobacter pylori infection in which azithromycin was substituted for metronidazole either as 250 mg b.i.d. or t.i.d. along with tetracycline 500 mg q.i.d. and bismuth subsalicylate 2 tablets q.i.d. for 14 days. H. pylori status was determined by histology before and 6 wk or more after therapy. RESULTS: Thirty men with documented H. pylori peptic ulcers completed therapy. Twenty-one also received ranitidine (300 mg in the evening) along with the antimicrobial therapy. H. pylori infection was successfully treated in 15 (50%) (95% CI = 31-69%). The cure rate was significantly higher with the 250-mg-t.i.d.-azithromycin dosage regime (83%) (95% CI = 52-98%) compared to the 250-mg-b.i.d.-dosage regime (28%) (95% CI = 10-53%) (p < 0.01). Troublesome side effects were experienced by the majority of those receiving azithromycin t.i.d. CONCLUSION: We conclude that although 750 mg or more of azithromycin might eventually be able to replace metronidazole or clarithromycin in standard triple therapy, additional studies are required to identify a regime that is both effective and tolerable.

Azithromycin↗
PubMed1995

Helicobacter pylori as a promoter of intestinal metaplasia and gastric cancer: an alluring hypothesis in search of evidence.

OBJECTIVES: To examine the current evidence supporting a role for Helicobacter pylori in the genesis of intestinal metaplasia and to offer suggestions for the design of studies that could be carried out to elucidate the pathogenesis of gastric cancer. METHOD: Literature review. CONCLUSIONS: The epidemiologic relationship between H. pylori and gastric cancer is widely accepted; however, the sequence of events leading to the development of carcinoma is unknown. A currently accepted model is that chronic active gastritis progresses to atrophic gastritis with intestinal metaplasia, dysplasia and eventually neoplasia. The relationship between H. pylori and intestinal metaplasia remains unclear, as several studies have yielded conflicting results.

Helicobacter Infections↗
PubMed1994

Helicobacter pylori: the new bug on the (paraffin) block.

A nameless spirillar organism in search of a disease only a few years ago, Helicobacter pylori has seen its fortunes suddenly reversed. After a rapid succession of name changes and some acrimonious disputes across continents, in less than a decade H. pylori has been catapulted to the centre stage of gastroenterological and microbiological research and has topped the most-wanted list of the pharmaceutical industry. The discovery of H. pylori has provided the momentum for the formation of the group that eventually created the Sydney System. Today, H. pylori is increasingly recognized as one of the most prevalent human pathogens worldwide. Its causal association with chronic active gastritis is undisputed and its role in the pathogenesis of peptide ulcer disease, although still poorly understood, is universally accepted. Furthermore, possible connections between chronic H. pylori infection and gastric carcinoma and primary gastric lymphoma are now being explored with increasing alacrity. With a few notable exceptions, pathologists have remained passive spectators of these exciting discoveries and have allowed gastroenterologists and microbiologists to set the pace in the quest for the determinants of gastritis, peptic ulcer and gastric cancer. This article is intended to outline some of the accepted facts on the development, progression, and pathology of H. pylori gastritis and to pose questions about this elusive infection. The authors hope that it might also contribute to stimulate further research, particularly on those aspects that are eminently suited to be addressed by pathologists.

Gastric Mucosa↗
PubMed1994

The gastric cardia in Helicobacter pylori infection.

Helicobacter pylori gastritis is believed to be both more prevalent and more severe in the antrum than in the corpus. The mucosa of the cardia is architecturally similar to that of the antrum. This study was designed to test the hypothesis that intensity of H pylori infection and the associated inflammation are similar in the cardia and the antrum and are greater in these locations than in the corpus. A total of 445 gastric biopsy specimens were obtained from predetermined sites from 50 subjects (42 with demonstrated H pylori infection). Slides were stained with a combined stain to simultaneously visualize H pylori, mucosal morphology, and inflammatory infiltrate. Numbers of H pylori, inflammatory responses, and intestinal metaplasia were graded on a scale from 0 to 5. Helicobacter pylori was detected in the cardia of 40 of the 42 infected subjects (95%). Helicobacter pylori density was similar in the three gastric regions. The intensity of chronic active gastritis was similar in the antrum and the cardia, and was higher in these locations than in the corpus (P < .005). Lymphoid follicles were significantly less prevalent in the cardia and in the corpus than in the antrum (P < .05). Helicobacter pylori infection was as prevalent in the cardia as in the rest of the stomach and its density was similar in all sites of antrum, corpus, and cardia. The inflammatory responses characteristic of chronic active gastritis, except for lymphoid follicles, were similar in the antrum and the cardia and in both these locations were more intense than in the corpus. The significance of these findings is discussed with respect to the relationship between H pylori infection and the genesis of gastric adenocarcinoma and lymphoma.

Adult↗
PubMed1994

Simultaneous visualization of Helicobacter pylori and gastric morphology: a new stain.

Although the histopathologic patterns associated with Helicobacter pylori infection have been described, details of the interaction between bacteria, epithelial cells, and inflammatory cells remain elusive. One of the limiting factors has been the lack of a staining technique that allows the simultaneous visualization of H pylori and tissue morphology. By combining three commonly available stains (Steiner, hematoxylin-eosin, and alcian blue at pH 2.5) into a single procedure we have developed a stain that permits the optimal detection of H pylori in tissue sections while simultaneously allowing the histopathologic evaluation of all salient characteristics of the gastric mucosa. This procedure is inexpensive, as easy to perform as any silver stain, and provides consistent results. This stain is as sensitive as the Warthin-Starry stain for the detection of H pylori and significantly more sensitive than hematoxylin-eosin alone (> 99% v 85% when compared with the hematoxylin-eosin stain in a series of 332 positive biopsy specimens; > 99% v 61% in 49 biopsy specimens with rare bacteria). This stain is particularly useful for the visualization of small numbers of bacteria, such as in the evaluation of posttreatment gastric biopsy specimens, in specimens with abundant mucus or debris, and in specimens from the corpus, where H pylori usually does not elicit strong inflammatory responses and, therefore, pathologists' index of suspicion tends to be low.

Biopsy↗
PubMed1994

Transitional cell carcinoma of fossa navicularis in a man with three other synchronous malignancies.

Transitional cell carcinoma arising from the anterior portion of the male urethra is rare, with less than 10 cases reported in the literature. Our patient had a high-grade, highly invasive transitional cell carcinoma originating in the fossa navicularis and extending proximally along the corpus spongiosum, the corpora cavernosa, and blood and lymphatic vessels. In addition, the patient had a concurrent low-grade prostatic adenocarcinoma, a large basal cell carcinoma of the nose, and a squamous cell carcinoma of the penile skin. The previously reported cases are reviewed, with particular reference to the possible association of these tumors with human papillomavirus infection.

Adenocarcinoma↗
PubMed1994

Short report: omeprazole-tetracycline combinations are inadequate as therapy for Helicobacter pylori infection.

BACKGROUND: Current triple antimicrobial therapies cure Helicobacter pylori infection in 60-90% of cases but are cumbersome. Addition of omeprazole to amoxycillin has been shown to enhance effectiveness when compared to amoxycillin alone. METHOD: We studied omeprazole 20 mg t.d.s. plus tetracycline 500 mg q.d.s. for 14 days (OMP/TCN) and omeprazole 40 mg in the morning plus tetracycline 500 mg q.d.s. along with bismuth subsalicylate tablets 2 q.d.s. (OMP/TCN/BSS) for 14 days. Forty-four patients (19 OMP/TCN, 25 OMP/TCN/BSS) with H. pylori peptic ulcer disease were studied. H. pylori status was evaluated at least 4 weeks after ending antimicrobial therapy. RESULTS: In the OMP/TCN group cure of H. pylori infection was achieved in 5/19 (26%). Adding bismuth to the regimen improved the results; 4 weeks after ending therapy cure of H. pylori infection was achieved in 12/25 (48%). CONCLUSIONS: Neither regimen can be recommended for routine cure of H. pylori infection. Although one cannot predict which antimicrobial therapies will be enhanced by the addition of omeprazole, these data suggest that future studies should evaluate drugs whose effectiveness is compromised by low pH.

Adult↗
PubMed1994

Clarithromycin-amoxycillin therapy for Helicobacter pylori infection.

BACKGROUND: More convenient therapies are needed to treat Helicobacter pylori infection successfully. Clarithromycin and amoxycillin are effective against H. pylori both in vivo and in vitro. Recent success with a high dose amoxycillin-metronidazole combination therapy led us to evaluate clarithromycin-amoxycillin dual therapy for H. pylori infection. METHODS: We tested the combination of clarithromycin 500 mg t.d.s. with meals plus amoxycillin 750 mg t.d.s. with meals for 10 days for its effect on H. pylori infection in 29 patients with documented H. pylori peptic ulcers. There were 27 men and 2 women, ranging in age from 23 to 77 years. H. pylori and ulcer status were evaluated at entry and at least 4 weeks after ending antimicrobial therapy. For ulcer healing, ranitidine 300 mg was given each evening for 6 weeks. H. pylori status was determined by CLOtest and histology. RESULTS: H. pylori infection was cured in 86% (95% CI = 78-99%). Compliance averaged 93% by pill count. Ten patients (34%) experienced mild side effects: eight reported dysgeusia and two had mild diarrhoea; none discontinued therapy because of side effects. CONCLUSION: We conclude that dual therapy with clarithromycin and amoxycillin is a safe and effective alternative regimen for the successful treatment of H. pylori infections.

Administration, Oral↗
PubMed1994

The significance of lymphoid follicles in the interpretation of gastric biopsy specimens.

Lymphoid follicles are a common feature of Helicobacter pylori-associated gastritis. Recently, by using gastric mapping, we demonstrated lymphoid follicles in all of 62 patients with H pylori infection. This study was designed to address (1) the prevalence of lymphoid follicles in routine gastric biopsy specimens, (2) their correlation with chronic active gastritis, and (3) their predictive value with respect to H pylori infection. Slides from 174 patients whose gastric biopsy findings carried a nonneoplastic diagnosis were evaluated for the presence of (1) chronic active gastritis, (2) lymphoid follicles, and (3) H pylori. When either follicles or active gastritis was found, but H pylori could not be identified by the hematoxylin-eosin stain, additional slides were prepared with a newly developed silver-hematoxylin-eosin-alcian blue stain. Active gastritis was present in 153 patients (88%). Helicobacter pylori was identified on hematoxylin-eosin-stained slides in 123 patients and by the modified Steiner stain in 11 additional patients. Thus, 87% of the patients with chronic active gastritis had histologically detectable H pylori infection. One or more lymphoid aggregates were present in 110 patients (82% of patients with H pylori and 72% of those with chronic active gastritis). Of these, 101 (92%) had H pylori infection. In six of the nine H pylori-negative patients with lymphoid aggregates, biopsy specimens were taken from the edges of an ulcer. In summary, except when biopsy specimens are obtained from the immediate vicinity of a gastric ulcer, lymphoid aggregates in a gastric biopsy specimen are virtually always associated with chronic active gastritis and provide a useful marker for H pylori infection.

Biopsy↗
PubMed1994

Clarithromycin, tetracycline, and bismuth: a new non-metronidazole therapy for Helicobacter pylori infection.

OBJECTIVE: Metronidazole resistance has become an increasing problem that has limited the usefulness of the original triple therapy. Our objective was to evaluate clarithromycin, a new macrolide compound active against Helicobacter pylori. METHODS: We evaluated a new clarithromycin triple therapy for H. pylori infection consisting of the combination of clarithromycin (500 mg t.i.d.), tetracycline (500 mg q.i.d.), and bismuth subsalicylate tablets (2 q.i.d.) for 14 days. Patients with ulcer also received concomitant ranitidine, 300 mg after the evening meal, for 6 wk. RESULTS: Thirty men with documented H. pylori infection were studied; 29 had peptic ulcer disease. Seven had previously failed antimicrobial therapy, including three with metronidazole-based triple therapy. H. pylori status was determined by histology. H. pylori status and ulcer status were evaluated 4 wk after the end of antimicrobial therapy. The ulcer was healed in 90%. The H. pylori infection was cured in 93%, including all three patients who previously failed metronidazole-based triple therapy. CONCLUSION: We conclude that the combination of clarithromycin, tetracycline, and bismuth is an effective new therapy for treatment of H. pylori infection.

Adult↗
PubMed1994

Adherence of monocytes and polymorphonuclear cells to infective larvae of Strongyloides stercoralis after complement activation.

The activation of the complement system by living Strongyloides stercoralis filariform larvae and their antigenic preparation was demonstrated in vitro through both classical and alternative pathways. This activation does not require the presence of specific antibodies but promotes the adhesion of peripheral blood monocytes (MNC) and polymorphonuclear cells (PMNC) to the larval surface. Larvae, totally coated by PMNC, showed a visible loss of motility after 2 hr incubation. Ethylenediamine tetraacetic acid, in contrast to ethylene glycol-bis beta-aminoethylether N,N,N,N-tetraacetic acid, abolished the adherence activity, suggesting the involvement of the alternative pathway in this process. Deposition of complement components C1q, C3, C4, C8, and properdin on the larval surface was demonstrated by immunofluorescence assays. In addition, complement activation by the larvae was demonstrated through C3 conversion and C4 cleavage assays, both depending on the number of larvae. On the other hand, complement activation by S. stercoralis antigen was determined by factor B and C4 cleavage, as well as C3 conversion assays. Our results suggest that the complement system as a first line of defense, in association with the effector cells, plays an important role in the nonspecific immune response of the host to S. stercoralis infection, especially considering the constant parasite recycling through the host tissues.

Animals↗