Cases reported "Helicobacter Infections"

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1/174. Molecular relationships of helicobacter pylori strains in a family with gastroduodenal disease.

    OBJECTIVE: Few studies have examined the genetic relationships of helicobacter pylori strains affecting family members. Our aim was to do so. methods: We characterized H. pylori isolates obtained from members of a single family presenting with various gastroduodenal diseases to examine H. pylori bacterial genetic similarity. Endoscopic evaluation with gastric mapping was performed on each individual to establish clinical and histological disease. Genomic dna extracted from each H. pylori isolate was used to generate dna fingerprints for each strain by REP-PCR. vacA genotypes and cagA presence were established by PCR. RESULTS: gastrointestinal diseases among the five members of this family included gastric adenocarcinoma in a 52-yr-old man (index patient), gastric MALT-lymphoma in the 73-yr-old mother; intestinal metaplasia (IV) and atrophic gastritis in the 48-yr-old brother; intestinal metaplasia (I-III) in the 47-yr-old brother, and a duodenal ulcer scar in the 42-yr-old sister. REP-PCR dna fingerprints of H. pylori isolates from the index patient, his mother, and both of his brothers were identical or highly similar. By contrast, the H. pylori dna fingerprint from the sister was markedly different from the H. pylori dna fingerprints from the other family members. All isolates had the genotype cagA-positive and vacA slb/ml mosaic genotype. CONCLUSIONS: The dna fingerprints of H. pylori strains obtained from members of this family with malignancy or premalignant histological disease were identical or highly similar and markedly different from the H. pylori dna fingerprint from the sibling with duodenal ulcer disease. All H. pylori isolates within the family possessed genetic markers of enhanced virulence (presence of the cagA gene and vacA sl/ml mosaicism). In addition to host genetics and environmental factors, these findings suggest that infection with genetically similar H. pylori strains is a significant factor in determining the clinical outcome of an infection with H. pylori.
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2/174. Eradication of helicobacter pylori infection did not lead to cure of duodenal mucosa-associated lymphoid tissue lymphoma.

    Duodenal mucosa-associated lymphoid tissue (MALT) lymphoma is very rare, and little is known about its clinical course or association with helicobacter pylori infection. This report describes the case of a 76-year-old man with a polypoid mass in the duodenal bulb, diagnosed as low-grade MALT lymphoma. H. pylori infection in the duodenal mucosa was confirmed by histology with silver stain. Endoscopic examination showed that the gross lesion regressed after the eradication of H. pylori despite its histopathologic persistence. Ten months later, however, cervical and intraperitoneal lymphadenopathy and bone marrow involvement was observed, and the pathologic diagnosis of the cervical lymph node was identical with that of the duodenal lesion.
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3/174. Septic shock due to Helicobacter fennelliae in a non-human immunodeficiency virus-infected heterosexual patient.

    Helicobacter fennelliae (formerly campylobacter fennelliae) has been reported to cause bacteremia in homosexual men with or without human immunodeficiency virus (hiv) infection. We report here a 48-year-old, non-hiv-infected, heterosexual man with diabetes mellitus and cirrhosis of the liver who developed bacteremia and septic shock due to H. fennelliae. The patient was treated successfully initially with intravenous ampicillin-sulbactam and ceftazidime, followed by ampicillin-sulbactam only. These agents were active in vitro against the isolate by E-test results. To our knowledge, this is the first documented case of septic shock due to H. fennelliae in a non-hiv-infected, heterosexual, immunocompromised patient.
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4/174. helicobacter pylori infection and persistent hyperemesis gravidarum.

    hyperemesis gravidarum is the most severe spectrum of gastrointestinal complaints in pregnant women. Our purpose is to describe an association of helicobacter pylori with hyperemesis gravidarum. Three pregnant women are described with the working diagnoses of hyperemesis gravidarum unresponsive to standard therapy. The medical management used to treat helicobacter pylori in these women are elaborated. The persistence of the symptomatology and/or hematemesis resulted in helicobacter pylori testing of these women. A 2-week course of antibiotics and a proton pump inhibitor or H2 receptor antagonist resulted in resolution of the hyperemesis. A discussion of the incidence, diagnosis, and management of helicobacter pylori in pregnancy is described. When the symptoms of hyperemesis gravidarum are persistent into the second trimester, active peptic ulcer disease from helicobacter pylori should be included in the differential diagnoses.
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5/174. Successful symptomatic management of a patient with Menetrier's disease with long-term antibiotic treatment.

    We present the case of a 79-year-old female patient with criteria typical for Menetrier's disease, i.e. enlargement of the gastric folds due to foveolar hyperplasia associated with severe protein-loss along with epigastric pain, nausea, vomiting and weight loss. Gastrin levels were within the normal range, but elevated helicobacter pylori antibody titers (83 microg/ml) were indicative of a recent infection. Histologic examination of a gastric polyp, which was removed in toto, revealed the presence of early gastric cancer of the mucosal type. After initiation of antibiotic treatment with clarithromycin (3 x 250 mg/day) and metronidazole (2 x 500 mg/day) in combination with lansoprazole (30 mg/day), the patient's condition improved rapidly along with abrogation of protein loss. Under maintenance treatment as indicated above, the patient has been free of symptoms now for a period of more than 2 years. On repetitive endoscopic follow-up, there was no change in gastric mucosa morphology either endoscopically or histologically, and also no evidence of recurrence of a malignant lesion. We conclude that this therapeutic regimen represented an effective alternative to surgical intervention in this patient and should be considered in similar cases.
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6/174. Recurrent bacteremia caused by a "Flexispira"-like organism in a patient with X-linked (Bruton's) agammaglobulinemia.

    Helicobacter spp., except for Helicobacter cinaedi, have only rarely been reported in cases of septicemia. A patient with X-linked (Bruton's) agammaglobulinemia was found to have persistent sepsis with a Helicobacter-like organism despite multiple courses of antibiotics. His periods of sepsis were associated with leg swelling thought to be consistent with cellulitis. The organism was fastidious and required a microaerophilic environment containing H(2) for growth. Optimal growth was observed at 35 to 37 degrees C on sheep blood, CDC anaerobe, and Bordet-Gengou agars. Serial subcultures every 4 to 5 days were required to maintain viability. The organism was strongly urease positive and showed highest relatedness to Helicobacter-like organisms with the vernacular name "Flexispira rappini" by 16S rRNA gene sequence analysis. Genomic dna hybridization studies, however, found 24 to 37% relatedness to "F. rappini" and even less to other Helicobacter spp. Although the organism phenotypically resembles "Flexispira" and Helicobacter, it is thought to represent a new taxon. The patient's infection was eventually cleared with a prolonged (5-month) course of intravenous imipenem and gentamicin.
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7/174. angioedema due to acquired C1-esterase inhibitor deficiency in a patient with helicobacter pylori infection.

    The first component of the classical pathway of the complement system, C1 is regulated by a serum protein, the C1-esterase inhibitor (C1-INH). Deficiency of this protein leads to the release of vasoactive mediators (C2 kinin and bradykinin) that increase vascular permeability and can induce edema formation in subcutaneous and submucosal tissues. The genetic variant of C1-INH deficiency is inherited as an autosomal dominant trait and causes hereditary angioneurotic edema. The acquired form of C1-INH deficiency is characterized by similar manifestations and can occur in association with lymphoproliferative diseases, malignancy, immune disorders, and infections. The authors present a case of acquired C1-INH deficiency in a patient with helicobacter pylori infection. Complete eradication of this pathogen was followed by the resolution of symptoms and normalization of serum complement levels. It seems therefore probable that in this patient, acquired C1-INH deficiency was related to helicobacter pylori infection. To our best knowledge, no similar observations have been published so far. Specific immune reactions are important contributing factors in H. pylori. Excessive consumption of complement by antibodies directed against H. pylori is a potential cause of C1-INH deficiency observed in our case.
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8/174. A case of prurigo and lichenified plaques successfully treated with proton pump inhibitor.

    A case of prurigo and lichenified plaques successfully treated with proton pump inhibitor is presented. She presented with pruritic eruptions, which showed marked lichenification and prurigo nodules, on her trunk and extremities. She had been treated with steroid ointment and H1-histamine receptor antagonist without success. Laboratory examinations revealed increased eosiophils and elevated lactate dehydrogenase. The skin biopsy specimen showed moderate acanthosis with spongiosis and lymphocytic and eosinophilic infiltration into the upper dermis. Because of vomiting and epigastralgia, endoscopical examination was performed, and an ulcer was found at the angle of her ventricle. A biopsy specimen disclosed a benign gastric mucosa with moderate inflammation within the lamina propria, and organisms consistent with helicobacter pylori. Treatment for gastric ulcer with proton pump inhibitor (omeprazole) and aluminium hydroxide gel improved her eruptions and her pruritus resolved. She was discharged with complete cure of her eruption and ventricular ulcer. Our case indicates that gastric lesions induced by helicobacter pylori infection may play an important role in dermatological diseases. proton pump inhibitors including omeprazole are one of the choices for the treatment of some dermatological diseases including prurigo and lichenified plaques.
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9/174. Rapidly growing primary gastric B-cell lymphoma after eradication of helicobacter pylori.

    helicobacter pylori (H. pylori) infection plays a decisive role in primary gastric B-cell lymphoma especially of mucosa-associated lymphoid tissue (MALT)-type. We treated a 47-year-old male patient with primary gastric B-cell lymphoma associated with H. pylori infection. Although antibiotic therapy for eradication of H. pylori caused great improvement in the low-grade MALT lymphoma-like lesion, the small areas of high-grade lesion rapidly formed a new bulky mass in only 8 weeks. This suggests that eradication of H. pylori is not effective for high-grade lymphoma.
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10/174. Characteristics and prevalence of helicobacter heilmannii infection in children undergoing upper gastrointestinal endoscopy.

    BACKGROUND: helicobacter heilmannii, described in 1983 as a new cause of chronic gastritis, has been reported rarely in children. The purpose of this study was to determine the clinical characteristics and the prevalence of H. heilmannii infection, in comparison with helicobacter pylori infection in children undergoing upper digestive endoscopy. methods: diagnosis of H. heilmannii was based on its morphologic characteristics in gastric biopsy specimens (two from the antrum, one from the fundus), whereas H. pylori infection was defined by histology and/or culture (one specimen from the antrum, one from the fundus). Respective prevalences of H. heilmannii and H. pylori were calculated in 518 patients studied prospectively who underwent systematic biopsies. RESULTS: The prevalence of H. pylori was 8.9% (46/518) and increased with age (from 2% before 3 years of age to 18% after 10 years). On the contrary, the prevalence of H. heilmannii infection was low, 0.4% (2/518), and no different from that published in adults. After completion of the study period, a third H. heilmannii-infected child was diagnosed. Characteristics of H. heilmannii infection could be studied in these three children 5, 9, and 14 years old. Two of three had abdominal pain and one had dysphagia. Nodular gastritis was observed at endoscopy in two children. H. heilmannii chronic active gastritis (n = 3) was localized in the antrum, associated with an interstitial infiltrate, and could not be distinguished from H. pylori gastritis (n = 46). CONCLUSION: Clinical characteristics, endoscopic features and gastric histopathology did not allow H. heilmannii to be distinguished from H. pylori gastritis in our pediatric population. H. heilmannii infection should be considered and carefully looked for during histologic examination of gastric specimens in cases of H. pylori-negative gastritis.
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