bluuebunny/crossref_metadata_2025_split huggingface dataset:
Rifampin is safe for treatment of pruritus due to chronic cholestasis: a meta‐analysis of prospective randomized‐controlled trials
Authors: Khurana Sandeep , Singh Pankaj 
Published: September 2006

Abstract: Objectives: To determine the safety and efficacy of rifampin for treatment of pruritus associated with cholestasis due to chronic liver disease.Methods: Medical literature was searched systematically using keywords as rifampicin, rifampin, rifamycin, cholestasis, pruritus, itching, and liver disease. Trials that compared the efficacy of rifampin with placebo/alternative for treatment of pruritus due to chronic cholestasis were selected for analysis. Primary outcomes were resolution of pruritus and development of side effects. Association was measured with the odds ratio (OR). Breslow–Day method was used to treat for homogeneity under null hypothesis that OR was consistent across all the trials. Corrected Mantel–Haenszel χ2 test was used to test if OR differed systematically from value of 1.Results: Five prospective randomized‐controlled cross‐over trials with 61 patients were identified. Treatment with rifampin led to complete or partial resolution of pruritus in 47 (77%) patients as compared with 12(20%) treated with placebo or alternative (OR 15.2, 95% confidence interval 5.2–45.6, P=0.001). Four (7%) patients treated with rifampin suffered side effects, which resolved after its discontinuation. There was no incidence of hepatotoxicity. Test of heterogeneity for primary end points among the trials was not significant (P=0.16).Conclusion: This meta‐analysis suggests that rifampin is safe and effective for treatment of pruritus due to chronic cholestasis. This analysis also suggests that use of rifampin for short duration is associated with a low risk of hepatotoxicity.
A Community‐Based Study of Helicobacter pylori Therapy Using the Strategy of Test, Treat, Retest, and Re‐treat Initial Treatment Failures
Authors: Lee Yi‐Chia , Wu Hui‐Min , Chen Tony Hsiu‐Hsi , Liu Tzeng‐Ying , Chiu Han‐Mo , Chang Chun‐Chao , Wang Hsiu‐Po , Wu Ming‐Shiang , Chiang Hung , Wu Meng‐Chen , Lin Jaw‐Town 
Published: September 2006

AbstractBackground:  Although eradication of Helicobacter pylori infection can decrease the risk of gastric cancer, the optimal regimen for treating the general population remains unclear. We report the eradication rate (intention‐to‐treat and per protocol) of a community‐based H. pylori therapy using the strategy of test, treat, retest, and re‐treat initial treatment failures.Materials and methods:  In 2004, a total of 2658 residents were recruited for 13C‐urea breath testing. Participants with positive results for infection received a standard 7‐day triple therapy (esomeprazole 40 mg once daily, amoxicillin 1 g twice daily, and clarithromycin 500 mg twice daily), and a 10‐day re‐treatment (esomeprazole 40 mg once daily, amoxicillin 1 g twice daily, and levofloxacin 500 mg once daily) if the follow‐up tests remained positive. Both H. pylori status and side‐effects were assessed 6 weeks after treatment.Results:  Among 886 valid reporters, eradication rates with initial therapy were 86.9% (95% confidence interval [CI]: 84.7–89.1%) and 88.7% (95%CI: 86.5–90.9%) by intention‐to‐treat and per protocol analysis, respectively. Re‐treatment eradicated infection in 91.4% (95%CI: 86–96.8%) of 105 nonresponders. Adequate compliance was achieved in 798 (90.1%) of 886 subjects receiving the initial treatment and in all 105 re‐treated subjects. Mild side‐effects occurred in 24% of subjects. Overall intention‐to‐treat and per protocol eradication rates were 97.7% (95%CI: 96.7–98.7%) and 98.8% (95%CI: 98.5–99.3%), respectively, which were only affected by poor compliance (odds ratio, 3.3; 95%CI, 1.99–5.48; p < .0001).Conclusions:  A comprehensive plan using drugs in which the resistance rate is low in a population combined with the strategy of test, treat, retest, and re‐treat of needed can result in virtual eradication of H. pylori from a population. This provides a model for planning country‐ or region‐wide eradication programs.
Polymorphisms in Cytokine Genes and Risk of Helicobacter pylori Infection among Jamaican Children
Authors: Tseng Fan‐Chen , Brown Elizabeth E. , Maiese Eric M. , Yeager Meredith , Welch Robert , Gold Benjamin D. , Owens Marilyn , Cranston Beverly , Hanchard Barrie , El‐Omar Emad , Hisada Michie 
Published: September 2006

AbstractBackground:  Infection by Helicobacter pylori is often acquired during childhood. Recent studies suggest that inflammatory cytokines may play a role in susceptibility to, and disease phenotype caused by, H. pylori infection, but the association of host genetic variability with risk of H. pylori infection has not been studied in children.Methods:  We investigated the relationship between the risk of H. pylori antibody positivity and cytokine gene polymorphisms among 199 two‐year‐old Jamaicans. H. pylori seropositivity was determined by a validated research enzyme‐linked immunosorbent assay. Real‐time Taqman® polymerase chain reaction was used to determine variants at 17 loci in 11 cytokine genes (IL1A, IL1B, IL2, TNF, TLR4, IL4, IL6, IL10, IL10RA, IL12A and IL13). We estimated the odds ratio and the 95% confidence interval for the association of genetic polymorphisms with H. pylori seropositivity, using logistic regression.Results:  Forty (20.1%) of 199 children were seropositive. Children's H. pylori seropositivity correlated highly with maternal H. pylori seropositivity (OR = 7.98, 95% CI = 1.05–60.60, p = .02). Children carrying IL1A−889T had a lower risk of H. pylori positivity, compared to those carrying −889C, with each T allele associated with 43% risk reduction (OR = 0.57, 95% CI = 0.33–0.99, p‐trend = .05). No other loci we examined were associated with the risk of H. pylori seropositivity.Conclusions:  The IL1A−889 T allele, known to express a higher level of cytokine IL‐1α, is associated with a lower risk of H. pylori infection among Jamaican children. Our finding supports the hypothesis that an upregulation of pro‐inflammatory cytokines may protect against persistent H. pylori colonization.
Helicobacter pylori Recurrence in Patients with Duodenal Ulcer: Clinical, Endoscopic, Histologic, and Genotypic Aspects. A 10‐Year Brazilian Series
Authors: Eisig Jaime N. , Zaterka Schlioma , Silva Fernando M. , Malfertheiner Peter , Mattar Rejane , Rodriguez Tomás N. , Hashimoto Cláudio L. , Iriya Kioshi , Laudanna Antonio A. , Moraes‐Filho Joaquim P.P. 
Published: September 2006

AbstractBackground:  Recurrence infection following successful eradication of Helicobacter pylori is usually low, except for countries with high prevalence of H. pylori. The aim of this study was to verify H. pylori recurrence rate in patients with duodenal ulcer after eradication and the possible relationship with environmental factors, histologic pattern of the mucosa and bacterial genotype.Materials and methods:  One‐hundred and ninety‐four patients with an active duodenal ulcer and who were successfully treated for H. pylori infection from 1990 to 1999 were studied. A questionnaire was answered about their living conditions, and a 14C‐urea breath test was performed. Patients with a positive breath test underwent an upper endoscopy to investigate for possible ulcer recurrence; gastric biopsy samples were than collected for rapid urease test and for histologic assessment. H. pylori vacA and cagA genotype was determined by polymerase chain reaction in those samples with positive urease test.Results:  H. pylori infection was detected in 11 patients (recurrence rate of 5.7%) that were not associated with the type of bacterial virulence. In 10 patients the ulcer was healed and all of them were clinically asymptomatic. In eight, histology showed an intensification of gastritis. All 11 patients had adequate housing and sanitary conditions and no other risk for H. pylori recurrence was identified.Conclusions:  The recurrence rate of H. pylori in Brazil was higher than that reported in developed countries, but lower than usually reported in developing ones. Ulcer relapse rarely occurs even in long‐term follow up.
Comparison of Amoxicillin–Metronidazole Plus Famotidine or Lansoprazole for Amoxicillin–Clarithromycin–Proton Pump Inhibitor Treatment Failures for Helicobacter pylori Infection
Authors: Murakami Kazunari , Okimoto Tadayoshi , Kodama Masaaki , Sato Ryugo , Miyajima Hajime , Ono Masami , Inoue Kunimitsu , Watanabe Koichiro , Otsu Satoshi , Fujioka Toshio 
Published: September 2006

AbstractBackground:  Proton pump inhibitor–amoxicillin–metronidazole is recommended as second‐line Helicobacter pylori therapy in Japan. The authors assessed the efficacy and safety of second‐line eradication using the H2‐receptor antagonist famotidine as a substitute for proton pump inhibitor.Materials and methods:  Sixty‐one patients who failed in first‐line H. pylori eradication using proton pump inhibitor–clarithromycin–amoxicillin were randomly assigned to either second‐line therapy including metronidazole: a 7‐day course of lansoprazole 30 mg, amoxicillin 750 mg, and metronidazole 250 mg, b.i.d. (lansoprazole group); or a 7‐day course of famotidine 40 mg, amoxicillin 750 mg, and metronidazole 250 mg, b.i.d. (famotidine group). Eradication was assessed for each group at least 4 weeks after completing eradication therapy. Drug susceptibility test was performed using 57 strains in pretreatment to clarithromycin, metronidazole, and amoxicillin.Results:  Prior to second‐line H. pylori eradication, the rate of resistance to clarithromycin was high at 84% (48/57). Similarly, resistance to metronidazole was low at 5.3% (3/57); however, no amoxicillin‐resistant strains were found.The eradication rates for both lansoprazole and famotidine treatment groups were high at 97% (29/30) and 94% (29/31), respectively.Conclusions:  Famotidine treatment including metronidazole–amoxicillin as second‐line therapy provided a high eradication rate similar to lansoprazole therapy. Famotidine is therefore expected to serve as a useful H. pylori eradication regimen in patients with proton pump inhibitor allergy, an economic benefit in terms of reduced health‐care costs is also anticipated.
Acute Symptomatic Gastritis Due to Helicobacter heilmannii
Authors: Al‐Hamoudi Waleed K. , Alpert Lesley , Szilagyi Andrew 
Published: September 2006

Abstract Helicobacter heilmannii is a Gram‐negative spiral‐shaped organism predominantly associated with zoonotic infection. Human pathology has also been described, but acute symptoms with complete resolution have been infrequently reported. We present a 50‐year‐old man in whom H. heilmannii gastritis presented as an acute febrile illness and was successfully treated with antibiotics and proton pump inhibitor. Epidemiology, diagnosis, and treatment of similar cases are reviewed.
Helicobacter pylori Infection and CagA Protein Translocation in Human Primary Gastric Epithelial Cell Culture
Authors: Lai Yo‐Ping , Yang Jyh‐Chin , Lin Tzu‐Zung , Lin Jaw‐Town , Wang Jin‐Town 
Published: September 2006

AbstractBackground:  Increasing evidence has shown that Helicobacter pylori CagA protein translocation into gastric epithelial cells plays an important role in the development of gastric inflammation and malignancy. Translocated CagA undergoes tyrosine phosphorylation in gastric adenocarcinoma cell line cells, and CagA involves disruption of cellular apical–junction complex in Madin–Darby canine kidney cells.Methods:  To elucidate whether these events take place in normal human gastric epithelium, we infected human primary gastric epithelial cells with H. pylori.Results:  Our results demonstrate that CagA protein was translocated into primary gastric epithelial cells and tyrosine phosphorylated. The translocated CagA induces cytoskeletal rearrangement and the disruption of tight junctions in primary gastric epithelial cells.Conclusions:  This study provides direct evidence of the modulation of gastric epithelial cells by CagA protein translocation, and advances our understanding of the pathogenesis of H. pylori infection.
Apoptosis in Helicobacter pylori Gastritis is Related to cagA Status
Authors: Cabral Mônica M.D.A. , Mendes Cláudia M.C. , Castro Lúcia P.F. , Cartelle Christiane T. , Guerra Juliana , Queiroz Dulciene M.M. , Nogueira Ana M.M.F. 
Published: September 2006

AbstractBackground:  Helicobacter pylori infection increases gastric epithelial cell apoptosis; however, the influence of cagA status is still controversial. We aimed to investigate if cagA status is related to apoptosis in H. pylori gastritis at different anatomic sites of the gastric mucosa.Materials and Methods:  We studied by immunohistochemistry (streptavidin–biotin method) pro‐apoptotic (Bax and Bak) and antiapoptotic (Bcl‐2 and Bcl‐x) proteins expression, scored from 0 to 4, in gastric biopsies, at the antrum (lesser and greater curvatures), incisura, and corpus (greater curvature) from 50 patients with H. pylori gastritis (22 males, 28 females, median age 40 years) and eight non‐infected patients (6 males, median age 39.6 years). H. pylori and cagA status were determined by polymerase chain reaction.Results:  Apoptotic proteins were expressed in a granular pattern, in the cytoplasm of foveolar cells; Bax and Bak expression was higher than Bcl‐2 and Bcl‐x in most cases and was significantly higher in patients infected by cagA‐positive strains than in those infected by cagA‐negative strains (p = .001). Bak expression was higher at the lesser curvature (antrum and incisura) than in the other regions (p = .002) and was correlated with atrophy. Anti‐apoptotic proteins were significantly more expressed at the antral lesser curvature than in the other regions of the stomach (Bcl‐2: p = .02; Bcl‐x: p < .001).Conclusions:  Infection with cagA‐positive strains is significantly associated with overexpression of pro‐apoptotic proteins in the gastric mucosa, mainly at the antral lesser curvature, which may have a role on atrophy development. Anti‐apoptotic proteins were also overexpressed at the lesser curvature, which may occur to keep epithelial cell turnover or might be related to malignant transformation.
In Vitro and In Vivo Complementation of the Helicobacter pylori Arginase Mutant Using an Intergenic Chromosomal Site
Authors: Langford Melanie L. , Zabaleta Jovanny , Ochoa Augusto C. , Testerman Traci L. , McGee David J. 
Published: September 2006

AbstractBackground:  Gene complementation strategies are important in validating the roles of genes in specific phenotypes. Complementation systems in Helicobacter pylori include shuttle vectors, which transform H. pylori at relatively low frequencies, and chromosomally based approaches. Chromosomal complementation strategies are susceptible to polar effects and disruption of other H. pylori genes, leading to unwanted pleiotropic effects.Materials and methods:  A new complementation strategy was developed for H. pylori by utilizing a suicide plasmid vector that contains fragments of an H. pylori intergenic region (hp0203–hp0204), a chloramphenicol acetyltransferase cassette (cat), and a multiple‐cloning site. Genes of interest could be cloned into the intergenic plasmid and the genes integrated into H. pylori by homologous recombination into the intergenic chromosomal region without disrupting any annotated H. pylori gene. The complementation system was validated using the gene encoding arginase (rocF).Results:  A rocF mutant unable to hydrolyze or consume l‐arginine regained these functions by complementation with the wild‐type rocF gene. Complemented strains also had restored arginase protein as determined by Western blot analysis. The complementation system could be successfully applied to multiple H. pylori strains. The intergenic region varied in length and sequence across 17 H. pylori strains, but the flanking‐3′ ends of the hp0203 and hp0204 coding regions were highly conserved. Inserting a cat cassette and wild‐type rocF into the intergenic region did not alter the ability of strain SS1 to colonize mice.Conclusions:  This complementation strategy should greatly facilitate genetic experiments in H. pylori.
Deficiency in OGG1 Protects against Inflammation and Mutagenic Effects Associated with H. pylori Infection in Mouse
Authors: Touati Eliette , Michel Valérie , Thiberge Jean‐Michel , Avé Patrick , Huerre Michel , Bourgade Franck , Klungland Arne , Labigne Agnès 
Published: September 2006

AbstractBackground:  Helicobacter pylori infection is associated with gastric cancer. Study with the Big Blue mouse model has reported a mutagenic effect associated with the H. pylori infection, as a result in part of oxidative DNA damage. The present work investigates the consequences of a deficiency in the OGG1 DNA glycosylase, responsible for the excision of 8‐oxo guanine, on the inflammatory and genotoxic host response to the infection.Materials and Methods:  Big Blue Ogg1–/– C57BL/6 mice were orally inoculated with H. pylori strain SS1 or vehicle only, and sacrificed after 1, 3, or 6 months. The serologic response, histologic lesions, mutant frequency, and spectra of mutations were assessed in the stomach and compared to what observed in the wild‐type (Wt) context.Results:  Inflammatory lesions induced in the gastric mucosa of H. pylori‐infected mice, corresponding to a moderate gastritis, were less severe in Ogg1–/– than in Wt Big Blue mice. Analysis of antimicrobial humoral immunity exhibited a lower IgG2a serum level (Th1 response) after 6 months of infection in Ogg1–/– than in the Wt mice. In these conditions, the H. pylori‐SS1 infection in the Ogg1–/– mice did not induce a mutagenic effect at the gastric epithelial cells level, either after 3 or 6 months.Conclusions:  The inactivation of the OGG1 DNA glycosylase in mouse leads to less severe inflammatory lesions and abolished the mutagenic effect at the gastric epithelial cells level, induced by the H. pylori infection. These data suggest for the OGG1deficiency a protective role against inflammation and genotoxicity associated to the H. pylori infection.
Monoclonal Gammopathy of Undetermined Significance and Russell Body Formation in Helicobacter pylori Gastritis
Authors: Wolkersdörfer Gernot W. , Haase Michael , Morgner Andrea , Baretton Gustavo , Miehlke Stephan 
Published: September 2006

AbstractBackground:  Infection by Helicobacter pylori has been linked to monoclonal gammopathy of undetermined significance (MGUS). MGUS is thought to develop due to chronic antigenic stimulation in people with a specific genetic predisposition.Methods and Results:  We describe a patient presenting with dyspepsia associated with H. pylori‐related erosive gastritis. Histopathologic findings revealed infiltration with plasma cells containing accumulated condensed intercisternal immunoglobulins, the so‐called ‘Russell bodies’. In addition, MGUS was present with total immunoglobulins within the normal range but a significantly decreased serum concentration of IgG subtype 3. Molecular analyses demonstrated IgH formation, T‐cell receptor γ rearrangement, and alterations within the IgHG3 gene sequence. Following H. pylori eradication, gastritis and dyspepsia gradually resolved but MGUS persisted for at least 22 months.Conclusions:  This is the first report to demonstrate that upon infection with H. pylori, an impaired secretory capacity of plasma cells due to specific molecular changes can present as Russell body gastritis. The molecular findings question a pathogenetic link between Russell bodies and H. pylori, but suggest genetic alterations in the immunoglobulin locus as the possible cause for both MGUS and Russell body gastritis.
Metabolic Aspects of Acid-Base Change
Authors: Lotspeich William D. 
Published: October 2006

The state of metabolic acidosis involves changes of a varied and subtle nature in other organs as well as in the kidney. This fact has been illustrated in metabolic studies with glutamine, a major substrate of the kidney and of various other organs.
In addition to the well-described increase in renal glutaminase enzymes, the hexose monophosphate-shunt enzymes also are much more active during metabolic acidosis; this phenomenon is limited to the kidney; its exact meaning remains speculative, but its possible relation to renal excretion of acid, lipogenesis, and gluconeogenesis during acidosis has been discussed.
In the kidney there are metabolic changes associated with ammonium chloride acidosis that affect the basic mechanisms of gene-directed growth. There is a renal regenerative process during this kind of acidosis that resembles in some respects the compensatory hypertrophy in the remaining kidney after unilateral nephrectomy, from which it also differs in important ways. Lastly, we must now regard the role of glutamine in renal metabolism as an affair that goes well beyond the specific needs of formation of ammonia during the normal and acidotic states. Glutamine enters the general metabolic mill of the kidney, its carbon skeleton is incorporated into all the major tissue components, and it is an important source material for gluconeogenesis in the kidney; all of these renal functions of glutamine are increased during metabolic acidosis.
Thus there is a fruitful field of exploration ahead, not only in the biochemical aspects of the renal response, but also in the metabolic interrelations among different organs during various types of acid-base change. This article, in concentrating on metabolic acidosis, gives only a glimpse of a broader picture to come.
Death as an Event: A Commentary on Robert Morison
Authors: Kass Leon R. 
Published: October 2006

1) We have no need to abandon either the concept of death as an event or the efforts to set forth reasonable criteria for determining that a man has indeed died.
2) We need to recover both an attitude that is more accepting of death and a greater concern for the human needs of the dying patient. But we should not contaminate these concerns with the interests of relatives, potential transplant recipients, or "society." To do so would be both wrong and dangerous.
3) We should pause to note some of the heavy costs of technological progress in medicine: the dehumanization of the end of life, both for those who die and for those who live on; and the befogging of the minds of intelligent and moral men with respect to the most important human matters.