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Whether Helicobacter pylori infection alters the risk of ulcer disease in patients receiving nonsteroidal anti‐inflammatory drugs (NSAIDs) or low‐dose aspirin is one of the most controversial topics in peptic ulcer research. This is an important management issue, particularly in countries where peptic ulcer disease is common and the prevalence of H. pylori infection is high. Current evidence shows that H. pylori infection increases the ulcer risk associated with NSAIDs or low‐dose aspirin. Eradication of H. pylori reduces the subsequent risk of endoscopic and complicated ulcers in patients who are about to start long‐term NSAIDs. Among patients with H. pylori infection and a history of ulcer bleeding who continue to use low‐dose aspirin, 1 week of eradication therapy prevents recurrent ulcer bleeding. Failure of eradication and concomitant use of NSAIDs, however, account for most cases of recurrent bleeding with low‐dose aspirin. The apparent protective effect of H. pylori in long‐term NSAIDs users reported in some studies was actually the weeding out of susceptible patients who were intolerant to NSAIDs. There is no convincing evidence that eradication of H. pylori has any clinically important adverse effect on the healing and prevention of ulcers in NSAIDs users.  相似文献   
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我非常高兴向大家推荐这份发展中国家幽门螺杆菌(H.priori)临床指南。该指南的编译是由数位在该领域具有丰富临床经验的世界知名专家共同完成的。  相似文献   
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Background  

Pneumocystis jiroveci pneumonia (PCP) is an important opportunistic infection among immunosuppressed patients, especially in those infected with human immunodeficiency virus (HIV). The clinical presentation of PCP in immunosuppressed patients have been well-reported in the literature. However, the clinical importance of PCP manifesting in the setting of an immunorestitution disease (IRD), defined as an acute symptomatic or paradoxical deterioration of a (presumably) preexisting infection, which is temporally related to the recovery of the immune system and is due to immunopathological damage associated with the reversal of immunosuppressive processes, has received relatively little attention until recently.  相似文献   
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Resting neutrophils may be "primed" to augmented effector function, eg, superoxide (O2-) production in the respiratory burst, upon a second stimulation with a variety of soluble agonists including formylated methionyl-leucyl-phenylalanine (FMLP) and phorbol myristate acetate (PMA). At priming concentrations of FMLP (5 x 10(-9) mol/L) that did not initiate O2- generation, two metabolic activities were noted: (1) approximately a threefold increase in the baseline intracellular calcium (Ca++i) level, that was not dependent on extracellular Ca++, and (2) a rapid rise in intracellular pH that was blocked by 5-(N,N- dimethyl) amiloride (DA), that had no effect on the Ca++i response to priming. Furthermore, there were no significant increases in inositol metabolites in cells primed and stimulated with FMLP compared with cells receiving the stimulating dose of FMLP alone and pretreatment with pertussis toxin (PT) (before the addition of the priming -5 x 10(- 9) mol/L dose of FMLP), whereas abolishing the response to FMLP during the second stage of stimulation, had (1) no effect on FMLP-primed cells subsequently stimulated with PMA, and (2) only partially ablated the rise in Ca++i initiated with FMLP. That FMLP priming involved distinctive processes to those of the well characterized FMLP-coupled Ca++-dependent activation cascade was shown by the full priming effect attained in a Ca++-free buffer, which did not sustain an O2- response to a second-stage FMLP stimulation, but sustained a primed response to PMA. These data demonstrate that FMLP primes human neutrophils by a Ca++-independent and PT-insensitive pathway, offering a functional model for studying heterogeneous FMLP receptor-coupled reactions.  相似文献   
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The prevalence of 3 mycoplasmas (Mycoplasma hominis, Ureaplasma urealyticum and Mycoplasma genitalium) was determined in a cohort of women with or without bacterial vaginosis (BV) and in their respective male partners. Heterosexual women with or without BV and their male partners were recruited and genital sampling for these microorganisms was performed. Seventeen women with BV and 21 women with normal flora, and their respective male partners, were recruited. M. hominis was present in 9 (53%) of 17 women with BV compared with none of 21 women without BV (P=0.0001). Of the 17 male partners of women with BV, 8 (47%) had M. hominis compared to 5 (24%) of 21 male partners of women without BV (not significant [n/s]). U. urealyticum was detected in 11 (65%) of 17 women with BV in comparison with 10 (48%) of 21 women without BV (n/s). U. urealyticum was present in 4 (24%) of 17 male partners of women with BV compared to 6 (29%) of 21 male partners of women without BV (n/s). M. genitalium was not detected in any of 15 women with BV and in only 2 (12%) of 17 women without BV (n/s). M. genitalium was present in 4 (25%) male partners of 16 women with BV in comparison with 3 (16%) male partners of 19 women without BV (n/s). Thus, M. hominis was the only mycoplasma detected significantly more often in women with, rather than in those without, BV. None of the mycoplasmas was found significantly more often in male partners of women with, rather than those without, BV. Overall, M. genitalium behaved somewhat similar to Chlamydia trachomatis. It was the least commonly occurring mycoplasma, a reflection perhaps of the relatively low incidence of partner change in this study population.  相似文献   
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