Helicobacter pylori infection in patients with autoimmune thrombocytopenic purpura

AIM:To compare the prevalence of Helicobacter pylori(Hpylon)infection in autoimmune thrombocytopenic purpura(AITP)patients with that of nonthrombocytopenic controls,and to evaluate the efficacy of the treatment in H pylori( )and H pylor(-)AITP patients.METHODS:The prevalence of gastric H pylori infection in38 adult AITP patients(29 female and 9 male;median age27 years;range 18-39 years)who consecutively admittedto our clinic was investagated.RESULTS:H pylori infection was found in 26 of 38 AITPpatients(68.5%).H pylori infection was found in 15 of 23control subjects(65.2%).The difference in H pylori infectionbetween the 2 groups was not significant.Thrombocytecount of H pylori-positive AITP patients was significantlylower than that of H pylori-negative AITP patients(P<0.05).Thrombocyte recovery of H pylori-positive group was lessthan that of H pylori-negative group(P<0.05).CONCLUSION:H pylori infection should be considerecd inthe treatment of AITP patients with H pylori infection.     

Does Helicobacter pylori infection play a role in lung cancer?

BACKGROUND: Helicobacter pylori infection is a world-wide common disease and leads to many gastrointestinal and respiratory illnesses. It is suggested that one of these respiratory illnesses is lung cancer. METHODS: Forty-three patients with non-small cell lung cancer and 28 control subjects have been included to this study. H. pylori status of the patients and controls was determined by immunoblot for the detection of IgG (RIDA Blot Helicobacter). All subjects were examined to evaluate the presence of VacA and CagA gene. RESULTS: Seropositivity of anti H. pylori IgG was significantly higher in cancer patients than in control groups, 40 (93%) and 12 (42%), respectively (P<0.01). Although both VacA and CagA seropositivity was high in lung cancer patients, only VacA positivity was statistically significant when compared with control subjects, 35 (81%) and 11 (42%), respectively (P<0.05). CONCLUSION: H. pylori infection may be associated with development of lung cancer.     

Does infection play a role in the pathogenesis of pulmonary vasculitis?

The pulmonary vasculitides are a heterogeneous group of systemic inflammatory diseases of unknown etiology with potential for significant morbidity. The syndromes with particular predilection for the respiratory tract are Wegener's granulomatosis, microscopic polyangiitis, and Churg-Strauss syndrome. The discovery of antineutrophil cytoplasmic antibodies (ANCA) in these disorders has facilitated their diagnosis and contributed to the understanding of their pathogenesis. Clinical studies and some animal models suggest a disease-modifying role for antimicrobial therapy in ANCA-associated vasculitis. Nasal colonization with Staphylococcal aureus is an independent risk factor for relapse of Wegener's granulomatosis. This evidence suggests infectious pathogens as potential triggers of a cascade of events that result in vascular inflammation. Multiple laboratory studies have contributed to a coherent and plausible theory about the pathogenesis of ANCA-associated vasculitis in which infection plays a critical role. In susceptible individuals immune tolerance may break down and ANCA production resulting from molecular mimicry ensues. In addition, bacterial superantigens may serve as potent stimulators of the immune system. In this context, ANCA directed against proteinase 3 or myeloperoxidase may interact with their target antigens expressed on the surface of activated neutrophils, leading to an enhanced and perpetuated inflammation of vessels. Despite significant advances, the precise connection between infections and pulmonary vasculitis remains poorly understood, and further studies into the pathogenesis of these diseases are needed.     

Does cytomegalovirus play a causative role in the development of various inflammatory diseases and cancer?

Human cytomegalovirus (HCMV) is a herpes virus that infects and is carried by 70-100% of the world's population. During its evolution, this virus has developed mechanisms that allow it to survive in an immunocompetent host. For many years, HCMV was not considered to be a major human pathogen, as it appeared to cause only rare cases of HCMV inclusion disease in neonates. However, HCMV is poorly adapted for survival in the immunosuppressed host and has emerged as an important human pathogen in AIDS patients and in patients undergoing immunosuppressive therapy following organ or bone marrow transplantation. HCMV-mediated disease in such patients has highlighted the possible role of this virus in the development of other diseases, in particular inflammatory diseases such as vascular diseases, autoimmune diseases and, more recently, with certain forms of cancers. Current research is focused on determining whether HCMV plays a causative role in these diseases or is merely an epiphenomenon of inflammation. Inflammation plays a central role in the pathogenesis of HCMV. This virus has developed a number of mechanisms that enable it to hide from the cells of the immune system and, at the same time, reactivation of a latent infection requires immune activation. Numerous products of the HCMV genome are devoted to control central functions of the innate and adaptive immune responses. By influencing the regulation of various cellular processes including the cell cycle, apoptosis and migration as well as tumour invasiveness and angiogenesis, HCMV may participate in disease development. Thus, the various drugs now available for treatment of HCMV disease (e.g. ganciclovir, acyclovir and foscarnet), may also prove to be useful in the treatment of other, more widespread diseases.     

Sj?gren's syndrome in relation to other autoimmune diseases.

Autoimmune diseases can be divided into primary autoimmune diseases, in which the immune system is over-reactive, leading to an oligoclonal B cell stimulation, and secondary autoimmune diseases, in which the immune system is completely normal but some autoantigens are slightly altered, and are thus considered to be foreign. Sj?gren's syndrome probably has characteristics of both types of autoimmune disease. The primary autoimmune diseases can be divided into organ-specific autoimmune diseases like thyroiditis, gastritis and adrenalitis, and generalised autoimmune diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis. Sj?gren's syndrome has characteristics of both types of primary autoimmune disease, and therefore occupies a central position among the other autoimmune diseases. The focal position of the disease in the present issue of The Netherlands Journal of Medicine is because of the symposium organized for the occasion of the fifth anniversary of the "Dutch Association of Patients with Sj?gren's Syndrome", of which this issue is the report.     

Does Helicobacter pylori infection play a role in iron deficiency anemia? A meta-analysis

AIM:To perform a meta-analysis of observational studies and randomized controlled trials(RCTs)on the association between Helicobacter pylori(H.pylori)and iron deficiency anemia(IDA).METHODS:A defined search strategy was used to search Medline,Embase,the Cochrane Library,Clinical Trials,Cochrane Central Register of Controlled Trials,Premedline and Healthstar.Odds ratio(OR)was used to evaluate observational epidemiology studies,and weighted mean difference(WMD)was used to demonstrate the difference between co...     

Does the microbiome play a causal role in spondyloarthritis?

The purpose of this study is to review the potential causal role of the microbiome in the pathogenesis of spondyloarthritis. The method used for the study is literature review. The microbiome plays a major role in educating the immune response. The microbiome is strongly implicated in inflammatory bowel disease which has clinical and genetic overlap with spondyloarthritis. The microbiome also plays a causal role in bowel and joint disease in HLA B27/human beta 2 microglobulin transgenic rats. The mechanism(s) by which HLA B27 could influence the microbiome is unknown but theories include an immune response gene selectivity, an effect on dendritic cell function, or a mucosal immunodeficiency. Bacteria are strongly implicated in the pathogenesis of spondyloarthritis. Studies to understand how HLA B27 affects bacterial ecosystems should be encouraged.     

Does the GH-IGF axis play a role in cancer pathogenesis?

Recent case-controlled studies have found increases in the serum levels of insulin-like growth factor-I (IGF-I) in subjects who had, or who eventually developed, prostate or premenopausal breast cancers. Since growth hormone (GH) increases IGF-I levels, concern has been raised regarding its potential role as a cancer initiation factor. The epidemiological studies, which indicate an association between serum IGF-I levels and cancer risk, have not established causality. In fact, several alternative explanations for the elevated serum IGF-I levels in cancer patients may be proposed based on human and animal models. First, an effect of IGF-I causing symptomatic benign tissue hyperplasia may result in an ascertainment bias leading to an initiation of procedures resulting in the diagnosis of asymptomatic cancers. Second, elevated serum IGF-I in cancer patients may originate within the tumor (as suggested by some animal studies). Thirdly, serum IGF-I may actually be a surrogate marker of tissue IGF-I levels or of nutritional factors, which are not under GH control and may be involved in cancer initiation. The role of GH in cancer initiation is further negated by the fact that in acromegaly, the incidence of cancer, other than possibly colonic neoplasia does not appear to be significantly increased. Furthermore, GH transgenic mice, with high IGF-I levels, do not develop breast, prostate, or colonic malignancies. It is known that IGFBP-3 can inhibit IGF action on cancer cells in vitro and also can induce apoptosis via an IGF-independent mechanism. Importantly, in addition to increasing IGF-I levels, GH also increases the serum levels of IGFBP-3 and serum IGFBP-3 levels have been shown to be negatively correlated with the risk of cancer in the above mentioned epidemiological studies and in a similar study on colon cancer. These studies suggest that cancer risk is increased in individuals in whom both high IGF-I levels and low IGFBP-3 levels are present. In subjects treated with GH, IGF-I and IGFBP-3 levels both rise together and are not within the elevated cancer-risk range, based on published studies. Long-term studies are needed to assess the potential risks, including the long-term cancer risk associated with GH therapy. These should take into account several factors, including the duration of exposure, the risk magnitude associated with the degree of serum IGF-I elevation, and the adjusted risk based on a concomitant increase in IGFBP-3 levels. Since GH treated patients often have sub-normal IGF-I serum levels, which normalize on therapy, one might predict that their cancer risk on GH therapy should not increase above the normal population. Until further research in the area dictates otherwise, on-going cancer surveillance and routine monitoring of serum IGF-I and IGFBP-3 levels in GH-recipients should be the standard of care. At present, the data that are available do not warrant a change in our current management of approved indications for GH therapy.     

Does growth hormone play a role in chronic heart failure?

Experimental and clinical studies have recently demonstrated that the growth hormone-insulin-like growth factor-I (GH-IGF-I) system is involved in the regulation of cardiac structure and function. Patients with acromegaly have an increased propensity of developing cardiovascular complications, such as ventricular hypertrophy with interstitial fibrosis. Conversely, patients with GH deficiency can exhibit ventricular dysfunction, increased vascular thickness, and an increased number of atheromatous plaques. In both groups of patients these abnormalities may be partially reverted by normalizing GH-IGF-I levels. In experimental or human chronic heart failure (CHF), GH administration increases ventricular mass and cardiac performance and reduces pulmonary vascular resistance. The mechanism by which this occurs is still unclear, but seems to involve calcium channels and non-endothelium-mediated vasodilatation. Randomized trials studying CHF patients contradict these results, highlighting that, in patients with heart failure, the response to GH therapy appears to be variable, and is probably influenced either by acquired GH resistance or by baseline levels of hormones. Due to the small number of patients examined to date, larger, randomized, controlled studies are needed.     

Depression and survival in chronic heart failure: Does gender play a role?

BACKGROUND: Data regarding the influence of depression on outcome in chronic heart failure are conflicting and neglect possible gender differences. AIMS: To investigate prevalence and prognostic importance of depression in a cohort of patients with symptomatic heart failure and to compare findings in males and females. METHODS: Depression was measured at study entry using a self-reported 9-item Patient Health Questionnaire (PHQ-9) in 231 consecutive outpatients. The median follow-up time was 986 (IQR=664-1120) days. RESULTS: The prevalence of suspected major depression was 13% (minor depression, 17%) and was not different between the sexes. Major (but not minor) depression was associated with an increased mortality risk (hazard ratio [HR]=3.3, 95% confidence interval=1.8-6.1, p<0.001). This relationship remained significant after adjustment for other prognostically relevant factors as age, sex, heart failure aetiology, degree and type of left ventricular dysfunction, and New York Heart Association functional class. However, testing the effect of the interaction between gender and depression failed to reach significance (p=0.37). CONCLUSION: Our data confirm a high prevalence of depression in chronic heart failure. Further, they prove an independent prognostic impact of major, but not minor, depression. Possible gender differences regarding the prognostic impact of depression require further investigation in a larger patient cohort.     

Can thrombelastography be a new tool to assess bleeding risk in patients with idiopathic thrombocytopenic purpura?

Thrombelastography (TEG) analyses the status of blood coagulation including abnormalities associated with low platelet count. The aim of this study was to investigate the changes in TEG parameters in idiopathic thrombocytopenic purpura (ITP) patients. Thirty nine patients with ITP (platelet count?相似文献