Molecular mimicry by Helicobacter pylori CagA protein may be involved in the pathogenesis of H. pylori-associated chronic idiopathic thrombocytopenic purpura

The eradication of Helicobacter pylori often leads to platelet recovery in patients with chronic idiopathic thrombocytopenic purpura (cITP). Although this clinical observation suggests the involvement of H. pylori, little is known about the pathogenesis of cITP. We initially examined the effect of H. pylori eradication on platelet counts in 20 adult Japanese cITP patients. Then, using platelet eluates as the probe in immunoblot analyses, we examined the role of molecular mimicry in the pathogenesis of cITP. Helicobacter pylori infection was detected in 75% (15 of 20) of cITP patients. Eradication was achieved in 13 (87%) of the H. pylori-positive patients, seven (54%) of which showed increased platelet counts within the 4 months following treatment. Completely responsive patients also showed significant declines in platelet-associated immunoglobulin G (PAIgG) levels. Platelet eluates from 12 (nine H. pylori-positive and three H. pylori-negative) patients recognized H. pylori cytotoxin-associated gene A (CagA) protein, and in three completely responsive patients, levels of anti-CagA antibody in platelet eluates declined after eradication therapy. Cross-reactivity between PAIgG and H. pylori CagA protein suggests that molecular mimicry by CagA plays a key role in the pathogenesis of a subset of cITP patients.     

Effect of Helicobacter pylori eradication on platelet recovery in patients with chronic idiopathic thrombocytopenic purpura

BACKGROUND: A relationship between Helicobacter pylori infection and idiopathic thrombocytopenic purpura (ITP) has previously been reported. We determined the prevalence of H pylori infection in Japanese patients with chronic ITP and the effect of its eradication on platelet count. METHODS: The study population comprised 53 Japanese adults with chronic ITP and a platelet count of less than 100 x 10(3)/ micro L. A (13)C-urea breath test was performed to determine H pylori infection status. Those patients who were H pylori positive gave written informed consent and received eradication therapy. The effect of H pylori eradication on platelet count was evaluated up to 6 months after therapy. Clinical parameters were compared between responders to the therapy (increase in platelet count) and nonresponders, as well as between H pylori-positive and -negative patients. RESULTS: Of the 53 patients with chronic ITP in the study, 39 (74%) were H pylori positive. Of the 32 infected patients who received treatment, H pylori was successfully eradicated in 27 patients (84%). In 10 (37%) of these patients, this resulted in a favorable platelet response. A partial response was seen in 5 additional patients (19%). A significant (P<.001) increase in platelet count was demonstrated in patients in whom H pylori was successfully eradicated but not in patients who were unsuccessfully treated or in untreated patients. Current corticosteroid therapy was reported more often in nonresponders than in responders. CONCLUSION: Eradication of H pylori may prove effective in increasing platelet count in H pylori-positive patients with chronic ITP.     

Purification of Placenta-Eluted Gamma Globulins and Their Strong Effect against Graft-versus-Host Reactions In Vitro and In Vivo

A retrospective study was performed to determine the prevalence of Helicobacter pylori (H pylori) infection, the effect of H pylori eradication on platelet counts, and the characteristic clinical features of chronic immune or idiopathic thrombocytopenic purpura (ITP) with H pylori infection. H pylori infection was found in 300 patients, a group that was significantly older (P < .005) and had more cases of hyperplastic megakaryocytes in the bone marrow (P = .01) than patients without H pylori infection. H pylori eradication therapy was performed in 207 H pylori-positive ITP cases, and the platelet count response was observed in 63% of the successful eradication group and in 33% of the unsuccessful eradication group (P < .005). In the successful group, the complete remission and partial remission rates were 23% and 42%, respectively, 12 months after eradication. In the majority of responders, the platelet count response occurred 1 month after eradication therapy, and the increased platelet count continued without ITP treatment for more than 12 months. H pylori eradication therapy was effective even in refractory cases, which were unresponsive to splenectomy. In conclusion, H pylori infection was involved in most ITP patients older than 40 years in Japan, and eradication therapy should be the first line of treatment in H pylori-positive ITP patients.     

The long-term efficacy of Helicobacter pylori eradication therapy in patients with idiopathic thrombocytopenic purpura

BACKGROUND AND AIM: A beneficial effect of Helicobacter pylori (H. pylori) eradication in patients with H. pylori-positive idiopathic thrombocytopenic purpura (ITP) has been reported by several investigators; however, it was not clear whether the recovered platelet count after H. pylori eradication was maintained for a long period. METHOD: Thirty-eight ITP patients who were examined for H. pylori infection were assessed. H. pylori-positive patients received a standard antibiotic therapy for H. pylori eradication. We investigated the long-term effect of H. pylori eradication on platelet recovery in patients with H. pylori-positive ITP. RESULTS: Of the 38 ITP patients, 26 (68.4%) were positive for H. pylori. The response rate of platelet recovery was 56.5% (13/23 patients). Twelve patients showed complete response (CR) and one showed partial response (PR). The mean platelet counts 6 months after eradication significantly increased from 31 x 10(9)/L to 129 x 10(9)/L in 23 H. pylori-eradicated patients (P < 0.001). The median platelet counts of responders 1, 2, 3, and 4 years after eradication were 168 x 10(9)/L (n = 10), 193 x 10(9)/L (n = 9), 168 x 10(9)/L (n = 7), and 243 x 10(9)/L (n = 4) after a mean follow-up of 25.8 months. CONCLUSION: Eradication therapy for H. pylori-positive patients with ITP was effective and a favorable effect was maintained for long periods.     

Current status of treatment for patients with idiopathic thrombocytopenic purpura in the Hokkaido area (evaluation of Helicobacter pylori eradication)

Treatment guidelines for patients with idiopathic thrombocytopenic purpura (ITP) have been changed recently due to the clinical application of Helicobacter pylori (H. pylori) eradication but there has been no detailed multi-center analysis of the hematological effects of H. pylori eradication. The Clinical Hematology Forum consists of 11 large hematological departments and divisions in the Hokkaido area. We sent questionnaires to these 11 hematological departments and divisions in March 2003 to obtain information on current treatment strategies for patients with ITP and hematological results after the eradication of H. pylori. Questionnaires were returned by 9 (81.8%) of the 11 departments. Doctors in all hospitals had experience in diagnosis and treatment of H. pylori infection. Diagnostic examinations for H. pylori infection were performed in 54.3% of the registered cases. H. pylori infection was detected in 68.1% of the examined cases, and eradication treatment was performed in 87.7% of H. pylori-positive patients. H. pylori was eradicated in 52 (83.9%) of the 62 patients in whom the results of treatment could be evaluated. Among the patients whose platelet counts were less than 10.0 x 10(4)/microl, platelet recovery was observed in 48.8% of cases with successful eradication, a percentage similar to previously reported percentages in Japan. There was no prognostic factor to predict good responders before eradication treatment. Since the side effects of eradication treatment, including gastrointestinal symptoms and skin eruptions, were not serious, this method might become a front-line treatment for patients with ITP. Patient selection for eradication as an up-front treatment, analysis of the pathophysiology of platelet recovery after eradication and long-term effects should be investigated to make new treatment guidelines for newly diagnosed patients with ITP.     

Does Helicobater pylori initiate or perpetuate immune thrombocytopenic purpura?

To determine the prevalence of Helicobacter pylori (H pylori) infection in North American patients with immune thrombocytopenic purpura (ITP) and the effect of H pylori eradication on the platelet count, a prospective study was performed. Seventy-four patients aged 10 years and older (mean age of 41 years) with chronic ITP and a platelet count below 60 x 10(9)/L were enrolled. H pylori infection was found in 22% of patients by means of a breath test and could not be predicted by gastrointestinal symptoms. H pylori-positive patients (52.5 years of age) were older than H pylori-negative patients (38.5 years of age; P =.0035). Fifteen of the 16 H pylori-positive patients were treated and the bacteria was eradicated in 14 (93%). After 3 months, a significant response (platelet count > 50 x 10(9)/L and doubling the initial count) was observed in only one patient. After a median follow-up of 11.5 months, none of the 14 patients had responded. Ten H pylori-negative patients treated with the same regimen also did not increase their platelet counts. In conclusion, unlike several previous reports, this study does not implicate H pylori in the pathogenesis of ITP since the prevalence of H pylori infection was low and eradication of H pylori did not positively influence the course of the ITP.     

Helicobacter pylori eradication in the management of patients with idiopathic thrombocytopenic purpura

PURPOSE: To investigate the relation between Helicobacter pylori infection and the clinical features of idiopathic thrombocytopenic purpura (ITP), and to examine the effects of H. pylori eradication on platelet counts. METHODS: A(13)C urea breath test for H. pylori infection was performed in a cohort of 137 consecutive patients with ITP. Patients who tested positive received standard eradication therapy if their platelet count was <50 x 10(9)/L or if they had symptoms of dyspepsia. RESULTS: H. pylori infection was detected in 64 patients (47%), and was not associated with dyspepsia or other clinical or laboratory features. Eradication therapy was successfully administered to 52 patients. Platelet responses were observed in 17 (33%) of these patients, which lasted for more than 1 year in 11 patients. Duration of ITP was shorter among responders than nonresponders. Only one response was observed among patients with severe thrombocytopenia (platelet count <30 x 10(9)/L). CONCLUSION: The prevalence of H. pylori infection in patients with ITP is similar to that found in the general population. Infection is not associated with distinctive features of the disease. H. pylori eradication may improve the platelet counts in adults in whom the ITP is of recent onset and in those with less severe degrees of thrombocytopenia, but was not effective in patients with chronic severe ITP.     

Autoimmune thrombocytopenic Purpura and Helicobacter pylori infection

BACKGROUND: The mechanisms triggering the production of platelet autoantibodies in autoimmune thrombocytopenic purpura (AITP) are poorly understood. Recently, marked improvements in platelet counts have been reported in patients with AITP and concurrent Helicobacter pylori infection after eradication of H pylori by a standard antibiotic regimen. We looked for an association between H pylori infection and AITP in adults. METHODS: Fifty-one adults of white French origin, negative for human immunodeficiency virus (mean +/- SD age, 40 +/- 19.8 years), with AITP and a platelet count of less than 50 x 10(3)/microL at onset were included. Thirty-five consecutive nonthrombocytopenic patients (mean +/- SD age, 43 +/- 22 years) of the same origin and with unknown H pylori status served as control subjects. Antibodies against H pylori were detected by means of an agglutination method in both patients and control subjects. Sex ratio, mean age, hemorrhagic manifestations, response to corticosteroid therapy, and final outcome were compared in H pylori-negative and H pylori-positive patients with AITP. To test for a possible molecular mimicry mechanism, we also used an immunoblot assay to look for specific H pylori antibodies in platelet eluates from 3 H pylori-positive patients with AITP. RESULTS: Seroprevalence of H pylori in patients with AITP (15 [29%]) was not significatively different from that in control subjects (10 [29%]). The H pylori-positive and H pylori-negative patients with AITP did not differ in main characteristics at AITP onset, response rate to corticosteroids, and final outcome. None of the 3 patients investigated had H pylori antibodies in platelet eluates. CONCLUSION: Although the role of H pylori in a subgroup of patients with AITP cannot be excluded, we found no evidence of an association between H pylori infection and AITP.     

<Emphasis Type="Italic">Helicobacter pylori</Emphasis> Infection and Idiopathic Thrombocytopenic Purpura

A treatment strategy for idiopathic thrombocytopenic purpura (ITP) is considered with the aim of cure or management of the bleeding tendency. In 1998, Gasbarrini et al reported a high prevalence of Helicobacter pylori infection in patients with ITP and showed that platelet recovery occurred after eradication therapy in most cases. Since then, many studies were performed to evaluate eradication therapy. This article discusses the incidence of H pylori infection in ITP, characteristic clinical features in H pylori-positive ITP, the effectiveness of eradication on platelet count increase, and the mechanisms of development of ITP by H pylori infection. Overall, there was a positive association between H pylori infection and ITP, and eradication of bacterium was accompanied by a significant increase in platelet counts in more than 50% of H pylori-positive ITP cases. These findings suggest that H pylori infection is involved in the mechanisms of thrombocytopenia in most cases of ITP in middle-aged and older patients. This approach could be beneficial to some ITP patients, but there were some uncertainties raised. To confirm the effectiveness of eradication therapy in H pylori-positive ITP, prospective studies conducted in several countries with a new treatment protocol are required, with a large number of ITP cases and longer follow-up.     

Clonally Expanded T-Cells in the Peripheral Blood of Patients with Idiopathic Thrombocytopenic Purpura and Helicobacter pylori Infection

Eradication of Helicobacter pylori leads to platelet recovery in some patients with idiopathic thrombocytopenic purpura (ITP). Therefore, the pathogenesis of a subgroup of ITP is probably associated with H pylori infection (H pylori-related ITP). If H pylori-related ITP is a definite subgroup of ITP, specific oligoclonal T-cells might accumulate in the peripheral blood (PB). To address this issue, we performed single-strand conformation polymorphism analysis of complementarity-determining region 3 (CDR3) of the T-cell receptor beta-chain genes of PB T-cells. Fourteen ITP patients with H pylori infection and 12 ageadjusted healthy volunteers were studied. Of the 14 patients, 8 patients (responders) exhibited a platelet response after successful H pylori eradication therapy, but 6 patients (nonresponders) did not. Vbeta5.2, Vbeta15, and Vbeta19 gene usage by clonally expanded T-cells in PB obtained before H pylori eradication therapy was significantly higher in responders than in nonresponders or healthy volunteers (Vbeta5.2, P = .023; Vbeta15, P = .004; Vbeta19, P = .036). Furthermore, an abrogation of clonally expanded T-cells was observed after therapy in some responders. These findings suggest that specific T-cell clones accumulate in H pylori-related ITP and that such clones may be associated with immune-mediated destruction of platelets.     

Helicobacter pylori eradication can induce platelet recovery in chronic idiopathic thrombocytopenic purpura

We prospectively investigated the prevalence of Helicobacter pylori (H. pylori) infection in a cohort of 54 adult Serbian patients with chronic idiopathic thrombocytopenic purpura (ITP), and examined the effects of its eradication on their platelet counts. H. pylori infection was diagnosed in 39/54 (72.2%) patients, using the 14C-urea breath test; and was significantly higher than in the healthy Serbian population (55% P < 0.05). H. pylori-positive patients were significantly older than H. pylori-negative patients (P = 0.006), though there were no significant differences regarding gender, disease duration, mean platelet counts, previous therapies and spleen status between H. pylori-positive and H. pylori-negative patients. Successful eradication was confirmed in 23/30 (77%) treated patients. Stable platelet recovery was registered in 6/23 eradicated patients (26.1%) and maintained for 18 months. Complete and partial remissions were achieved in two and four patients, respectively, including one highly refractory patient. A significant mean platelet recovery was seen 6 months after successful H. pylori eradication in the group of 23 patients (P < 0.05). No platelet recovery was registered in either H. pylori-negative (n = 15), untreated H. pylori-positive patients (n = 9) or H. pylori-positive non-eradicated patients (n = 7). Even though the pathogenetic mechanisms of H. pylori-induced thrombocytopenia remain obscure, the results of this small prospective study support the use of H. pylori eradication as an effective non-immunosuppressive treatment for chronic ITP.     

Helicobacter pylori impairs iron absorption in infected individuals

BACKGROUND: Infection with Helicobacter pylori is recognised as a major risk factor for chronic gastritis, peptic ulcer disease and gastric cancer. The association between H. pylori infection and iron deficiency anaemia has been established. Multiple mechanisms have been advocated to explain the relationship between H. pylori and iron status and their association might reduce iron deposit. AIM: Aim of this study was to investigate whether H. pylori infection affects iron absorption. METHODS: The study was designed on a prospective basis. Fifty-five subjects underwent upper gastrointestinal endoscopy and biopsy to investigate the presence of H. pylori and, when this was positive, also search of serum anti-CagA was performed. Tests included an oral iron absorption test with the administration of 1 mg/kg of Fe2+. Iron levels were measured before and 2 h after iron administration (delta iron). H. pylori-positive subjects were administered antibiotic therapy for 1 week and, 2 months later, the oral iron absorption test was repeated and urea-breath test was first performed. RESULTS: H. pylori-positive subjects had lower serum level of ferritin and lower delta iron compared to H. pylori-negative subjects. That difference is significant in anaemic women and is independent of the presence of serum anti-CagA antibodies. After H. pylori eradication iron absorption test was similar to those of non-infected subjects. CONCLUSION: H. pylori infection impairs iron uptake. That mechanism, together with others, may contribute to the depletion of iron in infected patients.     

Detection of H. pylori infection by ELISA and Western blot techniques and evaluation of anti CagA seropositivity in adult Turkish dyspeptic patients

INTRODUCTIONH pylori colonizes in the mucosa of the human stomach where it establishes a long-term infection associated with acute or chronic gastric inflammation, which may progress to peptic ulcer disease, atrophic gastritis with intestinal metaplasia, …     

Evaluation of Helicobacter pylori stool antigen test before and after eradication therapy

BACKGROUND AND AIM: The Helicobacter pylori stool antigen (HpSA) test is useful for initial diagnosis of H. pylori infection, but there is disagreement regarding its diagnostic accuracy after eradication therapy. The aim of the present study was to evaluate the diagnostic accuracy of the HpSA test before and after eradication therapy. METHODS: One hundred and thirty-six patients underwent upper gastrointestinal endoscopy with biopsies for the diagnosis of H. pylori infection using culture, histology and the rapid urease test. Fifty-four H. pylori-positive patients were treated with 1-week triple therapy. Six to 10 weeks after the end of therapy, the patients underwent re-endoscopy and received the same biopsy-based methods. In addition, the 13C-urea breath test was performed. The HpSA test was performed before and 6-10 weeks after the end of therapy. In 23 patients, the HpSA test was also performed at the end of therapy. RESULTS: Before therapy, the sensitivity and specificity of the HpSA test was 98.3% (95% confidence interval (CI): 95.9-100%) and 95.0% (95% CI: 75.1-99.9%), respectively. At the end of therapy, the HpSA tests were all negative both for eradication and non-eradication patients. The sensitivity and specificity of the HpSA test after eradication therapy were 90% (95% CI: 55.5-99.7%) and 97.7% (95% CI: 93.3-100%), respectively. CONCLUSIONS: The HpSA test is a useful method for the diagnosis of H. pylori infection before and after eradication therapy.     

Helicobacter pylori infection and chronic immune thrombocytopenic purpura: long-term results of bacterium eradication and association with bacterium virulence profiles

Eradication of Helicobacter pylori may lead to improvement of chronic immune thrombocytopenic purpura (ITP), although its efficacy over time is uncertain. We report the results of H pylori screening and eradication in 75 consecutive adult patients with ITP. We also used molecular methods to investigate lymphocyte clonality and H pylori genotypes in the gastric biopsies from 10 H pylori-positive patients with ITP and 19 H pylori-positive patients without ITP with chronic gastritis. Active H pylori infection was documented in 38 (51%) patients and successfully eradicated in 34 (89%) patients. After a median follow-up of 60 months, a persistent platelet response in 23 (68%) of patients with eradicated infection was observed; 1 relapse occurred. No differences in mucosal B- or T-cell clonalities were observed between patients with ITP and control participants. Of note, the frequency of the H pylori cagA gene (P = .02) and the frequency of concomitant H pylori cagA, vacAs1, and iceA genes (triple-positive strains; P = .015) resulted statistically higher in patients with ITP than in control participants. All asymptomatic H pylori-positive patients with ITP were suffering from chronic gastritis. Our data suggest a sustained platelet recovery in a proportion of patients with ITP by H pylori eradication alone. Overrepresentation of specific H pylori genotypes in ITP suggests a possible role for bacterium-related factors in the disease pathogenesis.     

Helicobacter pylori-associated chronic idiopathic thrombocytopenic purpura and low molecular weight H. pylori proteins

We examined the association between Helicobacter pylori infection and chronic idiopathic thrombocytopenic purpura (cITP) to clarify the development of H. pylori-associated cITP. cITP patients were classified into 3 different groups: Hp-negative (HP-N); Hp-positive, completely or partially responsive to treatment (CR); and Hp-positive and unresponsive to treatment (NR). Reactivity of antibodies to H. pylori before and after eradication was examined by immunoblotting. We used immunoblotting with immunoprecipitation to establish whether platelets form complexes with H. pylori proteins and if these complexes react with patients' sera. CR group showed large (>50 kDa) and low molecular weight protein bands, especially of 36, 27 and 17-kDa. These low molecular weight bands were detected significantly more in the CR group compared to other groups. When healthy human platelets were incubated with H. pylori lysate, they aggregated with the lysate, indicating that complexes were formed between the platelets and the lysate. The complexes immunoprecipitated with anti-human thrombocyte antibodies, and showed a 17 kDa band in the CR, but not in other groups. At least 3 low molecular weight proteins of H. pylori were involved in H. pylori-associated cITP. Immunocomplexes consisting of platelets, low molecular weight proteins of H. pylori and anti-H. pylori antibodies may represent an extra mechanism in development of H. pylori- associated cITP.     

Successful platelet recovery after the second eradication of Helicobacter pylori with metronidazole in two patients with chronic idiopathic thrombocytopenic purpura

There are many reports on the efficacy of Helicobacter pylori (H. pylori) eradication therapy in patients with H. pylori-positive chronic idiopathic thrombocytopenic purpura (ITP). We administrated metronidazole (MNZ), amoxicillin (AMPC), and a proton-pump inhibitor (PPI) as the second eradication therapy for two patients who failed in the first eradication therapy consisting of PPI, AMPC, and clarithromycin (CAM). Successful eradication and the rapid recovery of platelet counts within one month were achieved in both patients. Recently, H. pylori eradication is considered as the first-line therapy for H. pylori-positive chronic ITP patients. In Japan, the PPI + AMPC + CAM regimen is recognized as the standard eradication therapy for H. pylori. However, the PPI + AMPC + MNZ regimen is also useful for eradication and should be tried as the re-treatment regimen after failure of the first-line CAM-containing regimen.     

Anti-CagA and anti-VacA antibodies in Helicobacter pylori-infected patients with and without peptic ulcer disease in Serbia and Montenegro

BACKGROUND: The expression of two Helicobacter pylori proteins, CagA and VacA, is associated with more severe pathogenesis and clinical outcomes of the infection. However, this association varies among geographical regions and ethnic groups. We therefore evaluated CagA and VacA seroprevalence in H. pylori-positive dyspeptic patients in Serbia and Montenegro. METHODS: In 173 consecutive dyspeptic patients referred to endoscopy (67M, mean age 49 +/- 15, 76 smokers), immunoblot assay was used to detect serum antibodies against CagA and VacA. Presence of H. pylori infection was assessed using a rapid urease test (RUT), routine histology and serology (anti-IgG ELISA). Duodenal ulcer (DU) was diagnosed in 28, gastric ulcer (GU) in 3 and non-ulcer dyspepsia (NUD) in the remaining 142 patients. RESULTS: 129 (74.6%) patients were H. pylori-positive, 27 (96.4%) with DU, 3 (100%) with GU and 99 (69.7%) with NUD (P < 0.01); 121 (93.8%) patients carried anti-CagA antibodies and there was no difference between the DU and NUD groups. VacA antibodies were detected in sera of 50 (38.75%) and were more prevalent in patients with DU compared to the NUD group (P < 0.05). CONCLUSIONS: In Serbia and Montenegro there is high seroprevalence of CagA-positive H. pylori strains in dyspeptic patients with and without peptic ulcer, while VacA-positive strains are more closely related to peptic ulcer disease.     

Acquisition of Helicobacter pylori infection and reinfection after its eradication are uncommon in Indian adults.

BACKGROUND: Eradication of Helicobacter pylori infection is known to decrease the recurrence rate of peptic ulcer disease. Data from India on the acquisition rate of H. pylori infection and reinfection after eradication are scant. AIM: To study the rates of acquisition of H. pylori infection and of reinfection after eradication in Indian adult patients. METHODS: We evaluated 116 consecutive patients with dyspepsia undergoing endoscopy. Sixty-four of them were H. pylori-positive on gastric antral biopsy (rapid urease test and histology). Patients diagnosed to have H. pylori infection were treated with a four-drug regimen (omeprazole, bismuth subcitrate, tetracycline, furazolidine) for 2 weeks; those failing H. pylori eradication were treated with a second regimen (lansoprazole, amoxycillin, secnidazole) for one week. Patients who were H. pylori-negative to begin with and those who had successful H. pylori eradication were followed up clinically and endoscopically every 3 months for a median of one year. RESULTS: Ninety-six patients (50 H. pylori-positive) were available for study; the other 20 were lost to follow up after the first endoscopy. Fifty of the 96 (52%) were H. pylori-positive; four of these 50 patients did not follow up after first treatment. The eradication rate with the four-drug regimen was 89.1% (41/46). Four of the 5 non-responders eradicated H. pylori with the second regimen. At the end of median one year follow-up (range 9-15 months), one of the 45 patients (2.4%) who eradicated the organism developed reinfection; none of the 46 patients who were initially H. pylori-negative acquired new infection. CONCLUSIONS: The risk of reinfection after eradication is low in Indian subjects at the end of one year. The rate of acquisition of new infection is also low in the adult population.     

Cytokine profile of patients with chronic immune thrombocytopenia affects platelet count recovery after Helicobacter pylori eradication

Helicobacter pylori eradication induces platelet recovery in a subgroup of patients with chronic immune thrombocytopenia (cITP), but the mechanisms involved are still not understood. We aimed to evaluate the effect of H. pylori eradication on platelet response and to identify the associated serum cytokine profile in 95 patients with cITP. Serum cytokine concentrations were determined by enzyme‐linked immunosorbent assay prior to and 6 months after H. pylori eradication. Remission of cITP was observed in 17 (28·8%) of 59 patients in whom the bacterium was eradicated. Six months after treatment, a significant reduction in the concentrations of T‐helper (Th) 1 and Th17 cells and an increase in T regulatory (Treg) and Th2‐cell commitment cytokines were observed in patients who recovered, but not in those whose platelet count did not recover. Patients who had a platelet response to eradication of the bacteria had higher pre‐treatment serum levels of γ‐interferon (IFNG, IFN‐γ), transforming growth factor‐β (TGFB1, TGF‐β) and interleukin 17 (IL17A, IL‐17) than patients who did not respond, but only higher pre‐treatment TGFB1 levels was independently associated with platelet response. In conclusion, amelioration of cITP after eradication of H. pylori was linked to a more efficient suppression of Th1 and Th17 response and a more pronounced Treg cell response.