Incidence and Treatment Outcomes of Helicobacter pylori Infection in HIV-infected Patients

 

George PSEVDOS, Cristina BATOG, Victoria SHARP

 

George PSEVDOS, Cristina BATOG, Department of Infectious Diseases, St Lukes Roosevelt Medical Center, an affiliate of Columbia University College of Physicians and Surgeons, New York, NY, 10019, the United States

George PSEVDOS, Cristina BATOG, Victoria SHARP, Center for Comprehensive Care, New York, NY 10019, the United States

Correspondence to: George PSEVDOS, Department of Infectious Diseases, St Lukes Roosevelt Medical Center, an affiliate of Columbia University College of Physicians and Surgeons, New York, NY, 10019, the United States. GPsevdos@chpnet.org

Telephone: +01-212-523-6500         Fax: +01-212-523-7182

Received: October 19, 2012               Revised: January 9, 2013

Accepted: January 12, 2013

Published online: April 21, 2013

 

 

ABSTRACT

Helicobacter pylori is an established causative agent of peptic ulcer disease throughout the world. There is paucity of information regarding co-infection in HIV-infected individuals. We analyzed HIV-infected patients diagnosed with H. pylori infection in our institution over a six year period.

 

© 2013 ACT. All rights reserved.

 

Key words: Helicobacter pylori; HIV infection; Co-infection

 

Psevdos G, Batog C, Sharp V. Incidence and Treatment Outcomes of Helicobacter Pylori Infection in HIV-infected Patients. Journal of Gastroenterology and Hepatology Research 2013; 2(4): 552-554 Available from: URL: http://www.ghrnet.org/index./joghr/

 

 

DEAR EDITOR

Several studies have indicated Helicobacter pylori infections to be common in HIV- infected patients and prevalence of the disease to be higher in patients with CD4+ T-cell counts greater than 200/µL[1-2]. Nkuize et al, reviewed the characteristics of 48 HIV-infected patients with H. pylori infection who underwent upper endoscopic evaluations. They demonstrated co-infection to be more common in patients of Black African origin, in heterosexual individuals, in patients with a high BMI, high CD4+ T-cell counts, and low HIV viral loads[3].   There is little data on H. pylori treatment choices and outcomes of treatment in HIV-infected patients. Therefore, we retrospectively analyzed our HIV-infected patients that were diagnosed with H. pylori infection from 1/1/2004-12/31/2010. From 4918 HIV-infected patients seen in our clinic during the study period, 169 were diagnosed with H. pylori infection. All 169 patients had symptoms: Reflux esophagitis-like symptoms or dyspepsia, or dysphagia/epigastic discomfort. 150 patients were diagnosed by serology alone, 12 patients had also positive stool antigen, and 7 were diagnosed incidentally by a positive histology after undergoing diagnostic upper endoscopy and gastric biopsy. We analyzed demographic data,  HIV risk factors, CD4+ T cell counts, HIV viral loads, birth place/travel histories, incarceration history, upper endoscopies, and stool antigen studies. We reviewed the treatment choices used and their outcomes.

    The prevalence of H. pylori infection was 169/4918, 3.4%. Most were men, 106 (62.7%). See Table 1. The median age was 46 years.  The median CD4+ T-cell count was 429/µL (range 2-1486). Only 22 patients had CD4<200. 104 patients had undetectable HIV viral load. 77% of patients were on antiretroviral therapy. The majority of patients were African American (70/169, 41.4%) and Hispanic (85/169, 50.2%); only 13/169 (7.69%) were Caucasian, and 1/169 was Asian. The HIV-risk factors were 44% Heterosexual, 38% were men who have sex with men, 17% were IV drug users, and 1% acquired HIV via blood transfusion. 64 patients were born outside the United States (78% from Latin America/Caribbean), 16% Africa, 3% Asia), see figure 1, and 15 had travelled to known H. pylori endemic regions prior to the HIV diagnosis. 46 patients had history of incarceration in United States. 48 patients underwent upper endoscopic evaluation, 15 of them had upper endoscopy after treatment that confirmed eradication of infection.

 

    Treatment was offered in 129 patients. 40 patients either did not have stool antigen testing or were lost to follow up. The most common regimen used (in 113 patients) was a 14-days course of Amoxicillin-Clarithromycin and Proton Pump Inbibitor (PPI) known as the standard therapy. 8 patients used Bismuth-Metronizadole-Tetracycline regimen; 3 Clarithromycin-Metronidazole-PPI; 2 Clarithromycin-Tetracycline-PPI and 2 a levofloxacin based-PPI regimen. See figure 2.

    From the 129 patients, eight patients had evidence of treatment failure (persistent  positive stool antigen). All had failed amoxicillin-based therapies, and were receiving HAART; their mean CD4+ T cell count was 535 (218-1103), median was 472. One patient was retreated with the same regimen (amoxicillin/clarithromycin/PPI) and the stool antigen was again positive; he was then treated with sequential therapy, amoxicillin/PPI for five days, followed by five days of tinidazole/clarithromycin/PPI and the stool antigen became negative.  Two patients were retreated with tinidazole/amoxicillin/PPI but were lost to follow up. Four patients were retreated with Bismuth-Metronidazole-Tetracycline, one had resolution of symptoms, the other developed negative stool antigen, and the other two patients were lost to follow up. 1/129 patients died from unknown etiology on the 3rd day of H. pylori treatment. The  (13)C -Urea breath test (UBT) was not available, and the stool antigen test was obtained 2 months after treatment and after a chronic PPI was held for at least two weeks before obtaining the specimen. 15 patients underwent upper endoscopy and biopsy after treatment, and histological analysis confirmed eradication of the organisms.

    Successful eradication of H. pylori in HIV-infected patients had been documented[4]. Magen et al, showed 11 HIV-infected patients treated with amoxicillin based therapy to have a negative UBT eight weeks after completion of treatment. Persistent infection in non-HIV infected patients is also well documented[5]. Recent clinical trials and meta-analyses have also shown that the eradication rate of the standard triple therapy has declined to less than 80% and this is attributed to the increasing incidence of clarithromycin-resistant strains of H. pylori[6]. The respected European Helicobacter Study Group has recently released its guidelines for management of H. pylori infection; regional knowledge of clarithromycin resistance rates now dictates initial treatment strategies[7]. (For further details, the authors highly recommend reviewing the referenced guidelines).

    From our review of the literature we didnt find other reports of HIV-infected patients who had failed standard triple therapy for H. pylori infection. In our experience, use of bismuth or sequential therapy was successful in achieving eradication where the standard triple therapy had failed. Our study has many limitations stemming from its retrospective nature and from the fact that many patients were diagnosed on positive serology and symptoms alone. This fact points to the difficulties and challenges that physicians face in clinical practice as many patients didnt provide stool specimen, and UBT was not easily available. 

    H. pylori co-infection in our large urban HIV-infected population was not uncommon. It was found in patients that grew up or had travelled to endemic regions. Treatments were in general well tolerated, however, treatment failures to the standard triple therapy was noted. Physicians who treat H. pylori infection in HIV-infected patients should be aware of increasing incidence of clarithromycin resistant H. pylori stains. We strongly recommend pursuing test of cure in all HIV-infected patients who received the standard triple therapy, and if failure is detected, to follow appropriate retreatment strategies as outlined by recently released guidelines.

 

 

REFERENCES

1    Nkuize M, De Wit S, Muls V, Arvanitakis M, Buset M. Upper gastrointestinal endoscopic findings in the era of highly active antiretroviral therapy. HIV Med 2010; 11: 412-417

2    Fialho ABC, Braga-Neto MB, Guerra AJC, et al.  Low prevalence of H. pylori infection in HIV-positive patients in the Northeast of Brazil. BMC Gastroenterol 2011; 11: 13

3    Nkuize M, De Wit S, Muls V, Ntounda R, Gomez-Galdon M, Buset M.  Comparison of demographic characteristics and upper gastrointestinal endoscopy findings in HIV-positive, antiretroviral-treated patients with and without Helicobacter pylori infection. Helicobacter 2012; 17: 153-159

4    Magen E, Elbirt D, Agmon-Levin N, Mishal J, Sthoege Z. Eradication of Helicobacter pylori can facilitate immune reconstitution in HIV-1 infected immunological non-responders. Int J Infect Dis 2010; 14: e322-e327

5    McColl KE. Helicobacter pylori Infection. N Engl J Med 2010; 362: 1597-1604

6    Seng-Kee C, Feng-Woei T, Ping-I H, Deng-Chyang Wu.  A new look at Anti-Helicobacter pylori therapy. World J Gastroenterol 2011; 17: 3971-3975

7    Malfertheiner P, Megraud F, OMorain CA, et al  Management of Helicobacter pylori infectionthe Maastricht IV/Florence Consensus Report. Gut 2012; 61: 646-664

 

Peer reviewer: Osamu Handa, Department of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Kawaramachi-Hirokoji, Kamigyo, Kyoto. 602-8566, Japan.

 

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