Background The current literature suggests that there has been a decrease in opportunistic diseases among HIV‐infected patients since the widespread introduction of highly active antiretroviral therapy (HAART) in 1995. Objectives The aim of the study was to investigate the impact of HAART and CD4 lymphocyte count on diseases of the upper gastrointestinal (UGI) tract, digestive symptoms, and endoscopic and histological observations. Methods A review of 706 HIV‐infected patients who underwent GI endoscopy was undertaken. The cohort was divided into three groups: group 1 (G1), pre‐HAART, consisting of 239 patients who underwent endoscopy between January 1991 and December 1994; group 2 (G2), early HAART, consisting of 238 patients who underwent endoscopy between January 1999 and December 2002; and group 3 (G3), recent HAART, consisting of 229 patients who underwent endoscopy between January 2005 and December 2008. Parameters studied included age, gender, opportunistic chemoprophylaxis, antiretroviral therapies, CD4 cell counts, symptoms, observations at the first UGI endoscopy and histology. Results When G1, G2 and G3 were compared, significant increases were seen over time in the following parameters: the percentage of women, the mean CD4 cell count, and the frequencies of reflux symptoms, gastroesophageal reflux disease (GERD), inflammatory gastropathy, gastric ulcer and Helicobacter pylori (HP) infection. Significant decreases were seen in the frequencies of the administration of anti‐opportunistic infection prophylaxis, odynophagia/dysphagia, acute/chronic diarrhoea, candida oesophagitis, nonspecific oesophageal ulcer and Kaposi sarcoma. No significant change was observed in the other parameters, i.e. digestive bleeding, duodenal ulcer and inflammatory duodenopathy. Conclusion These results suggest a correlation between the improvement of immunity as a result of more efficient antiviral therapy and the decrease in the frequency of digestive diseases in AIDS, mainly opportunistic pathologies. However, HP infection, reflux symptoms and GERD have increased in the HAART era.

Helicobacter pylori is a worldwide infection, but little is known about the efficacy of treatment for H. pylori infection in HIV-positive patients. The goal of this work was to evaluate outcomes after first-line H. pylori treatment and identify risk factors for failure in HIV-positive patients. MethodsThis registry study of unmatched H. pylori-infected HIV-positive patients and HIV-negative obese pre-bariatric surgery controls was performed in a tertiary university hospital. Cases were enrolled from 2006 to 2017, controls from 2007 to 2014, and both received standard of care. An additional 'optimal' subgroup of cases was enrolled prospectively from 2017 to 2019 which was treated only on the basis of antibiogram, drug interaction search and additional support by one referent physician. Helicobacter pylori eradication failure rates were compared according to clinical, microbiological and pathological parameters and treatment. ResultsWe analysed 258 HIV-positive patients and 204 HIV-negative control patients. Helicobacter pylori eradication failure rates were markedly greater in cases (24.1%) than in controls (8.8%). The proportions of levofloxacin and metronidazole resistance were greater in cases than in controls (P < 0.05). Among cases treated with H. pylori triple therapy (S3T), the 'optimal' subgroup experienced a 9.5% failure rate vs. 28.6% with other strategies (P = 0.01). Risk factors for failure were H. pylori treatment strategy, exposure to antiretroviral treatment, and alcohol status. Overall, positive HIV status was a risk factor for S3T eradication failure. ConclusionsPatients co-infected with H. pylori and HIV frequently failed to eradicate H. pylori and this was related to treatment strategy, antiretroviral exposure and lifestyle.

BackgroundPatients infected with human immunodeficiency virus (HIV) are living longer due to the availability of more potent treatments. However, prescription of antibiotics to treat or prevent infections in these patients may increase the likelihood of co-infection with antibiotic-resistant species.AimTo compare antimicrobial susceptibility of Helicobacter pylori (H. pylori) in HIV-positive and HIV-negative patients and assess risk-factors for resistance.MethodsWe prospectively collected data from consecutive HIV-positive and HIV-negative patients undergoing upper gastrointestinal endoscopy. Patients with H. pylori-positive gastric biopsies who had never received H. pylori treatment were included.ResultsOf the 353 patients included, 93 were HIV-positive and 260 HIV-negative. Among the HIV-positive patients, 56 (60%) had been infected for <10 years, the median CD4+ count was 493 cells/μl and median viral load was 61 copies/mL; 66 (71%) were receiving antiretroviral therapy. HIV-positive patients were more often male (p = 0.009), had a lower body mass index (p<0.0001), and had less frequently received antibiotics during the 12-months prior to the endoscopy (p<0.0001) than HIV-negative patients. HIV-positive patients were more likely to have H. pylori resistant to levofloxacin (p = 0.0004), metronidazole (p = 0.01), or multiple antibiotics (p = 0.006). HIV-positive Black Africans were more likely to have resistant strains than were HIV-negative Black Africans (p = 0.04). Ethnicity and HIV status were independent risk factors for H. pylori resistance in all patients and acquired immune deficiency syndrome (AIDS) and sex were risk factors in HIV-positive patients.ConclusionsThere was a higher prevalence of primary H. pylori-resistant strains in HIV-positive than in HIV-negative patients. AIDS and sex were predictors of H. pylori resistance in HIV-positive patients.

Treatment of anal dysplasia appears to be safe and to offer short-term efficiency. However, its long-term efficiency remains unknown, especially in the HIV-positive population in which spontaneous clearance is lower and rate of recurrence higher.

Prolonged cART (≥24 months) is associated with fewer anal HSIL.

Epidemiological data on hepatitis delta virus (HDV) infection in Belgium are lacking. A multicenter questionnaire-based registry on HDV infection was collated between March 1, 2008 and February 28, 2009. It consisted of patients coinfected with hepatitis B virus (HBV) and HDV. The data samples were compared to those of a concurrent registry on HBV infection. Prospective data of patients with HBV-HDV coinfection were collected. Active HBV replication is defined as HBeAg positivity or HBV DNA > 2,000 IU/ml. Forty-four patients from 15 centers were registered. A comparison of 29 patients infected with HDV (registered in the concurrent HBV registry) was made against 785 HBV mono-infected patients. The seroprevalence of patients coinfected with HBV and HDV in Belgium is reported to be 3.7% (29/785), consisting solely of the HBV-HDV coinfected patients in the HBV registry. This rises to 5.5% (44/800) if all patients infected with HDV from the two registries combined are included. The patients coinfected with HBV and HDV had higher (P < 0.05) ALT values and more advanced liver disease (Metavir score ≥F2), but had less active HBV replication and lower HBV DNA titers when compared with the patients infected only with HBV. Additionally, the majority of HBV-HDV coinfected patient was male, and 13.6% (6/44) of the patients that were coinfected HBV and HDV were also infected with HCV. In conclusion, this study provided much needed epidemiological data on the current state of HDV infection in Belgium.

In CHC, insulin resistance is independently associated with the presence of genotypes 1/4. Ethnicity is not independently associated with metabolic disorders in patients with CHC.

In the antiretroviral therapy era, HIV-H. pylori coinfection is associated with a greater incidence of duodenal ulcers and higher CD4 counts, higher BMI, less comorbidity, and less frequent use of macrolides.