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Ford N.,WHO | Vitoria M.,WHO | Penazzato M.,WHO | Doherty M.,WHO | And 15 more authors.
The Lancet HIV | Year: 2015

Background Morbidity associated with HIV infection is poorly characterised, so we aimed to investigate the contribution of diff erent comorbidities to hospital admission and in-hospital mortality in adults and children living with HIV worldwide. Methods Using a broad search strategy combining terms for hospital admission and HIV infection, we searched MEDLINE via PubMed, Embase, Web of Science, LILACS, AIM, IMEMR and WPIMR from inception to Jan 31, 2015, to identify studies reporting cause of hospital admission in people living with HIV. We focused on data reported after 2007, the period in which access to antiretroviral therapy started to become widespread. We estimated pooled proportions of hospital admissions and deaths per disease category by use of random-eff ects models. We stratifi ed data by geographical region and age. Findings We obtained data from 106 cohorts, with reported causes of hospital admission for 313 006 adults and 6182 children living with HIV. For adults, AIDS-related illnesses (25 119 patients, 46%, 95% CI 40-53) and bacterial infections (14 034 patients, 31%, 20-42) were the leading causes of hospital admission. These two categories were the most common causes of hospital admission for adults in all geographical regions and the most common causes of mortality. Common region-specifi c causes of hospital admission included malnutrition and wasting, parasitic infections, and haematological disorders in the Africa region; respiratory disease, psychiatric disorders, renal disorders, cardiovascular disorders, and liver disease in Europe; haematological disorders in North America; and respiratory, neurological, digestive and liver-related conditions, viral infections, and drug toxicity in South and Central America. For children, AIDS-related illnesses (783 patients, 27%, 95% CI 19-34) and bacterial infections (1190 patients, 41%, 26-56) were the leading causes of hospital admission, followed by malnutrition and wasting, haematological disorders, and, in the African region, malaria. Mortality in individuals admitted to hospital was 20% (95% CI 18-23, 12 902 deaths) for adults and 14% (10-19, 643 deaths) for children. Interpretation This review shows the importance of prompt HIV diagnosis and treatment, and the need to reinforce existing recommendations to provide chemoprophylaxis and vaccination against major preventable infectious diseases to people living with HIV to reduce serious AIDS and non-AIDS morbidity. © 2015. World Health Organization. Published by Elsevier Ltd/Inc/BV. All rights reserved.


O'Brien D.P.,Medecins Sans Frontieres | O'Brien D.P.,Royal Melbourne Hospital | Ford N.,World Health Organisation | Vitoria M.,World Health Organisation | And 6 more authors.
Tropical Medicine and International Health | Year: 2014

Background: Buruli Ulcer (BU)-HIV co-infection is an important emerging management challenge for BU disease. Limited by paucity of scientific studies, guidance for management of this co-infection has been lacking. Methods: Initiated by WHO, a panel of experts in BU and HIV management developed guidance principles for the management of BU-HIV co-infection based on review of available scientific evidence, current treatment experience, and global recommendations established for management of HIV infection and tuberculosis. Results: The expert panel agreed that all BU patients should be offered quality provider-initiated HIV testing and counselling. In areas with high prevalence of malaria and/or bacterial infections, all patients with HIV co-infection should be started on cotrimoxazole preventative therapy. Combination antibiotic treatment for BU should be commenced before starting antiretroviral therapy (ART) and provided for 8 weeks duration. The suggested combination is rifampicin (10 mg/kg daily up to a maximum of 600 mg/day) plus streptomycin (15 mg/kg daily). An alternative regimen is rifampicin plus clarithromycin (7.5 mg/kg twice daily up to a maximum of 1000 mg daily) although due to drug interactions with antiretroviral drugs this regimen should be used with caution. ART should be initiated in all BU-HIV co-infected patients with symptomatic HIV disease (WHO clinical stage 3 or 4) regardless of CD4 cell count and in asymptomatic individuals with CD4 count ≤500 cells/mm3. If CD4 count is not available, BU-HIV co-infected individuals with category 2 or 3 BU disease should be offered ART. For eligible individuals, ART should be commenced as soon as possible within 8 weeks after commencing BU treatment, and as a priority in those with advanced HIV disease (CD4 ≤ 350 cells/mm3 or WHO stage 3 or 4 disease). All co-infected patients should be actively screened for tuberculosis before commencing BU treatment and before starting ART. Programmes should implement a monitoring and reporting system to document the outcomes of BU-HIV interventions. Conclusions: Knowledge of the clinical and epidemiological interactions between BU and HIV disease is limited. While awaiting more urgently needed evidence, current management practice of both diseases has been useful to build simple 'common sense' preliminary guidance on how to manage BU-HIV co-infection. © 2014 John Wiley & Sons Ltd.


Boyd A.,French Institute of Health and Medical Research | Maylin S.,Laboratoire Of Virologie | Maylin S.,University Paris Diderot | Moh R.,Treichville University Hospital | And 19 more authors.
Journal of Gastroenterology and Hepatology (Australia) | Year: 2016

Background and Aim: In Sub-Saharan Africa, seroclearance of hepatitis B surface antigen (HBsAg) and hepatitis B "e" antigen (HBeAg), including their quantifiable markers, have rarely been evaluated during long-term antiviral treatment among patients coinfected with HIV and hepatitis B virus (HBV). Methods: In this prospective cohort study from two randomized-control trials in Côte d'Ivoire, 161 antiretroviral-naïve HIV-HBV coinfected patients starting lamivudine (n=76) or tenofovir/emtricitabine (n=85) containing antiretroviral therapy were included. HBV DNA was quantified using an in-house assay (detection limit=12copies/mL) and HBsAg quantification (qHBsAg) using the Elecsys assay. Results: Overall, 33 (20.5%) patients were HBeAg positive, 121 (75.2%) had detectable HBV DNA, and 92/93 (98.9%) harbored HBV genotype E. Median treatment duration was 35.5months (interquartile range: 24.3-36.4). Among HBeAg-positive patients, cumulative proportion with HBeAg seroclearance was 46.3% (n=14). Overall, cumulative proportion of HBsAg seroclearance was 6.6% (n=10). Lower baseline qHBsAg levels and strong 12-month declines in qHBsAg were significantly associated with HBsAg seroclearance for both HBeAg-negative and HBeAg-positive patients. When taken at certain levels, these determinants provided moderate sensitivity (Se) and specificity (Sp) in predicting HBsAg seroclearance at month 36 (≤1000IU/mL at baseline, Se=0.80, Sp=0.80; ≥1.0log10IU/mL drop at month 12, Se=0.57, Sp=1.00). Instead, qHBsAg levels ≤100 or ≤10IU/mL at month 12 were optimal (both Se=0.90 and Sp=1.00). Detectable HBV-DNA provided fairly high Se and Sp when evaluated at baseline (Se=1.00, Sp=0.80), but not at month 12 (Se=0.80, Sp=0.40). Conclusions: HBsAg seroclearance rates are not common in patients from Sub-Saharan Africa treated with anti-HBV containing antiretroviral therapy. qHBsAg levels at 12months of treatment may accurately predict HBsAg seroclearance. © 2016 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing Asia Pty Ltd.

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