14 research outputs found

    Technical efficiency of peripheral health units in Pujehun district of Sierra Leone: a DEA application

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    BACKGROUND: The Data Envelopment Analysis (DEA) method has been fruitfully used in many countries in Asia, Europe and North America to shed light on the efficiency of health facilities and programmes. There is, however, a dearth of such studies in countries in sub-Saharan Africa. Since hospitals and health centres are important instruments in the efforts to scale up pro-poor cost-effective interventions aimed at achieving the United Nations Millennium Development Goals, decision-makers need to ensure that these health facilities provide efficient services. The objective of this study was to measure the technical efficiency (TE) and scale efficiency (SE) of a sample of public peripheral health units (PHUs) in Sierra Leone. METHODS: This study applied the Data Envelopment Analysis approach to investigate the TE and SE among a sample of 37 PHUs in Sierra Leone. RESULTS: Twenty-two (59%) of the 37 health units analysed were found to be technically inefficient, with an average score of 63% (standard deviation = 18%). On the other hand, 24 (65%) health units were found to be scale inefficient, with an average scale efficiency score of 72% (standard deviation = 17%). CONCLUSION: It is concluded that with the existing high levels of pure technical and scale inefficiency, scaling up of interventions to achieve both global and regional targets such as the MDG and Abuja health targets becomes far-fetched. In a country with per capita expenditure on health of about US$7, and with only 30% of its population having access to health services, it is demonstrated that efficiency savings can significantly augment the government's initiatives to cater for the unmet health care needs of the population. Therefore, we strongly recommend that Sierra Leone and all other countries in the Region should institutionalise health facility efficiency monitoring at the Ministry of Health headquarter (MoH/HQ) and at each health district headquarter

    Development and Validation of a Risk Score for Chronic Kidney Disease in HIV Infection Using Prospective Cohort Data from the D:A:D Study

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    Ristola M. on työryhmien DAD Study Grp ; Royal Free Hosp Clin Cohort ; INSIGHT Study Grp ; SMART Study Grp ; ESPRIT Study Grp jäsen.Background Chronic kidney disease (CKD) is a major health issue for HIV-positive individuals, associated with increased morbidity and mortality. Development and implementation of a risk score model for CKD would allow comparison of the risks and benefits of adding potentially nephrotoxic antiretrovirals to a treatment regimen and would identify those at greatest risk of CKD. The aims of this study were to develop a simple, externally validated, and widely applicable long-term risk score model for CKD in HIV-positive individuals that can guide decision making in clinical practice. Methods and Findings A total of 17,954 HIV-positive individuals from the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) study with >= 3 estimated glomerular filtration rate (eGFR) values after 1 January 2004 were included. Baseline was defined as the first eGFR > 60 ml/min/1.73 m2 after 1 January 2004; individuals with exposure to tenofovir, atazanavir, atazanavir/ritonavir, lopinavir/ritonavir, other boosted protease inhibitors before baseline were excluded. CKD was defined as confirmed (>3 mo apart) eGFR In the D:A:D study, 641 individuals developed CKD during 103,185 person-years of follow-up (PYFU; incidence 6.2/1,000 PYFU, 95% CI 5.7-6.7; median follow-up 6.1 y, range 0.3-9.1 y). Older age, intravenous drug use, hepatitis C coinfection, lower baseline eGFR, female gender, lower CD4 count nadir, hypertension, diabetes, and cardiovascular disease (CVD) predicted CKD. The adjusted incidence rate ratios of these nine categorical variables were scaled and summed to create the risk score. The median risk score at baseline was -2 (interquartile range -4 to 2). There was a 1: 393 chance of developing CKD in the next 5 y in the low risk group (risk score = 5, 505 events), respectively. Number needed to harm (NNTH) at 5 y when starting unboosted atazanavir or lopinavir/ritonavir among those with a low risk score was 1,702 (95% CI 1,166-3,367); NNTH was 202 (95% CI 159-278) and 21 (95% CI 19-23), respectively, for those with a medium and high risk score. NNTH was 739 (95% CI 506-1462), 88 (95% CI 69-121), and 9 (95% CI 8-10) for those with a low, medium, and high risk score, respectively, starting tenofovir, atazanavir/ritonavir, or another boosted protease inhibitor. The Royal Free Hospital Clinic Cohort included 2,548 individuals, of whom 94 individuals developed CKD (3.7%) during 18,376 PYFU (median follow-up 7.4 y, range 0.3-12.7 y). Of 2,013 individuals included from the SMART/ESPRIT control arms, 32 individuals developed CKD (1.6%) during 8,452 PYFU (median follow-up 4.1 y, range 0.6-8.1 y). External validation showed that the risk score predicted well in these cohorts. Limitations of this study included limited data on race and no information on proteinuria. Conclusions Both traditional and HIV-related risk factors were predictive of CKD. These factors were used to develop a risk score for CKD in HIV infection, externally validated, that has direct clinical relevance for patients and clinicians to weigh the benefits of certain antiretrovirals against the risk of CKD and to identify those at greatest risk of CKD.Peer reviewe

    Association of Lower Exposure Risk With Paucisymptomatic/Asymptomatic Infection, Less Severe Disease, and Unrecognized Ebola Virus Disease: A Seroepidemiological Study.

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    BackgroundIt remains unclear if there is a dose-dependent relationship between exposure risk to Ebola virus (EBOV) and severity of illness.MethodsFrom September 2016 to July 2017, we conducted a cross-sectional, community-based study of Ebola virus disease (EVD) cases and household contacts of several transmission chains in Kono District, Sierra Leone. We analyzed 154 quarantined households, comprising both reported EVD cases and their close contacts. We used epidemiological surveys and blood samples to define severity of illness as no infection, pauci-/asymptomatic infection, unrecognized EVD, reported EVD cases who survived, or reported EVD decedents. We determine seropositivity with the Filovirus Animal Nonclinical Group EBOV glycoprotein immunoglobulin G antibody test. We defined levels of exposure risk from 8 questions and considered contact with body fluid as maximum exposure risk.ResultsOur analysis included 76 reported EVD cases (both decedents and survivors) and 421 close contacts. Among these contacts, 40 were seropositive (22 paucisymptomatic and 18 unrecognized EVD), accounting for 34% of the total 116 EBOV infections. Higher exposure risks were associated with having had EBOV infection (maximum risk: adjusted odds ratio [AOR], 12.1 [95% confidence interval {CI}, 5.8-25.4; trend test: P < .001) and more severe illness (maximum risk: AOR, 25.2 [95% CI, 6.2-102.4]; trend test: P < .001).ConclusionsThis community-based study of EVD cases and contacts provides epidemiological evidence of a dose-dependent relationship between exposure risk and severity of illness, which may partially explain why pauci-/asymptomatic EBOV infection, less severe disease, and unrecognized EVD occurs
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