Prevalence of HPV Infection in Racial-Ethnic Subgroups of Head and Neck Cancer Patients.

The landscape of HPV infection in racial/ethnic subgroups of head and neck cancer (HNC) patients has not been evaluated carefully. In this study, a meta-analysis examined the prevalence of HPV in HNC patients of African ancestry. Additionally, a pooled analysis of subject-level data was also performed to investigate HPV prevalence and patterns of p16 (CDNK2A) expression amongst different racial groups. Eighteen publications (N = 798 Black HNC patients) were examined in the meta-analysis, and the pooled analysis included 29 datasets comprised of 3,129 HNC patients of diverse racial/ethnic background. The meta-analysis revealed that the prevalence of HPV16 was higher among Blacks with oropharyngeal cancer than Blacks with non-oropharyngeal cancer. However, there was great heterogeneity observed among studies (Q test P<0.0001). In the pooled analysis, after adjusting for each study, year of diagnosis, age, gender and smoking status, the prevalence of HPV16/18 in oropharyngeal cancer patients was highest in Whites (61.1%), followed by 58.0% in Blacks and 25.2% in Asians (P<0.0001). There was no statistically significant difference in HPV16/18 prevalence in non-oropharyngeal cancer by race (P=0.682). With regard to the pattern of HPV16/18 status and p16 expression, White patients had the highest proportion of HPV16/18+/p16+ oropharyngeal cancer (52.3%), while Asians and Blacks had significantly lower proportions (23.0% and 22.6%, respectively) [P <0.0001]. Our findings suggest that the pattern of HPV16/18 status and p16 expression in oropharyngeal cancer appears to differ by race and this may contribute to survival disparities.

Iron supplementation in HIV-infected Malawian children with anemia: a double-blind, randomized, controlled trial.

BACKGROUND: It is unknown whether iron supplementation in human immunodeficiency virus (HIV)-infected children living in regions with high infection pressure is safe or beneficial. A 2-arm, double-blind, randomized, controlled trial was conducted to examine the effects of iron supplementation on hemoglobin, HIV disease progression, and morbidity. METHODS: HIV-infected Malawian children aged 6-59 months with moderate anemia (hemoglobin level, 7.0-9.9 g/dL) were randomly assigned to receive 3 mg/kg/day of elemental iron and multivitamins (vitamins A, C, and D) or multivitamins alone for 3 months. Participants were followed for 6 months. RESULTS: A total of 209 children were randomly assigned to treatment, and 196 (93.8%) completed 6 months of follow-up. Iron supplementation was associated with greater increases in hemoglobin concentrations (adjusted mean difference [aMD], 0.60; 95% confidence interval [CI], .06-1.13; P = .03) and reduced the risk of anemia persisting for up to 6 months follow-up (adjusted prevalence ratio, 0.59; 95% CI, .38-.92; P = .02). Children who received iron had a better CD4 percentage response at 3 months (aMD, 6.00; 95% CI, 1.84-10.16; P = .005) but an increased incidence of malaria at 6 months (incidence rate, 120.2 vs 71.7; adjusted incidence rate ratio [aIRR], 1.81 [95% CI, 1.04-3.16]; P = .04), especially during the first 3 months (incidence rate, 78.1 vs 36.0; aIRR, 2.68 [95% CI, 1.08-6.63]; P = .03). CONCLUSIONS: Iron supplementation in anemic HIV-infected children has beneficial effects on hemoglobin, anemia, and immunity but increases the risk of malaria. Thus, iron supplementation in HIV-infected children living in malaria-endemic areas should only be provided in combination with adequate protection from malaria. CLINICAL TRIALS REGISTRATION: ISRCTN-62947977.

Iron deficiency in children with HIV-associated anaemia: a systematic review and meta-analysis.

We conducted a systematic review and meta-analysis to determine the prevalence of iron deficiency in HIV-infected children from high- and low-income settings and compared it with that of HIV-uninfected controls. We searched five major databases for primary studies reporting on anaemia and iron markers in HIV-infected children. A pooled analysis was done using random-effects models, with Forest plots and heterogeneity test estimates provided. Fifteen articles (2778 children) met the inclusion criteria. In the pooled analysis, mean overall prevalence of iron deficiency in HIV-infected children was 34% (95%CI 19-50%). Prevalence rates were similar in high-income (31%; 95%CI 2-61%) and low-income settings (36%; 95%CI 17-54%) (p=0.14). Studies that included a HIV-uninfected control population (n=4) were only available from low-income settings and showed less iron deficiency in HIV-infected children (28%) than in HIV-uninfected children (43%); OR 0.50 (0.27-0.94); p=0.03. The findings suggest that HIV-infected children are less likely to be iron deficient when compared with HIV-uninfected children. Possible explanations for this include HIV-induced haematosuppression and associated hypoferraemia, with adequate iron stores. Nevertheless iron deficiency is a common co-morbidity in HIV. Studies are needed to determine the role of iron deficiency in HIV-associated anaemia and the effects of iron supplementation in this population.

Intermittent preventive therapy for malaria with monthly artemether-lumefantrine for the post-discharge management of severe anaemia in children aged 4-59 months in southern Malawi: a multicentre, randomised, placebo-controlled trial.

BACKGROUND: Young children with severe malarial anaemia in Africa are at high risk of readmittance to hospital or death within 6 months of discharge. We aimed to assess whether 3 months of chemoprevention with artemether-lumefantrine reduced this risk. METHODS: We did a randomised, placebo-controlled, multicentre trial in four hospitals in Malawi testing the efficacy and safety of intermittent preventive therapy post-discharge (IPTpd) in children aged 4-59 months admitted for severe malarial anaemia. All convalescent children who had completed a blood transfusion received artemether-lumefantrine at discharge and were randomly assigned by a computer-generated sequence to receive placebo or artemether-lumefantrine at 1 month and 2 months after discharge, providing about 1 month and 3 months of protection, respectively. Patients and study staff were masked throughout the study. The primary endpoint was a composite of all-cause mortality or hospital readmittance because of all-cause severe anaemia or severe malaria between 1 and 6 months after enrolment. This trial is registered, number ISRCTN89727873. RESULTS: Of 1414 children enrolled, 708 were assigned to receive placebo and 706 the intervention. By 6 months, 192 children (14%) had died or were readmitted with severe malaria or severe anaemia. 1-6 months after randomisation, 109 primary events occurred in 85 children in the placebo group and 86 in 74 children in the intervention group (adjusted protective efficacy [PE] 31%, 95% CI 5-50; absolute rate reduction 11·7 per 100 children years, 95% CI 1·8-18·9; p=0·024). The protective effect was greatest during the IPTpd period (1-3 months), when 58 primary events occurred in 49 children in the placebo group and 37 in 34 children in the intervention group (PE 41%, 10-62; p=0·01), but was not sustained after the third month (4-6 months, PE 17%, -27 to 45; p=0·395). When episodes in the first month were included--ie, before the first dose of IPTpd, when both groups benefited from the post-treatment prophylactic effect of artemether-lumefantrine provided at discharge--the overall cumulative PE by 6 months was 26% (-2 to 46; p=0·06). INTERPRETATION: In areas with intense malaria transmission, chemoprevention with IPTpd given to children with severe malarial anaemia might reduce rates of readmittance to hospital for severe anaemia or malaria. Studies to confirm these findings and to investigate different delivery mechanisms and cost-effectiveness are needed. FUNDING: The Netherlands African Partnership for Capacity Development and Clinical Interventions Against Poverty Related Diseases, the UBS-Optimus Foundation, and the Gates Malaria Partnership.