ALBERT

Description: Progressive inflammation and anemia are common in tuberculosis (TB) and linked to poor clinical outcomes. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have inflammation-resolving properties, whereas iron supplementation in TB may have limited efficacy and enhance bacterial growth. We investigated effects of iron and EPA/DHA supplementation, alone and in combination, on inflammation, anemia, iron status markers and clinical outcomes in Mycobacterium tuberculosis-infected C3HeB/FeJ mice. One week post-infection, mice received the AIN-93 diet without (control) or with supplemental iron (Fe), EPA/DHA, or Fe+EPA/DHA for 3 weeks. Mice supplemented with Fe or EPA/DHA had lower soluble transferrin receptor, ferritin and hepcidin than controls, but these effects were attenuated in Fe+EPA/DHA mice. EPA/DHA increased inflammation-resolving lipid mediators and lowered lung IL-1α, IFN-γ, plasma IL-1β, and TNF-α. Fe lowered lung IL-1α, IL-1β, plasma IL-1β, TNF-α, and IL-6. However, the cytokine-lowering effects in the lungs were attenuated with Fe+EPA/DHA. Mice supplemented with EPA/DHA had lower lung bacterial loads than controls, but this effect was attenuated in Fe+EPA/DHA mice. Thus, individually, post-infection EPA/DHA and iron supplementation lowered systemic and lung inflammation and mitigated anemia of infection in TB, but not when combined. EPA/DHA also enhanced bactericidal effects and could support inflammation resolution and management of anemia.

Description: Low and high plasma glutamine levels are associated with increased mortality. This study aimed to measure glutamine levels in critically ill patients admitted to the intensive care unit (ICU), correlate the glutamine values with clinical outcomes, and identify proxy indicators of abnormal glutamine levels. Patients were enrolled from three ICUs in South Africa, provided they met the inclusion criteria. Clinical and biochemical data were collected. Plasma glutamine was categorized as low (700 µmol/L). Three hundred and thirty patients (median age 46.8 years, 56.4% male) were enrolled (median APACHE II score) 18.0 and SOFA) score 7.0). On admission, 58.5% had low (median 299.5 µmol/L) and 14.2% high (median 898.9 µmol/L) plasma glutamine levels. Patients with a diagnosis of polytrauma and sepsis on ICU admission presented with the lowest, and those with liver failure had the highest glutamine levels. Admission low plasma glutamine was associated with higher APACHE II scores (p = 0.003), SOFA scores (p = 0.003), C-reactive protein (CRP) values (p 〈 0.001), serum urea (p = 0.008), and serum creatinine (p = 0.023) and lower serum albumin (p 〈 0.001). Low plasma glutamine was also associated with requiring mechanical ventilation and receiving nutritional support. However, it was not significantly associated with length of stay or mortality. ROC curve analysis revealed a CRP threshold value of 87.9 mg/L to be indicative of low plasma glutamine levels (area under the curve (AUC) 0.7, p 〈 0.001). Fifty-nine percent of ICU patients had low plasma glutamine on admission, with significant differences found between diagnostic groupings. Markers of infection and disease severity were significant indicators of low plasma glutamine.

Description: This study aims to determine the prevalence of risk of malnutrition on admission and discharge in African hospitals, and to identify the association with selected indicators. In this multi-center prospective cohort study, adult patients from hospitals in South Africa, Kenya, and Ghana were screened on admission and discharge and contacted 3 months post-discharge. Relevant morbidity and mortality outcomes were assessed. At risk of malnutrition was indicated if NRS-2002 score ≥3. Adult patients (n = 2126; 43.11 years, IQR: 31.95–55.60; 52.2% female) were screened on admission and 61% were identified as at risk of malnutrition. The proportion of at-risk patients for the three hospitals in Kenya and Ghana (66.2%) were significantly higher than that of the three South African hospitals (53.7%) (Chi2 = 31.0; p 〈 0.001). Discharge risk of malnutrition was 71.2% (n = 394). Mean length of stay (LOS) was 6.46 ± 5.63 days. During hospitalization, 20.6% lost ≥5% body weight, 18.8% were referred for nutrition support, and discharge BMI (23.87 ± 7.38 kg/m2) was significantly lower than admission BMI (24.3 ± 7.3 kg/m2) (p 〈 0.001). Admission nutrition risk was associated with lower admission and discharge BMI (p 〈 0.001), longer LOS (p 〈 0.001), increased 3-month re-admission rates (Chi2 = 1.35; p = 0.245) and increased mortality (Chi2 = 21.68; p 〈 0.001). Nearly two-thirds of patients were at risk of malnutrition on admission. This was associated with longer LOS and greater hospital mortality. The nutritional status of patients deteriorated during hospitalization. Routine screening practices with appropriate nutrition support action should be implemented as a matter of urgency.

Description: Chronic kidney disease (CKD) is increasing in sub-Saharan Africa. Undernutrition has been prevalent amongst end stage CKD patients, with limited data on the prevalence of obesity. The aim of this study was to assess the nutritional status of CKD patients using various methods sensitive to over and under-nutrition. Stage 3 to 5 CKD patients (glomerular filtration rate (GFR) 〈 60 mL/min/1.73 m2) attending a pre-dialysis clinic in Cape Town, were enrolled. Exclusion criteria included infectious and autoimmune conditions. Sociodemographic, clinical and biochemical data were collected, and anthropometric measurements were performed. Dietary intake was measured with a quantified food frequency questionnaire (FFQ). Statistical Package for the Social Sciences (SPSS) version 26 was used for statistical analysis. Seventy participants, with mean age of 41.8 ± 11.8 years, 52.9% females and 47.1% males were enrolled. Participants enrolled mainly had stage 5 kidney failure. Thirty percent were overweight (21) and 25 (36%) were obese, 22 (60%) of females were overweight and obese, while 13 (39.4%) of males were predominantly normal weight. Abdominal obesity was found in 42 (60%) of participants, mainly in females. Undernutrition prevalence was low at 3%. Dietary assessment showed a high sugar and protein intake. There was a high prevalence of overweight, obesity and abdominal obesity in CKD stage 35 patients, with unhealthy dietary intake and other nutritional abnormalities.

Description: The etiology of multifactorial morbidities such as undernutrition and anemia in children living with the human immunodeficiency virus (HIV) (HIV+) on antiretroviral therapy (ART) is poorly understood. Our objective was to examine associations of HIV and iron status with nutritional and inflammatory status, anemia, and dietary intake in school-aged South African children. Using a two-way factorial case-control design, we compared four groups of 8 to 13-year-old South African schoolchildren: (1) HIV+ and low iron stores (inflammation-unadjusted serum ferritin ≤ 40 µg/L), n = 43; (2) HIV+ and iron sufficient non-anemic (inflammation-unadjusted serum ferritin 〉 40 µg/L, hemoglobin ≥ 115 g/L), n = 41; (3) children without HIV (HIV-ve) and low iron stores, n = 45; and (4) HIV-ve and iron sufficient non-anemic, n = 45. We assessed height, weight, plasma ferritin (PF), soluble transferrin receptor (sTfR), plasma retinol-binding protein, plasma zinc, C-reactive protein (CRP), α-1-acid glycoprotein (AGP), hemoglobin, mean corpuscular volume, and selected nutrient intakes. Both HIV and low iron stores were associated with lower height-for-age Z-scores (HAZ, p 〈 0.001 and p = 0.02, respectively), while both HIV and sufficient iron stores were associated with significantly higher CRP and AGP concentrations. HIV+ children with low iron stores had significantly lower HAZ, significantly higher sTfR concentrations, and significantly higher prevalence of subclinical inflammation (CRP 0.05 to 4.99 mg/L) (54%) than both HIV-ve groups. HIV was associated with 2.5-fold higher odds of iron deficient erythropoiesis (sTfR 〉 8.3 mg/L) (95% CI: 1.03–5.8, p = 0.04), 2.7-fold higher odds of subclinical inflammation (95% CI: 1.4–5.3, p = 0.004), and 12-fold higher odds of macrocytosis (95% CI: 6–27, p 〈 0.001). Compared to HIV-ve counterparts, HIV+ children reported significantly lower daily intake of animal protein, muscle protein, heme iron, calcium, riboflavin, and vitamin B12, and significantly higher proportions of HIV+ children did not meet vitamin A and fiber requirements. Compared to iron sufficient non-anemic counterparts, children with low iron stores reported significantly higher daily intake of plant protein, lower daily intake of vitamin A, and lower proportions of inadequate fiber intake. Along with best treatment practices for HIV, optimizing dietary intake in HIV+ children could improve nutritional status and anemia in this vulnerable population. This study was registered at clinicaltrials.gov as NCT03572010.