Alan Sive

A prospective, cross-sectional study of anaemia and peripheral iron status in antiretroviral naïve, HIV-1 infected children in Cape Town, South Africa

BackgroundAnaemia is a common manifestation of paediatric HIV infection. Although there are many causes, anaemia of chronic diseases is the most frequent type. In poor countries iron deficiency is widespread. It is probable that many HIV-infected children in these countries are also iron deficient. This study describes the relationship between paediatric HIV infection and anaemia, and documents the peripheral iron status of antiretroviral naive, HIV-infected children.MethodsSixty children were evaluated prospectively. Investigations included CD4+ count, haemoglobin concentration (Hb), red blood cell (RBC) morphology, and iron studies.ResultsAnaemia was present in 73% of children. Compared to mild HIV infection, median Hb was lower in children with moderate clinical infection (104 g/L v 112 g/L, p = 0.04) and severe clinical infection (96 g/L v 112 g/L, p = 0.006), and more children with severe infection were anaemic (92% v 58%, 0.04). There was a significant relationship between immunological status and Hb. 68% had abnormal RBC morphology. Significantly more children with moderate and severe disease, and severe immunosuppression had abnormal RBC morphology. 52% were iron-depleted, 20% had iron-deficient erythropoiesis and 18% iron deficiency anaemia (IDA). 16% (7/44) of anaemic children had microcytosis and hypochromia. Median soluble transferrin receptor concentration was significantly higher in those with microcytic hypochromic anaemia (42.0 nmol/L v 30.0 nmol/L, p = 0.008).ConclusionsBoth the proportion of anaemic children and the median Hb were associated with disease status. Iron depletion and IDA are major problems in HIV-infected children in South Africa.

Growth and micronutrient disturbances in stable HIV-infected children in Cape Town.

Abstract This prospective study of 60 stable, HIV-infected children in an economically deprived setting was designed to document anthropometric and micronutrient disturbances. Investigations included CD4+ counts, anthropometry and plasma levels of albumin, transthyretin, retinol-binding protein (RBP), vitamins A, B6, E and B12, and folate, zinc and copper. The median age was 25 months. Thirty-two per cent had mild, 48% moderate and 20% severe clinical features, and 80% were moderately or severely immunosuppressed. Twenty-eight per cent had a weight Z-score <-2.0 and 58% a height Z-score <-2.0. Many children had micronutrient deficiencies: albumin (70%), transthyretin (100%), RBP (85%), vitamins A (80%), B6 (37%), E (37%) and B12 (5%), zinc (20%) and copper (25%). Sixty-two per cent had two or more trace element or vitamin deficiencies. There was a weak association between micronutrient status and disease status. Micronutrient concentrations did not correlate with chronological age, height-for-age or weight-for-age. CRP was elevated in 53% but did not correlate with any of the micronutrient concentrations. Micronutrient deficiencies were more common and micronutrient concentrations lower in children over 24 months of age.

Red blood cell antioxidant enzyme concentrations in kwashiorkor and marasmus.

Kwashiorkor may occur when an imbalance between pro- and antioxidants in malnourished children results in an excess of free radicals. The concentrations of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH) and glutathione peroxidase (GPX) were measured in erythrocytes of 22 children with kwashiorkor on admission to hospital and repeated on days 5, 10 and 30 of recovery. The concentrations were compared with those in 22 children with marasmus and in 20 children who were normally nourished but had infective illness necessitating their hospitalization. CAT and SOD were similar in all groups and did not change during recovery. GSH and GPX were significantly lower in kwashiorkor than in the other groups. Concentrations of thiobarbituric acid-reactive substances (TBARS), a marker of lipid peroxidation, were significantly elevated in children with kwashiorkor. During clinical recovery, GSH but not GPX concentrations rose despite an increase in plasma selenium levels and decreased concentrations of TBARS. These findings suggest that the antioxidant status of children with kwashiorkor differs from that of well nourished and marasmic children. Whether these differences are the cause of the consequence of the clinical picture is unresolved.

Comparison of enteral and intramuscular vitamin A supplementation in preterm infants

Vitamin A deficiency associated with preterm delivery is not readily reversible using the recommended supplement of 1500 IU per day. It has been reported that 2000 IU of intramuscular vitamin A administered on alternate days for 28 days will correct the deficiency. The objective of this study was to compare this regime with the practice in our nursery of giving 5000 IU of vitamin A per day with the early introduction of feeds. The vitamin A status of ten preterm infants (mean gestation 30.5 weeks) who received intramuscular vitamin supplementation was compared with that of nine infants (mean gestation 30.7 weeks) given enteral vitamin A. Vitamin A status was evaluated on the 32nd day of life using plasma retinol and retinol-binding protein (RBP) concentrations and a modified relative dose response (RDR) test. Plasma retinol and RBP concentrations were similar in the two groups shortly after birth revealing vitamin A deficiency. By the 32nd day of life, plasma retinol and RBP concentrations had risen significantly in both groups and in 70% the modified RDR was normal. Differences between the groups were not observed irrespective of the method of vitamin A administration. None of the infants developed clinical or biochemical vitamin A toxicity. In most preterm infants who tolerate feeds, vitamin A deficiency can be corrected safely by supplementing the feeds with 5000 IU of vitamin A per day.

Plasma zinc, copper, selenium, ferritin and whole blood manganese concentrations in children with kwashiorkor in the acute stage and during refeeding.

Plasma zinc, copper, selenium, ferritin and whole blood manganese concentrations were measured in 22 children with kwashiorkor on admission to hospital and on days 5, 10 and 30 of refeeding. Twenty similarly aged, healthy, well nourished children served as controls. The mean (SEM) zinc, copper and selenium concentrations of 7.5 (0.93), 10.8 (0.64) and 0.29 (0.02) mumol/l, respectively, in the children with kwashiorkor on admission were all significantly lower than the values of 13.7 (0.66), 25.6 (1.72) and 0.72 (0.04) mumol/l in the controls. In contrast, the erythrocyte manganese level of 1.67 (0.09) micrograms/gHb and the median ferritin concentration of 293 micrograms/dl were significantly higher than in the controls. After 30 days there was full clinical recovery with significant weight gain and a return of the plasma albumin, caeruloplasmin, copper and ferritin to normal. However, manganese remained elevated and zinc and selenium concentrations remained significantly low. Our results suggest that nutritional rehabilitation of children with kwashiorkor is incomplete by 30 days and cannot be judged purely by a return of the plasma proteins to normal. Addition of selected trace elements to the diet may hasten full recovery.