Objective: To examine the effects of stunting in early childhood on blood pressure in later childhood. Design: A cohort study. Setting: Kingston, Jamaica. Subjects: Seven to eight year old children, 120 stunted (height for age`À2 s.d. of the NCHS references) and 224 non-stunted (height for age b À1 s.d. of the NCHS references) at age 9 ± 24 months. Methods: Stunted and non-stunted children were identi®ed at age 9 ± 24 months by house to-house survey of poor neighbourhoods in Kingston, Jamaica. Blood pressure and anthropometry were measured at age 7 ± 8 y. Birth weight was obtained from hospital records (73%) or maternal recall. Results: The stunted children remained shorter and thinner than the non-stunted ones. In multiple regression analysis adjusting for size and pulse rate, the stunted children had higher systolic blood pressure (P`0.05). Birth weight was not a signi®cant predictor of systolic blood pressure. Conclusion: Stunting in early childhood may increase the risk of elevated systolic blood pressure in later life.
SUMMARY Objectives We aimed to characterize neurological outcomes and determine the prevalence of HIV encephalopathy in a cohort of HIV-infected children in Jamaica. Methods Data for 287 HIV-infected children presenting between 2002 and 2008 were reviewed and neurological outcomes characterized. A nested case–control study was conducted between July and September 2009 used 15 randomly selected encephalopathic HIV-infected children aged 7–10 years and 15 matched controls (non-encephalopathic HIV-infected). Their neurocognitive functions were evaluated using clinical assessment and standardized tests for intelligence, short term memory (visuo-spatial and auditory), selective attention, and fine motor and coordination functions. Outcomes were compared using Fisher’s exact test and the Mann–Whitney U-test. Results Sixty-seven (23.3%) children were encephalopathic. The median age at diagnosis of HIV encephalopathy was 1.6 years (interquartile range (IQR) 1.1–3.4 years). Predominant abnormalities were delayed milestones (59, 88.1%), hyperreflexia (59, 86.5%), spasticity (50, 74.6%), microcephaly (42, 61.7%), and quadriparesis (21, 31.3%). The median age of tested children was 8.7 years (IQR 7.6–10.8 years) in the encephalopathic group and 9 years (IQR 7.4–10.7 years) in the non-encephalopathic group. Encephalopathic children performed worse in all domains of neurocognitive function (p < 0.05). Conclusions A high prevalence of HIV encephalopathy was noted, and significant neurocognitive dysfunction identified in encephalopathic children. Optimized management through the early identification of neurological impairment and implementation of appropriate interventions is recommended to improve quality of life.
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