Micronutrient and cytokine interaction in congenital pediatric HIV infection Review uri icon

Overview

MeSH Major

  • HIV Infections
  • Micronutrients
  • Nutritional Status
  • Tumor Necrosis Factor-alpha

abstract

  • Malnutrition is a frequent manifestation of HIV infection that has received comparatively little attention despite growing clinical importance with improved treatment and lengthened survival times. Fundamental relationships and mechanisms of HIV viral interaction in nutrient metabolism remain to be established. In an attempt to begin to fill the void of information relative to pediatric HIV infection, we have summarized the extant knowledge with regard to micronutrients and present some of the data from studies performed in our laboratory. Previous studies have shown both that vitamin A deficiency is associated with increased mortality in HIV+ intravenous drug users and that maternal vitamin A deficiency is a risk factor for transmission in congenital exposure. Our most significant finding is that 70% of children congenitally exposed to HIV are vitamin A-deficient in the first months of life compared to age-matched controls whether they are HIV-infected or not. About 25% of our patient population was found to have growth or developmental delay, frequently without other signs of progression and in the presence of an intact T-cell compartment. In addition, we found evidence of cytokine imbalance, specifically elevated plasma levels of TNF which has been implicated in loss of lean body mass. Inflammatory reactions in the mucosa and increased TNF production in association with regional HIV infection may compromise gastrointestinal absorption. Based on the review of the literature and our research findings, it is clear that understanding the interaction between nutrients and both the regional and systemic immune system is vital for intervention and effective nutrient repletion in congenital HIV infection.

publication date

  • October 1996

Research

keywords

  • Review

Identity

Language

  • eng

PubMed ID

  • 8861931

Additional Document Info

start page

  • 2674S

end page

  • 2679S

volume

  • 126

number

  • 10 SUPPL.