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Iron status in HIV-1 infection: implications in disease pathology
BACKGROUND: There had been conflicting reports with levels of markers of iron metabolism in HIV infection. This study was therefore aimed at investigating iron status and its possible mediation of severity of HIV- 1 infection and pathogenesis. METHOD: Eighty (80) anti-retroviral naive HIV-1 positive...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3551638/ https://www.ncbi.nlm.nih.gov/pubmed/23245266 http://dx.doi.org/10.1186/1472-6890-12-26 |
Sumario: | BACKGROUND: There had been conflicting reports with levels of markers of iron metabolism in HIV infection. This study was therefore aimed at investigating iron status and its possible mediation of severity of HIV- 1 infection and pathogenesis. METHOD: Eighty (80) anti-retroviral naive HIV-1 positive and 50 sero-negative controls were recruited for the study. Concentrations of serum total iron, transferrin, total iron binding capacity (TIBC), CD(4)(+) T -lymphocytes, vitamin C, zinc, selenium and transferrin saturation were estimated. RESULTS: The mean CD(4)(+) T-lymphocyte cell counts, serum iron, TIBC, transferrin saturation for the tests and controls were 319 ± 22, 952 ± 57 cells/μl (P < 0.001), 35 ± 0.8, 11.8 ± 0.9 μmol/l (P < 0.001), 58.5 ± 2.2, 45.2 ± 2.4 μmol/l (P < 0.005) and 68.8 ± 3.3, 27.7 ± 2.2%, (P <0.001), respectively, while mean concentrations of vitamin C, zinc and selenium were 0.03 ± 0.01, 0.3 ± 0.04 (P < 0.001), 0.6 ± 0.05, 11.9 ± 0.26 μmol/l (P < 0.001) and 0.1 ± 0.01, 1.2 ± 0.12 μmol/l (P < 0.001) respectively. Furthermore, CD(4)(+) T-lymphocyte cell count had a positive correlation with levels of vitamin C (r = 0.497, P < 0.001), zinc (r = 0.737, P < 0.001), selenium (r = 0.639, P < 0.001) and a negative correlation with serum iron levels (r = −0.572, P < 0.001). CONCLUSION: It could be inferred that derangement in iron metabolism, in addition to oxidative stress, might have contributed to the depletion of CD(4)(+) T cell population in our subjects and this may result in poor prognosis of the disease. |
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