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TitelAnalysis of antibody and cytokine markers for leprosy nerve damage and reactions in the INFIR cohort in India  
AuteursR. Jadhav, L. Suneetha, R. Kamble, V. Shinde, K. Devi, M.V. Chaduvula, R. Raju, S. Suneetha, P.G. Nicholls, W.H. van Brakel, D.N.J. Lockwood
Jaar2011
TijdschriftPLoS Neglected Tropical Diseases
Jaargang5
Serienummer3
Pagina's8
OrganisatieKIT - Royal Tropical Institute
OnderwerpHealth and Nutrition
Trefwoordendisease prevention and control, health
SamenvattingBACKGROUND: The ILEP Nerve Function Impairment in Reaction (INFIR) is a cohort study designed to identify predictors of reactions and nerve function impairment (NFI) in leprosy. AIM OF THE STUDY: Antibodies to mycobacteria, nerve components and serum cytokine were measured as potential markers for their possible association with reactions and NFI. Patients and Methods: 303 newly diagnosed leprosy patients from two centres in North India were enrolled. Antibodies to PGL-1, LAM (IgG1 and IgG3), ceramide, S100 and TNFa levels were measured using ELISA techniques. RESULTS: S-100, PGL IgG and IgM antibody levels were lowest in patients with BT leprosy and highest in patients with lepromatous leprosy. LAM IgG1 and LAM IgG3 antibody levels were highest in patients with BL leprosy. Ceramide antibody levels were not correlated with type of leprosy. Levels of all the antibodies tested and TNF a were lowest in patients with only skin reaction. PGL IgM antibody levels were elevated in patients with skin reactions and NFI. Old sensory NFI is associated with significant elevation of PGL IgG, LAM IgG and S100 antibody levels. CONCLUSION: These results reveal that the antibody response to mycobacterial antigens, nerve antigens and cytokines are in a dynamic flux and could collectively contribute to NFI in leprosy. The association of multiple markers with old NFI may indicate the contribution of different pathological processes.  
TaalEngels
CategorieResearch
Soort documentArtikel
Rechten© 2011 Jadhav et al. This work is licensed under a Creative Commons Attribution Licence.
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