Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 1995
Serum IgE in patients with human immunodeficiency virus infection.
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Mazza D S, Grieco M H, Reddy M M, Meriney D
Аннотация
BACKGROUND: Dysregulation of IgE synthesis has been noted in the past in several immunodeficiency states. More recently, analysis of IgE synthesis and atopy in patients who are infected with the human immunodeficiency virus (HIV) has been conflicting.
OBJECTIVE: To determine whether IgE dysregulation occurs in HIV-infected patients and if so, whether this dysregulation is antigen-specific and accompanied by any significant changes in T and B cell markers.
METHODS: Thirty-six HIV-infected patients were enrolled in the study. Twenty-nine patients completed the study. All patients completed an allergy questionnaire and physical examination. Interval visits occurred every 3 months. Blood was obtained at baseline and every 3 months for total IgE, antigen-specific IgE to eight environmental allergens and lymphocyte markers. Study was not blinded.
RESULTS: Analysis of results at baseline and 1 year revealed a subset of patients who had marked elevations in serum IgE protein. This increase was not accompanied by any detectable antigen-specific IgE to the measured allergens nor was any significant change noted in lymphocyte markers. Student's paired t tests were used for data analysis.
CONCLUSION: In a subset of patients with HIV infection, acquired dysregulation of IgE synthesis occurs that results in increased circulatory levels of IgE protein not attributable to atopic allergens or associated with detectable changes in lymphocyte markers.
OBJECTIVE: To determine whether IgE dysregulation occurs in HIV-infected patients and if so, whether this dysregulation is antigen-specific and accompanied by any significant changes in T and B cell markers.
METHODS: Thirty-six HIV-infected patients were enrolled in the study. Twenty-nine patients completed the study. All patients completed an allergy questionnaire and physical examination. Interval visits occurred every 3 months. Blood was obtained at baseline and every 3 months for total IgE, antigen-specific IgE to eight environmental allergens and lymphocyte markers. Study was not blinded.
RESULTS: Analysis of results at baseline and 1 year revealed a subset of patients who had marked elevations in serum IgE protein. This increase was not accompanied by any detectable antigen-specific IgE to the measured allergens nor was any significant change noted in lymphocyte markers. Student's paired t tests were used for data analysis.
CONCLUSION: In a subset of patients with HIV infection, acquired dysregulation of IgE synthesis occurs that results in increased circulatory levels of IgE protein not attributable to atopic allergens or associated with detectable changes in lymphocyte markers.