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Background Although patients with idiopathic CD4+ T-lymphocytopenia and serious opportunistic infections have been described previously, the clinical and immunologic features of this condition have not been well defined.
Methods We studied in detail five patients with idiopathic CD4+ T-lymphocytopenia. The studies included serologic testing, culture, and polymerase chain reaction for the human immunodeficiency virus (HIV) types 1 and 2, serologic testing for the human T-cell lymphotropic virus (HTLV) types I and II, lymphocyte phenotyping, immunoglobulin quantitation, and lymphocyte-transformation assays, as well as attempts to isolate a retroviral agent. The results were compared with those in HIV-infected persons matched for CD4+ T-cell counts and with those in normal controls. We also studied the spouses of patients and the blood donors for one patient.
Results In these five patients, there was no evidence of either HIV or HTLV infection. All the patients had both low percentages and low counts of CD4+ T cells, with relative increases in percentages, but not counts, of CD8+ cells. Numbers of B cells and natural killer cells were generally normal. As compared with HIV-infected persons, our patients had lower percentages and counts of CD8+ cells and more lymphopenia. CD4+ counts were relatively stable over time. Instead of the high immunoglobulin levels seen in HIV infection, these patients had normal or slightly low levels of immunoglobulins. The lymphocyte-transformation response to mitogens and antigens was depressed. Results in spouses and blood donors were normal.
Conclusions Idiopathic CD4+ T-lymphocytopenia differs from HIV infection in its immunologic characteristics and in its apparent lack of progression over time. Nothing about the immunologic or viral-culture studies performed in these patients or about their family members or blood donors suggests that a transmissible agent causes this condition.
Source Information
From the Immunology Branch, Division of HIV/AIDS (T.J.S., B.M.J., J.K.A.N.), and the Retrovirus (R.B.L., T.R.) and Herpesvirus (A.C.M.) Branches, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta; the Divisions of Allergy, Immunology, and Infectious Diseases, William Beaumont Hospital, Royal Oak, Mich. (C.B.L.); the Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine, Atlanta (J.A.S.); and the University of Arkansas for Medical Sciences, Little Rock (R.A.M.). Presented in part at the Keystone Symposia on Molecular and Cellular Biology, Keystone, Colo., March 27-April 4, 1992, and the Eighth International Congress of Immunology, Budapest, Hungary, August 23-28, 1992.The use of trade names is for identification only and does not imply endorsement by the Public Health Service or the Department of Health and Human Services.
Address reprint requests to Dr. Spira at the Division of HIV/AIDS, Mailstop D-08, National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Rd., Atlanta, GA 30333.
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