BACKGROUND: The classical triad of Job's syndrome (Hyper-IgE syndrome), a congenital immunodeficiency disorder, includes recurrent "cold" abscesses, pneumonias and extreme elevations of the serum IgE concentration. CASE REPORT: A 49-year-old HIV-1 infected patient with a viral load of 268,852 copies/ml plasma and a CD4+ T lymphocyte concentration of 2 cells/microliter blood was admitted to our clinic for antibiotic therapy and incision and drainage of several large abscesses. The patient suffered for approximately 5 years from recurrent pneumonias, abscesses and multiple allergies. The serum IgE level was over 100-fold elevated and, after analysis of archived serum samples, had not been influenced by fluctuations in the plasma viral load or changes in the CD4+ T lymphocyte concentration in previous years. No stigmata of Job's syndrome were present prior to the patient's HIV-1 infection. Observations on other patients with AIDS and recurrent abscesses suggest that in these patients hyperimmunoglobulinemia E is related to a cytokine class switch from a TH1 to a TH2 profile as CD4+ T lymphocytes are depleted. CONCLUSIONS: Following CD4+ T lymphocyte depletion, it has been rarely documented that HIV-1 infected patients may develop clinical symptoms and a hyperimmunoglobulinemia E, similar to patients with the congenital immunodeficency of Job's syndrome.
BACKGROUND: The classical triad of Job's syndrome (Hyper-IgE syndrome), a congenital immunodeficiency disorder, includes recurrent "cold" abscesses, pneumonias and extreme elevations of the serum IgE concentration. CASE REPORT: A 49-year-old HIV-1 infectedpatient with a viral load of 268,852 copies/ml plasma and a CD4+ T lymphocyte concentration of 2 cells/microliter blood was admitted to our clinic for antibiotic therapy and incision and drainage of several large abscesses. The patient suffered for approximately 5 years from recurrent pneumonias, abscesses and multiple allergies. The serum IgE level was over 100-fold elevated and, after analysis of archived serum samples, had not been influenced by fluctuations in the plasma viral load or changes in the CD4+ T lymphocyte concentration in previous years. No stigmata of Job's syndrome were present prior to the patient's HIV-1 infection. Observations on other patients with AIDS and recurrent abscesses suggest that in these patientshyperimmunoglobulinemia E is related to a cytokine class switch from a TH1 to a TH2 profile as CD4+ T lymphocytes are depleted. CONCLUSIONS: Following CD4+ T lymphocyte depletion, it has been rarely documented that HIV-1 infectedpatients may develop clinical symptoms and a hyperimmunoglobulinemia E, similar to patients with the congenital immunodeficency of Job's syndrome.