Recently, a new epidemic illness, the acquired immunodeficiency syndrome, has dramatically emerged in the United States, Europe, and Haiti. The syndrome represents an unprecedented epidemic form of immunodeficiency involving prominent defects of the T-lymphocyte arm of the immune system. Pneumocystis carinii pneumonia, other opportunistic infections, and the previously rare cancer, Kaposi's sarcoma, are the most conspicuous illnesses that have this profound state of immune compromise as their underlying basis. Two years after the onset of clinical illness the case-fatality rate may exceed 90%. A steadily growing body of epidemiologic evidence indicates an infectious (probably viral) cause of the immunodeficiency although the responsible agent(s) remains obscure. Critical issues surrounding the diagnosis, screening of blood products, treatment of complicating infections and cancers, and prognosis for immunologic recovery in affected persons are unresolved. The identification of the cause of acquired immunodeficiency syndrome and the institution of effective preventive measures require the urgent attention of the medical and scientific community worldwide.

The Acquired Immunodeficiency Syndrome

Acquired Immunodeficiency Syndrome (AIDS)

Patients with acquired immune deficiency syndrome (AIDS) frequently present with signs and symptoms referable to the head and neck. Three hundred ninety-nine patients with AIDS presented at the University of California, San Francisco and its affiliated hospitals from 1980 to April 1984. One hundred sixty-five patients (41%) with AIDS presented with, or had on initial evaluation, head and neck manifestations. Of that group, 58 (35%) had cutaneous, oral, and pharyngeal lesions of Kaposi's sarcoma; 51 (31%) had oral, pharyngeal, esophageal, or laryngeal candidiasis; 36 (22%) had chronic cough and shortness of breath; 13 (8%) had rapidly enlarging neck masses; and 7 (4%) had herpes simplex lesions. With the increasing number of cases of AIDS it is important for the otolaryngologist to be aware of these presentations.

Otolaryngologic and head and neck manifestations of acquired immunodeficiency syndrome (AIDS).

Acquired immune deficiency syndrome in childhood.

We evaluated the human T-cell lymphotropic virus type III/Iymphadenopathy-associated virus (HTLV-III/LAV) antibody and immune status of 88 persons living with and/or sexual partners of 43 hemophiliacs, 12 of whom had AIDS, five of whom had AIDS-related complex (ARC), 17 of whom were clinically well but HTLV-III/LAV antibody positive, and nine of whom were well and HTLV-III/LAV antibody negative. No nonhemophilic household contacts (0/50) of healthy hemophiliacs were HTLV-III/LAV antibody positive; two of 33 nonhemophilic AIDS/ARC contacts were positive. One was a spouse and one a sexual partner of a hemophiliac. One of these antibody-positive contacts herself had AIDS, and one had ARC. Antibody-negative, nonhemophilic contacts of AIDS/ARC and of antibody-positive hemophiliacs had significantly lower numbers of lymphocytes, T helper lymphocytes, and T suppressor lymphocytes than did contacts of antibody-negative hemophiliacs. We conclude that risk of HTLV-III/LAV transmission may exist for spouses and/or sexual contacts of hemophiliacs with AIDS/ARC, but we cannot now determine the risk for contacts of asymptomatic hemophiliacs. ( JAMA 1986;255:212-215)

HTLV-III/LAV antibody and immune status of household contacts and sexual partners of persons with hemophilia.

Recently, hemophiliac patients receiving factor VIII concentrate therapy have developed the acquired immunodeficiency syndrome. Because abnormalities of cell-mediated immunity are found in this syndrome, we evaluated the peripheral blood immunologic status of 24 patients with classic hemophilia and 5 patients with factor IX deficiency. Both groups had decreased percentages and numbers of helper-inducer lymphocytes (OKT4+) and increased percentages of suppressor-cytotoxic T-lymphocytes (OKT8+) which resulted in depressed OKT4/T8 ratios. Abnormalities of the T-lymphocyte subpopulation were most severe in 7 patients with factor VIII deficiency with lymphadenopathy who also had increased Ia+ cells and profoundly suppressed lymphocyte mitogenic responses. No correlation was found between OKT4/OKT8 ratios or lymphocyte responses to mitogen and the amount of factor VIII concentrate used per year. Evaluation of five wives of factor-VIII-deficient patients who had abnormal OKT4/OKT8 ratios showed decreased percentages of OKT4 cells, but normal lymphocyte mitogenic responses. Serum levels of IgG were elevated in factor-VIII-deficient patients but not their wives or factor-IX-deficient patients. We conclude that T-lymphocyte subpopulation abnormalities and lymphocyte mitogenic responses are depressed in asymptomatic hemophiliac patients receiving either factor VIII or factor IX concentrates. These abnormalities are most severe in otherwise asymptomatic hemophiliac patients who have developed lymphadenopathy.

An Immunologic Evaluation of Hemophiliac Patients and Their Wives: Relationships to the Acquired Immunodeficiency Syndrome

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An Immunologic Evaluation of Hemophiliac Patients and Their Wives: Relationships to the Acquired Immunodeficiency Syndrome