Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 23 out of 227 patients with positive serological tests for the human immunodeficiency virus (10%), seen between June 1987 and May 1988, lingual lesions of hairy leukoplakia (HL) were found. HL was present in 16/188 drug abusers (9%) and in 7/19 homosexuals (32%). In 3 cases HL was the only clinical manifestation of disease, in 11 it was associated with other symptoms of acquired immunodeficiency syndrome related complex (ARC), and in 9 it was found in patients with a previous or concomitant diagnosis of acquired immunodeficiency syndrome. The mean count of CD4 lymphocytes in the 23 patients was 0.22 X 10(9)/l. The diagnosis was made on the basis of the characteristic clinical features. In 3 cases biopsy was carried out, and parakeratosis and vacuolization of the spinous layer cells were found. Remarkably, particles of the herpesvirus group were also found. The lesions oscillated in size or even spontaneously disappeared, at least transiently; however, in the patients treated with zidovudine the improvement appeared to be more significant. The detection of HL discloses a likely infection by the HIV; it is usually associated with other features of ARC and/or severe immune depression, and it requires the institution of antiretroviral treatment.
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PMID:[Hairy leukoplakia: a new disease of the oral mucosa associated with infection by the human immunodeficiency virus]. 274 11

To examine neuropsychological deficits associated with the human immunodeficiency virus (HIV), 25 asymptomatic homosexual men and sexual partners of intravenous drug users and 25 seronegative homosexual men and nonhigh-risk heterosexuals were assessed on measures of fine motor control, visual scanning, attention, depression, and global psychological functioning. Analysis suggested that HIV infection is associated with reduced fine motor control. Seropositivity is associated with elevated depression and global psychological maladjustment. When depression and global adjustment were analyzed as covariates, motor slowing was evident in the seropositive group. These findings suggest an association between motor slowing and HIV infection in asymptomatic subjects and point to the necessity of measuring affect at least as a control variable. Further study is needed to determine whether the fine motor deficit evident in this sample is limited to distinct subgrouping of the over-all sample.
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PMID:Motor slowing in asymptomatic HIV infection. 276 96

Mononuclear leukocytes from human immunodeficiency virus (HIV)-seronegative and -seropositive homosexual men lysed HIV-infected U937 cells to a significantly greater degree than uninfected U937 cells. Depletion of cell subsets with monoclonal antibodies and complement indicated that the effector cells were primarily of the CD16+ phenotype. Acid-stable alpha interferon (IFN-alpha) production induced by the HIV-infected cells correlated with, although was not an absolute requisite for, preferential lysis of the infected targets. The activity of these CD16+, natural killer (NK) cells decreased in relation to the duration of HIV infection and the presence of acquired immunodeficiency syndrome. Pretreatment of peripheral blood mononuclear cells from HIV-seronegative subjects, but not HIV-seropositive men, with IFN-alpha or recombinant interleukin-2 enhanced lysis of both uninfected and HIV-infected U937 cells. These results suggest that IFN-alpha-associated, NK-like mechanisms are active in the cytotoxic response against HIV-infected cells and that HIV infection results in an early and progressive depression of such responses. Prospective investigations may be useful in determining the role of this NK cell response in the natural history and pathogenesis of HIV infection and the efficacy of therapeutic modalities.
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PMID:Association of alpha interferon production with natural killer cell lysis of U937 cells infected with human immunodeficiency virus. 291 35

The clinical and immunologic findings in a 57-year-old woman with hypogammaglobulinemia are described. The immunodeficiency occurred 11 years after surgical removal of an invasive lymphocytic thymoma. The typical findings of hypogammaglobulinemia as a thymoma-associated clinical syndrome are absence of peripheral blood B-lymphocytes and deficiency of plasma cells in bone marrow. However, in our patient peripheral blood B-lymphocytes and plasma cells in bone marrow were within normal limits, while the total number of peripheral blood mononuclear cells was subnormal. This subnormality was found to be a diminution of peripheral blood T-helper cells. Our patient was anergic to a battery of skin test antigens and her lymphocytes showed a decreased in vitro response to mitogen stimulation. In particular, the response to phytohemagglutinin (PHA) was low, but could be improved by the addition of interleukin-2 to the culture medium. Cocultures between patient B-cells and normal T-cells revealed normal function of patient B-cells. However, cocultures between patient T-cells and normal B-cells showed a significant depression of mitogen-induced immunoglobulin synthesis. These results are suggestive of T-helper cell dysfunction. Consequently, in our case the hypogammaglobulinemia was assumed to be secondary to deficient T-helper cell function.
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PMID:[Immune defect following thymoma. Case description and review]. 293 5

Recent data indicate that the lymphadenopathy-associated virus (LAV) is morphologically similar to animal lentiviruses, such as equine infectious anemia and visna viruses. This finding, together with the cross-reactivity of the core proteins of LAV with those of the equine infectious anemia virus and a similarity in genome structure and biological properties, allows LAV to be placed in the retroviral subfamily of Lentivirinae. Molecular data indicate a high degree of genetic variation of the virus, especially in the envelope gene, which have important implications for the origin of the virus (the T4 lymphotropism may be a recently acquired property) and for future immunization. Another problem is the role of viral infection in the induction of irreversible immunodeficiency. This syndrome occurs in a minority of infected persons, who generally have in common a past of antigenic stimulation and of immune depression before LAV infection.
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PMID:Lymphadenopathy-associated virus: from molecular biology to pathogenicity. 299

Psychiatric symptoms among patients with acquired immune deficiency syndrome (AIDS) may be functional reactions to contracting a fatal and stigmatizing disease or may be secondary to malignancies and opportunistic infections in the central nervous system (CNS). More recent evidence indicates that HTLV-III, the virus that causes AIDS, directly infects the CNS and may cause psychiatric symptoms before signs of immunodeficiency, cognitive impairment, or neurological abnormalities emerge. AIDS-related organic mental syndromes may mimic functional disorders such as chronic mild depression and acute psychosis. Both of these common presentations are illustrated with detailed case reports, and diagnostic and management guidelines are provided.
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PMID:Neuropsychiatric manifestations of AIDS-spectrum disorders. 300 46

Zoster is uncommon before the age of 50 years in immunologically normal individuals, but it occurs with increased frequency in people who are immunosuppressed. A retrospective review of 300 patients with acquired immunodeficiency syndrome associated with Kaposi's sarcoma, revealed that 8% had prior zoster, a rate that is sevenfold greater than historic controls of the same age. We prospectively examined forty-eight patients, with no known immunodeficiency or signs of AIDS or AIDS related complex (ARC), who presented with zoster localized to the thoracic region. Forty-one patients had known risk factors for AIDS and thirty-five had antibody to the AIDS-associated virus (AAV) at the time of presentation. One seropositive subject had no known risk factors. Absolute lymphocyte counts, lymphocyte OKT4/OKT8 ratios, and lymphocyte mitogen responses were all depressed in subjects with antibody to AAV when compared with seronegative individuals. Seven of thirty-three AAV antibody-positive subjects, who could be followed longitudinally, developed AIDS from 1 to 28 months (mean = 13) after zoster. One antibody-negative subject seroconverted to become AAV seropositive 16 months after zoster and developed Kaposi's sarcoma 1 month later. These eight subjects had persistently low lymphocyte OKT4/OKT8 ratios and elevated beta-2 microglobulin. In patients at risk for AIDS, the occurrence of zoster may be one sign that heralds the marked depression of cellular immunity associated with AIDS or ARC.
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PMID:Herpes zoster: a possible early clinical sign for development of acquired immunodeficiency syndrome in high-risk individuals. 301 55

Patients with multiple myeloma are generally immunodeficient, with pronounced depression in primary antibody responses. We have attempted to delineate the reasons for the humoral immunodeficiency by analyzing the specificity repertoire of the surface immunoglobulin (Ig)-positive B cells in patients with multiple myeloma or monoclonal gammopathy of undetermined significance (MGUS), in comparison with normal donors. B lymphocytes from 26 patients with multiple myeloma, 12 patients with MGUS, and 8 normal donors were transformed with Epstein-Barr virus (EBV) and cultured at limiting dilution for clonal analysis. The Ig secreted by each clone was analyzed for class and anti-tetanus toxoid (TT) specificity to determine the frequencies of IgM, IgG, anti-TT IgM, and anti-TT IgG antibody-secreting clones. Our objective was to establish whether the inability to mount humoral responses to common environmental pathogens was due to a lack of specific B cells or to inhibition of B-cell function. Our results indicate that the quantitative B-cell deficiency in patients was due to a nonrandom loss of selected sets of B cells. Although most patients had a reduced aggregate number of B cells, the number of TT-specific B cells was normal. There was, on average, a threefold increase in the proportion of the B-cell specificity repertoire devoted to recognition of TT. Forty-four percent of the patients with MGUS were also affected. In addition, the TT-specific B cells in multiple myeloma patients were severely compromised in their ability to secrete antibody or to differentiate to antibody-secreting cells in vivo. This arrest in differentiation appears to be extrinsic to the B cells, as they were fully able to secrete anti-TT antibody after transformation and culture in vitro. We postulate the existence of an autoimmune inhibitory network mediating the arrest in B-cell differentiation and the humoral immune deficiency.
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PMID:Humoral immune deficiency in multiple myeloma patients due to compromised B-cell function. 302 34

The eradication of a high-response Factor VIII inhibitor in patients with severe hemophilia A is extremely rare even with prolonged immunosuppressive therapy. This report presents a patient with severe hemophilia A, in whom the disappearance of such an inhibitor coincided with the development of the acquired immunodeficiency syndrome (AIDS). Laboratory studies demonstrated a marked decrease in helper T-cells and marked depression of cell-mediated immunity by in vivo and in vitro testing. In addition, humoral immune responses were abnormal. Thus, anamnestic antibody formation to different antigens was absent and in vitro pokeweed mitogen-induced immunoglobulin synthesis by the patient's B-cells was markedly impaired even in the presence of normal T-cells. These findings indicate that the disappearance of the Factor VIII inhibitor and the lack of an anamnestic antibody response to infused Factor VIII observed in this patient may be secondary to a humoral immunodeficiency associated with AIDS.
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PMID:Disappearance of a high response factor VIII inhibitor in a hemophiliac with AIDS. 312 44

This article discusses clinical, immunologic, and etiologic considerations in the acquired immunodeficiency syndrome (AIDS) and the relationship of AIDS to other immunodeficiency diseases. The outstanding clinical feature of AIDS is the occurrence of opportunistic infections in individuals with no prior known cause of immunodeficiency. Such infections have included Pneumocystis carinii, oral thrush from Candida albicans, cytomegalovirus, atypical mycobacteria, cryptosporidium, and Herpes simplex virus. Central nervous system invasion by Cryptococcus neoformans and Toxoplasma gondi has also been reported. Persistent quantitative and functional depression of T4 cells is the immunologic hallmark of full-blown AIDS. Another prominent feature is in vitro spontaneous hyperactivity of B cells. AIDS patients lose cutaneous delayed hypersensitivity reactions both to recall and to new antigens, and T-cell-mediated cytotoxicity is diminished. The mounting number of T8 cells and diminution in T4 cells causes an inversion in the normal T4:T8 ratio. It has been hypothesized that the host defense mechanism is the attempt of the cytotoxic T8 cells to destroy the virus-infected T4 cells. 2 groups of investigators have discovered a lymphocytotropic retrovirus from blood and node lymphocytes of AIDS patients: lymphadenopathy-associated virus (LAV) or human T-lymphotropic virus type III (HTLV-III). Among the primary immunodeficiencies, AIDS most closely resembles the defect observed in purine nucleoside phosphorylase deficiency, an inherited autosomal recessive phenomenon. There is evidence that multiple infections or antigen overload characterize all the risk groups for AIDS. Moreover, antigen overload in experimental animals and man has been shown to suppress immune responses and to down-regulate Ia antigen expression on monocytes. This may prove to be a necessary precondition for the development of AIDS.
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PMID:The acquired immunodeficiency syndrome (AIDS). 315 26


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