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)

HIV disease often leads to neuropsychiatric disturbance, either through direct infection of the brain by the virus or through CNS disease secondary to immunodeficiency. Neuropsychiatric complications of AIDS and AIDS-related disorders may present clinically as acute or chronic organic mental syndromes, or may mimic functional psychiatric illness, in particular depression, anxiety, or psychotic states. Two cases of hypomanic states in homosexual men suffering from AIDS are reported. Neither of the two men had a personal or family history of affective disorder. In one man, hypomanic symptoms were caused by early HIV encephalopathy; he rapidly developed typical HIV dementia with a marked downhill course. In the second case, a clear connection between the hypomanic symptoms and direct HIV brain involvement was not established.
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PMID:Two cases of hypomania in AIDS. 316 73

Neuropsychological examination was performed on 13 patients and 10 matched controls to assess the brain involvement of patients with human immunodeficiency virus (HIV) infection. HIV-infected patients showed a significant decline in visuomotor, visuoconstructive and practical abilities as well as in motor-free visuospatial performance and repeating a long sentence. These findings could not be explained by the concomitant mental depression of these patients. Neither were they associated with any particular stage of HIV infection. The results suggest that mild cognitive changes may be detected even in the early stages of HIV infection, when examined by appropriate neuropsychological methods.
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PMID:Cognitive changes as early signs of HIV infection. 317 82

Pathogenesis of HIV infection and expression of retroviral proteins are gradually being elucidated. Antibody to HIV is a marker of past or present viral infection. The virus can be isolated from cultured lymphocytes of seropositive but not seronegative patients. Sero-epidemiological studies show that the majority of infected patients are asymptomatic carriers without biological sign of immune depression. Some then show immune abnormalities such as a decrease of CD4 cells in the blood; some patients present with lymphadenopathies or signs of AIDS-related complexes. Frank AIDS is a late stage of the disease. Some cofactors increase the immunodeficiency and then accelerate the passage from asymptomatic carrier to persistent generalized lymphadenopathies or AIDS by spreading the virus into target cells, susceptible T4 cells, bone marrow precursors, or brain. These AIDS patients then present with opportunistic infections and/or malignancies like Kaposi's sarcoma, lymphoma, and/or brain diseases (dementia or encephalitis).
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PMID:HIV target cells: effect of their infection by HIV on the pathogenesis of AIDS. 326 Sep 82

The epidemic form of Kaposi's sarcoma (KS) that occurs in patients with the acquired immune deficiency syndrome (AIDS) produces lesions that, histopathologically, are indistinguishable from those of classical KS or of the endemic form of the disease seen in children and adults in certain areas of Africa. There are, however, important differences in the pathogenesis of the disease in the different groups affected by the neoplasm. Compared with classical KS in people of eastern European and Mediterranean descent, which commonly takes a protracted, indolent course, the epidemic Kaposi's sarcoma (EKS) is far more aggressive. However, the KS seen in adults in endemic areas of Africa may also become florid and rapidly progressive after years of quiescence. Some degree of immune dysfunction is thought to be a factor in all forms of KS, with immune depression being the hallmark of EKS and the setting in which it occurs. Cytomegalovirus (CMV) is thought to be at least a cofactor in the disease, but it has also been suggested that the etiologic agent of AIDS, human immunodeficiency virus (HIV), may also play a role in EKS.
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PMID:Pathophysiology and epidemiology of epidemic Kaposi's sarcoma. 329 18

Bone marrow transplantation (BMT) is often followed by significant morbidity and mortality due to protracted immunodeficiency. We have hypothesized that the bone marrow-ablative regimen may delay the recovery of normal immune function following transplantation by impairing the interaction of host endothelial cells with circulating graft-derived lymphocytes. This report compares the relative effects of busulfan (an alkylating drug) and gamma-irradiation on the tissue-specific localization potential of lymphocytes and the eventual recovery of immune function within syngeneic murine transplant recipients. Localization of normal lymphocytes into peripheral lymph nodes of irradiated BMT recipients was markedly less (less than 50%) than in busulfan-treated or normal mice over the first 2 months post-BMT. This finding correlated with irradiation-induced endothelial cell edema and microvascular occlusions within lymphocyte-receptive areas of the nodal microvasculature. The effect of both preparative regimens on the recovery of contact hypersensitivity (CHS) was also analyzed. This response recovered more quickly (between 1 and 2 months) in busulfan-pretreated animals. Further experiments demonstrated that the decrease in CHS responsiveness appeared, in part, related to a depression in the capacity of lymphocytes to localize into skin sites of antigen deposition within irradiated mice. The impairment of tissue-specific lymphocyte localization may represent a novel mechanism by which whole body irradiation can contribute to delayed immunologic reconstitution following bone marrow transplantation.
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PMID:Recovery of contact hypersensitivity responses following murine bone marrow transplantation: comparison of gamma-irradiation and busulfan as preparative marrow-ablative agents. 331 44

We evaluated 100 human immunodeficiency virus (HIV) antibody-positive persons from the only alternate test site in Los Angeles. Thirty-five subjects complained of systemic symptoms suggestive of HIV infection and 65 were completely asymptomatic. Irrespective of symptoms, the group as a whole demonstrated clinical and laboratory evidence of immunodeficiency. Eighty had generalized lymphadenopathy, 16 onychomycosis, six oral candidiasis, and two biopsy-proved Kaposi's sarcoma. Seventy-seven were anergic to seven intradermal antigens. Despite normal white blood cell counts in most subjects, the T-helper-cell count was less than 300/mm3 in 48% of asymptomatic and 46% of symptomatic subjects. The degree of immune depression was less severe but approximated that of patients with acquired immunodeficiency syndrome after Pneumocystis carinii pneumonia. We believe these findings justify the need for comprehensive medical evaluation and follow-up care for seropositive persons from alternate test sites.
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PMID:Clinical features of 100 human immunodeficiency virus antibody-positive individuals from an alternate test site. 350 Jun 85

Although supported by a number of experimental models, the assumption assigning a crucial role to the immune system in the antineoplastic defense mechanisms has not been convincingly demonstrated so far for human tumors. Should the theory be correct, severe functional impairment of the immune system would obviously result in the occurrence of tumors with abnormally high frequency. Registry holdings systematically collecting pertinent information on the malignancies developed in patients with primary immunodeficiency diseases or in organ transplant recipients maintained on therapeutically-induced immune depression, as well as the observation of tumors occurring in patients treated with immunosuppressive agents and of second malignancies arising after radio- and/or chemotherapy of the primary tumor consistently indicate that depressed immunity is usually associated with an increased incidence of cancer as compared with that expected in the general control populations. However, not all types of tumors are increased to the same extent, in that lymphoreticular neoplasias (especially non-Hodgkin's lymphomas), acute leukemias as second tumors and, among solid neoplasms, squamous cell carcinomas are those most frequently reported. These observations suggest that even deeply impaired tumoricidal immune mechanisms may facilitate the growth of certain tumors only, especially of those arising from the cells of the immune system itself, in remarkable contrast with their frequency in the general population. Oncogenesis may be favoured in various states of depressed immunity by a number of ways. Their elucidation might have bearing on the comprehension of the more general phenomenon of the neoplastic transformation.
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PMID:[Immunological deficiency syndromes, immunosuppression by drugs and occurrence of neoplasms: a casual association?]. 409 54

Alpha- and gamma-interferon (IFN) production by peripheral blood mononuclear cells (PBMC) from 18 patients affected by primary immunodeficiency syndromes was examined and compared with that of 20 normal donors. Patients included 8 with common variable immunodeficiency (CVI), 2 with congenital agammaglobulinemia, 4 with ataxia-telangiectasia, 2 with hyper-IgE syndrome, 1 with chronic EBV infection, 1 with combined immunodeficiency, and 1 with immunodeficiency with hyper-IgM. No spontaneous IFN production was observed in either patients and controls. Newcastle disease virus-induced alpha-IFN production was found to be normal in all patients. Gamma-IFN was induced by both galactose oxidase and staphylococcal enterotoxin (B). Gamma-interferon production was low or undetectable in patients with ataxia-telangiectasia, in immunodeficiency with hyper-IgM, and in hyper-IgE syndrome. No major defect of gamma-IFN was found in other types of immunodeficiency, despite the presence of occasional low producers (1 of 8 CVI patients and 1 case of congenital agammaglobulinemia). No correlation was found between IFN production and natural killer activity in individual patients. The analysis of lymphocyte subsets by monoclonal antibodies revealed gross imbalances of helper/inducer and suppressor/cytotoxic subpopulations, but no overall correlation could be established with gamma-IFN production. The observation of major defects in gamma-IFN yield only in diseases with depression of T cell-mediated immunity might contribute to a better understanding of the pathogenetical mechanisms in these diseases. Moreover, future studies should monitor these in vitro functions and their modifications by in vitro or in vivo manipulations.
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PMID:Interferon production in primary immunodeficiencies. 609 14

A 31-year-old Frenchman had an acquired immunodeficiency syndrome (AIDS) with profound depression of cellular immunity and relative sparing of humoral immunity. The clinical picture included intractable secretory diarrhoea, vomiting, abdominal pain, and weight loss. Gastrointestinal cryptosporidiosis was present and a perfusion technique showed profuse secretion of fluid in the proximal small bowel. The patient also had recurrent Salmonella typhimurium septicaemia, cytomegalovirus infection, and cerebral toxoplasmosis and he died within 13 months. This patient did not belong to any of the groups known to be affected by this type of acquired immunodeficiency (homosexuals, drug addicts, haemophiliacs, Haitians) but had been transfused with Haitian blood 4 years before onset of symptoms. This case supports the notion that some forms of AIDS may be transmitted by blood, with a long incubation period.
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PMID:Acquired immunodeficiency with intestinal cryptosporidiosis: possible transmission by Haitian whole blood. 613 90

Low levels of serum complement subcomponent C1q may accompany primary humoral immunodeficiency diseases such as sex-linked agammaglobulinemia, severe combined immunodeficiency, and common varied immunodeficiency. This selective depression of C1q is proportional to the degree of hypogammaglobulinemia, and is corrected in severe combined immunodeficiency by bone marrow transplantation or in hypogammaglobulinemia by immunoglobulin infusions, possibly because C1q is stabilized by IgG by reversible interactions which reduce extravascular degradation. In this study it is shown that a pH 4.0 treated intravenous gamma-globulin (ivGG) and a reduced and alkylated ivGG can equally increase levels of serum IgG, but that only the pH 4.0 preparation can raise C1q levels into the normal range. These findings show that some of the methods used to produce immunoglobulins suitable for intravenous use may hinder the ability of these molecules to stabilize Clq. The clinical implications of this observation remain unclear.
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PMID:Normalization of serum C1q after intravenous immunoglobulin infusions in hypogammaglobulinemia: dependence upon methods of immunoglobulin preparation. 620 68


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