Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human herpesvirus type six (HHV-6), previously called human B-cell lymphotropic virus (HBLV), was first isolated in 1986 from patients with various lymphoproliferative disorders, some related to the acquired immunodeficiency syndrome. In order to investigate the epidemiology of HHV-6 in the Horn of Africa, we studied 281 young adults living in the city of Djibouti during June 1988. Of these, 181 belonged to various groups at risk for human immunodeficiency virus (HIV), while 100 represented the normal young adult population. Sera were screened and titrated for antibodies against HHV-6 by an indirect fluorescent antibody assay. The percentage seropositivity for HHV-6 was 71 in the normal population, 75 in the population at risk for HIV, and 93 in the population of subjects with a confirmed positive HIV Western blot. Mean titres of positive sera were similar in all population groups. No correlation existed between HHV-6 seropositivity and age, sex, tribe, habitat, and risk factors for HIV. A positive correlation was noted between HHV-6 and patients complaining of fatigue.
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PMID:HHV-6 in Djibouti--an epidemiological survey in young adults. 216 Nov 34

During autumn- and winter epidemics respiratory syncytial (RS) virus accounts for the majority of respiratory infections in infants and young children. In case of an acute lower respiratory tract infection, RS virus can induce serious symptoms. These are age-dependent. The most important symptoms in babies and toddlers are dyspnea, wheezing, cyanosis and apneas. In the case of respiratory insufficiency or fatigue, as well as recurrent apneas, mechanical ventilation is required. Diagnosis can be made using a direct immunofluorescence technique with monoclonal antibodies. To control the risk of nosocomial RS virus infections, isolation precautions are necessary. The overall mortality is low (less than 1%), but may be strikingly higher in children at risk: babies less than one month of age, preterm babies, infants with congenital heart- or pre-existent respiratory diseases, and those with severe immunodeficiency syndromes. In these subgroups therapy with ribavirin (Virazole) may be beneficial, although until now there is no strong evidence for the effectiveness of this antiviral agent. The majority of the children will have recurrent symptoms of dyspnea and wheezing over the subsequent years following the RS virus infection. In acute lower respiratory RS virus infection, there may be IgE mediated hypersensitivity reactions to viral agents, with release of chemical mediators of airway obstruction. The pathophysiological mechanisms might be comparable to those in patients with asthma.
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PMID:[Once more a discussion of the RSV affair]. 218 Jan 18

A 43-year-old homosexual man visited his dentist with painful, nodular, ulcerated lesions on the soft palate, right buccal mucosa, and right posterior maxillary gingiva. Serologic studies for exposure to human immunodeficiency virus, performed before biopsy, were positive. Biopsy of the maxillary gingiva demonstrated sheets of histiocytes containing small intracellular yeasts, which on culture were identified as Histoplasma capsulatum. Bilateral leukoplakic lesions with some vertical furrowing involving the lateral borders of the tongue were also noted. Histologically, hyperkeratosis and fungal hyphae were identified. The patient was treated for histoplasmosis with amphotericin B, which resulted in significant improvement of the oral lesions. He was subsequently hospitalized for fatigue and dyspnea and was found to have Pneumocystis carinii pneumonia. Pulmonary status deteriorated within a 3-week period, and the patient died. Autopsy findings were negative for histoplasmosis but positive for necrotizing and cavitary P. carinii pneumonia, pulmonary and hepatic herpes simplex infections, and pulmonary and intestinal cytomegalovirus infection.
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PMID:Oral histoplasmosis as a presenting disease in acquired immunodeficiency syndrome. 223 84

Relationships between nutrition and infection are generally complex, bidirectional, and not perfectly worked out. Healthy people can adapt to simple decreases in intake or increases in expenditure. However, the imposition of infection with associated cytokines may impair such adaptations, resulting in wasting of lean tissue. In human immunodeficiency virus (HIV) infection, nutritional abnormalities are common. Lean body mass depletion is associated temporally with death in a subset of acquired immune deficiency syndrome (AIDS) patients. Weakness, fatigue, and anorexia are important symptomatic complaints affecting quality of life. Pathophysiologic mechanisms remain speculative, although there is reason to suspect four theoretic factors: decreased intake, malabsorption, hypermetabolism, and altered metabolism. More than one disturbance may be necessary for clinical wasting to develop; ie, a primary abnormality plus a failure of homeostatic adaptation. Excess cytokine production also may be involved, but this is uncertain. Therapeutics remain empiric in the absence of known mechanisms. Current options are restricted to diet adjustments or supplements, treatment of underlying diseases (where possible), and rarely, parenteral alimentation. Promising investigational possibilities include an appetite stimulant (megestrol acetate) and therapies to oppose cytokine production or actions, but definitive beneficial effects on nutritional status, subjective performance, disease activity, or survival have not yet been demonstrated. Advances in clinical therapeutics await an improved understanding of pathophysiologic mechanisms and carefully designed clinical trials testing proposed interventions.
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PMID:Current approach to the treatment of human immunodeficiency virus-associated weight loss: pathophysiologic considerations and emerging management strategies. 225 24

AIDS-related gastrointestinal disease is common, presenting a challenge to all nutritional support clinicians. Patients frequently suffer from weight loss, diarrhea, malabsorption, and cachexia. Many factors complicate the course of AIDS-related gastrointestinal disease, including decreased food intake (resulting from fatigue and malaise), increased metabolic demand and nutritional requirements, and identifiable gastrointestinal pathology. Gastrointestinal pathology is well-documented, and in approximately 50% of persons with AIDS-related gastrointestinal disease, a causative agent can be identified. In general, treatment of AIDS-related gastrointestinal disease is not always curative. Much of the chronic gastrointestinal dysfunction is caused by recurring opportunistic pathogens that are resistant to chemotherapy. Often, patient care and long-term management can focus only on fluid and electrolyte balance, nutritional support, and symptom control. Even clinically stable patients have been diagnosed as chronically malnourished and, for reasons that remain unclear, are prone to rapid nutritional deterioration during disease exacerbations. Published reports of nutritional assessment and intervention in persons with AIDS are now appearing in the literature. However, the eventual mortality associated with AIDS still results in a hesitancy on the part of many clinicians to prescribe aggressive nutritional support, especially parenteral nutrition. Who to treat and at what stage of illness becomes the question. As new agents, such as AZT, are prescribed on a more frequent basis for persons with AIDS, the use of nutritional support as adjunctive therapy early in the course of disease becomes an issue. Although improving nutrition has not been shown to reverse any of the cellular immunodeficiency caused by HIV infection, quality of life may be improved. In specific cases, nutritional support, whether through diet counseling, food programs, or intervention with enteral or parenteral nutrition, appears to improve strength and endurance, thus enhancing quality of life.
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PMID:Gastrointestinal manifestations of the acquired immunodeficiency syndrome. 249 50

A mononucleosis-like illness is frequently recognized retrospectively as the first manifestation of infection with human immunodeficiency virus-type 1 (HIV-1). This acute but transient retroviral syndrome may include symptoms such as malaise, fever, sweats, myalgia, arthralgia, maculopapular rash, diarrhea, and lymphocytic meningitis. We observed two intravenous drug users who developed a severe, febrile illness with subsequent oral thrush (one also had biopsy-proven esophageal candidiasis). Both patients had weight loss, arthralgia, myalgia, and fatigue. These symptoms occurred two weeks after needle-sharing and persisted for 7 weeks in one patient and 10 weeks in the other. Both patients had serologic evidence for both acute HIV-1 and cytomegalovirus infection. Cytomegalovirus enhances HIV-1 replication in vitro, presumably by stimulating HIV-1 gene expression. Thus, the observed syndrome suggests that this viral interaction may be clinically significant because it appears to cause severe additional morbidity, which is not typical for primary infection with HIV-1. After 6 months of follow-up, one patient is completely asymptomatic but shows markedly reduced CD4+ lymphocytes. The other patient developed persistent lymphadenopathy after the acute illness, but is feeling well 21 months after infection.
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PMID:Co-infection with human immunodeficiency virus-type 1 (HIV-1) and cytomegalovirus in two intravenous drug users. 215 58

Early pathological abnormalities in human immunodeficiency virus (HIV-1)-related dementia have not been well documented. We report a homosexual man with fatigue and intermittent diarrhea in whom early HIV-1-related dementia was demonstrated during neurological screening in the Multicenter AIDS Cohort Study. Within 4 months he died of massive epistaxis, and the brain revealed astrocytosis of white matter and mild pallor of myelin staining in the absence of inflammation, multinucleated giant cells, and brain atrophy.
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PMID:Neuropathological changes in early HIV-1 dementia. 281 44

EBV infection may have a wide range of clinical consequences: it is often asymptomatic; some cases-generally adolescents-develop the classic "infectious mononucleosis" syndrome; in rare cases the illness takes a severe, fatal course. EBV is also implicated in some geographic areas, in Burkitt' lymphoma and naso-pharyngeal carcinoma. Recent research has enrich our knowledge on the viral genome and the various viral antigen, but some problems are still unsolved. The "normal" immunological response to EBV infection is briefly summarized; then the abnormal immunological pattern is considered in relation to some conditions such as age, congenital and acquired immunodeficiencies and unusual clinical syndromes. Recently a group of not well defined, persistent illnesses (fever, fatigue, headache etc.) has been correlate to a "chronic" EBV infection. It becomes more and more evident that different clinical manifestations of EBV infection are always connected with a particular immunological response; between the "normal" cases and those with well defined immunodeficiency probably large group exists in which minor immunological abnormalities are responsible for a partial derepression of the virus.
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PMID:[Epstein-Barr virus infection. Old and new immunological aspects]. 282 32

A 29 year old white homosexual man presented with a two and a half week history of severe sore throat, fever, and extreme fatigue. His symptoms did not respond to antibiotics. He had mild bilateral conjunctivitis, a rash over his chest and back, and enlarged lymph nodes, but examination of the nervous system yielded normal results. He had low total white cell and platelet counts. The results of enzyme linked immunosorbent assay for human immunodeficiency virus (HIV) were equivocal when HIV IgM was detected in serum. Despite treatment with ampicillin his temperature remained high and he developed abnormal neurological signs, including a paraparesis and hyperreflexia of the arms. HIV was isolated from lymphocytes from blood and cerebrospinal fluid. Over the next six weeks the patient improved and was discharged. Two months later abnormal neurological signs persisted in his legs. Although various neurological syndromes associated with seroconversion to HIV have been described, this is probably the first report of a patient with myelopathy at the time of seroconversion.
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PMID:Acute myelopathy associated with primary infection with human immunodeficiency virus. 288 58

Tumor necrosis factor (TNF) has demonstrated antitumor activity against a variety of tumors and is particularly cytotoxic to capillary endothelial cells, which are the presumed cell of origin of Kaposi's sarcoma. We evaluated the toxicity and clinical antitumor and antiretroviral effects of recombinant TNF administered at a once weekly dose of 100 micrograms/m2 intravenously for 8 weeks in five men with AIDS-related Kaposi's sarcoma and without prior opportunistic infection. One patient was removed from study at week 4 due to rapid progression of Kaposi's sarcoma, another patient with stage IV disease and a pretreatment CD4 count of 11 developed fever, hypotension, and pneumonia at week 7 and died 8 days after discontinuing recombinant TNF. No pathogenic organisms were isolated. He had marked eschar formation of his Kaposi's sarcoma lesions, particularly in areas previously exposed to radiation therapy. Uniform toxicities included fevers, rigors, and headaches during drug infusion that were ameliorated by prophylactic meperidine hydrochloride and acetaminophen. All experienced fatigue and three had arthralgias. One patient had transient hypotension which corrected with i.v. fluids. No significant hematologic, hepatic, or renal toxicities were seen. All patients had some progression of their Kaposi's sarcoma on study. There was no change in CD4 or CD8 count or in CD4:CD8 ratios. Serum human immunodeficiency virus (HIV) p24 antigen levels increased greater than 50% in three patients. We conclude that, as a single agent, at a dose of 100 micrograms/m2 recombinant TNF by i.v. infusion has no obvious antitumor or antiretroviral effects in patients with AIDS-related Kaposi's sarcoma.
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PMID:Intravenous recombinant tumor necrosis factor in the treatment of AIDS-related Kaposi's sarcoma. 291 61


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