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)

Though not conclusive, our primary findings indicate that a feature common to many of our tumor and ICD patients is depressed cortisol production. Additionally, the response to ACTH adrenal cortex stimulation tests, at 2-hour intervals between rest and stimulation, have ranged from negative to substantially less than would be expected in normal subjects. Peripheral plasma cortisol values for dogs, at rest and 2 hours after ACTH stimulation, respectively, have been reported as 2-10 and 25-30 mug/dl, 3-8 and 7.5-18 mug/dl, and 1-12.5 and 9.5-22 mug/dl. For representative patients, our resting values have been 1.2-5.2 mug/dl, vs 1.2-7.6 mug after ACTH stimulation (Table 2). Altogether we have studied 42 cases in detail, and we feel that a post-ACTH level of 8.0 mug/dl or less is a conservative indication of adrenocortical insufficiency; all levels have been between 1 and 8 mug/dl. We believe these low cortisol levels indicate either a genetically-induced adrenal cortical insufficiency (evident at 2 months to 1 year of age) or an immune complex adrenal cortical suppression (occurring after 1 year of age in association with other immunodeficiency disorders). Our studies demonstrate a need for biphasic therapy. We have found it necessary to not only initiate cortisone acetate therapy to support the deficient adrenal cortical secretion, but also use other immunosuppressive drugs to control the ICD. If the target organ has been suppressed or destroyed, the need for supplementation is obvious. However, other immune-injury moieties must be suppressed also, eg, ANA, anti-IgG antibodies, etc.
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PMID:Canine immune complex diseases. 13 91

Several investigators have suggested that early diagnosis of human immunodeficiency virus (HIV) infection in infants could be accomplished with a modified, more-sensitive, acid-dissociated p24 antigen enzyme-linked immunosorbent assay (ELISA) technique (p24 antigen immune complex dissociation [ICD]). We compared detection of HIV infection by HIV culture, PCR, and p24 antigen ICD assays in 46 infants by using samples collected independently. The detection sensitivity of the p24 antigen ICD assay was 0% with cord blood samples (2 HIV-positive infants), 38% with plasma samples from infants under 3 months of age (8 HIV-positive infants), and 58% overall (12 HIV-positive infants). By contrast, the sensitivities of HIV culture and PCR were 50% for cord blood samples, 75% for plasma samples from infants under 3 months of age, and 83% overall. These results indicate that the p24 antigen ICD does not offer the sensitivity necessary for this assay to be used as an indicator of HIV infection in infants.
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PMID:Sensitivity of immune complex-dissociated p24 antigen testing for early detection of human immunodeficiency virus in infants. 771 18

Human immunodeficiency virus (HIV)-associated nephropathies are characterized by renal immune cell interstitial infiltration in patients with peripheral T-cell depletion. Since interstitial inflammation may mediate cytokine-induced fibrosis, we evaluated the immune cell population in the interstitium and glomeruli in renal biopsy tissue from 10 HIV-infected patients with focal segmental glomerulosclerosis (HIVFGS), staining renal biopsy specimens for UCHL-1 (a T-cell marker), OPD4 (predominantly a T helper-cell marker), PG-M1 (a macrophage marker), and L26 (a B-cell marker), and comparing them with renal tissue specimens from patients with HIV-associated immune complex glomerulonephritis (ICD) and from uninfected patients with FGS. Five fields comprising 0.2 mm2 were examined at a magnification of x400, a total area of 1 mm2. Total immune cells were estimated as the sum of UCHL-1, L-26, and PG-M1 cells. The T helper to suppressor (H/S) ratio was estimated as OPD4/(UCHL-1 - OPD4) lymphocytes. Tubular interstitial infiltrate was variable but dense in the majority of the infected biopsies, and was mild to moderate in all uninfected cases. The proportion of interstitial macrophages was greater in biopsy specimens from patients with HIVFGS than in those with HIVICD. In contrast, there was a greater percentage of B cells in the infiltrate in HIVICD compared with HIVFGS. Although there were fewer immune cells in whole glomeruli compared with 1 mm2 interstitium, macrophages were the predominant cells in glomeruli. B lymphocytes were generally absent in glomeruli in infected tissue, a pattern similar to uninfected tissue. The blood H/S ratio in HIV-infected patients was 0.2 +/- 0.03.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Macrophages in human immunodeficiency virus-associated kidney diseases. 797 17

To examine recent changes in longevity and the causes of death among persons with hemophilia A, we evaluated death certificate data for persons who died in the United States from 1968 through 1989 and had hemophilia A or congenital Factor VIII disorder (ICD code 286.0) listed on the death certificate as one of the multiple causes of death. Multiple-cause-of-death mortality data for the United States from 1968 to 1989 were examined to compare death rates by year, focusing on death rates and causes of death for 1979-1981, 1983-1985, and 1987-1989. Gender, age group, race, geographic region, and median age at death of persons with hemophilia A and human immunodeficiency virus (HIV)-related disease listed as a cause of death were compared with those with hemophilia A without HIV-related disease. From 1968 through 1989, 2,792 hemophilia A deaths were reported. The death rate increased from 0.5 to 1.3 per 1,000,000 persons. From 1979-1981 through 1987-1989, mortality increased in all age groups above 9 years of age and age at death shifted markedly to lower ages. Median age at death decreased from 57 years in 1979-1981 to 40 years in 1987-1989. The percentage of deaths due to hemorrhage or diseases of the circulatory system decreased markedly as the result of the increase in deaths associated with HIV infection or infections other than HIV infection. Spread of HIV-1 infection in persons with hemophilia A has disrupted the reduction in mortality seen with factor replacement therapy, implementation of home care, and use of comprehensive hemophilia treatment centers. It is hoped that advances in the care of HIV-infected persons will improve survival in the hemophilia community.
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PMID:Changes in longevity and causes of death among persons with hemophilia A. 814 Nov 17

Progressive cognitive impairment in human immunodeficiency virus (HIV) infection, called acquired immunodeficiency syndrome (AIDS) dementia complex (ADC), significantly influences the social prognosis of afflicted patients. The frequency and character in different stages of the infection are controversially discussed. In previous studies, differences in the selection of patients and methods of testing led to widely differing results. For these reasons, in the present prospective study on 45 HIV-infected patients, a structured psychiatric interview (SIDAM) was conducted based on the algorithm of diagnosing dementia in DSM-III-R and the ICD-10 guidelines. The psychopathological findings are expressed in syndrome scores; the results are summarized in a total score (SISCO). The interview contains the Mini-Mental State Examination. The degree of psychosocial functioning was estimated on the global assessment of functioning, Axis V of DSM-III-R. In stages preceding AIDS, only slight cognitive dysfunction was found compared with age- and education-matched normal controls, and this caused no relevant disturbance of psychosocial functioning. In 9 patients with manifest AIDS, dementia was diagnosed with DSM-III-R criteria and ICD-10 guidelines (30% of the AIDS patients). They showed marked impairment of intellectual ability, memory, verbal ability and calculation and constructional ability and fewer cortical focal symptoms (aphasia and apraxia). Corresponding to previous studies, major cognitive dysfunction in HIV infection can be characterized as subcortical dementia.
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PMID:Cognitive impairment, dementia and psychosocial functioning in human immunodeficiency virus infection. A prospective study based on DSM-III-R and ICD-10. 842 19

Epidemiological hypotheses on disease etiology, generated by the observation of geographic distribution and time trends, can be confirmed or refuted by analytical investigations on specific risk factors. In the case of leukemias, lymphomas and myelomas, however, hypothesis generation is limited by the use of the ICD classification in mortality and incidence statistics. We compared recent incidence data in different parts of the world and at different times for leukemias, lymphomas and myelomas. The incidence rate of non-Hodgkin's lymphomas (NHL) is increasing in most Western countries, while trends for the other hematolymphopoietic malignancies are strikingly stable. To formulate hypotheses on the causes of this pattern would require a more appropriate classification of descriptive data. Excesses of non-Hodgkin's lymphomas have been observed in populations exposed to phenoxy-acetic acid herbicides, to insecticides and to organic solvents. Some of these exposures, in particular TCDD, which is a contaminant of phenoxy herbicides, DDT and chlorinated solvents, have been reported to alter cell-mediated immunity. The incidence of NHL is also increased among subjects with HIV infection and subjects undergoing heart or kidney transplantation, all of whom experience immunodeficiency. A hypothesis that has been put forward recently is that the NHL increase is related to increased exposure to sunlight, which has immunosuppressive effects. From a mechanistic point of view, one can hypothesize that NHL is caused by exposures that induce proliferation and immortalization of B-cells, followed by T-cell impairment entailing cell-mediated immune deficiency.
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PMID:Incidence and time trends for lymphomas, leukemias and myelomas: hypothesis generation. Working Group on the Epidemiology of Hematolymphopoietic Malignancies in Italy. 864 39

Hospital discharge data from 1980 to 1989 from the National Center for Health Statistics, National Hospital Discharge Survey (NHDH), and two commercially generated hospital discharge data sources (PAS and McAuto) were analyzed to document nationally the increased rate of opportunistic candidal infections among hospitalized patients in the 1980s and to identify the major risk factors. National projections were made by year. Age-, sex-, race-, and disease-specific denominators were generated from NHDS data. ICD-9-CM codes derived from discharge diagnoses were used to identify patients with oropharyngeal candidiasis, disseminated candidiasis, human immunodeficiency virus (HIV) infection/AIDS, or malignancies and transplants. Between 1980 and 1989, rates of oropharyngeal candidiasis increased 4.7 times (from 0.34 to 1.6 cases per 1,000 admissions per year), and the number of deaths among patients with oropharyngeal candidiasis increased fivefold. Although the highest rates were among pediatric patients (3 cases per 1,000 pediatric admissions), the greatest rate increases were among 15- to 44-year-old patients (13-fold) and males (fivefold). Between 1983 and 1989, the rates of oropharyngeal candidiasis among patients with HIV infections/AIDS rose more than 22 times (from 0.02 to 0.45 case per 1,000 admissions; NHDS data). Over the whole decade, the rates of disseminated candidiasis increased 11 times (from 0.013 to 0.15 case per 1,000 admissions). Between 1985 and 1989, the rate of this complication among patients with HIV infection/AIDS increased 10-fold, compared with only a twofold rate increase among patients with malignancies or transplants. The rate of debilitating and life-threatening candidiasis among hospitalized patients increased considerably over the 1980s. This rate increase was significant among patients with HIV infection/AIDS and patients undergoing transplantation or immunosuppressive therapy for malignancies.
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PMID:Opportunistic candidiasis: an epidemic of the 1980s. 864 37

A quantitative human immunodeficiency virus type 1 (HIV-1) RNA polymerase chain reaction assay has been validated analytically and clinically in > 13,000 samples. The assay is highly reproducible with intra- and inter-assay precision of 16% and 19%, respectively. In 1,542 of 1,548 subjects with CD4+ counts of 0-500 cells per mm3, viral RNA levels were quantifiable and ranged from approximately 3,000-52,200,000 copies per milliliter. Median plasma HIV-1 RNA values were inversely proportional to CD4+ counts from 0-400 cells per mm3. When patients were off antiretroviral therapies for approximately 14 days prior to the initial baseline RNA PCR evaluation, the mean variance between the two baseline values was 23% (0.1 log). Of these patients, 95% had a sufficient plasma viral load to quantitate a 10-fold (1 log) diminution in viral load caused by antiviral therapy. In contrast, only 20% and 45% of these subjects had sufficient p24 and ICD p24 levels to detect a 50% diminution in circulating virus. The high precision and reproducibility of this quantitative RNA PCR assay provide an enhanced means of evaluating therapeutic drug regimens for HIV-1.
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PMID:Validation of a quantitative RNA PCR assay for HIV-1 in human plasma. 888 5

Results of polymerase chain reaction (PCR) and p24 antigen detection after immune complex dissociation (p24-ICD) were compared with antibody results after 18 months of age for human immunodeficiency virus (HIV) diagnosis in 345 prospectively followed, perinatally exposed infants. Of 59 infected and 286 uninfected infants tested at 1-6 months of age, sensitivity and specificity were, respectively, 100% and > 97% for PCR and 90% and > 97% for p24-ICD. Testing was done on > or = 2 occasions in the first 6 months of life in 43 infected infants; 77% had > or = 2 positive results with the same test. Of these infants, 68% had 2 positive p24-ICD tests. In uninfected infants, 96% had only negative tests; none had > 1 positive. By 6 months, all uninfected infants with > or = 2 PCR results could have been diagnosed. HIV status can be determined by PCR by age 6 months in most HIV-exposed infants. p24-ICD should not be used alone, because of its lower sensitivity, but may be useful in areas without advanced laboratory support.
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PMID:Diagnosis of perinatal human immunodeficiency virus infection by polymerase chain reaction and p24 antigen detection after immune complex dissociation in an urban community hospital. 918 Jan 71

The human and simian immunodeficiency virus (HIV-1 and SIVmac) transmembrane proteins contain unusually long intracytoplasmic domains (ICD-TM). These domains are suggested to play a role in envelope fusogenicity, interaction with the viral matrix protein during assembly, viral infectivity, binding of intracellular calmodulin, disruption of membranes, and induction of apoptosis. Here we describe a novel mutant virus, SIVmac-M4, containing multiple mutations in the coding region for the ICD-TM of pathogenic molecular clone SIVmac239. Parental SIVmac239-Nef+ produces high-level persistent viremia and simian AIDS in both juvenile and newborn rhesus macaques. The ICD-TM region of SIVmac-M4 contains three stop codons, a +1 frameshift, and mutation of three highly conserved, charged residues in the conserved C-terminal alpha-helix referred to as lentivirus lytic peptide 1 (LLP-1). Overlapping reading frames for tat, rev, and nef are not affected by these changes. In this study, four juvenile macaques received SIVmac-M4 by intravenous injection. Plasma viremia, as measured by branched-DNA (bDNA) assay, reached a peak at 2 weeks postinoculation but dropped to below detectable levels by 12 weeks. At over 1.5 years postinoculation, all four juvenile macaques remain healthy and asymptomatic. In a subsequent experiment, four neonatal rhesus macaques were given SIVmac-M4 intravenously. These animals exhibited high levels of viremia in the acute phase (2 weeks postinoculation) but are showing a relatively low viral load in the chronic phase of infection, with no clinical signs of disease for 1 year. These findings demonstrated that the intracytoplasmic domain of the transmembrane Env (Env-TM) is a locus for attenuation in rhesus macaques.
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PMID:The intracytoplasmic domain of the Env transmembrane protein is a locus for attenuation of simian immunodeficiency virus SIVmac in rhesus macaques. 1084 63


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