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)

The level of interferon-gamma (IFN-gamma) in pleural fluid has been reported to be increased in pleural tuberculosis. Nevertheless, its diagnostic value has not yet been well-established, and immunocompromised patients have not previously been evaluated. The aim of this study was to determine the value of the IFN-gamma level in pleural fluid for diagnosing tuberculous pleurisy in immunocompetent and immunocompromised patients. Three hundred and eighty eight consecutive patients were studied prospectively (73 with tuberculous pleural effusions, including nine with concurrent human immunodeficiency virus (HIV) infection and one after liver transplantation, and 315 with nontuberculous effusions). IFN-gamma was measured by radioimmunoassay. The sensitivity of the test, using a 3.7 U.mL-1 cut-off point, was 0.99 (95% confidence interval (95% CI) 0.93-1.00) and the specificity was 0.98 (95% CI 0.96-1.00). The sensitivity of the test did not differ in HIV-positive and HIV-negative patients. Patients with lymphoma, vasculitis or vascular connective tissue disease did not have abnormal IFN-gamma values. In conclusion, the level of interferon-gamma in pleural fluid is a very good diagnostic marker of tuberculous pleural effusion, even in immunocompromised patients.
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PMID:Interferon-gamma in 388 immunocompromised and immunocompetent patients for diagnosing pleural tuberculosis. 898 Sep 81

Tuberculous pleural effusions occur in up to 30% of patients with tuberculosis. It appears that the percentage of patients with pleural effusion is comparable in human immunodeficiency virus (HIV)-positive and HIV-negative individuals, although there is some evidence that HIV-positive patients with CD4+ counts <200 cells x mL(-1) are less likely to have a tuberculous pleural effusion. There has recently been a considerable amount of research dealing with the immunology of tuberculous pleurisy. At present, we have more evidence that activated cells produce cytokines in a complex pleural response to mycobacteria. Intramacrophage elimination of mycobacterial antigens, granuloma formation, direct neutralization of mycobacteria and fibrosis are the main facets of this reaction. With respect to diagnosis, adenosine deaminase and interferon gamma in pleural fluid have proved to be useful tests. Detection of mycobacterial deoxyribonucleic acid (DNA) by the polymerase chain reaction is an interesting test, but its usefulness in the diagnosis of tuberculous pleurisy needs further confirmation. The recommended treatment for tuberculous pleurisy is a 6 month regimen of isoniazid and rifampicin, with the addition of pyrazinamide in the first 2 months. HIV patients may require a longer treatment. The general use of corticosteroids is not recommended at this time, but they can be used in individuals who are markedly symptomatic.
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PMID:Pleural tuberculosis. 915 Mar 38

Within 1987-1995 the authors observed 16 cases of tuberculosis in HIV-infected patients which accounted for 26.7% of AIDS patients treated by them. 14 cases were diagnosed intravitally, 2 postmortem. Infiltrative, generalized, cavernous, intrathoracic lymph node, intraabdominal lymph node tuberculosis and tuberculous pleurisy were identified in 5, 6, 2, 1, 1 and 1 patients, respectively. 6 patients from the above are still alive and are receiving treatment (5 of them with infiltrative tuberculosis), 10 died. Tuberculosis course and outcomes in HIV-infected subjects depended on the stage of their immunodeficiency. In moderate immunodeficiency (CD4-lymphocyte > 200/mm3) tuberculosis ran, as a rule, as local and infiltrative, sensitive to specific therapy. In severe damage to immune system (CD4 < 100/mm3) tuberculosis acquired a generalized course, sometimes fulminant, resistant to treatment. It is inferred that HIV-infected subjects with immunodeficiency need tuberculosis prophylaxis with isoniazide or rifampicin.
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PMID:[Tuberculosis in patients with HIV infection]. 932 99

The inflammatory response to infection is necessary for host defense but can contribute to the systemic toxicity and lung injury that may result from pneumonia. In some settings, adjunctive treatment of lower respiratory infections with anti-inflammatory agents can reduce morbidity. Corticosteroids have a well-documented role in the management of Pneumocystis carinii pneumonia complicating human immunodeficiency virus (HIV) infection. Corticosteroids also were found to reduce systemic symptoms of tuberculosis in a number of older studies, but their role as adjuncts to contemporary antimicrobial therapy are less clear. Corticosteroids also may be effective under some circumstances in the treatment of inflammatory sequelae of respiratory tract infection, such as tuberculous pleurisy, bronchiolitis obliterans organizing pneumonia, or prolonged acute respiratory distress syndrome. Nonsteroidal anti-inflammatory drugs may have limited applications in the modulation of chronic airway inflammation. Strategies targeting specific cytokines have not been effective to date, but remain active areas of investigation.
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PMID:Anti-inflammatory treatment of acute and chronic pneumonia. 1130 15

Tuberculous pleuritis has increased worldwide, especially in developing countries, as a consequence of human immunodeficiency virus co-infection. Tuberculous pleuritis is a delayed hypersensitivity reaction against mycobacterial antigens in the pleural space. Mycobacteria are detected in less than 50% of pleural samples, but the characteristic pleural involvement, granulomas with or without caseous necrosis, is evident in 56 to 80% of cases from samples obtained by percutaneous pleural biopsy. Of several pleural fluid parameters studied, adenosine deaminase and interferon gamma (IFN-gamma) have the best diagnostic yield, while polymerase chain reaction remains a promising test. Treatment of patients with tuberculous pleuritis is discussed. Tuberculous empyema is a rare form of tuberculous pleuritis. It consists of a purulent infection of the pleural cavity with detectable bacilli in pleural fluid. Diagnosis is easily established clinically and bacteriologically. Treatment is to adequately drain the pleural space and achieve lung reexpansion, in conjunction with antituberculous chemotherapy. The efficacy of different surgical techniques is discussed.
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PMID:Tuberculous pleural effusion and tuberculous empyema. 1608 8

To define the incidence and spectrum of extra pulmonary tuberculosis (EPTB) and the trend of pulmonary tuberculosis (PTB) among human immunodeficiency virus (HIV) infected patients in the University of Ilorin teaching hospital, a tertiary care centre in Nigeria. Review of all PTB cases diagnosed by Ziehl-Neelsen staining technique and EPTB diagnosed by tissue histology and/or cytology between January 2000 and December 2004. HIV/TB coinfection occurred in 40% (297 cases) of the 744 new cases of tuberculosis (TB) seen in the last 5 years, HIV/PTB occurred in 79% and HIV/EPTB occurred in 21%. About 47 new cases of HIV/PTB and 12 of HIV/EPTB were diagnosed per year. Tuberculous pleurisy with effusion; 23%, tuberculous meningitis; 16% and genital tuberculosis; 10% as (tuberculous: orchitis, endometritis and frozen pelvis) were common form of extra pulmonary presentation. The chance of mixed presentation was 3 times higher amongst the HIV positive than HIV negative patients; 27 vs. 11: X2 = 6.99, OR 3.25; 95% CI = 1.32-8.14, p-value = 0.008. Similarly the chance of miliary tuberculosis was 4 1/2 times higher in the HIV positive group; 9 vs. 2: X2 = 4.29, OR 4.67; 95% CI = 0.90-45.93, p-value = 0.03. Both conditions recorded the lowest CD4+ cells count; 88 cells/ul and 93.6.6 cells/ul, thus serving as features of advanced HIV illness. PTB and EPTB are common amongst the HIV infected patients; miliary spread and mixed presentation are signs of severe immunosuppression.
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PMID:Human immunodeficiency virus-associated tuberculosis: pattern and trend in the University of Ilorin Teaching Hospital. 1772 13

Although the infectious diseases tuberculosis (TB) and cryptococcosis both cause formation of single or multiple nodules in immunodeficient hosts, cases of co-infection of these diseases are rarely seen. We report a patient who was co-infected with TB and cryptococcosis. A male patient with no clinical evidence of immunodeficiency presented with a 3-week history of abdominal distension accompanied by oedema of recurring lower extremities. The patient was diagnosed with tuberculous peritonitis and tuberculous pleurisy by an abdominal puncture biopsy. Several months after being treated for TB, the patient was diagnosed with Cryptococcus infection and received antifungal treatment. Computed tomographic and magnetic resonance imaging findings suggested that treatment was effective. This case illustrates the challenges encountered during assessment of neoplasms associated with TB and cryptococcosis. Differential diagnosis requires an abdominal puncture biopsy. Diagnosis of Cryptococcus infection also requires a positive cryptococcal culture and positive India ink staining analysis. Notably, our patient also showed no obvious symptoms of cryptococcosis after receiving anti-TB treatment. Accordingly, in this report, we discuss the possible pathogenic mechanisms that underlie the coincidence of both types of inflammatory lesions. We emphasize the need for a greater awareness of atypical presentations of TB accompanied by Cryptococcus infection.
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PMID:Tuberculous peritonitis and pleurisy accompanied by pulmonary cryptococcosis: A case report. 2975 4