Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with advanced renal cell carcinoma, previously failed maximal treatment with standard chemo-hormonal-radiation therapies, were treated with plant lectin phytohemagglutinin (PHA)-stimulated autologous peripheral blood lymphocytes in a 10-year study with a 16-year follow up period. In a phase I-II setting, 52 patients were given subcutaneously 40-80 x 10(6) PHA-stimulated lymphocytes weekly for 3 weeks and then escalated to a maximum number of 80 x 10(9) lymphocytes over the next 9 weeks at 3 week intervals. In vitro blastogenesis under study conditions (10 micrograms/ml PHA for 72 hr) measured by [3H]thymidine uptake was optimal with lymphocyte stimulating indexes approaching 300. Lymphocytes obtained from patients with breast cancer, melanoma and renal cell carcinoma responded to PHA similarly to those from normal volunteers. All patients that responded developed erythematous reactions at the sites of injection; malaise, joint paint and chill-fever for 24-48 hr. The patients that responded the best were those with at least 1 positive reaction out of 4 skin tests (tuberculosis, yeast, dermatophytin, mumps) prior to therapy. All toxicity was transient and did not exceed Grade I based on criteria of the Southwest Oncology Group. The majority of patients developed a lymphopenia in the first 24 hr followed by a lymphocytosis 48-72 hr later. For some patients the lymphocytosis was as much as 30% atypical lymphocytes. Of 41 evaluable patients, there were 5 complete responses, 8 partial responses, 3 stable diseases, and 25 progressive disease. The overall response rate was 32% and the median survival was 2.8 years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adoptive immunotherapy of advanced renal cell cancer using PHA-stimulated autologous lymphocytes. 826 79

Twenty-two hospitalized HIV seropositive patients were studied prospectively between July 1991 and January 1992. The majority of the patients were intravenous drug users (IVDUs). Their age ranged from 20 to 38 years with a male preponderance of 12 to 1. Anemia, lymphopenia and thrombocytopenia were observed in 100%, 36% and 41%, respectively. The common pathogens like malaria parasites, Mycobacterium tuberculosis, Entamoeba histolytica, Streptococcus and Salmonella were isolated/identified rather than opportunistic organisms.
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PMID:Some characteristics of hospitalized HIV seropositive patients in Myanmar. 836 94

T cells and their sub-populations were evaluated with respect to reactive, intermediate and unreactive forms of tuberculosis as classified by Lenzini. Significant CD4 lymphopenia and a reduction of CD4/CD8 ratios were found in patients with reactive tuberculosis. It was observed that there was a B lymphocytosis, CD8 lymphocytosis and a reduction of CD4/CD8 ratio in patients with intermediate and unreactive forms of tuberculosis. The T lymphocytes and CD4 subset were unchanged. There was no significant difference in the lymphocytes and sub-populations among the intermediate and unreactive groups.
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PMID:T lymphocytes in pulmonary tuberculosis. 848 3

Infection with the human immunodeficiency virus (HIV) has changed both the epidemiology and natural history of tuberculosis. Despite a generally good response to effective antituberculous therapy, the prognosis remains poor. The objective of this analysis was to determine the independent predictors of survival in HIV-infected Ugandan adults with smear-positive pulmonary tuberculosis. A total of 191 HIV-infected Ugandan adults with smear-positive pulmonary tuberculosis were enrolled into a clinical trial of chemotherapy for tuberculosis. The subjects received either rifampin, isoniazid, and pyrazinamide for two months, followed by rifampin and isoniazid for six months (n = 101) or streptomycin, thiacetazone, and isoniazid for two months followed by thiacetazone and isoniazid for eight months (n = 90). After standard measurements were made at baseline, the group was followed at regular intervals for a mean of 16 months to determine survival. During the course of follow-up, 82 (43%) of the patients died, six within the first month of therapy. The one-year survival proportion was 68% with an estimated median survival of 26 months and did not differ according to treatment regimen. The hazard for death was biphasic, high early in the course of therapy, and then again after about one year. After controlling for the treatment regimen, four independent predictors of survival were found: anergy to purified protein derivative, atypical chest roentgenogram, previous HIV-related condition, and lymphopenia. In this cohort of Ugandan adults, four simple and inexpensive predictors of survival were found. These factors suggest that the degree of immunosuppression was a major determinant of survival.
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PMID:Predictors of survival in human immunodeficiency virus-infected patients with pulmonary tuberculosis. The Makerere University-Case Western Reserve University Research Collaboration. 866 64

A 67-year-old male was hospitalized because of nonspecific symptoms and bilateral pleural effusions. He gave no history of cough, dyspnea or thoracic pain. The blood counts showed moderate anemia and high-grade lymphopenia. The tuberculin test and the anergy-panel were both negative. Testing for HIV was negative. Analysis of pleural fluid showed an exudate with 47% lymphocytes and absence of acid-fast bacilli on Ziehl-Neelsen smear. On histologic examination, the pleural tissue showed no evidence of granuloma. However, cultures for mycobacteria of pleural tissue yielded M. tuberculosis. In this case of pleural tuberculosis, leading symptoms were absent and the tuberculin test was negative in the presence of active tuberculosis. In addition, the cells in the pleural effusion were not predominantly lymphocytic. Patients presenting with unclear effusion should undergo extensive investigations, including a tuberculin test, and anergy panel, pleural fluid cultures, and pleural biopsy with cultures for microorganisms, with the object of establishing or ruling out pleural tuberculosis.
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PMID:[An unusual presentation of tuberculosis]. 901 35

The formation of immunodeficiency whose likely mechanism is apoptosis of some immunocompetent cells was studied in 35 patients with caseous pneumonia. The leading clinical sign of apoptosis in acutely progressive tuberculosis is significant lymphopenia (4-10%). Immunological studies indicated a substantial reduction in the count of T lymphocytes and their regulatory subpopulations of different phenotypes. In vitro mitogenic induction causes a decline of activated CD3+, CD4+, and CD8+ cells on the average by 10-40%, a decrease in the proliferative and synthetic functions, as compared with those in patients with infiltrative tuberculosis of the lung and healthy donors. Cytochemical findings in the same patients show that half the lymphocytes in the blood samples from patients with caseous pneumonia has profound intracellular metabolic disturbances. These cells are unavailable and undergo apoptosis, which determines immunodeficiency in patients with acutely progressive tuberculosis.
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PMID:[Increased apoptosis of immunocompetent cells as a possible mechanism in the development of immunodeficiency in patients with acutely progressive tuberculosis]. 901 75

Adenosine deaminase (ADA) deficiency typically causes severe combined immunodeficiency (SCID) in infants. We report metabolic, immunologic, and genetic findings in two ADA-deficient adults with distinct phenotypes. Patient no. 1 (39 years of age) had combined immunodeficiency. She had frequent infections, lymphopenia, and recurrent hepatitis as a child but did relatively well in her second and third decades. Then she developed chronic sinopulmonary infections, including tuberculosis, and hepatobiliary disease; she died of viral leukoencephalopathy at 40 years of age. Patient no. 2, a healthy 28-year-old man with normal immune function, was identified after his niece died of SCID. Both patients lacked erythrocyte ADA activity but had only modestly elevated deoxyadenosine nucleotides. Both were heteroallelic for missense mutations: patient no. 1, G216R and P126Q (novel); patient no. 2, R101Q and A215T. Three of these mutations eliminated ADA activity, but A215T reduced activity by only 85%. Owing to a single nucleotide change in the middle of exon 7, A215T also appeared to induce exon 7 skipping. ADA deficiency is treatable and should be considered in older patients with unexplained lymphopenia and immune deficiency, who may also manifest autoimmunity or unexplained hepatobiliary disease. Metabolic status and genotype may help in assessing prognosis of more mildly affected patients.
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PMID:Adenosine deaminase deficiency in adults. 910 4

This study surveys the extent and severity of haematological abnormalities which occurred in 380 patients with pulmonary tuberculosis. Full blood count, bone marrow aspiration smears, and bone marrow trephine biopsy was analyzed by authors. Anaemia was present in 32 percent of patients. Leucocytosis with neutrophilia occurred in 18 percent. Leucopenia with neutropenia, and lymphopenia was observed in 16 percent in patients with very severe clinical tuberculosis. Elevated platelet count occurred in 8 percent with deep vein thrombosis in legs in 50 percent. Dysmyelopoietic syndrome was diagnosed in one case by bone marrow trephine biopsy. There was a close correlation between the haematological abnormalities and the severity of clinical findings of pulmonary tuberculosis. This survey has revealed that haematological abnormalities are relatively common in severe pulmonary tuberculosis. It seems that body weight loss, white blood cell count, haemoglobin level and erythrocyte sedimentation rate are useful indices of severity of the tuberculosis. The return of these indices to a normal level is a good indication of disease control in that they correlate with sputum conversion to acid-fast bacilli negative.
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PMID:[Hematologic abnormalities in pulmonary tuberculosiss]. 918 73

We determined in 14 patients with pleural tuberculosis total lymphocyte count, T subsets and NK cells (CD56) in pleura and blood and it was found a preferential accumulation in pleura of CD3 T lymphocytes, TCR alpha beta, mainly CD4 subset, but not T or NK cells. In 5 pleuritis it was studied 40% of V beta TCR subfamilies in blood and pleura and in 2 pulmonary tuberculosis and one pleuritis all V beta and V alpha TCR subfamilies (trough PCR), without be observed a clear clonal expansion. It was not observed correlation among a) pleural and blood lymphocyte cellularity b) the amount of pleural effusion and the existence of lymphopenia or tuberculinic anergia c) levels of ADA and percentage of CD3 and CD4 cells in pleura. In 7 out 11 pleuritis a high expression of IL-2 receptor (CD25) was observed. In 24 patients with pleural and pulmonary tuberculosis there was not correlation between levels of SIL-2R and IL-6 and radiographic extension.
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PMID:[Lymphocyte activation in tuberculous pleuritis . Correlation with adenosine deaminase (ADA), peripheral blood lymphocytes, T cell receptor subfamilies, radiographic extension and levels of Il-6 and soluble Il-2 receptor]. 954 1

A 29-year-old Caucasian woman presented to hospital with a 2-day history of diarrhoea, anorexia and rigors. Investigations showed abnormal liver function tests, hyponatremia, hypoalbuminaemia and lymphopenia. The initial chest radiograph was normal. A bone marrow trephine biopsy showed non-caseating granulomata and she subsequently developed miliary shadowing on the chest radiograph. A transjugular liver biopsy confirmed the presence of acid-alcohol fast bacilli. Despite starting triple therapy for miliary tuberculosis she remained febrile and developed massive hepatosplenomegaly, jaundice and pancytopenia. Standard triple therapy was substituted with ethambutol, streptomycin and oral prednisolone and the patient made a dramatic recovery. The clinical symptoms of miliary tuberculosis are frequently non-specific and the onset of the illness is often insidious. The liver is involved in almost all patients with miliary tuberculosis, but massive hepatosplenomegaly and jaundice are rare. Standard triple-therapy should be discontinued when there is significant liver dysfunction, and corticosteroids should be considered for patients with miliary tuberculosis who fail to respond to conventional therapy.
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PMID:Massive hepatosplenomegaly, jaundice and pancytopenia in miliary tuberculosis. 957 Jun 66


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