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)

In a previously healthy 13-year-old girl with disseminated blastomycosis, immunodeficiency was considered because of lymphopenia and the slow response of her lung disease to therapy with amphotericin B. Cellular immunity was found to be profoundly impaired, with absent delayed cutaneous hypersensitivity to several common antigens, a decreased count of thymus-dependent lymphocytes in the peripheral blood and a greatly diminished in-vitro proliferative response of lymphocytes to phytohemagglutinin (PHA). Humoral immunity was intact. Two additional types of therapy were assessed: subcutaneous injection of transfer factor was associated with an unsustained increase in lymphocyte counts and a positive cutaneous response to PHA but no clinical change; parenteral alimentation to ensure an adequate energy intake was associated with rapid clinical improvement, the development of delayed hypersensitivity to four additional antigens, and the return of lymphocyte counts and proliferative response to normal. These findings suggest that increased energy intake rather than transfer factor therapy was responsible for the child's recovery, and they emphasize the importance of adequate nutrition in the maintenance of intact cellular immunity.
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PMID:Cellular immunity and nutrition in refractory disseminated blastomycosis. 9 21

The clinical course of cytomegalovirus (CMV) pneumonia in seven consecutive bone marrow transplant (BMT) recipients during a 24-month period was studied. Retrospective analysis of clinical data on the recipients with CMV pneumonia during the illness and prospective follow-up of those who recovered from the pneumonia was performed. Those who had CMV as the sole pathogen and with lymphocytosis in the BAL or the peripheral blood during the illness recovered from the pneumonia. On the contrary, those who had mixed bacterial or fungal infection with peripheral lymphopenia died. Persistent lymphocytosis in the BAL and the peripheral blood, in the absence of CMV infection, was observed in the survivors. Two subsequently developed restrictive lung disease and two had relapse of their primary malignancy. These data suggest that CMV pneumonia in BMT patients is associated with significant long-term sequelae. The phenomenon of persistent lymphocytosis in the BAL and the peripheral blood, in the absence of CMV infection, supports Grundy's hypothesis that CMV pneumonia in BMT recipients is an immunopathologic condition.
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PMID:Long-term sequelae after recovery from cytomegalovirus pneumonia in allogeneic bone marrow transplant recipients. 131 48

We analysed BALF cell findings in 9 patients (group A: 5 patients without lung disease after bone marrow transplantation (BMT), group B: 4 patients with lung disease after BMT) before and after BMT. Before BMT, BALF cell findings in group A were almost normal, whereas a relative increase of lymphocytes was seen in group B. Although total cell counts and cell composition in group A changed little after BMT, CD4/CD8 ratios in BALF lymphocytes decreased. In contrast, a relative increase of lymphocytes and neutrophils was seen in group B and there was variation of CD4/CD8 ratios in BALF lymphocytes after BMT. We there studied the BALF lymphocytes of 3 patients in group A and 4 patients in group B after BMT by means of 2-color analysis. Among CD4+ cell populations, CDw 29+ cells were decreased in both groups after BMT. A relative increase of BALF-CD4+ HLA-DR+ cells and CD8+ HLA-DR+ cells was seen in group A, but was not seen in group B. These findings suggest that there is abnormality of local immunity in the lung after BMT.
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PMID:[Analysis of bronchoalveolar lavage fluid in patients before and after bone marrow transplantation]. 162 96

Accumulation of inflammatory and immune cells within lung parenchyma would constitute the initial step in producing the alveolar structural abnormalities. It is usually assumed that alveolitis, as assessed by broncho-alveolar lavage (BAL), represents a biological assessment of lung disease activity. The aim of this study, using monoclonal antibodies, is to characterize the T lymphocytes alveolitis in the lung and in peripheral blood in 3 well-defined populations: 1 degree) control subjects (n = 7); 2 degrees) patients with biopsy proven mediastino-pulmonary sarcoidosis (sarc) (n = 73), classified according to their clinical activity as active, inactive, chronic, and treated; 3 degrees) patients with extrinsic alveolar alveolitis (EAA) (n = 19). For the same BAL volume, the % of CD4+ cells and the CD4/CD8 ratio are increased in chronic and active sarc, contrasting with an increase in the % of CD8+ cells and a decrease in the CD4/CD8 ratio in the EAA. In absolute values, there are 2 times as many CD4+ cells and 5 times as many CD8+ cells in EAA than in sarcoidosis. In sarcoidosis, corticotherapy tends to normalize the CD4/CD8 ratio although the intensity of the lymphocytic alveolitis is not affected. In the peripheral blood, lymphopenia is observed only in the active form of sarc. in the CD4+ population, without any significant change in the CD4/CD8 ratio compared to the other groups. The number and distributions of BAL. T lymphocytes subsets may constitute a biological indicator for diagnostic orientation, but they do not distinguish sufficiently between the different groups of sarcoidosis to be of any prognostic value.
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PMID:[T lymphocyte subsets in alveolar lavage and peripheral blood in sarcoidosis and extrinsic allergic alveolitis]. 296 92

The ability of alveolar macrophages (AM) to release hydrogen peroxide (H2O2), an indicator of AM function, was studied in five children with the acquired immunodeficiency syndrome (AIDS) related complex and, for comparison, in 11 children without disorders of the lung parenchyma. In the AIDS-related complex group, pulmonary manifestations were mild, and lung involvement was suspected by moderate clinical and/or radiological features. None had a past history of opportunistic infections; neither did any have lymphopenia. Cytologic study of the bronchoalveolar lavage (BAL) fluid revealed increased cellularity with increased percentage of lymphocytes. The study of H2O2 release was performed on unstimulated AM and on AM stimulated by phorbol myristate acetate (PMA). Under both experimental conditions, the amount of H2O2 accumulated in the medium was significantly increased in the group with AIDS-related complex (P less than 0.001). As no enhanced oxidative activity has been reported in AM from patients with full-blown AIDS, an increased ability of AM to release oxygen metabolites from children with AIDS-related complex may reflect an initial and temporary step in the course of the LAV/HTLV-III pulmonary disease. Determining AM activation might be a reliable method of assessing the evolution of lung disorder in AIDS.
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PMID:Activation of alveolar macrophages from children with the acquired immunodeficiency syndrome-related complex. 323 46

Bronchoalveolar lavage (BAL) cell populations were determined in 47 immunosuppressed patients during episodes of pulmonary disease. Thirty six patients had AIDS and 11 had conventional causes of immunosuppression. Pulmonary disease was due to a variety of infectious and noninfectious causes and was similar in both groups. In the AIDS patients, the mean BAL cell proportions were 64.2 +/- 3.7 percent alveolar macrophages (MACS), 28.7 +/- 3.4 percent lymphocytes, 3.5 +/- 1.8 percent polymorphonuclear cells (PMN) and 1.6 +/- 0.6 percent eosinophils (EOS). The non-AIDS group had similar findings in the BAL, with 59.3 +/- 8.3 percent MACS, 34.8 +/- 7.2 percent lymphocytes, 5.5 +/- 1.7 percent PMN and 0.4 +/- 0.2 percent EOS. The most striking finding in each group was a significant increase in both the proportion and absolute number of lymphocytes compared to controls. This was in marked contrast to the peripheral blood findings of lymphopenia. There was no characteristic cell profile diagnostic of any specific pulmonary disease. There was also no direct relationship of the cells present to respiratory symptoms, roentgenographic abnormalities or survival from pulmonary disease. This study demonstrates that although there was wide individual variation in lavage findings, a local pulmonary inflammatory reaction consisting predominantly of lymphocytes occurs in the immunosuppressed host during episodes of lung disease. The significance of this lymphocyte alveolitis and the complex host pathogen interaction responsible for determining the cell populations present in the lungs of these patients requires further study.
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PMID:Pulmonary cell populations in the immunosuppressed patient. Bronchoalveolar lavage findings during episodes of pneumonitis. 402 44

Profound lymphocytopenia (greater than 2,000 lymphocytes/mm3) occurring within two days of rash in 69 South African black children with measles predicted either death or progression to chronic lung disease in 51 (77%) of 66 children who were followed for at least six weeks. Lymphocytopenia was significantly associated with the presence of histocompatibility leukocyte antigen (HLA) AW32 (P = 0.01), with a relative risk of 5.5. There was a trend toward an association between the presence of particular antigens in the HLA complex and the various indices of humoral and cellular immunity studied. These findings are discussed in terms of variation in the clinical spectrum of the disease and in relation to the evolution of HLA polymorphism.
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PMID:Measles, histocompatibility leukocyte antigen polymorphism, and natural selection in humans. 691 75

Lymphocyte subpopulations in peripheral blood and bronchoalveolar lavage fluid (BAL) were examined in 29 patients with AIDS (26 men, three women; median age 32 [16-55] years). Patients in group 1 (n = 12) had no lung disease, in group 2 (n = 11) had Pneumocystis carinii pneumonia, in group 3 (n = 6) had other lung disease. There were 13 men and two women (median age 48 [21-80]) in the control group (bronchoscoped for mild pulmonary symptoms: no abnormal findings in the BAL). Compared with the control group, patients with AIDS had a significant deficiency in helper cells, both in blood (7-23% vs 50%; P < 0.01) as well as in the BAL (7-24% vs 52%; P < 0.001). There was a correlation of the percentage helper cell proportion in peripheral blood and BAL (for both group 1 and 2, rs = 0.75; P < 0.05). The proportion of helper cells in peripheral blood and BAL in AIDS patients was significantly lower in those with than without lung disease (group 1: 23% blood, 24% BAL vs group 2: 9% blood, 7% BAL; group 3: 7% blood, 7% BAL; P < 0.02 blood, P < 0.004 BAL). The percentage proportion of suppressor cells was greater in both blood and BAL in AIDS patients (group 1: blood 47%, BAL 63%; group 2: blood 44%, BAL 76%; group 3: blood 52%, BAL 75%) than in the controls (blood 28%, BAL 33% [P < 0.01], but there was no correlation between peripheral blood and BAL. In addition, the absolute number of suppressor cells in the lavage (30 cells/microliters in group 1 and 3, 65 cells/microliters in group 2) was significantly higher than in the controls (8 cells/microliters).--In AIDS patients there occurs a lymphocytosis in the BAL, while in blood there is a lymphopenia. The concordant decrease in helper cells in blood and BAL is decisive for the severity of any pulmonary infections.
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PMID:[Lymphocyte subpopulations in bronchoalveolar lavage fluid in AIDS]. 811 8

Use of methotrexate to treat rheumatoid arthritis is associated with pulmonary adverse effects in 3% to 5% of cases. In addition to immunoallergic lung disease, bronchitis and pneumonia due to pyogenic organisms, opportunistic lower respiratory tract infections have been reported, including, to our knowledge, 18 cases of Pneumocystis carinii pneumonia. We report two new cases of P. carinii pneumonia in methotrexate-treated rheumatoid arthritis patients. One case occurred in a 62-year-old woman with a nine-year history of seropositive rheumatoid arthritis treated for the last seven months with methotrexate, 15 mg per week, and prednisone, 10 mg/d. The other patient was a 58-year-old woman who had been diagnosed with rheumatoid arthritis 18 months earlier and had been receiving 15 mg per week of methotrexate for eight months in combination with 12.5 mg of prednisone per day. Both patients had negative tests for the human immunodeficiency virus. Symptoms consisted of fever, cough and dyspnea, with interstitial infiltrates on chest films, hypoxia, and lymphopenia (700 and 600/mm3, respectively). The diagnosis was confirmed by bronchoalveolar lavage. Both patients recovered under treatment with trimethoprim-sulfamethoxazole. An analysis of the 20 cases of P. carinii pneumonia reported to date in methotrexate-treated rheumatoid arthritis patients demonstrated a number of characteristics: the rheumatoid arthritis was of recent onset in some cases (a few months in one patient); lymphopenia was present in two thirds of cases; one-third of patients were not receiving corticosteroid therapy; the dosage and duration of methotrexate therapy varied widely, from 5 to 30 mg per week and two to 48 months; and four patients died.
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PMID:Pneumocystis carinii pneumonia in rheumatoid arthritis patients treated with methotrexate. A report of two cases. 881 57

To study the role of Fas-Fas ligand (FasL) interaction-mediated apoptosis in lymphocyte homeostasis, we generated a mutant fas allele allowing conditional inactivation of the fas gene through Cre-mediated recombination. Experiments in which Fas was ablated in T cells, B cells, T and B cells, or in a more generalized manner demonstrated that the development of lymphoproliferative disease as seen in Fas-deficient mice requires Fas ablation in lymphoid and nonlymphoid tissues. Selective inactivation of Fas in T cells led to a severe lymphopenia over time, accompanied by up-regulation of FasL on activated T cells and apoptosis of peripheral lymphocytes. In addition, the mutant animals developed a fatal wasting syndrome caused by massive leukocyte infiltration in the lungs together with increased inflammatory cytokine production and pulmonary fibrosis. Inhibition of Fas-FasL interaction in vivo completely prevented the loss of lymphocytes and initial lymphocyte infiltration in the lungs. Thus, FasL-mediated interaction of activated, Fas-deficient T cells with Fas-expressing cells in their environment leads to break down of lymphocyte homeostasis and development of a lung disease strikingly resembling idiopathic pulmonary fibrosis in humans, a common and severe disease for which the mutant mice may serve as a first animal model.
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PMID:T cell-specific ablation of Fas leads to Fas ligand-mediated lymphocyte depletion and inflammatory pulmonary fibrosis. 1514 35


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