Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fatal graft-versus-host disease (GVHD) developed in a patient with Hodgkin's disease treated with combined chemotherapy and radiotherapy following the transfusion of 2 U of packed red blood cells. Clinical features of the GVHD included the development of exfoliative dermatitis, progressive hepatic dysfunction, aplastic anemia, and finally progressive fatal pneumonia. GVHD was documented by skin biopsy and chimerism by HLA typing. The HLA phenotype of the patient's skin fibroblasts [A3, Bw44 (w4)/A2, B15 (w4)] was appropriate for parental haplotypes and probably represented her true HLA phenotype. Lymphocytes from the patient (peripheral blood and lymph node biopsy) were of a different HLA phenotype (A3; Bw35, w38, w4, w6; Cw4), which was inappropriate for parental HLA haplotypes but identical to the HLA phenotype of one of the blood donors. The HLA-DR typing of the patient's family and of the blood donor demonstrated that the patient and the donor probably were HLA-DR identical (DRw5/DRw6), although no B lymphocytes could be obtained from the patient for direct DR typing. We are currently irradiating all blood products administered to patients with Hodgkin's disease receiving intensive treatment. Further observations will be necessary to determine whether transfusions to other cancer patients with immunodeficiency states should be restricted to irradiated blood products.
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PMID:Fatal graft-versus-host disease following blood transfusion in Hodgkin's disease documented by HLA typing. 736 71

A total of 28 patients with chronic myelogenous leukemia (CML) in chronic phase (CP) received bone marrow allografts from HLA-matched siblings at the University of Florida between August 1984-July 1992. The present study compares the disease-free survival (DFS) for those patients who were transplanted before or after August 1988 using the same conditioning regimen. The analysis shows significant difference in 3-year DFS for those patients transplanted post- vs. pre-August 1988 (69.6% vs. 20%, respectively; P = 0.006). A decrease in pneumonitis due to different etiologies from pre-August 1988 (6/13, 46%) to post-August 1988 (1/15, 7%) was statistically significant (P = 0.029). A decrease, although statistically insignificant, in the overall incidence and severity of acute and chronic graft vs. host disease (GVHD) after August 1988 was also noticed. This study indicates significantly improved outcome for patients with CML in CP who have been treated in the University of Florida after August 1988. Better supportive care and prophylaxis for GVHD most likely contributed to such improvement.
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PMID:Improved survival of patients with chronic myelogenous leukemia undergoing allogeneic bone marrow transplantation. 748 9

The treatment effect of immunoselected allogeneic CD34+ blood cells was evaluated in two patients with poor graft function following BMT without evidence for immune-mediated rejection. Patient A had no signs of hematopoietic recovery up to day +34 post-BMT and patient B had normal leukocyte counts only with G-CSF support and remained platelet transfusion-dependent for > 200 days post-BMT. PBPC from the HLA-identical sibling BM donors were mobilized with G-CSF (2 x 5 micrograms/kg sc daily) for 5 days. Aphereses were performed on days 4 and 5 of G-CSF administration. CD34+ cells were separated from the pooled PBPC concentrates by immunoadsorption with the anti-CD34 moAb 12.8 in a biotin-avidin system. Patient A received 0.4 x 10(6) CD34+ and 4.3 x 10(5) CD3+ cells/kg body weight and patient B 3.4 x 10(6) CD34+ and 1.4 x 10(5) CD3+ cells/kg body weight. The trilineage repopulation of BM and the rapid improvement of peripheral blood parameters correlated with CD34+ cell infusion. Patients' blood and BM cell analyses proved the donor origin. Patient A died from CMV pneumonitis and multiorgan failure 27 days after CD34+ cell infusion (day +61 post-BMT). Patient B is still stable and in remission 260 days after CD34+ cell infusion (day +478 post-BMT). Neither patient suffered further exacerbation of GVHD). Thus, immunoselected allogeneic CD34+ blood cells might be appropriate for treatment of post-BMT graft failure.
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PMID:Treatment of poor marrow graft function with allogeneic CD34+ cells immunoselected from G-CSF-mobilized peripheral blood progenitor cells of the marrow donor. 753 62

Bronchoalveolar lavage was performed in patients with chronic eosinophilic pneumonia of unknown origin diagnosed histopathologically, and the alveolar fluid cells were investigated before and during corticosteroid therapy. The counts of eosinophils in bronchoalveolar lavage fluid decreased markedly during steroid therapy compared with before therapy, and the ratios of interleukin 2 receptor-positive T cells and HLA DR-positive T cells to all T lymphocytes in the lavage fluid also decreased. Both before and during steroid therapy, many macrophages in bronchoalveolar lavage fluid phagocytosed EG2-positive granules and stained immunohistochemically as CD71-positive 'responsive macrophages'. The decrease of activated T lymphocytes and the active phagocytosis of eosinophil granules by macrophages might play an important role in the mechanism of healing in chronic eosinophilic pneumonia.
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PMID:Analysis of bronchoalveolar lavage cells in chronic eosinophilic pneumonia before and during corticosteroid therapy. 754 15

Surface antigens on peripheral blood eosinophils from 23 patients with bronchial asthma, 6 with eosinophilic pneumonia and 8 controls were examined using a new direct method. Peripheral blood eosinophils in bronchial asthma and eosinophilic pneumonia showed higher complexity and/or granularity than those from controls. The percentage expression of HLA DR, CD4 and CD45RO on peripheral blood eosinophils from patients with bronchial asthma were increased compared with those from patients with eosinophilic pneumonia and from the controls. These results suggest that peripheral blood eosinophils in bronchial asthma may play a role in immunoregulation via the expression of human leukocyte antigens, such as HLA-DR, CD4 and CD45RO, that interact with lymphocytes, and may function as antigen-presenting cells. Furthermore this study suggests that there may be different phenotypes of eosinophils with differing surface antigens and intercellular reactions between eosinophils and lymphocytes.
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PMID:Surface antigens on eosinophils in bronchial asthma and eosinophilic pneumonia. 754 26

Cytomegaloviraemia diagnosed by early antigen detection or conventional viral culture from blood occurred 7-71 days (median 41 days) after transplant in 25 of 38 consecutive patients undergoing bone marrow transplantation (BMT) from HLA-identical siblings for haematological malignancies where patient and/or donor were CMV-seropositive. Prophylactic ganciclovir, high-dose intravenous acyclovir or immunoglobulin were not administered. Viraemia was treated with a short 3-week course of ganciclovir (10 mg/kg x 1 week, 5 mg/kg x 2 weeks). Clearance of viraemia occurred 3-47 days (median 6 days) after starting anti-viral therapy in 20 patients (18 with ganciclovir, 2 with foscarnet), and before therapy in 3 patients. The remaining 2 patients received inadequate anti-viral therapy for various reasons and died of CMV pneumonitis. There was no clinical evidence of CMV disease in the 13 patients who did not develop viraemia. One patient treated with ganciclovir before adequate haematological recovery died of graft failure. A second episode of viraemia occurred in four patients, and a third in one. We conclude that a short 3-week course of ganciclovir is adequate in most patients developing cytomegaloviraemia after allogeneic BMT. Treatment is not necessary in all patients but some inadequately treated patients develop CMV disease. Ganciclovir is tolerated well but may cause severe myelosuppression if used prior to adequate marrow recovery.
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PMID:Three weeks of ganciclovir for cytomegaloviraemia after allogeneic bone marrow transplantation. 767 Apr 5

Chediak-Higashi syndrome is a rare condition characterized by susceptibility to bacterial infections, defective natural killer activity, and episodes of macrophage activation known as accelerated phases. Chemotherapy can induce transient remission of the accelerated phase, but relapses become less and less sensitive to treatment and ultimately lead to death. Allogenic bone marrow transplantation (BMT) has been proposed as a curative treatment for Chediak-Higashi syndrome. We report the outcome of BMT in 10 such children. Seven received marrow from an HLA-identical related donor and three from an HLA-nonidentical related donor. Three patients died, two from a new accelerated phase after rejection of transplanted bone marrow and one from cytomegalovirus (CMV) pneumonia. Six of seven recipients of HLA-identical marrow and one of three recipients of HLA-nonidentical marrow are alive and well without treatment 1.5 to 13 years after transplantation (median, 6.5 years). No manifestations of accelerated phases have occurred in these seven patients, and significant natural killer activity is detectable. Interestingly, BMT prevented recurrence of accelerated phases in patients with limited numbers of donor-type leukocytes after transplantation. Ocular and cutaneous albinism were not corrected after transplantation. None of the patients developed serious toxic reactions to the BMT conditioning regimen or have long-term sequelae. These results show that HLA-identical BMT is an acceptable curative treatment for Chediak-Higashi syndrome, whereas HLA-nonidentical BMT remains an experimental approach.
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PMID:Treatment of Chediak-Higashi syndrome by allogenic bone marrow transplantation: report of 10 cases. 775 66

Cytomegalovirus (CMV) pneumonia is associated with the development of secondary immunosuppression with resultant bacterial and fungal superinfections. Because class II HLA expression within the lung may be important in normal pulmonary cell-mediated immunity, the association of CMV infection of alveolar epithelial cells (AEC) with an absence of HLA class II antigens was tested. Using dual-labeling immunohistochemistry to detect CMV, AEC, endothelial cells, macrophages, and HLA class II antigens, lung tissue from patients whom died with CMV pneumonia was examined. Seventy-five percent of infected cells were AEC. In contrast to adjacent noninfected AEC, which expressed HLA-DR antigens, 91% of infected AEC were negative. There was no difference in this expression pattern between patients with or without AIDS. The absence of HLA class II antigens on infected AEC may account, in part, for the secondary immunosuppression associated with CMV pneumonia.
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PMID:Cytomegalovirus infection is associated with absence of alveolar epithelial cell HLA class II antigen expression. 779 81

Eleven patients underwent bone marrow transplant (BMT) from an HLA-identical sibling following single dose total body irradiation (TBI), with in vivo and ex vivo T cell depletion (TCD). In spite of CMV prophylaxis with acyclovir and high-dose i.v. Ig, 10 of 11 patients developed CMV antigenemia, at a median interval from BMT of 34 days (range 16-72 days) and five died with CMV disease. Foscarnet was then given prophylactically in 11 additional TCD patients to test whether we could (1) prevent CMV reactivation, and (2) reduce transplant-related mortality. Foscarnet was given daily from days +10 to +15 (180 mg/kg/day), then thrice weekly (90 mg/kg/day) until day +100. Five patients developed CMV antigenemia at a median interval from BMT of 42 days (range 16-65 days); one progressed to CMV pneumonitis and died. The risk of developing CMV antigenemia within day 100 is currently 91% for the historical control group and 45% for the foscarnet group (p = 0.005). At diagnosis of CMV, the median number of CMV antigen-positive cells was 6.5 (range 1-13) vs 1 (range 1-5) in acyclovir vs foscarnet patients (p = 0.02) and the median highest number of CMV antigen-positive cells was 7 (range 3-110) vs 1 (range 1-12), respectively, (p = 0.03). The actuarial 1 year transplant-related mortality (TRM) is 49% and 13% in the two groups (p = 0.08). This study suggests that foscarnet prophylaxis starting on day +10 post-BMT may be helpful in reducing the risk of CMV disease and early mortality following TCD BMT.
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PMID:CMV prophylaxis with foscarnet in allogeneic bone marrow transplant recipients at high risk of developing CMV infections. 792 Mar 15

We report a clinically isolated toxoplasma pneumonitis in a child treated by HLA haplo-mismatched BMT. Conditioning consisted of TBI, cytarabine and melphalan. The BM graft was T-depleted and the boy received iv moAb antiLFA1 and antiCD2. The clinical course of pneumonitis was characterised by an early onset (day 28) and a rapidly overwhelming course. Donor and recipient had pre-graft IgG Ab against toxoplasma without IgM. These Abs had completely disappeared from the serum of the patient at the time of pneumonitis. PCR amplification detected the B1 gene of Toxoplasma gondii in the patient's PBMC from day 28.
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PMID:Lung toxoplasmosis after HLA mismatched bone marrow transplantation. 799 72


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