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)

To evaluate the usefulness of immunohistochemistry for studies of brain tissues taken from patients with a clinically established diagnosis of brain death, we examined 8 brains that had been removed and fixed in formalin between 13 h and 5 days after diagnosis of brain death (Table). As a control we also examined the brain of a patient who had suffered extensive infarction with a 28-day clinical course and died of pneumonia. Routine examination of each of the brains revealed old to recent tissue necrosis associated with macrophages, capillary proliferation and/or astrocytic gliosis. The streptavidin-biotin immunoperoxidase method was applied to the materials using four monoclonal antibodies: antiglial fibrillary acidic protein (GFAP), anti-vimentin (vimentin), LN-1 and LN-3. GFAP was stained in reactive astrocytes even 5 days after diagnosis of brain death (Fig. 3, 7). Vimentin (Fig. 2, 4) was stained in reactive astrocytes until 3 days after diagnosis of brain death. LN-1 (Fig. 5) produced positive staining in resting microglias until 3 days after diagnosis of brain death. LN-3 (Fig. 1, 6, 8), which detects human leukocyte antigen-DR, stained reactive microglias and macrophages even 5 days after diagnosis of brain death. From our findings, it is considered that immunohistochemical examination is useful even in brains from patients diagnosed as brain-dead.
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PMID:[Application of immunohistochemistry to the dead brain]. 129 31

We treated 17 patients with chronic myeloid leukemia (CML) by bone marrow transplantation using marrow from human leukocyte antigen (HLA)-matched unrelated donors. Patients were conditioned with a combination of in vivo monoclonal antibodies, chemotherapy with daunorubicin (n = 7) or busulfan (n = 10) and cyclophosphamide, and both total body and total lymphoid irradiation. Donor marrow was depleted of T cells by incubation with monoclonal antibodies of the Campath series. Fourteen (88%) of 16 evaluable patients had sustained engraftment. Four (27%) of the 15 evaluable patients developed acute graft-versus-host disease (GVHD) of grade II or greater, and 4 of 12 evaluable patients developed chronic GVHD. Three patients developed hematological and two developed cytogenetic evidence of relapse. Eight patients (47%) survive at a median follow-up of 32 months (range 10-51 months), giving an actuarial survival of 44%. Five patients remain alive without evidence of hematological or cytogenetic relapse, giving an actuarial disease-free survival of 27%. Pneumonitis caused or contributed to death in six of the nine patients who died. We conclude that T-cell depletion can prevent the severest forms of GVHD but also increases the risk of relapse after transplant with unrelated donors, as it does with HLA-identical siblings. Nevertheless the use of matched unrelated donors should be considered for CML patients who lack HLA-identical siblings.
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PMID:Bone marrow transplantation for chronic myeloid leukemia: the use of histocompatible unrelated volunteer donors. 233 31

The clinical, radiographic, and pathologic correlates of acute respiratory failure due to Pneumocystis carinii pneumonia were studied in 12 renal transplant patients treated with cyclosporin (CS) and prednisone. Six patients required only supplemental oxygen, while the other six patients developed the adult respiratory distress syndrome (ARDS) requiring prolonged mechanical ventilation despite similar predisposing factors and prompt initiation of therapy. Ten (83%) patients survived. Increased frequency of human leukocyte antigen (HLA) DR6 was noted in six of the 11 patients tested. The resolution of radiographic infiltrates was significantly slower in ARDS patients; however, there was no apparent difference in the severity of early alveolar damage between the two groups. There was also no association between the development of ARDS due to P. carinii pneumonia and the mean daily dose of CS and prednisone, the presence of cytomegalovirus infection or pneumonia, HLA-DR6 antigen, or initial hypoxemia.
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PMID:Acute respiratory failure due to Pneumocystis carinii pneumonia: clinical, radiographic, and pathologic course. 388 75

We report here a case of 33 year-old-man with refractory bilateral pneumothoraces during the treatment for interstitial pneumonitis 6 months after bone marrow transplantation (BMT). He was diagnosed as having acute myelogenous leukemia (AML) M1. He was treated with chemotherapy, and cerebral irradiation. BMT was performed in August 1989 from a sibling donor whose human leukocyte antigen was matched, ABO blood type mismatched. Preconditioning regimen was cyclophosphamide and total body irradiation (TBI). BMT was successful without major graft versus host disease. Thereafter he complained of respiratory symptom and was admitted on June 14 1990. Computed tomogram (CT) scan showed interstitial and alveolar shadows. We started the treatment against bacterial infection, Pneumocystis carinii, cytomegalovirus (CMV) and against interstitial pneumonitis with bolus dose of steroid. The transbronchial lung biopsy specimen revealed interstitial pneumonitis without typical CMV nor pneumocystis carinii pneumonia. Although a CT scan showed improvement of pneumonitis, bilateral pneumothoraces occurred. The adhesion therapy became successful after the reduction of steroid dosage. A pneumothorax rarely occurs after BMT. In this case it is speculated that TBI might be responsible for interstitial pneumonitis, and the steroid might have inhibited the adhesion therapy of pneumothorax.
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PMID:[Refractory bilateral pneumothoraces complicated with interstitial pneumonitis after bone marrow transplantation]. 836 73

We conducted serial studies on peripheral blood lymphocytes from four patients with acute Coxiella burnetii infection. These studies revealed that the proportion of gammadelta T cells in these patients significantly increased after the onset of disease (mean, 16%; range, 13%-30%) as compared with that in five healthy controls (mean, 4%; range, 0.5%-7%; P < .0055) and that in five controls with pneumonia (mean, 2%; range, 1%-3%; P < .0014). Most of the gammadelta T cells from these patients expressed the Vgamma9 Vdelta2 gene product. During the acute phase of disease, most gammadelta T cells expressed the activation marker human leukocyte antigen DR but not CD25. During this phase, gammadelta T cell activation was higher than alphabeta T cell activation. Our findings indicate that gammadelta T cells are predominantly involved in the acute immune response to C. burnetii.
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PMID:The number and proportion of Vgamma9 Vdelta2 T cells rise significantly in the peripheral blood of patients after the onset of acute Coxiella burnetii infection. 911 59

We studied the efficacy and safety of a risk-adapted approach with ganciclovir to prevent cytomegalovirus (CMV) pneumonia in 41 CMV-seropositive recipients of genotypically human leukocyte antigen-identical bone marrow transplants. Prophylaxis with ganciclovir, at a dosage of 2.5 mg/kg twice a day for 14 days, was started when patients were treated with high-dose steroids for acute graft-versus-host disease (i.e., they were considered at high risk for CMV pneumonia), or the drug was given as preemptive therapy when CMV antigenemia developed (i.e., the patients were considered at intermediate risk for CMV pneumonia). Twelve patients (29%) were treated prophylactically and seven patients (17%) preemptively. Only five patients (26%) received a second course of ganciclovir (given preemptively to four patients). Twenty-two patients (54%) never received ganciclovir because they did not fall within these risk groups. None of the 41 patients developed CMV pneumonia. Ganciclovir-related granulocytopenia did not occur (course 1) or was very mild (course 2). We conclude that this approach appears to prevent the development of CMV pneumonia after bone marrow transplantation.
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PMID:A risk-adapted approach with a short course of ganciclovir to prevent cytomegalovirus (CMV) pneumonia in CMV-seropositive recipients of allogeneic bone marrow transplants. 914 90

The obligate intracellular pathogen Chlamydia pneumoniae is associated with chronic respiratory, atherosclerotic, and rheumatic disease. The alveolar macrophage (AM) is a potential target cell for the pathogen and may contribute to respiratory immunopathology. We therefore investigated in vitro the interaction between chlamydiae and macrophages with cocultures of C. pneumoniae and AM from 12 healthy volunteers. Inflammatory responses were evaluated through lucigenin-amplified chemiluminescence; secretion of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin 8 (IL-8); and expression of intercellular adhesion molecule-1 (ICAM-1) and human leukocyte antigen-DR (HLA-DR). C. pneumoniae readily induced productive infection in the AM. Inclusions containing replicating pathogens could be maintained for up to 120 h. Morphologically similar infection patterns were seen ex vivo in AM collected from six patients with known C. pneumoniae pneumonia. AM responded to the infection with a marked, dose-dependent release of reactive oxygen species, TNF-alpha, IL-1beta, and IL-8. ICAM-1 expression remained unchanged, but HLA-DR was significantly upregulated. Our data indicate that the release of antimicrobial mediators cannot prevent chlamydial infection and replication in AM, but may be involved in amplification of the local inflammatory response in C. pneumoniae pneumonia.
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PMID:Interaction of Chlamydia pneumoniae and human alveolar macrophages: infection and inflammatory response. 980 36

Azathioprine is a drug commonly used for the treatment of inflammatory bowel disease, organ transplantation and various autoimmune diseases. Hepatotoxicity is a rare, but important complication of this drug. The cases reported to date can be grouped into three syndromes: hypersensitivity; idiosyncratic cholestatic reaction; and presumed endothelial cell injury with resultant raised portal pressures, venoocclusive disease or peliosis hepatis. The components of azathioprine, 6-mercaptopurine and the imidazole group, may play different roles in the pathogenesis of hepatotoxicity. The strong association with male sex, and perhaps with human leukocyte antigen type, suggests a genetic predisposition of unknown type. Many of the symptoms of hepatotoxicity, such as nausea, abdominal pain and diarrhea, can be nonspecific and can be confused with a flare-up of inflammatory bowel disease. As well, the subtype resulting in portal hypertension can occur without biochemical abnormalities. A 63-year-old man with Crohn's disease who is presented developed the rare idiosyncratic form of azathioprine hepatotoxicity, but also had a severe disabling steroid myopathy, peripheral neuropathy, resultant deep venous thrombosis and pulmonary embolism related to immobility, and a nosocomial pneumonia. His jaundice and liver enzyme levels improved markedly on withdrawal of the drug, returning to almost normal in five weeks. Treating inflammatory bowel disease effectively while trying to limit iatrogenic disease is a continuous struggle. Understanding the risks of treatment is the first important step. There must be a low threshold for obtaining liver function tests, especially in men, and alertness to the need to discontinue the drug or perform a liver biopsy should patients on azathioprine develop liver biochemical abnormalities, unexplained hepatomegaly or signs of portal hypertension.
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PMID:Cholestatic hepatocellular injury with azathioprine: a case report and review of the mechanisms of hepatotoxicity. 981 67

Acute eosinophilic pneumonia (AEP) is a recently described illness and the number of case reports has increased during the last few years. However, the role of interleukin (IL)-5 and activated lymphocytes in the pathogenesis or activity of AEP is still not clear. The clinical features, lymphocyte surface analysis and IL-5 concentrations in bronchoalveolar lavage fluid (BALF) and peripheral blood (PB) of a young female patient with AEP are described before and at 2 weeks, 4 weeks and 6 months after a 3-day course of i.v. methylprednisolone. Serum and BALF concentrations of IL-5 before treatment were 5,200 and 8,400 pg x mL(-1), respectively. Activated CD4 lymphocytes bearing CD25 and human leukocyte antigen (HLA)-DR in BALF were higher than in PB. Treatment caused a rapid fall in these cells and levels of IL-5 in BALF returned to normal levels in parallel with clinical improvement. There was no evidence of recurrence after cessation of steroid therapy. In contrast, eosinophilia in BALF persisted for 4 weeks after steroid therapy in spite of normalization of the chest radiograph and arterial blood gases. The number of CD8+CD11b- (suppressor/cytotoxic) T-cells subsequently increased while the number of CD8+CD11b+ cells decreased. These results suggest that activated CD4 cells and interleukin-5 elevation contribute to the development of acute eosinophilic pneumonia rather than persistent eosinophilia in the lung and that a short course of steroid therapy may effectively control acute eosinophilic pneumonia.
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PMID:Activation of lymphocytes and increased interleukin-5 levels in bronchoalveolar lavage fluid in acute eosinophilic pneumonia. 1083 52

In contrast to solid organ transplantation (Tx), the incidence of post-transplant lymphoproliferative disease (PTLD) after hematopoietic stem cell Tx (HSCT) is generally low. This risk, however, is significantly elevated in patients receiving human leukocyte antigen (HLA) mis-matched or T-cell-depleted grafts, or after treatment for severe graft-versus-host disease (GvHD). An 18-yr-old patient with positive Epstein-Barr virus (EBV) serology received a fully matched, unmanipulated bone marrow graft from an unrelated EBV-positive donor for treatment of acute myeloid leukemia (AML) in second complete remission. GvHD prophylaxis was performed with cyclosporin A (CsA) and a short course of methotrexate. Four months after Tx, the patient developed ulcerative tonsillitis that was unresponsive to antibiotic treatment. Diarrhea appearing simultaneously was interpreted as gastrointestinal GvHD and steroids were added to CsA. A few days later the patient was admitted to hospital because of generalized seizure and pneumonia. Despite reduction of immunosuppression, intensification of anti-viral treatment, and subsequent mechanical ventilation, the patient died of acute respiratory distress 6 days later. Autopsy demonstrated disseminated EBV-induced, multi-nodular lymphoma infiltration of the entire colon but no signs of GvHD. Moreover, both lungs, paratracheal lymph nodes, kidneys, thyroid gland, and liver were infiltrated with large B-cell non-Hodgkin's lymphomas. This case underlines the rapid and aggressive course of EBV-induced disseminated PTLD after HSCT, initially mimicking intestinal GvHD because of massive colonic lymphoma infiltration. Tissue biopsies should be performed early for establishing correct diagnosis, thus enabling specific therapy, e.g. infusion of donor leukocytes with cytotoxic T-lymphocytes.
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PMID:Epstein-Barr virus-associated post-transplant lymphoproliferative disease after bone marrow transplantation mimicking graft-versus-host disease. 1127 9


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