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)

Anti-neutrophil antibodies have been described in a variety of clinical conditions associated with neutropenia. However, relatively little is known about the antigenic specificities of naturally occurring anti-neutrophil autoantibodies. We investigated the possibility that anti-neutrophil antibodies specific for the neutrophil adhesion glycoprotein (GP) complex CD11b/CD18 might be present in the sera of some patients with autoimmune neutropenia. These membrane GPs have been shown to be highly immunogenic in the production of murine monoclonal antibodies against neutrophil antigens. Moreover, autoantibodies to the platelet membrane GP complex IIb/IIIa, another member of the integrin family of cell adhesion proteins, have been demonstrated in immune thrombocytopenic purpura. Sera from 50 patients known to have anti-neutrophil IgG antibodies were evaluated using an immunobead "antigen capture" assay, modeled after a method used to identify anti-platelet GPIIb/IIIa autoantibodies. This assay detected anti-CD11b/CD18 autoantibodies in seven of the 50 sera. Each of these seven sera demonstrated decreased IgG binding to the neutrophils of a patient with congenital deficiency of CD11b/CD18. The patient with the highest levels of anti-CD11b/CD18 suffered recurrent skin infections and cellulitis, and died of respiratory failure during one of multiple episodes of pneumonia. Purified IgGs from five of these patients demonstrated effects on adhesion and/or opsonin receptor-mediated functions when tested with intact neutrophils in vitro. Our findings indicate that some patients with autoimmune neutropenia have autoantibodies specific for the functionally important neutrophil adhesion proteins CD11b/CD18. Our findings also raise the possibility that these autoantibodies may, in some cases, interfere with neutrophil function, thereby amplifying the risk of infection associated with neutropenia.
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PMID:Identification of autoantibodies specific for the neutrophil adhesion glycoproteins CD11b/CD18 in patients with autoimmune neutropenia. 167 88

A 17 year old male was admitted because of pancytopenia. Bone marrow aspiration revealed myelodysplasia, no increase of blast cells and excessive expansion of megakaryocytic lineage. Although mild increase of bone marrow reticulin fiber was observed, no hepatosplenomegaly was recognized. Therefore he was diagnosed as refractory anemia (RA) or MDS with myelofibrosis and treated with low dose Ara-C regimen. Remission was achieved in June 1987, but the relapse occurred in Oct. 1987. His bone marrow at the relapse showed more remarkable dysplastic change than before. Sequential bone marrow examinations thereafter, revealed an increase of megakaryocytic lineage, especially immature dysplastic megakaryocytes, leading to the appearance of the abnormal megakaryoblasts (detected with anti GP IIb/IIIa antibody) as well as uncharacterized blast cells in his terminal stage. Transformation from MDS to megakaryocytic leukemia was strongly suggested. He died of severe pneumonia in March 1989. The invasion of abnormal immature megakaryocytic cells including megakaryoblasts was observed in liver, spleen and lymph nodes at autopsy. There are several reports on cases having a common hematological features such as 1) pancytopenia in peripheral blood, 2) myelodysplasia, 3) excessive growth of megakaryocytic lineage, 4) myelofibrosis without hepatosplenomegaly, although other clinical features were different. We propose all these cases should be reviewed at the point of MDS mainly involved in megakaryocytic lineage.
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PMID:[Myelodysplasia predominantly involving in megakaryocytic lineage successfully treated with low-dose Ara-C]. 194 32

AIMS: This study evaluated the treatment of early coronary stent thrombosis with intracoronary urokinase or the platelet glycoprotein IIb/IIIa receptor inhibitor ReoPro (abciximab). METHODS AND RESULTS: Seventy-four patients (126 stents) were treated immediately after identification of early (0-30 days) coronary stent thrombosis. Twenty-nine patients were treated with intracoronary urokinase (UK) (UK alone in 19; UK and additional balloon angioplasty in 10) and another 45 patients were given ReoPro((R)) (abciximab) (0.25 mg/kg as a bolus alone in 26, abciximab with additional balloon angioplasty in 19) within 30 days of stent implantation. TIMI grade 3 flow was obtained in 23 patients (79%) in the UK group and in 38 (84%) in the abciximab group (nonsignificant). Three patients (10%) in the UK group and one (2%) in the abciximab group underwent repeat percutaneous transluminal coronary angioplasty (PTCA) (nonsignificant). Five patients (17%) in the UK group and three (7%) in the abciximab group were referred for urgent coronary artery bypass graft surgery (CABG) because of residual thrombus and refractory ischemia (nonsignificant). Repeat revascularization was necessary in eight patients (28%) in the UK group versus four (9%) in the abciximab group (p < 0.05). Five patients (17%) in the UK group and eight (18%) in the abciximab group developed myocardial infarction (nonsignificant). Five patients (17%) in the UK group (cardiogenic shock (three), cerebral hemorrhage (one) and pneumonia (one)) and three (6.6%) in the abciximab group (cardiogenic shock (two), heart failure (one)) died within 30 days (nonsignificant). Overall, noncardiac complications (bleeding including surgical repair of groin) were observed in 11 patients (38%) in the UK group and three (7%) in the abciximab group (p < 0.001). CONCLUSION: Compared to urokinase, abciximab reduced the need for repeat revascularization procedures and the risk of noncardiac events, including bleeding complications in patients with early coronary stent thrombosis.
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PMID:Comparison of ReoPro((R)) (abciximab) versus intracoronary thrombolysis for early coronary stent thrombosis. 1247 Mar 68

Abciximab, a platelet glycoprotein (GP) IIb/IIIa inhibitor, has been shown to improve clinical outcomes in patients undergoing percutaneous coronary intervention. However, there is a well-documented increase in bleeding risk associated with the use of this agent. Spontaneous pulmonary hemorrhage is a particularly rare and easily misdiagnosed complication that requires early diagnosis to ensure patient survival. A 61-year-old man presented to the emergency department with chest pain and inferolateral ST elevation on electrocardiogram. A paclitaxel drug-eluting stent was then placed in the left circumflex artery, without complications. Abciximab (a bolus of 0.25 mg/kg followed by an infusion of 10 mg/min for 12 h) was given. Approximately 20 min later, the patient developed dyspnea and hemoptysis. A chest radiograph revealed new bilateral diffuse interstitial infiltrates, and the patient was started on empirical antibiotics for pneumonia. Because of increasing dyspnea and somnolence, the patient was intubated and bronchoscopy was performed, revealing serial hemorrhagic returns from the left lower lobe, diagnostic of diffuse alveolar hemorrhage and judged to be secondary to abciximab, given the time course. All antiplatelet and antithrombotic agents were stopped. The patient stabilized over the next several days, with some recurrent hemoptysis, and was successfully extubated seven days later. Prognosis remains poor in GP IIb/IIIa inhibitor-induced pulmonary hemorrhage, and early diagnosis is critical so that antithrombotic and antiplatelet agents may be discontinued in a timely manner. A high degree of suspicion is required when treating a patient who presents with dyspnea and new radiological infiltrates after receiving a GP IIb/IIIa inhibitor.
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PMID:Abciximab-induced alveolar hemorrhage after percutaneous coronary intervention. 1827 91

As mechanisms of sepsis pathophysiology have been elucidated with time, sepsis may be considered nowadays, as an uncontrolled inflammatory and pro-coagulant response to a pathogen. In this cascade of events, platelets play a key role, via interaction with endothelial cells and modulation of both innate and adaptive immune system. In that manner, inhibition of platelet function could represent a useful tool for attenuating inflammatory response and improving outcomes. Data on current antiplatelet agents, including acetylsalicylic acid, P2Y12 inhibitors and GPIIb/IIIa antagonists, in animal models are promising. Clinical data in patients hospitalized for pneumonia, at risk for acute lung injury, and/or critically ill revealed an association between antiplatelet therapy and reduction in both short-term mortality and prevalence of acute lung injury, as well as, the need for intensive care unit admission, without a concomitant increased bleeding risk. In need of innovative approach in the treatment of sepsis, further prospective, interventional, randomized trials are pivotal to establish potential use of antiplatelet agents in this context.
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PMID:Use of antiplatelet agents in sepsis: a glimpse into the future. 2410 87