Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Complications are the major causes of illness and death after burning and most of them stem from the burn wound. Their origin and importance are reviewed with emphasis on problems and growing points in knowledge. Fluid leakage from the circulation into the burn is the cause of hypovolemic shock, but the underlying permeability changes in the burn are only partly understood. Other nonbacterial complications include acute cardiac failure, acute anemia, hemolytic jaundice, renal failure, encephalopathy, complex hypermetabolic effects including pseudodiabetes, gastric and duodenal ulceration, deep vein thrombosis and pulmonary embolism, pulmonary and glomerular microthrombosis, hepatic jaundice, and arterial thrombosis. Involvement of the airway in conflagrations carries special hazards like glottic edema and inhalation of irritant fumes. Nowadays, bacterial causes are dominant and these remain the main challenge. Bacterial infection and invasion of the burn are usually responsible for septicemia, bronchopneumonia, and pyelonephritis although other sources also contribute. Indirect manifestations of septicemia include paralytic ileus, acute gastric dilatation, toxic myocarditis, and some cases of renal failure. Therapeutic complications like agranulocytosis, thrombocytopenia, and colitis occur at times. High concentrations of oxygen given therapeutically can produce fatal aseptic hypoxic pneumonitis.
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PMID:A review of the complications of burns, their origin and importance for illness and death. 44 73

A 59-year-old chronic alcoholic male, with no cardiac past history, was hospitalised with septicemia 5 months after the endoscopic removal of 2 benign intestinal polyps. The diagnosis of tricuspid endocarditis was possible only 2 months later on the basis of echocardiography requested because of the onset of a tricuspid systolic murmur. Blood cultures revealed the presence in succession of streptococcus D fecalis then bovis. Antibiotics, changed several times because of the onset of complications (allergy, agranulocytosis), failed to deal with the problem of infection as shown by the development of several septic pulmonary emboli which finally resulted in total tricuspidectomy with neither immediate nor secondary valve replacement. The authors use this clinical case to review the characteristics of tricuspid endocarditis, the incidence of which is on the increase in certain etiological contexts (staphylococcal endocarditis in drug addicts or secondary to central vascular lines). They stress that the clinical picture is often confusing since the murmur of tricuspid incompetence is absent in 2/3 of cases. Echocardiography must therefore be requested routinely in all septicemias, thus enabling earlier diagnosis and assessment of the risk of pulmonary embolism (risk if vegetation greater than 10 mm). The nature of the organism responsible may be suggestive of certain etiologies. Thus malignant disease of the colon should be sought if the bacterium is a streptococcus D bovis. Apart from antibiotics, treatment must include effective anticoagulation to decrease the risk of embolic recurrence.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Isolated tricuspid endocarditis. Apropos of a case caused by Streptococcus D bovis and faecalis occurring after coloscopy]. 190 45

A report of 27 drug induced agranulocytosis is presented in a period of 13 years. The rate of the disease was 0.12% of the total number of patients. Cases due to cytostatical and radiation treatment were not included. According to bone-marrow cellularity patients were divided into hypo- and hyper-cellular groups. The clinical findings were similar in both groups and the majority of patients recovered. Two patients died, both in the hypocellular group: the first due to mycotic pulmonary infection, the other after massive pulmonary embolism but after complete haematological recovery. Bone-marrow plasmocytosis was slightly expressed in the hypocellular group. The normal leukocyte number appeared after treatment within 3-25 days. Recurrent agranulocytosis was observed in four patients and permanent leukopenia developed in five. The leukocyte-agglutination test was positive in 10 cases only, but the leukocyte migration test was positive in all investigated cases except two. Five patients had a previous history with idiosyncrasy. Treatment was started with antibiotics, corticosteroids and with antimycotic drugs. Sterile island and granulocyte-transfusion was applied in seriously ill patients with septicemic complications only.
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PMID:[Occurrence and clinical course of drug-induced agranulocytosis]. 258 75

We describe 3 cases of acute graft-versus-host (GVH) disease in patients with acute myeloid leukaemia following transfusions taken from non-HLA-identical healthy donors. The leucocyte transfusions were given because of severe bone marrow aplasia and granulocytopenia following leukaemia induction treatment. The first patient had an acute GVH reaction with an erythrodermia-like skin reaction all over and associated with severe abdominal cramping, enlarged liver and pathological liver function tests. The second patient had a relatively mild skin reaction and enlarged liver. Both died of severe pulmonary infection. The third patient also had a mild skin reaction and enlarged liver. He died of pulmonary embolism. The diagnosis of GVH of the latter 2 cases was made on skin biopsy. The autopsy samples revealed in all cases a heavy lymphocytic infiltration of the kidneys and liver portal area. Until more precise guidelines can be established, irradiation of blood cell products given to patients with neutropenia due to leukaemia induction treatment should be considered.
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PMID:Graft-versus-host reaction in 3 adult leukaemia patients after transfusion of blood cell products. 658 Jul 18

Respiratory failure is the main cause of death in patients undergoing bone marrow transplantation (BMT). In this paper, clinical and research aspects as well as diagnostic, prophylactic and therapeutic strategies concerning the various forms of pulmonary and bronchial complications, which may evolve after BMT, are discussed. Both cytomegalovirus (CMV)-induced interstitial pneumonia (PM) and the idiopathic pneumonia syndrome rarely occur in the cytopenic phase post-BMT. Haematological reconstitution with donor type cells seems to be a prerequisite to the development of these complications, suggesting a key role of immunological reactions. While CMV pneumonia can be effectively treated or prevented by ganciclovir, the idiopathic syndrome is usually fatal. Due to improved prophylaxis and therapy, lethal interstitial PM due to Pneumocystis carinii, herpes simplex, varizella zoster or Toxoplasma gondii as well as lethal PM caused by bacteria or Candida species are comparatively rare events. Aspergillus species, on the other hand, have emerged as frequent causative pathogens in lethal PM during the past years. Prolonged granulocytopenia and prolonged medication with corticosteroids are major risk factors of pulmonary aspergillosis, which is usually fatal; effective prophylaxis may be achieved by sterile air supply during the hospital stay and by inhalation of amphotericin B thereafter. Pulmonary haemorrhage, as diagnosed by bronchoalveolar lavage (BAL), may develop due to the toxicity of the conditioning regimen, or may be secondary to infectious PM of various kind. Congestive heart failure or the application of cytokines might give rise to the development of pulmonary oedema. Patients with hepatic veno-occlusive disease have a high risk of subsequent pulmonary complications, possibly on the basis of toxic lung injury. Venous thromboembolism or air embolism may occur; they are usually venous catheter-associated. Pleural effusions may develop secondary to infection, congestive heart failure, veno-occlusive disease, pulmonary embolism or malignancy. Patients with bronchiolitis obliterans, which leads to progressive respiratory failure, present with an obstructive pattern in lung function tests and hyperinflated lungs on chest radiographs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The lung as a critical organ in marrow transplantation. 772 20

Clozapine (Clozaril), a tricyclic dibenzodiazepine, causes fewer extrapyramidal side effects than do other antipsychotic drugs. Because it can induce agranulocytosis, however, clozapine is indicated only for schizophrenia that is not responsive to other therapies. To describe the drug's effects on mortality, we compared rates of various causes of death in 67,072 current and former clozapine users. We linked data from a national registry of clozapine recipients to the National Death Index and Social Security Administration Death Master Files, obtained death certificates, and calculated mortality rates for underlying causes of death using standardization to adjust for age, sex, and race. During 1991-1993, there were 396 deaths in 85,399 person-years for patients ages 10-54 years. Mortality was lower during current clozapine use than during periods of non-use. Mortality from suicide was decreased in current clozapine users by comparison with past users [rate ratio (RR) = 0.17; 95% confidence interval (CI) = 0.10-0.30]. During clozapine use, there were elevations in mortality rates for less common causes of death, including pulmonary embolism (RR for current exposure compared with past clozapine use = 5.2) and respiratory disorders (RR = 2.9). Clozapine appears to reduce mortality in severe schizophrenics, mostly by decreasing suicide rates.
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PMID:Mortality in current and former users of clozapine. 934 68

Esophageal cancer frequently expresses cyclooxygenase-2 (COX-2) enzyme. In preclinical studies, COX-2 inhibition results in decreased cell proliferation and potentiation of chemotherapy and radiation. We report preliminary results of a phase II study conducted by the Hoosier Oncology Group in patients with potentially resectable esophageal cancer. All patients received cisplatin at 75 mg/m2 given on days 1 and 29 and fluorouracil (5-FU) at 1000 mg/m2 on days 1 to 4 and 29 to 32 with radiation (50.4 Gy beginning on day 1). Celecoxib (Celebrex) was administered at 200 mg orally twice daily beginning on day 1 until surgery and then at 400 mg orally twice daily until disease progression or unexpected toxicities, or for a maximum of 5 years. Esophagectomy was performed 4 to 6 weeks after completion of chemoradiation. The primary study endpoint was pathologic complete response (pCR). Secondary endpoints included response rate, toxicity, overall survival, and correlation between COX-2 expression and pCR. Thirty-one patients were enrolled from March 2001 to July 2002. Respective grade 3/4 toxicities were experienced by 58%/19% of patients, and consisted of granulocytopenia (16%), nausea/vomiting (16%), esophagitis (10%), dehydration (10%), stomatitis (6%), and diarrhea (31%). Seven patients (24%) required initiation of enteral feedings. There have been seven deaths so far, resulting from postoperative complications (2), pulmonary embolism (1), pneumonia (1), and progressive disease (3). Of the 22 patients (71%) who underwent surgery, 5 had pCR (22%). We conclude that the addition of celecoxib to chemoradiation is well tolerated. The pCR rate of 22% in this study is similar to that reported with the use of preoperative chemoradiation in other trials. Further follow-up is necessary to assess the impact of maintenance therapy with celecoxib on overall survival.
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PMID:Cisplatin, fluorouracil, celecoxib, and RT in resectable esophageal cancer: preliminary results. 1568 29

Acute right ventricular (RV) failure following pulmonary embolism (PE) is a strong predictor of poor clinical outcome. Present studies test for an association between RV failure from experimental PE, inflammation, and upregulated chemokine expression. Additional experiments test if neutrophil influx contributes to RV dysfunction. PE was induced in male rats by infusing 24 microm microspheres (right jugular vein) producing mild hypertension (1.3 million beads/100 g, PE1.3), or moderately severe hypertension (2.0 million beads/100 g, PE2.0). Additional rats served as vehicle sham (0.01% Tween 20, Veh). In vivo RV peak systolic pressures (RVPSP) increased significantly, and then declined following PE2.0 (51 +/- 1 mm Hg 2 h; 49 +/- 1, 6 h; 44 +/- 1, 18 h). RV generated pressure of isolated, perfused hearts was significantly reduced in PE2.0 compared with PE1.3 or Veh. MCP-1 protein (ELISA) was elevated 21-fold and myeloperoxidase activity 95-fold in RV of PE2.0 compared with Veh or PE1.3. CINC-1, CINC-2, MIP-2, MCP-1, and MIP-1alpha mRNA also increased in RV of PE2.0. Histological analysis revealed massive accumulation of neutrophils (selective esterase stain) and monocyte/macrophages (CD68, ED-1) in RV of PE2.0 hearts in regions of myocyte damage. Electron microscopy showed myocyte necrosis and phagocytosis by inflammatory cells. LV function was normal and did not show increased inflammation after PE2.0. Treatment with anti-PMN antibody reduced RV MPO activity and prevented RV dysfunction. Conclusions-PE with moderately severe pulmonary hypertension (PE2.0) resulted in selective RV dysfunction, which was associated with increased chemokine expression, and infiltration of both neutrophils and monocyte/macrophages, indicating that a robust immune response occurred with RV damage following experimental PE. Experimental agranulocytosis reduced RV, suggesting that neutrophil influx contributed to RV damage.
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PMID:Cardiac inflammation contributes to right ventricular dysfunction following experimental pulmonary embolism in rats. 1681 20