Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.11.1.7 (peroxidase)
 65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 88-year-old man was admitted because of the left chest pain due to herpes zoster for 1 week. Blood analyses and immunoelectrophoresis revealed anemia, severe neutropenia, rouleaux formation and IgM, lambda-type monoclonal gammopathy. The HE staining and peroxidase-anti-peroxidase staining of biopsy specimens of the cervical lymph node swelling appeared from the fifth hospital day, revealed an increase in atypical lymphocytes bearing IgM, lambda-type immunoglobulin. Then a diagnosis of primary macroglobulinemia was made. Although the patient's clinical findings transiently improved after chemotherapy with prednisolone and vindesine, he died of a septic shock which appeared after klebsiella pneumonia and sepsis. We reported an unusual case of primary macroglobulinemia with severe neutropenia, leading to a rapid development of septic shock after the chemotherapy.
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PMID:[Primary macroglobulinemia with severe neutropenia, leading to a rapid development of septic shock]. 249 64

We report a case of acute myelofibrosis (AMF) developing into acute myelomegakaryoblastic leukemia. A 33-year-old woman was admitted to our hospital because of fever and chest pain. On physical examination, hepatosplenomegaly was not noticed. Pancytopenia and a small number of blast cells were observed in the peripheral blood. Poikilocytosis was not detected. Bone marrow examination revealed dry tap on aspiration, and moderate increase in reticulin fiber on biopsy. The diagnosis of AMF was made. Eight months later, blast cells markedly increased. Surface marker was investigated and MCS-2 (CD13), C17 (CDw41) and P2 (CDw41) were found to be positive. Electron microscopic examination revealed that blast cells were composed of PPO-positive cells and MPO-positive cells. Based on these findings, it was considered that the patient developed acute myelomegakaryoblastic leukemia. Recently AMF is thought to be a state to have the ability to develop into various types of acute leukemia. Adequate therapy may be required before the development of leukemia.
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PMID:[Acute myelofibrosis terminating in acute myelomegakaryoblastic leukemia]. 259 46

Cardiac rupture occurs in 10 per cent of patients who die with acute myocardial infarction, but the pathogenesis remains unclear. Twenty randomly selected patients with cardiac rupture were reviewed retrospectively at autopsy, and the findings were compared with those of 20 age- and sex-matched control subjects who had died of acute transmural myocardial infarction without rupture. The times from the onset of chest pain to death were similar in the two groups (5.7 +/- 5.8 days for patients with rupture versus 4.2 +/- 4.9 days for control subjects), and there were no differences in the incidences of systemic hypertension, diabetes mellitus, hypercholesterolemia, history of myocardial infarction, or angina pectoris. The severity of coronary atherosclerosis was different in the two groups, with 55 per cent of the patients with cardiac rupture having single-vessel disease and 70 per cent of the patients without cardiac rupture having disease in three vessels. Additionally, the incidence of thrombosis was greater in patients with cardiac rupture than in those without. The inflammatory cell response in each patient was quantitated microscopically (number and type of leukocytes) in ten high-power fields. The inflammatory response was greater in patients with cardiac rupture. The number of eosinophils in the inflammatory response was significantly (P less than 0.01) greater in hearts associated with cardiac rupture (29.5 +/- 4 per cent) than in control hearts (11.7 +/- 3.1 per cent). It is postulated that eosinophils rich in arylsulfatase B, peroxidase, glucuronidase, beta-glycerophosphatase, major basic protein, and eosinophilic cationic protein may further weaken the necrotic myocardium and, in part, determine whether acute myocardial infarction will eventually result in cardiac rupture.
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PMID:Association of eosinophils with cardiac rupture. 399 34

A 77-year-old man, in whom chronic myeloid leukemia (CML) had been diagnosed in October 1990, was admitted to hospital with right chest pain in November 1992. Bone marrow examination revealed the chronic phase of CML. Chest X-ray showed right pleural effusion. The cells from pleural effusion were positive for CD7, CD13, CD33, CD41a, including CD33, CD41a-double positive cells in 57.5%. Southern blot analysis revealed 3'bcr rearrangement. Electron microscopic examination showed the presence of platelet peroxidase. An abnormal karyotype with various additional chromosomes was observed. This is a rare case of extramedullary pleural myelo-megakaryoblastic biphenotypic crisis during the chronic phase of CML.
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PMID:[Extramedullary pleural myelo-megakaryoblastic crisis during hematological chronic phase in chronic myeloid leukemia]. 813 19

We reported two cases of silicosis exhibiting MPO-ANCA associated disorder. Case 1 was a 69 year-old man with silicosis and chronic interstitial pneumonia. He was admitted because of fever, dry cough, left chest pain, dyspnea and body weight loss. He was diagnosed as acute exacerbation of interstitial pneumonia, pericarditis and gastrointestinal bleeding. Case 2 was a 67 year-old man with silicosis. He repeated attack of fever, hoarseness, dysphagia and headache. The cell counts of cerebrospinal fluid increased and the thickness of cerebellar tent and left dura mater was observed in the brain MRI. Therefore, he was diagnosed as pachymeningitis and neuropathy of cranial nerves. Both cases were complicated by silicosis and the laboratory findings showed high serum levels of P-ANCA, ANA and rheumatoid factor and inflammatory responses, indicating they were suspected vasculitis. The two cases were treated by steroid and immunosuppressive therapy and had good clinical response. Silicosis may affect multiple organ involvement associated with P-ANCA.
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PMID:[Two cases of silicosis exhibiting MPO-ANCA associated disorder]. 1069 8

A 69-year-old woman was admitted with sudden chest pain and high fever. Electrocardiography showed negative T waves in the precordial leads. Subsequently, pleural and pericardial effusion developed, but the symptoms and signs subsided without specific therapy. On day 31, fever, left shoulder pain and pleural effusion reappeared. 67Ga scintigraphy showed abnormal uptake in the chest and left shoulder. Blasts were detected in the peripheral blood on day 44, and in the pleural effusion and bone marrow on day 45. The blasts were positive for Philadelphia chromosome, CD10, CD19, CD33, CD34 and IgH-chain rearrangement and negative for myeloperoxidase. The clinical picture of the preceding pleuropericarditis was that of viral or idiopathic origin, but its relationship with acute lymphoblastic leukemia was unclear. Inflammatory chemokines in the pleural space may have induced invasion of the leukemic cells.
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PMID:[Philadelphia chromosome-positive acute lymphoblastic leukemia preceded by acute pleuropericarditis]. 1157 6

We report two patients with scleroderma, 73-year-old female and 67-year-old female, who developed anti neutrophil cytoplasmic autoantibody (ANCA) associated rapid progressive glomerulonephritis (RPGN). Both patients have had a long history of scleroderma (23 and 14 years, respectively) when ANCA-associated glomerulonephritis occurred. In the first patient, scleroderma was localized in both fingers. She has been followed-up as CREST syndrome rather than systemic sclerosis. The complaints on admission were leg edema and left chest pain in the first patient, and a pyrexia and dyspnea in the second patient. Both patients showed pulmonary manifestation (pleural effusion in the first patient, interstitial pneumonia and alveolar hemorrhage in the second patient, respectively) and rapid progressive glomerulonephritis. Both patients died in spite of corticosteroid therapy. Autopsy findings in the second patient demonstrated crescentic glomerulonephritis and alveolar hemorrhage. Our cases demonstrated that MPO-ANCA associated glomerulonephritis could be associated with limited scleroderma as well as systemic scleroderma. In these condition, the prognosis will be poor if scleroderma seemed to be stable.
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PMID:[Anti-neutrophil cytoplasmic autoantibody-associated rapid progressive glomerulonephritis complicated with both limited and diffuse scleroderma]. 1259 16

We report a case with microscopic polyangiitis (MPA) complicated by varicella zoster encephalitis. A 60-year-old woman caught a common cold and had acute otitis media in April 1998. Proteinuria and hematuria with hyaline cast were noted at the routine medical check in May, and she was referred to our hospital because of high fever and chest pain. MPA was diagnosed with acute progressive renal failure, pleuritis and elevated anti-neutrophil cytoplasmic myeloperoxidase antibody (MPO-ANCA). Corticosteroid therapy was administered under hemodialysis but MPA was flared several times with various symptoms including interstitial pneumonitis, alveolar hemorrhage and erythema multiforme exudativum. During the course of the disease she developed disseminated varicella zoster and encephalitis. Positive polymerase chain reaction to varicella zoster in cerebrospinal fluid helped to differentiate her encephalitis from central nervous system symptoms due to microscopic angiitis and herpes simplex encephalitis. Combination of corticosteroid and acyclovir therapies for MPA and varicella zoster encephalitis under hemodialysis were successful. The diagnostic process and therapies to these complicated contexts were thought to be very important.
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PMID:[Successfully treated case with microscopic polyangiitis complicated severe varicella zoster virus infection including encephalitis and disseminated varicella zoster]. 1459 66

To risk-stratify patients with chest pain who are admitted to emergency rooms and for whom initial evaluation is not conclusive, the use of cardiac markers has become a standard procedure. A recently introduced early plasma marker for acute myocardial infarction (AMI) is the 14.5-kDa cytoplasmic heart-type fatty acid-binding protein (FABP). To fully exploit its early release from injured myocardium, a rapid method for repeated measurements or continuous monitoring of FABP in plasma is desirable. Such an on-line method could be an immunosensor based on displacement. The aim of the present study was to further investigate the principles underlying the displacement assay of FABP, both in buffer and in plasma. Batches of sepharose-bound FABP were loaded with an antibody-horseradish peroxidase (HRP) conjugate (anti-FABP). Continuous measurement of FABP was mimicked by repeated addition of FABP containing solutions followed by several washing steps. In the presence of free FABP the antibody-HRP complex dissociated and was subsequently quantified. Significant displacement in the presence of free FABP was observed in both buffer and human plasma. Anti-FABP could be intermittently displaced in the same batch, for at least 9 h, and the displacement was concentration-dependent. These results show the feasibility of a sensor based on the displacement principle to be used for the diagnosis of AMI in emergency medicine.
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PMID:Development of a displacement immunoassay for human heart-type fatty acid-binding protein in plasma: the basic conditions. 1462 71

The existing markers for myocardial necrosis, such as cardiac troponin, creatine kinase-MB, and myoglobin are thought to be released into blood following irreversible myocardial necrosis. Thus results of these tests are usually negative for patients with acute coronary syndromes (ACS) who present to the emergency department (ED) within the first 3 hours after the onset of chest pain. Given the need to make early therapeutic and triage decisions, biomarkers that can be used to diagnose and/or risk stratify ACS patients during their initial ED presentation will be important. Active research in this area has identified several classes of biomarkers that show promise for early detection of disease. These include tests for the presence of acute inflammation and infiltration (e.g., high sensitivity-C-reactive protein, myeloperoxidase), plaque instability (e.g., pregnancy-associated plasma protein-A, placental growth factor), platelet activation (e.g., whole blood choline, platelet density, CD40 ligand), and myocardial ischemia (e.g., ischemia modified albumin, free fatty acids, serum choline, and B-type natriuretic peptide). Each of these tests has demonstrated some utility for early diagnosis. However, as most lack specificity for myocardial disease, routine use may require a multi-marker approach.
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PMID:Markers for early detection of cardiac diseases. 1611 68


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