Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019079 (hemoptysis)
6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A few hours after a 15 km march a 19-year-old man developed a fever of 40 degrees C, accompanied by hemoptysis, tarry stools and pain in the thigh. On physical examination there was tenderness and swelling over the shoulders, upper arms and thighs as well as petechiae, bruises, hepatomegaly, pain on percussion over the kidney region and signs of hypovolaemia. There was leukocytosis (18,800/microliters) and increased creatinase activity (3900 U/l, rising to 66,300 U/l after 24 h). The platelet count fell from 147,000 to 11,000/microliters, the fibrinogen level to 0.25 milligrams. On the second day serum creatinine was 4.1 mg/dl, urine volume 50 ml/24 h, urinary myoglobin concentration 120,000 micrograms/l. The Quick value dropped to under 3%, while liver enzymes and bilirubin concentration rose. The rhabdomyolysis caused acute respiratory failure, despite symptomatic treatment of the acute renal failure and consumption coagulopathy, but after 8 weeks of intensive treatment the patient was discharged without symptoms. No cause other than the preceding physical exertion was found for the rhabdomyolysis. Muscle biopsy revealed unspecific changes 4 1/2 months after discharge.
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PMID:[Complications of an idiopathic rhabdomyolysis (Meyer-Betz syndrome) after physical exertion]. 786 81

Anti-basement membrane antibody (anti-BM Ab) mediated disease is reported to be a rare disorder frequently leading to severe deterioration of renal function. It was our purpose to work out parameters necessary to predict the outcome reliably and to examine, who will benefit most from therapy. Data from 35 patients were evaluated retrospectively. Diagnosis was based on the detection of linear IgG staining (n = 28) along the glomerular basement membrane (GBM) in renal biopsies and/or on the demonstration of anti-BM Ab both by ELISA and immunoblotting (n = 35). Patients were followed up for at least 6 months. Several variables were analysed as to whether they are appropriate prognostic factors. Twenty patients (57%) presented with Goodpasture's syndrome, 13 (37%) had anti-GBM glomerulonephritis alone, whereas two patients suffered solely from pulmonary haemosiderosis. Frequent initial symptoms were haemoptysis (n = 18), haematuria (n = 26), proteinuria (n = 26) and elevated serum creatinine (n = 27). Among all, 10 patients improved, having stable renal function. Twenty-one patients developed end-stage renal failure and four died. Parameters indicating a poor prognosis were a serum(s)-creatinine greater than 600 mumol/l and crescent formation in more than 50% of the glomeruli on renal biopsy. By combining these two parameters the outcome could be reliably predicted. The initial antibody titre and cigarette smoking were without predictive value. In conclusion, the earlier therapy starts, the better will be the result. Patients presenting early with a serum creatinine < 200 mumol/l and without severe glomerular alterations gained the most benefit from therapy, indicating that outcome may be improved by early diagnosis.
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PMID:Course and prognosis of anti-basement membrane antibody (anti-BM-Ab)-mediated disease: report of 35 cases. 808 49

A 77-year-old man was admitted because of hemoptysis. Chest roentgenograms initially showed progressive infiltrative shadows, which improved spontaneously in 3 months. Transbronchial lung biopsy specimens obtained during the first admission revealed alveolar hemorrhage with neither granuloma nor vasculitis. Alveolar hemorrhage associated with renal dysfunction recurred 9 months later. Serum creatinine level was elevated to 3.5 mg/dl. No other organ than lungs or kidneys was involved. Renal biopsy was performed to confirm the pathological diagnosis of crescentic glomerulonephritis. Anti-basement-membrane antibody was negative, whereas anti-neutrophil-cytoplasmic antibody was positive for perinuclear pattern (P-ANCA) by indirect immunofluorescent (IF) method. He was diagnosed as having idiopathic crescentic glomerulonephritis complicated with alveolar hemorrhage, and the presence of anti-myeloperoxidase (MPO) antibody in serum was anticipated. Anti-MPO antibody level in his serum evaluated by ELISA was markedly elevated. Although myeloperoxidase has been considered as a common antigen to P-ANCA and anti-MPO antibody, the determination of P-ANCA has been clinically unreliable because of equivocal results. In contrast, the presence of anti-MPO antibody is highly specific for idiopathic crescentic glomerulonephritis complicated with alveolar hemorrhage or its incomplete variant case. Also, it is a better index of disease activity. Therefore, there is a possibility that those patients diagnosed as having idiopathic pulmonary hemosiderosis or pulmonary-renal syndrome may be categorized into the one disease, anti-MPO antibody-associated disease, and the measurement of anti-MPO antibody may lead to prompt treatment prior to the histological diagnosis.
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PMID:[A case of crescentic glomerulonephritis associated with anti-myeloperoxidase antibody presenting as alveolar hemorrhage]. 818 51

The requirements for a diagnosis of Goodpasture's syndrome (GPS) include: (1) the presence of glomerulonephritis, (2) alveolar bleeding, and (3) the presence of anti-glomerular basement membrane (anti-GBM antibody). Among Japanese case, the 2 patients reported here were rare in that they satisfied all of these requirements. In case 1 (a 40-year-old male), the disease developed with initial signs of proteinuria and hematuria. The patient developed hemoptysis after hospitalization. The interval from onset to hospitalization was 38 days. The serum creatinine (CRN) level was 3.6 mg/dl on admission. The pathological findings were rated as full-circumferential, cellular crescentic nephritis, and the patient did not display oliguria. The renal and pulmonary impairments in this case were markedly improved by glucocorticoid (prednisolone PSL, 60 mg/day), cyclophosphamide therapy (50 mg/day) and plasma exchange (PE 10 times). In case 2 (a 58-year-old male), the initial signs developed as proteinuria and hematuria, followed by rapidly progressive renal functional deterioration and hemoptysis occurred. Compared to Case 1, the interval from onset to hospitalization was longer in Case 2 (125 days) and the CRN level was also higher (10.7 mg/dl). Case 2 was rated as full-circumferential, fibrous crescentic nephritis, and the patient was oliguric. Although the pulmonary impairment was reduced by pulse therapy and 10 PEs, recovery of renal function has not been achieved, still necessitating maintenance hemodialysis at present. In case 1, the disease relapsed at 4.5 years after remission, presenting with aggravated renal function and hemoptysis. In this case, low-dose PSL therapy had been discontinued at 3 months before the relapse.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Two cases of Goodpasture's syndrome--clinicopathological studies and relapse. 833 6

A 69-year-old woman was admitted to our hospital because of hemoptysis, skin eruption, and gastrointestinal bleeding. A chest X-ray film revealed infiltrates in the left upper lung field. Analysis of bronchoalveolar lavage fluid revealed alveolar hemorrhage. Examination of skin biopsy specimens demonstrated leukocytoclastic vasculitis. Fiberoptic examination of the colon showed diffuse reddish and edematous mucosa. Histological examination of biopsy specimens from the sigmoid colon showed necrotizing vasculitis. The serum creatinine level was high: 2.2 mg/dl. Examination of transcutaneous renal biopsy specimens revealed crescentric glomerulonephritis. A test for perinuclear anti-neutrophil cytoplasmic antibody was negative, but a test for cytoplasmic anti-neutrophil cytoplasmic antibody was positive. The latter strongly suggests a diagnosis of Wegener's granulomatosis, although the association is not absolute. We diagnosed pulmonary-renal syndrome associated with anti-neutrophil cytoplasmic antibody. The findings in this case were compatible with microscopic polyangiitis.
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PMID:[Alveolar hemorrhage, skin eruption, and gastrointestinal bleeding accompanied by crescentric glomerulonephritis in a patient with cytoplasmic anti-neutrophil cytoplasmic antibody]. 881 Jul 61

A 28 years old male patient presented, after a history of previous recurrent hemoptysis, with diffuse bilateral air space consolidation at chest radiography (CXR). Within 48 hours, partial respiratory insufficiency developed and required intubation. On a clinical and roentgenographic basis, the diagnosis of a Goodpasture syndrome was suspected. Plasmapheresis and immunosuppressive therapy with prednisone and cyclophosphamide were started immediately. Three days after admission, macrohematuria developed and serum creatinine began to rise to a maximum of 3.9 mg/dl. Totally, 13 plasmaphereses were performed within 27 days. Clinical, laboratory and radiological findings improved markedly. 30 days after admission, the patient was discharged and followed on an outpatient basis. Serum creatinine eventually decreased to 1.1 mg/dl. Initially, circulating antibodies against glomerular basement membrane (GBM) were positive, controls remained negative. Renal biopsy was performed after the acute phase and showed glomerulonephritis and linear immunoglobulin deposition along the GBM. Radiologic findings at CXR and high resolution computed tomography are demonstrated.
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PMID:[Goodpasture syndrome: treatment initiation with plasmapheresis before histologic diagnostic verification]. 908 44

A 22-year-old woman was admitted to our hospital for evaluation of fever, renal dysfunction, and a 3-month-history of macrohematuria. Laboratory evaluation revealed proteinuria (1.8 g/day), hypoproteinemia, microcytic microchromic anemia, renal failure (blood urea nitrogen 30.3 mg/dl, serum creatinine 4.0 mg/dl), and positive serum antiglomerular basement membrane (anti-GBM) antibody. Renal biopsy revealed cellular crescents in all 8 glomeruli and partial rupture of the GBM. The interstitium showed severe inflammatory cell infiltration. Immunofluorescent examination revealed linear deposits of IgG and C3 along the GBM. Pulmonary biopsy revealed linear deposits of IgG along the alveolar basement membrane in the immunofluorescent examination. A diagnosis of Goodpasture's syndrome was made because all of the diagnostic criteria were fulfilled. After admission, the patient's renal function deteriorated rapidly. Hemodialysis was started, and the patient was treated with methylprednisolone pulse therapy and oral prednisolone with double filtration plasma pheresis (DFPP). However, her renal function did not improve. On the 30th hospital day, she showed hemoptysis, and a chest X-ray and CT revealed massive bilateral pulmonary hemorrhage. Despite treatment with pulsed methylprednisolone, oral prednisolone (80 mg/day), and DFPP, the pulmonary hemorrhage improved only transiently, worsening again 5 days later. Cyclophosphamide pulse therapy was administered. After this treatment, the patient's pulmonary manifestations and pulmonary hemorrhage improved. At the present time she is on maintenance dialysis therapy without pulmonary manifestations. These findings suggest that cyclophosphamide pulse therapy is effective against Goodpasture's syndrome with massive pulmonary hemorrhage showing resistance to other conventional therapy.
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PMID:[A case of Goodpasture's syndrome with massive pulmonary hemorrhage ameliorated by cyclophosphamide pulse therapy]. 1050 44

Aspergillosis comprises a variety of manifestations of infection. These guidelines are directed to 3 principal entities: invasive aspergillosis, involving several organ systems (particularly pulmonary disease); pulmonary aspergilloma; and allergic bronchopulmonary aspergillosis. The recommendations are distilled in this summary, but the reader is encouraged to review the more extensive discussions in subsequent sections, which show the strength of the recommendations and the quality of the evidence, and the original publications cited in detail. Invasive aspergillosis. Because it is highly lethal in the immunocompromised host, even in the face of therapy, work-up must be prompt and aggressive, and therapy may need to be initiated upon suspicion of the diagnosis, without definitive proof (BIII). Intravenous therapy should be used initially in rapidly progressing disease (BIII). The largest therapeutic experience is with amphotericin B deoxycholate, which should be given at maximum tolerated doses (e.g., 1-1.5 mg/kg/d) and should be continued, despite modest increases in serum creatinine levels (BIII). Lipid formulations of amphotericin are indicated for the patient who has impaired renal function or who develops nephrotoxicity while receiving deoxycholate amphotericin (AII). Oral itraconazole is an alternative for patients who can take oral medication, are likely to be adherent, can be demonstrated (by serum level monitoring) to absorb the drug, and lack the potential for interaction with other drugs (BII). Oral itraconazole is attractive for continuing therapy in the patient who responds to initial iv therapy (CIII). Therapy should be prolonged beyond resolution of disease and reversible underlying predispositions (BIII). Adjunctive therapy (particularly surgery and combination chemotherapy, also immunotherapy), may be useful in certain situations (CIII). Aspergilloma. The optimal treatment strategy for aspergilloma is unknown. Therapy is predominantly directed at preventing life-threatening hemoptysis. Surgical removal of aspergilloma is definitive treatment, but because of significant morbidity and mortality it should be reserved for high-risk patients such as those with episodes of life-threatening hemoptysis, and considered for patients with underlying sarcoidosis, immunocompromised patients, and those with increasing Aspergillus-specific IgG titers (CIII). Surgical candidates would need to have adequate pulmonary function to undergo the operation. Bronchial artery embolization rarely produces a permanent success, but may be useful as a temporizing procedure in patients with life-threatening hemoptysis. Endobronchial and intracavitary instillation of antifungals or oral itraconazole may be useful for this condition. Since the majority of aspergillomas do not cause life-threatening hemoptysis, the morbidity and cost of treatment must be weighed against the clinical benefit. Allergic bronchopulmonary aspergillosis (APBA). Although no well-designed studies have been carried out, the available data support the use of corticosteroids for acute exacerbations of ABPA (AII). Neither the optimal corticosteroid dose nor the duration of therapy has been standardized, but limited data suggest the starting dose should be approximately 0.5 mg/kg/d of prednisone. The decision to taper corticosteroids should be made on an individual basis, depending on the clinical course (BIII). The available data suggest that clinical symptoms alone are inadequate to make such decisions, since significant lung damage may occur in asymptomatic patients. Increasing serum IgE levels, new or worsening infiltrate on chest radiograph, and worsening spirometry suggest that corticosteroids should be used (BII). Multiple asthmatic exacerbations in a patient with ABPA suggest that chronic corticosteroid therapy should be used (BIII). Itraconazole appears useful as a corticosteroid sparing agent (BII). (ABSTRACT TRUNCATED)
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PMID:Practice guidelines for diseases caused by Aspergillus. Infectious Diseases Society of America. 1117 Sep 29

This report describes a case of a 49-year-old man with cough, recurrent hemoptysis, and dyspnea during 18 months, presenting with radiological findings of alveolar infiltrate and cystic lesions in left upper lobe. Laboratory studies revealed normocytic hypochromic anemia and normal coagulation tests. C-reactive protein and mucoproteins were negative. Serum protein electrophoresis and complement, urinalysis, serum creatinine, creatinine clearance, and 24-hour urine protein were normal. Tests for antineutrophil cytoplasmic antibodies and anti-glomerular-basement membrane antibodies were negative. Tests for connective tissue diseases were all negative. Histological findings were consistent with those of idiopathic pulmonary hemosiderosis. Radiological findings are discussed.
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PMID:Idiopathic pulmonary hemosiderosis with cystic lesions: a rare presentation. 1087 99

A 63-year-old man was referred to our hospital for rapid deterioration of his renal function. He had worked as a metal founder for more than 40 years, and had been diagnosed as having silicosis. Laboratory data on admission showed severe anemia, thrombocytopenia, and end-stage renal failure (BUN 88.8 mg/dl, serum creatinine 9.0 mg/dl). Myeloperoxidase anti-neutrophil cytoplasmic antibody(MPO-ANCA) was also detected in his sera. On the next day after admission, he complained of sudden dyspnea and hemoptysis. Mechanical ventilation with pure oxygen was insufficient to improve hypoxia without concomitant use of percutaneous cardio-pulmonary support(PCPS) and continuous hemofiltration(CHF). We diagnosed his condition as MPO-ANCA-associated rapidly progressive glomerulonephritis with diffuse alveolar hemorrhage. Treatment with plasmapheresis, pulse methylprednisolone and pulse cyclophosphamide effectively improved his hemoptysis as well as chest X-ray findings and blood gas analysis. However on his later clinical course, he was complicated with superimposed complex infection and passed away. Autopsy findings showed crescentic glomerulonephritis in the kidneys and silica nodules in the lungs. Recently it has been postulated that some relationship exists between ANCA-associated(especially MPO-ANCA-associated) glomerulonephritis and silica exposure. The reported cases of glomerulonephritis in the patients with silica exposure showed a rapidly progressive clinical course and pauci-immune necrotizing crescentic glomerulonephritis in their histology. Gregorini et al. reported that 12 of 37 (32%) male patients with RPGN had either silicosis or significant silica exposure, and 7 of 8 patients examined were ANCA-positive(6 of 7 were MPO-ANCA-positive). Therefore silica seems to cause glomerulonephritis by disrupting the immune response. Including this case mentioned above, we have experienced 10 cases of MPO-ANCA-associated glomerulonephritis, at least 3 cases out of which had suffered from silicosis in the past(30%). These results indicate that silicosis should be considered a relevant pathogen of MPO-ANCA-associated glomerulonephritis beyond the race.
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PMID:[A case of silicosis with MPO-ANCA-associated glomerulonephritis and alveolar hemorrhage]. 1143 4


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