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 38-year-old man was hospitalized for proteinuria, and pitting edema. He had noticed Raynaud's phenomenon at about age fifteen. One month prior to admission, his urine contained protein and the serum creatinine was 3.0 mg/dl. On admission, sclerodactylia, digital pitting scar of fingertips, digital bone absorption and pulmonary fibrosis were observed and a diagnosis of progressive systemic sclerosis (PSS) was made. Laboratory investigations revealed: 24-hour urine protein excretion 3 g; serum creatinine 5.6 mg/dl; creatinine clearance 13.5 ml/min; antinuclear factor strongly positive in a speckled pattern; antibodies to nRNP positive with a titer of 1: 20, 480; antibodies to DNA, Sm, SS-A, SS-B, Scl-70, centromere and Jo-1 negative; serum complement normal. A renal biopsy revealed focal and segmental necrotizing glomerulonephritis with 70% crescents but no vascular changes. Circulating antiglomerular basement membrane antibodies were negative. Immunofluorescence disclosed granular deposits of IgM and C3 in the mesangium and along the capillary walls. Treatment was begun with methylprednisolone pulse therapy. After 5 month, serum creatine and creatinine clearance were 1.9 mg/dl and 35 ml/min, respectively. A year after the discharge, he was readmitted for hemoptysis and worsening of proteinuria and microhematuria. A chest radiograph demonstrated bilateral alveolar consolidation. Serum creatinine was elevated to 3.5 mg/dl. The continuous hemoptysis resulted in a severe dyspnea associated with a rapid fall in the hemoglobin. On the fourth hospital day, the PaO2 was 41 Torr on oxygen by mask that necessitated mechanical ventilation and pulse therapy was started. However, the patient died on the ninth hospital day of respiratory failure due to pulmonary hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of progressive systemic sclerosis complicated by crescentic glomerulonephritis and diffuse pulmonary hemorrhage]. 147 23

Because of its clinical polymorphism and the difficulties to made a bacteriological and/or serological diagnosis, leptospirosis is an affection always non-detected. Nevertheless it is daily met affection in French Polynesia. Based on a homogenous series of 120 observations gathered from 1984 to 1990, all of them bacteriologically and/or serologically confirmed, we studied the different clinical and evolutive features of that disease. Fever is present in 91.6 p.c., cephalgia in 79.16 p.c. and myalgia in 70.83 p.c. Admission was necessary once out of four times. The four syndromes we observed in Tahiti are: infections syndrome, meningeal syndrome (30 p.c.) associated to an hyperproteinic grade in the C.S.F. (40 p.c.) and a lymphocytic reaction (60 p.c.). Liver syndrome, with hepatalgia (58.33 p.c.) and pain at the mass motion of liver (65 p.c.), that is an important sign in the local context; jaundice (28.33 p.c.) on the presence of which we must not based a diagnosis of leptospirosis: Biological renal syndrome displayed by transitory renal insufficiency with proteinuria, hematuria and leucocyturia. Neurological complications are mainly of encephalitic manifestations (5.8 p.c.). Hemorrhagic syndrome is expressed in digestive hemorrhage (8.33 p.c.) epistaxis (6.66 p.c.) and hemoptysis (6.66 p.c.). Cardiovascular manifestations are expressed in collapsus in 5.83 of the cases. Pulmonary abnormalities are frequent: cough (26.66 p.c.) and non specific X Ray image (19.16 p.c.). All patients are treated by Penicillin G (10 to 20 millions per day) by parenteral route with enteral alternative for an average of 10 days. Recovery was fast (7 to 10 days). In 65.8 p.c., slower in 15 p.c. (15 to 20 days); failure at first stage was observed in 10 p.c. of the cases, and relapse at medium or long term occurred under treatment in 8 cases (6.66 p.c.). Three dead were deplored (mortality 2.5 p.c.).
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PMID:[Leptospirosis in French Polynesia: 120 case reports]. 160 50

Eleven patients with Wegener's granulomatosis were seen at this Institute over a period of 20 years. There were six men and five women. The average age of presentation was 38.3 years, and the mean duration of symptoms was 10.5 months. Constitutional symptoms (82%), cough (82%), ocular symptoms (64%), arthralgias (55%), rhinorrhoea (55%), haemoptysis (45%), nasal granuloma (45%), otorrhoea (36%), sinusitis (36%), skin lesions (27%), and renal failure (27%) were the clinical manifestations encountered. All patients had an elevated ESR, and 55% had leucocytosis. Proteinuria and haematuria were observed in 64% and 55% respectively. Chest radiographs were abnormal in 82%. In four patients the disease had a fulminant course and the patients died before adequate treatment was given. Two patients received corticosteroids alone and have since been lost to follow up. Five (45%) received adequate cytotoxic therapy and have done well for 8-46 months (mean, 24.8 months) after diagnosis. Wegener's granulomatosis in India is apparently similar to that seen elsewhere, but the high incidence of tuberculosis interferes with early diagnosis and treatment.
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PMID:Wegener's granulomatosis in north India. An analysis of eleven patients. 343 65

A young woman presented with arthralgia, a rash and dramatic haemoptysis, and renal involvement was indicated by proteinuria, haematuria and a rising serum creatinine. A systemic vasculitic disorder was suspected initially, but the diagnosis of Henoch-Schonlein purpura was established by the finding of mesangial IgA deposits on renal biopsy. Immunofluorescent study of renal biopsy material is vital to diagnosis where the clinical features of Henoch-Schonlein purpura and those of the systemic vasculitides with renal involvement prove to be indistinguishable.
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PMID:Henoch Schonlein purpura presenting with pulmonary haemorrhage. 356 74

Granulomatous necrosing ulcerations in the upper respiratory tract, a generalized arteritis developing lung infarcts, and a focal glomerulonephritis in this sequence characterize the classic progression of Wegener's granulomatosis (WG). Two cases of this rarely observed disease are being reviewed, comparing the typical course of illness with a non-typical form hard to diagnose. On the basis of these cases, considering the available publications, the clinical-roentgenological peculiarities, autoptical findings, and therapeutical possibilities of this usually fatal WG are set forth. Ulcerations of the mucous membrane of the nose and oral cavity or chronic sinusitis, haemoptysis with melted round foci of the lung, which can be roentgenologically proved, as well as increasing pulmonary insufficiency, proteinuria, and haematuria with subsequent renal failure are signs and symptoms of WG. Problems of diagnosis are discussed and difficulties in diagnosing are put forward. Histological confirmation in the early phase of the illness is desirable.
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PMID:[Clinical course of Wegener's granulomatosis]. 688 Feb 92

A 62-year-old man was admitted to our hospital because of low-grade fever and hemoptysis. Chest roentgenogram revealed diffuse infiltrative shadows with air bronchograms. Bronchoalveolar lavage fluid demonstrated bloody fluid, including many hemosiderin-laden macrophages. In addition, his laboratory data on admission revealed elevation of serum creatinine and BUN, and proteinuria and hematuria on urinalysis. Renal needle biopsy showed atrophic glomeruli and mesangial proliferative glomerulonephritis without crescent formation. A history of wheezing and slight eosinophila was also present, and we therefore suspected allergic granulomatous angitis. We performed airway sensitivity and reversibility tests, which were positive, and so we judged that he had an asthmatic component. Perinuclear antineutrophil cytoplasmic antibody (P-ANCA) was positive (x 1000) with ELISA. We diagnosed diffuse alveolar hemorrhage with mesangial proliferative glomerulonephritis and bronchial asthma. His general condition improved with oral administration of corticosteroid (50 mg/day) and immunosuppressive agent (cyclophosphamide; 50 mg/day), and his major symptoms disappeared within a few days.
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PMID:[A case of diffuse alveolar hemorrhage accompanied by mesangial proliferative glomerulonephritis with positive perinuclear anti-neutrophil cytoplasmic antibody]. 780 59

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

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

An unusual case of a patient with Goodpasture's disease presenting with hemoptysis, severe iron deficiency anemia and microscopic hematuria and proteinuria is described. Both circulating and tissue anti-glomerular basement membrane (GBM) antibodies were present, and renal function remained normal throughout. Immunosuppressive therapy was given for subclinical pulmonary hemorrhage with successful resolution of anemia and disappearance of the circulating anti-GBM antibody. Nine months after presentation he developed nephrotic range proteinuria and a repeat renal biopsy revealed membranous glomerulonephritis with no evidence of his original disease. Both the Goodpasture's associated HLA-DR2 and the membranous associated HLA-DR3 class II antigens were present. The association of antibody mediated and immune complex glomerulonephritis is discussed. The simultaneous presence of HLA-DR2 and HLA-DR3 may predispose to this association.
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PMID:Progression from Goodpasture's disease to membranous glomerulonephritis. 853 89

We encountered two patients with pulmonary hemorrhage who had high levels of myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA). Patient 1 was a 69-year-old woman. Both were admitted to our hospital complaining of hemoptysis. Microscopic hematuria was detected in patient 1, and proteinuria and renal insufficiency were detected in patient 2. Chest X-ray films showed bilateral patchy infiltrates in patient 1, and right middle-lower infiltrates in patient 2. In both patients the levels of MPO-ANCA were high and the results of tests for anti-basement membrane antibodies were negative. These patients were suspected to have pulmonary-renal vasculitic syndrome with a high level of MPO-ANCA. In patient 1, because the level of MPO-ANCA decreased after treatment with steroid therapy, we believe that measuring the level of MPO-ANCA was useful in the management of the disease. Rapidly progressive glomerulonephritis developed in patient 2, and was exacerbated despite hemodialysis, steroid therapy, and plasma exchange therapy. Use of the term microscopic polyangiitis (MPA) was first proposed by yhe Chapel Hill Consensus Conference in 1993. MPA, which was formerly called microscopic polyarteritis nodosa, connotes pauci-immune necrotizing vasculitis affecting arterioles, venules, or capillaries, and this condition is strongly associated with ANCA. Patients with pulmonary-renal vasculitic syndrome who have MPO-ANCA may be given a diagnosis of MPA. Therefore, we diagnosed MPA in these two patients. Testing for ANCA may be useful in patients with pulmonary hemorrhage and renal involvement.
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PMID:[Two patients with pulmonary hemorrhage associated with myeloperoxidase-antineutrophil cytoplasmic antibody]. 907 Nov 67


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