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)

In May 1984 a 58-year-old woman presented with a broad spectrum of clinical symptoms including malaise, arthralgia, hemoptysis and dyspnea, proteinuria and hematuria and a vasculitic necrotizing rash. Bronchial biopsies revealed subglottic granulomatous lesions and renal biopsies showed necrosis, extracapillary proliferation and crest formation, confirming the diagnosis of Wegener granulomatosis. Positive c-ANCA and anti-proteinase 3 subfraction (anti-PR3) titers were first analysed in 1991. Clinical remission was achieved by standard immunosuppressive therapy and renal function was stabilised. Several minor relapses were treated with pulsed intravenous cyclophosphamide but the symptoms could not be completely controlled. Eight years after the onset of disease, a dramatic increase in anti-PR3 titers was observed (34438 U/ml, normal range < 10, ELISA), followed 3 months later by a clinically apparent relapse. Immunosuppressive therapy was reinstituted without clinical improvement. At this point plasmapheresis resulted in an amelioration of clinical symptoms as well as a reduction in anti-PR3 titers. Concomitant immunosuppressive therapy was administered with oral corticosteroids. Forty days later anti-PR3 titers increased, reaching 75000 U/ml twelve months later, however this time without associated clinical symptoms. During the following months the patient had a further transient deterioration of pulmonary and renal function due to secondary bacterial infection which was successfully treated with antibiotics. A nephritic sediment was not present during these episodes. Curiously, the anti-PR3 titers have remained excessively elevated for the last three years.
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PMID:Dissociation between high anti-PR3 titers (c-ANCA) and the clinical course of disease in a case of Wegener granulomatosis. 982 23

A 51-year-old man presenting with hemoptysis was admitted to our hospital. Chest radiography revealed air space consolidation in the right lung field. Laboratory data showed anemia, hypoxemia, and no evidence of inflammatory signs, bleeding tendency, renal dysfunction, or collagen vascular diseases. Tests of anti-GBM antibody, P-ANCA, and C-ANCA were negative. Microscopic examination of the lung tissue specimens obtained by video assisted thoracic surgery revealed hemorrhage and numerous hemosiderin-laden macrophages in the alveoli. No deposition of immunoglobulin and vasculitis were seen. These findings were consistent with a diagnosis of idiopathic pulmonary hemosiderosis. Steroid therapy had a limited effect, and the patient died. Idiopathic pulmonary hemosiderosis of adult onset is rare in Japan.
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PMID:[A case of idiopathic pulmonary hemosiderosis of adult onset]. 1106 Oct 83

A 77-year-old man was in good health until he complained of fatigue 3 weeks before presentation. Two weeks before admission, he developed gradually worsening shortness of breath. One week before admission, he developed a cough that initially was nonproductive but later was associated with hemoptysis.His past medical history was remarkable for a history of colon cancer (Dukes' stage III), for which he underwent a hemicolectomy and treatment with adjuvant chemotherapy in 1993. He had a myocardial infarction in 1986 and underwent coronary artery bypass surgery in 1999. He also had a history of hypertension, type 2 diabetes, and gout. He smoked in the past but had stopped more than 30 years ago.He was initially evaluated by his primary care physician, who noted that he complained of diaphoresis but denied fevers, chills, or contact with others who were ill. His physical examination was remarkable for bilateral crackles that were more pronounced on the right. A chest radiograph demonstrated bilateral pulmonary infiltrates (Figure 1). He was treated with amoxicillin. The next day, however, his physician noted that his dyspnea had worsened and that his oxygen saturation on room air was poor. He was therefore admitted for further evaluation. The amoxicillin was discontinued, and he was treated with levofloxacin, followed by ceftriaxone and azithromycin as his pulmonary status continued to deteriorate. He received intravenous diuretic agents, which failed to improve his respiratory status. During the initial phase of hospitalization, he was anemic, with a hematocrit of 21.3%. His serum creatinine level, which had been 1.0 mg/dL in 1999, was now 2.5 mg/dL. Urinalysis was remarkable for the presence of numerous red blood cells. His oxygen requirement increased, and he eventually required a 100% nonrebreather mask. A computed tomographic scan of the chest demonstrated prominent alveolar opacities throughout the right upper, middle, and lower lobes, with similar opacities in the left upper and left lower lobes (Figure 2). An echocardiogram showed an ejection fraction of 50%, as well as mild mitral regurgitation. Serologies were remarkable for an antinuclear antibody titer of 1:320 and a P-antineutrophil cytoplasmic antibody (P-ANCA) titer of greater than 1:320. C-ANCA was negative. Anti-glomerular basement membrane and anti-human immunodeficiency virus antibodies were undetectable.
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PMID:Cases from the medical grand rounds of the Osler Medical Service at Johns Hopkins University. 1207 15

A case of a cavitary lung lesion in the right middle lobe of a 34-year-old woman who presented with hemoptysis is presented. The patient had a 2-year history of Wegener granulomatosis that had been treated with cyclophosphamide and corticosteroids. Although the patient gradually achieved remission of her disease, she developed new pulmonary symptoms and a cavitary lesion in her right lung. Further workup revealed elevated C- and P-ANCA titers. Following partial resection of her right lung, she was found to have an aspergilloma and no evidence of active Wegener granulomatosis. Pulmonary aspergillosis was felt to be the cause of both the hemoptysis and the cavitary lesion. We postulate that C-ANCA and P-ANCA were falsely positive in this case. Although rare, false positive C-ANCA and P-ANCA have been reported in pulmonary fungal infections.
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PMID:Positive C-ANCA and cavitary lung lesion: recurrence of Wegener granulomatosis or aspergillosis? 1686 47

This case describes a 40-year-old man complaining of general malaise, dyspnea with hemoptysis and anuria. Laboratory data indicated renal failure and the presence of systemic inflammation. His chest radiograph and computed tomography showed bilateral diffuse interstitial alveolar infiltration. These findings indicated acute deterioration of chronic renal dysfunction complicated by interstitial pneumonitis. He initially received daily conventional hemodialysis (HD), an antibiotic and oxygen therapy. However, his renal and pulmonary function continued to deteriorate. Antineutrophil cytoplasm antibodies against myeloperoxidase (MPO-ANCA) and antibodies against proteinase 3 (PR3-ANCA) were negative. We suspected that his pulmonary-renal syndrome was caused by ANCA-negative vasculitis. We applied mechanical ventilation, pulsed methylprednisolone therapy and continuous hemodiafiltration (CHDF) combined with HD. PaO(2)/FiO(2) ratio and mean pulmonary arterial pressure gradually improved after initiation of CHDF. He was finally separated from mechanical ventilation after 44 days in the hospital. He is currently alive with the support of conventional HD.
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PMID:A case report of pulmonary-renal syndrome treated with continuous hemodiafiltration and hemodialysis. 1709 3

We report the case of a 55-year-old male patient who presented with non-specific pulmonary symptoms (cough, haemoptysis, fever up to 39 degrees C, night sweats and weight loss). After empirical antibiotic therapy prescribed by his primary care physician, the patient showed no improvement in symptoms. Laboratory findings were: elevated C-reactive protein and C-ANCA, leukocytosis and thrombocytosis, and anaemia. Chest radiography showed disseminated nodules bilaterally. On multidetector-row computed tomography (MDCT), the bronchial walls showed a significant thickening and extensive peribronchiolar consolidations. Bronchoscopy revealed diffuse erythema of the tracheobronchial mucosa with diffusely scattered white plaques. Histopathology described a multifocal ulcerative bronchitis with underlying chronic bronchitis. These findings in combination with the laboratory data lead to the diagnosis of Wegener's granulomatosis. Consequently, we started with an immunosuppressive therapy. Chest radiography after 10 days showed marked resolution of the infiltrates. Within 1 month, the patient became asymptomatic.
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PMID:Atypical bronchial thickening and ulceration: a rare radiological finding in Wegener's granulomatosis. 1776 50

Wegener's granulomatosis was diagnosed in 2 boys, aged 17 and 16 years. The first presented with pain in the right flank, without coughing or dyspnoea. He did have peaks of fever, night sweats, weight loss, headache, and epistaxis. The second presented with progressive dyspnoea, haemoptysis, malaise, and headache. Because an infection was suspected, both were given antibiotics, but without effect. Chest X-rays revealed infiltrative abnormalities. A lung biopsy in the first patient and a nasal biopsy in the second revealed a granulomatous inflammation, and both patients had an elevated titre of antineutrophilic cytoplasmic antibodies (ANCA), with a cytoplasmic pattern, and an elevated result of the ELISA test for antiproteinase-3 (PR3). Both patients recovered after aggressive immunosuppressive treatment. Wegener's granulomatosis is a systemic necrotising vasculitis, mostly localised in airways and kidneys. The disease is very rare in children, but may be life-threatening. Therefore, in children with pulmonary problems resistant to antibiotics, it is important to consider a diagnosis of Wegener's granulomatosis and test for ANCA and PR3.
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PMID:[Wegener's granulomatosis in 2 adolescents]. 1776 12

A 80-year-old man was admitted to our hospital because of coughing, hemosputum and dyspnea. As a chest X-ray showed infiltrates of the right lung, he was diagnosed as bacterial pneumonia and treated with antibiotics. However, after a few days, he exhibited hemoptysis and developed severe dyspnea, while laboratory findings showed rapid elevation of the serum creatinine level (5.55 mg dL). Computed tomography (CT) revealed large areas of ground glass opacity in the right lung, hence the hemoptysis was considered to be due to alveolar hemorrhage. As he had been diagnosed as chronic renal failure a few years before this admission and we also noticed that interstitial pneumonia with a slightly elevated level of C-reactive protein had existed from that time, ANCA-associated vasculitis was suspected to be the underlying pathogenesis. Accordingly, he was started on methylprednisolone pulse therapy and temporary hemodialysis resulted in improvement of dyspnea and renal function. PR3-ANCA was 12.4 EU, so he was diagnosed as PR3-ANCA-associated vasculitis. After a few days, he suddenly complained of abdominal pain, developing hypotension and anemia. Abdominal CT showed an irregular low-density mass in the right muscle, so he was diagnosed as rectus muscle hematoma. Surgery was performed and a massive hematoma was found in the rectus muscle without any ruptures of macroscopic vessels in the abdomen. Bleeding could not be stopped followed by multiple organ failure and the patient died four days postoperatively. Rectus muscle hematoma is an uncommon cause of acute abdomen, and has been reported in about 100 cases in Japan. It occurs because of a tear in epigastric vessels and is usually managed conservatively with a good prognosis, although hemodynamically unstable cases require surgery. To the best of the authors' knowledge, this is the first case of rectus muscle hematoma complicated with ANCA-associated vasculitis.
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PMID:[Autopsy case of PR3-ANCA-associated vasculitis complicated with rectus muscle hematoma]. 1971 63

A 73-year-old man who had been diagnosed with bronchiectasis in 2002 was admitted to our hospital with hemoptysis in March 2003. Upon detecting P. aeruginosa from his sputum culture, we diagnosed his condition as an exacerbation of a chronic respiratory infection with bronchiectasis. Levofloxacin was effective and his infection condition was resolved. In June 2006 he was admitted to our hospital again with hemoptysis and complaining of fever. This time, Levofloxacin was not effective. After admission, fourth-generation cephem, carbapenem, and new quinolone antibiotics were ineffective. However, micafungin sodium seemed to combat the infection. The patient was negative for PR-3 ANCA in laboratory testing, but histological findings of a transbronchial lung biopsy and middle nasal concha supported a diagnosis of Wegener's granulomatosis. Antitubercular drugs and antibiotics have been reported as effective against Wegener's granulomatosis, but we found no evidence of benefits with antifungal agents such as micafungin sodium. Recently however, a case has been reported of murine systemic vasculitis caused by Candida albicans extract. Our case suggests the possible involvement of fungus in the pathogenesis and progression of Wegener's granulomatosis.
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PMID:[A case of Wegener's granulomatosis]. 2005 88

The authors present a clinical case of 55 years old female patient with limited form of Wegener's granulomatosis (WG), which first manifestation was non-erosive polyarthritis with rheumatoid factor positive that antedates one decade the pulmonary manifestations. She had acute episodes with purulent expectoration, fever and hemoptysis, with resolution in a week. The chest x-rays demonstrated migratory bilateral pulmonary infiltrates. Transthoracic lung biopsy was performed and revealed capilaritis and signs of old and recent hemorrhage. At that time, autoimmunity study was repeated and showed positive for rheumatoid factor, negative anti-cyclic citrullinated peptide antibodies (anti-CCP) and high sustained PR3 anti-neutrophil cytoplasmic antibodies. The diagnosis of WG was established and cyclophosphamide started. This patient had a less common presentation and a less common histological pattern compared to the typical necrotizing granulomatous inflammation. She was treated with immunosuppression therapy which could have contributed to a mild clinical expression and a lower diagnostic yield. In suspicious cases, repeat the autoimmunity study, when facing new findings, could confirm the correct diagnosis.
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PMID:Wegener's granulomatosis and alveolar hemorrhage - case report. 2443 35


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