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)

Abciximab, a platelet glycoprotein (GP) IIb/IIIa inhibitor, has been shown to improve clinical outcomes in patients undergoing percutaneous coronary intervention. However, there is a well-documented increase in bleeding risk associated with the use of this agent. Spontaneous pulmonary hemorrhage is a particularly rare and easily misdiagnosed complication that requires early diagnosis to ensure patient survival. A 61-year-old man presented to the emergency department with chest pain and inferolateral ST elevation on electrocardiogram. A paclitaxel drug-eluting stent was then placed in the left circumflex artery, without complications. Abciximab (a bolus of 0.25 mg/kg followed by an infusion of 10 mg/min for 12 h) was given. Approximately 20 min later, the patient developed dyspnea and hemoptysis. A chest radiograph revealed new bilateral diffuse interstitial infiltrates, and the patient was started on empirical antibiotics for pneumonia. Because of increasing dyspnea and somnolence, the patient was intubated and bronchoscopy was performed, revealing serial hemorrhagic returns from the left lower lobe, diagnostic of diffuse alveolar hemorrhage and judged to be secondary to abciximab, given the time course. All antiplatelet and antithrombotic agents were stopped. The patient stabilized over the next several days, with some recurrent hemoptysis, and was successfully extubated seven days later. Prognosis remains poor in GP IIb/IIIa inhibitor-induced pulmonary hemorrhage, and early diagnosis is critical so that antithrombotic and antiplatelet agents may be discontinued in a timely manner. A high degree of suspicion is required when treating a patient who presents with dyspnea and new radiological infiltrates after receiving a GP IIb/IIIa inhibitor.
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PMID:Abciximab-induced alveolar hemorrhage after percutaneous coronary intervention. 1827 91

A 26-year-old woman with a history of idiopathic thrombocytopaenic purpura and a 1-year history of blood-streaked sputum presented after a severe episode of haemoptysis with dyspnoea. Chest imaging revealed diffuse ground glass and bronchovascular nodules. Bronchoscopy revealed bilateral diffuse alveolar haemorrhage (DAH). Sputum and bronchoalveolar lavage studies were negative for infectious aetiologies. A transthoracic echocardiogram revealed Libman-Sacks endocarditis with severe mitral regurgitation and physical examination revealed retinal artery occlusion and Osler's nodes. The patient had an increased anticardiolipin Immunoglobulin IgG and anti-B2 glycoprotein IgG, suggesting antiphospholipid syndrome (APLS). The patient was then started on high-dose methylprednisolone and had an improvement in her dyspnoea and haemoptysis. She was also started on anticoagulation as treatment for Libman-Sacks endocarditis. APLS should be considered as a possible underlying aetiology for unusual presentations of DAH with concurrent Libman-Sacks endocarditis in non-intravenous drug users with existing autoimmune disorders.
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PMID:Diffuse alveolar haemorrhage and Libman-Sacks endocarditis: a rare presentation of antiphospholipid syndrome. 2973 98

A 26 year old female presented for recurrent blood tinged sputum during the previous year with development of frank hemoptysis three days prior to admission. Diffuse alveolar hemorrhage (DAH) was confirmed with serial lavages. The patient had no history of autoimmune disease, vascular thrombosis or pregnancy morbidity including miscarriages or pre-eclampsia. High dose steroids were initiated along with noninvasive ventilatory support. Transthoracic echocardiogram showed severe mitral regurgitation and a vegetation on the mitral valve; transesophageal echocardiogram determined the lesion highly suggestive of Libman-Sachs endocarditis. Blood cultures were negative. Immunological evaluation established the patient was negative for: anti-nuclear antibody, anti-double-stranded DNA antibody, rheumatoid factor, anti-smith antibody, anti-cyclic citrullinated peptide, anti-neutrophil cytoplasmic antibodies, anti-glomerular basement membrane antibodies. Further evaluation revealed elevated levels of anticardiolipin immunoglobulin G and anti-beta 2 glycoprotein immunoglobulin G which continued to increase for months after hospitalization. She was diagnosed with DAH secondary to acute mitral regurgitation caused by Libman-Sachs endocarditis in the presence of primary antiphospholipid antibody syndrome. DAH is an important disease to understand given its high mortality rate. Few case reports relating the presence of Libman-Sachs endocarditis induced by antiphospholipid antibody syndrome leading to DAH have been published. Unique here is the absence of rheumatologic markers thus supporting a diagnosis of primary antiphospholipid antibody syndrome (APS). This patient had no findings associated with rheumatological disorders potentially making this diagnosis easily overlooked. This case further illustrates the importance of evaluating patients with APS presenting with DAH as there are multiple etiologies that lead to this pathology thus different treatment avenues are to be considered during management.
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PMID:Primary antiphospholipid syndrome associated Liebman-Sachs endocarditis leading to diffuse alveolar hemorrhage: A case report. 3019 Nov 20