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)

Over a period of four years, 23 patients had the diagnosis of chronic pulmonary hypertension made on the basis of elevated resting pulmonary arterial pressures above 30 mmHg mean. Clinical features included dyspnea (100%), previous thromboembolism (43%), congestive failure (39%), venous thrombosis (35%), syncope (30%), lung disease (22%), recent trauma (22%), hemoptysis (17%) and precordial pain (17%). Pulmonary angiograms showed embolic occlusion in all but four patients, who were considered to have primary pulmonary hypertension. KimRay-Greenfield((R)) vena caval filters were inserted in 18 patients. Three of them were in refractory shock at the time, and only the one who had successful intraluminal catheter embolectomy survived. These patients have been followed an average of 23 months with two embolic deaths, one from the right atrium and one bypassing a filter misplaced in the right iliac vein (overall mortality 22%). There has been no other known recurrent embolism, but one patient developed hematuria from the filter. The five patients who did not receive a filter have all died after intervals up to 18 months. Recurrent thromboembolism was documented in three and suspected in one patient with known embolic disease who died suddenly. Regardless of etiologic factors, pulmonary hypertension with cor pulmonale is associated with a high incidence of fatal thromboembolism. In our experience, maximal protection is afforded by long-term anticoagulation therapy and the placement of a venacaval filter.
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PMID:KMA-Greenfield filter placement for chronic pulmonary hypertension. 44 9

Primary pulmonary hypertension, as defined by the World Health Organization, specifically includes three entities: primary plexogenic arteriopathy, pulmonary veno-occlusive disease, and silent recurrent thromboembolism. Pulmonary hemorrhage may occur in each of these syndromes but is not usually a prominent symptom. The hemorrhage is probably the result of a variety of causes and related to the specific morphologic characteristics of the pulmonary vasculature in these diseases. In primary plexogenic arteriopathy, hemoptysis and pulmonary hemosiderosis occur mainly in advanced disease with dilatation lesions and plexiform lesions. In veno-occlusive disease, pulmonary hemorrhage occurs chiefly in adult patients and is almost certainly capillary in origin. In recurrent thromboembolism, hemoptysis is considerably more common in the symptomatic form than in the silent form, probably because hemorrhagic infarction and anticoagulant therapy play a greater role in the former situation.
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PMID:[Arterial hypertension and veno-occlusive disease. Connections with pulmonary hemorrhage]. 281 4

Elevation of pulmonary arterial pressure may be secondary to many diseases of the lungs, chest wall, and heart. From a pathophysiologic viewpoint, pulmonary hypertension is secondary to vascular obstruction, vasoactivity, increased circulation, and passive forces. Clinically, the entities that result in secondary pulmonary hypertension present with a picture that identifies the primary disease. Patients with primary pulmonary hypertension may be difficult to identify. Pulmonary hypertension may present early with dyspnea and fatigue, while syncope and hemoptysis are late symptoms. In many instances, pulmonary hypertension can be diagnosed utilizing physical examination and noninvasive tests. Eventually, right heart catheterization is necessary to confirm the diagnosis and to monitor trials of therapy with vasodilators. Treatment may be specific (closure of a septal defect, thromboendarterectomy) or generic (vasodilators). These have been used recently for both secondary and primary pulmonary hypertension in an effort to reduce pulmonary vascular resistance, thereby decreasing right ventricular afterload and improving cardiac output and oxygen delivery. The success of these treatments has not been demonstrated.
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PMID:Pulmonary hypertension: etiology and clinical evaluation. 333 61

Authors described a case of 26-year old patient with history of progressing dyspnea and repetitive syncopes. In history is intermittent hemoptysis and dyspnea from 1990. Diagnosis of thromboembolic disease was suspected. Clinical picture was dominated by dyspnea, central cyanosis, sinus tachycardia without pulmonary signs of hearth failure. On ecg there is right heart hypertrophy. Echocardiographic examination shows dilatation of right heart, systolic pressure in a. pulmonalis about 90 mmHg and tricuspidal regurgitation of the III. degree. Phlebothrombosis was not found. Complete hemocoagulation examination excluded a primary procoagulating hematologic disease. Pulmonary angiography did not confirm thromboembolic disease but found a high grade pulmonary hypertension--mean pulmonary arterial pressure of 93 mmHg. After complex pneumological examination, including HRCT, and other examinations the diagnosis of primary pulmonary hypertension was made. Patient is indicated to lung transplantation. (Fig. 4, Ref. 9.)
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PMID:[Primary pulmonary hypertension]. 1103 5

Pulmonary capillary hemangiomatosis (PCH) is a rare cause of primary pulmonary hypertension characterized by thin-walled microvessels infiltrating the peribronchial and perivascular interstitium, the lung parenchyma, and the pleura. These proliferating microvessels are prone to bleeding, resulting in accumulation of hemosiderin-laden macrophages in alveolar spaces. Here we report 2 cases of PCH with pulmonary hypertension, 1 of them associated with mechanical intravascular hemolysis, a feature previously reported in other hemangiomatous diseases, but not in PCH. Case 2 was diagnosed by pulmonary biopsy; to our knowledge the patient is the second adult to be treated with interferon alpha-2a. Review of the literature identified 35 patients with PCH and pulmonary hypertension. The prognosis is poor and median survival was 3 years from the first clinical manifestation. Dyspnea and right heart failure are the most common findings of the disease. Hemoptysis, pleural effusion, acropachy, and signs of pulmonary capillary hypertension are less common. Chest X-ray or computed tomography scan usually shows evidence of interstitial infiltrates, pulmonary nodules, or pleural effusion. Hemodynamic features include normal wedge pressures. Radiologic and hemodynamic findings are undifferentiated from those of pulmonary veno-occlusive disease but differ from other causes of primary pulmonary hypertension. Epoprostenol therapy, considered the treatment of choice in patients with primary pulmonary hypertension, may produce pulmonary edema and is contraindicated in patients with PCH. Regression of lesions was reported in 1 patient treated with interferon therapy and 2 other patients stabilized, including our second patient. PCH was treated successfully by lung transplantation in 5 cases. Early recognition of PCH in patients with suspected primary pulmonary hypertension is possible based on clinical and radiologic characteristics. Diagnosis by pulmonary biopsy is essential for allowing appropriate treatment.
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PMID:Pulmonary capillary hemangiomatosis associated with primary pulmonary hypertension: report of 2 new cases and review of 35 cases from the literature. 1244 98

A 29-year-old woman with primary pulmonary hypertension presented with recurrent hemoptysis. Contrast-enhanced CT of the chest demonstrated the enhanced mass surrounded by consolidation related to parenchymal hemorrhage. Pulmonary angiography suggested that the mass was a pulmonary artery false aneurysm. After a microcatheter was superselectively inserted into the parent artery of the false aneurysm, the false aneurysm was successfully treated by transcatheter embolization with coils. Her hemoptysis has never recurred.
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PMID:Transcatheter embolization of pulmonary artery false aneurysm associated with primary pulmonary hypertension. 1525 21

An 18-year-old woman presented with primary pulmonary hypertension (PPH) and was hospitalized because of hemoptysis and was referred to our department for a differential diagnosis pulmonary thromboembolism. Doppler ultrasonography of the lower extremities was normal. Echocardiography and cardiac catheterization showed right ventricular dilatation and increased pulmonary artery pressure without anatomic (intracardiac) shunt. The mean pulmonary arterial pressure was 110 mm Hg. Tc-99m MAA lung perfusion scans showed nonsegmental patchy defects. Extrapulmonary renal uptake and increased systemic deposition of radiotracer were seen in the MAA scintigraphy. It could be related to a functional intrapulmonary shunt resulting in increasing pressure in the pulmonary artery in PPH.
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PMID:Renal uptake on lung perfusion scintigraphy in a patient with primary pulmonary hypertension. 1582 3

We report a case of primary pulmonary hypertension supported with non-invasive positive pressure ventilation (NPPV). A 20-year-old woman was diagnosed as primary pulmonary hypertension at the age of 15 and we prepared for registration of cadaver lung transplantation at the age of 20. She suffered from hemoptysis and was transferred to our ICU. We performed NPPV with continuous positive airway pressure of 4-6 cmH2O. Her systolic pulmonary artery pressure estimated with echocardiography was reduced, lung congestion on chest X ray was improved, and arterial oxygenation was improved. Considering that her condition would deteriorate only with medical therapy, we planned living donor lung transplantation. However, she died from massive hemoptysis before lung transplantation.
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PMID:[Case of primary pulmonary hypertension supported with non-invasive positive pressure ventilation]. 1880 6