Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe pulmonary hypertension due to tumor cell microemboli or lymphangitic carcinomatosis is a rare complication of malignant disease. In most of the reported cases, a clinical picture of subacute cor pulmonale developed. A 57-year-old man with deep vein thrombosis in his left calf developed acute progressive dyspnea with hypoxemia, cyanosis and the clinical picture of acute cor pulmonale, while he was on full heparinization. Respiratory failure with the need for mechanical ventilatory support developed within 2 days. Chest radiography revealed the development of acute cardiac enlargement, dilated pulmonary artery and diffuse opacities in the fields of both lungs. Open lung biopsy disclosed massive tumor cell microemboli and lymphangitic carcinomatosis. No parenchymal metastases were found. This case is extremely rare because of the rapid development of the patient's respiratory signs and symptoms of acute cor pulmonale due to pulmonary tumor cell microemboli and lymphangitic carcinomatosis. It is also most atypical because of the rare pulmonary radiographic presentation.
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PMID:Acute cor pulmonale due to tumor cell microemboli. 931 Oct 58

Cationic lipid-mediated intravenous gene delivery shows promise in treating pulmonary diseases including lung tumor metastases, pulmonary hypertension, and acute respiratory distress syndrome. Nevertheless, clinical applications of cationic lipidic vectors via intravenous administration are limited by their transient gene expression. In addition, repeated dosing is not effective at frequent intervals. In an effort to elucidate the mechanism of gene inactivation, we report in this study that cationic lipid-protamine-DNA (LPD) complexes, but not each component alone, can induce a high level of cytokine production, including interferon-gamma and tumor necrosis factor-alpha. Furthermore, we demonstrate that LPD administration triggers apoptosis in the lung, a phenomenon that may be mediated in part by the two cytokines. Treatment of mice with antibodies against the two cytokines prolongs the duration of gene expression and also improves lung transfection on a second administration of LPD. Although the mechanism underlying LPD-induced cytokine production is unclear, methylation of the DNA significantly decreased the level of both interferon-gamma and tumor necrosis factor-alpha, suggesting that unmethylated CpG sequences in plasmid DNA play an important role. These data suggest that decreasing the CpG-mediated immune response while not affecting gene expression may be a useful therapeutic strategy to improve cationic lipid-mediated intravenous gene delivery to the lung.
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PMID:Effect of immune response on gene transfer to the lung via systemic administration of cationic lipidic vectors. 1033 36

We report a middle-aged woman who died 2 days after presenting with dyspnea and severe pulmonary hypertension of unknown etiology. Her symptoms were highly suggestive of pulmonary embolism, but clinical evaluations for that disease yielded negative results. Autopsy revealed a Krukenberg tumor of the left ovary, representing metastatic gastric carcinoma from an occult primary lesion. Although the lungs exhibited no gross evidence of pulmonary emboli or neoplasia, microscopic examination revealed diffuse microscopic metastases in the pulmonary arterial vasculature. The pulmonary arteries exhibited fibrocellular intimal proliferation with smooth muscle colonization of the luminal neoplastic lesions and associated microthrombi. This disease entity, known as tumor-related thrombotic pulmonary microangiopathy, results in generalized microvascular obliteration and subsequent pulmonary hypertension. It is a rare condition that is distinct from ordinary pulmonary thromboembolism and primary pulmonary hypertension. Tumor-related thrombotic pulmonary microangiopathy should be considered diagnostically by the autopsy pathologist in cases of rapidly evolving pulmonary hypertension in a middle-aged or elderly individual, or respiratory failure of unknown cause, especially if there is a history of a visceral malignancy.
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PMID:Tumor-related thrombotic pulmonary microangiopathy: review of pathologic findings and pathophysiologic mechanisms. 1091 85

Primary tumours of the heart are rare. The majority of these tumours are benign, with myxomas located in the left atrium being the most common form. Almost all malignant tumours are sarcomas and occur preferentially in the right side of the heart. An exception to this rule is leiomyosarcoma, a rare form of primary cardiac sarcoma that occurs predominantly in the left atrium, as does cardiac myxoma. The case of a 53-year-old woman who presented with symptoms of mitral valve stenosis and pulmonary hypertension is reported. Cardiac catheterization, angiography and echocardiography revealed a left atrial mass that was interpreted as atrial myxoma. At the time of operation, the myxoid appearance of the tumour mass further supported this assumption. The tumour, including a wide rim of atrial septum, was removed with cautery. Histopathological examination unexpectedly showed that the tumour was not an atrial myxoma but rather a myxoid variant of a primary leiomyosarcoma. Immunohistochemistry and electron microscopy confirmed the diagnosis. Local radiotherapy was considered but deemed contraindicated in view of the longstanding pulmonary hypertension. Two months after excision, a repeat echocardiogram indicated recurrence of tumour in the left atrium, and the patient died a few days later. The preferential left atrial location and the frequently myxoid appearance of primary leiomyosarcomas of the heart make it particularly difficult to differentiate them preoperatively from atrial myxomas. The authors recommend resection of all atrial myxoid tumours with a wide (at least 1 cm) margin, combined with intraoperative frozen section diagnosis, because complete surgical resection appears to correlate with prolonged survival in the few reported cases of atrial leiomyosarcomas. In cases of incomplete initial resection or local recurrence in the absence of metastatic disease, heart transplantation may be a valid option in appropriately selected patients.
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PMID:Myxoid leiomyosarcoma of the left atrium: a rare malignancy of the heart and its comparison with atrial myxoma. 1126 66

A 69-year-old male presented with symptoms of fulminant lung embolism and, despite immediate therapy with plasminogen activator, died of acute right heart failure. At autopsy multiple tumor cell emboli were detected in small pulmonary vessels in addition to widespread liver metastases from an urothelial carcinoma. - In a 23-year-old female a malignant gastric ulcer and multiple liver metastases were diagnosed at initial presentation. She too died from pulmonary hypertension due to a series of lung embolisms which occurred despite heparin therapy. At autopsy, many small pulmonary arteries were filled with adenocarcinoma cells; the primary gastric tumor and liver metastases were confirmed. These cases demonstrate that the shedding of tumor cells from hepatic metastases can obstruct the pulmonary vessels and lead to acute cor pulmonale. Tumor cell emboli should be considered in the differential diagnosis of acute pulmonary hypertension, especially in patients with a known tumor. They may, however, also represent the first clinical signs of previously unrecognized malignancy.
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PMID:[Tumor cell embolism to pulmonary arteries]. 1155 62

Chronic lung disease in humans is frequently complicated by the development of secondary pulmonary hypertension, which is associated with increased morbidity and mortality. Hypoxia, inflammation and increased shear stress are the primary stimuli although the exact pathways through which these initiating events lead to pulmonary hypertension remain to be completely elucidated. The increase in pulmonary vascular resistance is attributed, in part, to remodelling of the walls of resistance vessels. This consists of intimal, medial and adventitial hypertrophy, which can lead to encroachment into and reduction of the vascular lumen. In addition, it has been reported that there is a reduction in the number of blood vessels in the hypertensive lung, which could also contribute to increased vascular resistance. The pulmonary endothelium plays a key role in mediating and modulating these changes. These structural alterations in the pulmonary vasculature contrast sharply with the responses of the systemic vasculature to the same stimuli. In systemic organs, both hypoxia and inflammation cause angiogenesis. Furthermore, remodelling of the walls of resistance vessels is not observed in these conditions. Thus it has been generally stated that, in the adult pulmonary circulation, angiogenesis does not occur. Prompted by previous observations that chronic airway inflammation can lead to pulmonary vascular remodelling without hypertension, we have recently shown, using quantitative stereological techniques, that angiogenesis can occur in the adult pulmonary circulation. Pulmonary angiogenesis has also been reported in some other conditions including post-pneumonectomy lung growth, metastatic disease of the lung and in biliary cirrhosis. Such angiogenesis may serve to prevent or attenuate increased vascular resistance in lung disease. In view of these more recent data, the role of structural alterations in the pulmonary vasculature in the development of pulmonary hypertension should be carefully reconsidered.
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PMID:The structural basis of pulmonary hypertension in chronic lung disease: remodelling, rarefaction or angiogenesis? 1243 Sep 58

A 47-year-old man was admitted to our hospital because of progressive dyspnea and cough. Physical examination and chest radiographs showed the signs of cor pulmonale. A lung scan using perfused radionuclide revealed multiple peripheral perfusion defects and catheterization of the right heart showed severe pulmonary hypertension. A diagnosis of severe pulmonary embolism was made. Despite intensive care with anti-coagulation therapy, the patient died on the third-hospital day. Autopsy disclosed gastric cancer in the pylorus with metastases to the regional lymph nodes. There were no macroscopic pulmonary artery emboli or parenchymal lesions, but more than 60% of the small arteries and arterioles were occluded by casts of tumor cells. Cor pulmonale due to a pulmonary tumor embolism is a rare complication of cancer. This case is particularly unusual because the embolus-caused cor pulmonale was the initial manifestation of clinically occult, but pathologically advanced, gastric cancer.
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PMID:[An autopsy case of cor pulmonale due to a pulmonary tumor embolism as the first clinical manifestation of occult gastric cancer]. 1264 14

We describe a patient wih subacute cor pulmonale caused by tumor emboli in the lungs. A 64-year-old female suffering from a subacute progressive cough and shortness of breathing died of severe pulmonary hypertension seven days after admission. Neither chest CT scans nor lung perfusion scintigraphy showed any abnormal findings. Microscopic examination after an autopsy revealed diffuse intravascular tumor emboli occluding not only the small pulmonary arteries and arterioles, but also the lymphatic vessels, which were suggested to be metastases of a breast carcinoma resected five years previously. Thus, pulmonary tumor embolism should be considered in the differential diagnosis of primary pulmonary hypertension, particularly in patients with a past history of cancers.
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PMID:Subacute cor pulmonale due to tumor embolism. 1520 57

Neuroblastoma is a tumor of the sympathetic ganglia and adrenal medulla that rarely metastasizes to the placenta. A 21-year-old gravida 3, para 1 at 28 weeks' gestation had an incidental finding of a 3.8-cm fetal renal mass on prenatal ultrasound. Within 1 week, the fetus developed hydrops and was delivered for nonreassuring fetal assessment. The mother developed mirror syndrome as manifested by hypertension, oliguria, and edema. The hydropic infant developed pulmonary hypertension, sepsis, and renal failure. On day of life 4, life support was discontinued. Pathological examination of the placenta revealed disseminated small round blue cells consistent with neuroblastoma. Metastasis of congenital neuroblastoma to the placenta is exceedingly rare, and cases discovered prenatally have resulted in significant maternal morbidity and 100% neonatal mortality.
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PMID:Mirror syndrome resulting from metastatic congenital neuroblastoma. 1758 17

This case involved a 38-year-old man who was referred to our hospital with general fatigue, appetite loss, weight loss, cough and exertional dyspnea. Within a couple of days, he was admitted due to advanced dyspnea and general fatigue. Severe hypoxemia was identified and acute right heart failure developed on admission. Treatment was initiated using oxygen, antibiotics and heparin sodium, but the patient died of sudden cardiopulmonary arrest 30 h after admission. Autopsy revealed advanced gastric cancer and widespread tumor embolism together with fibrocellular intimal proliferation and thrombus formation in the small arteries. Pulmonary tumor thrombotic microangiopathy (PTTM) with gastric cancer was diagnosed. PTTM is characterized by widespread fibrocellular intimal proliferation of the small pulmonary arteries and arterioles in patients with metastatic carcinoma. Microscopic pulmonary tumor emboli frequently occur in patients with malignant tumors, but very few cases of PTTM have been reported. PTTM should be considered in the differential diagnosis of acute dyspnea or pulmonary hypertension. In cases of acute cor pulmonal, the existence of malignant cells can be examined using pulmonary arterial wedge aspiration cytology where feasible, in addition to positron emission tomography with F-2-deoxy-2-fluoro-D-glucose, which can be used to investigate certain primary tumors and associated metastatic disease. The suitability of gastroendoscopy to screen for malignancies should be examined.
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PMID:[Pulmonary tumor thrombotic microangiopathy caused by signet ring cell carcinoma in gastric cancer]. 1768 68


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