Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostaglandin D2 (PGD2) produced by platelets can inhibit aggregation via activation of platelet adenylate cyclase. PGD2 activation of platelet cyclase in platelet membrane fractions was studied in 20 consecutive patients hospitalized with acute deep-vein thrombosis and/or pulmonary embolism. In nine patients, PGD2-stimulated enzyme activity was decreased at all concentrations of PGD2 studied. This altered enzyme sensitivity was specific for PGD2 as basal enzyme activity, and prostaglandin E1, prostaglandin I2, and sodium fluoride stimulated adenylate cyclase was normal. The effect of PGD2 on platelet aggregation and 14C-serotonin release was also studied in one patient where a four-fold higher concentration of PGD2 was required to inhibit collagen-induced 14C-serotonin release. Binding studies using [3H]PGD2 as a radioligand indicated that this patient's platelets bound 10 fmole PGD2/10(8) platelets compared to 30 fmole/10(8) platelets in a normal control. Five patients had follow-up studies between 2 and 7 mo after their acute thrombotic event, and PGD2-stimulated adenylate cyclase activity returned towards normal in four. Since PGD2 is synthesized in platelets at concentrations sufficient to inhibit aggregation and activate adenylate cyclase, diminished platelet sensitivity to this prostaglandin could result in "hyperactivity" and contribute to the thrombosis observed in these patients.
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PMID:Diminished platelet adenylate cyclase activation by prostaglandin D2 in acute thrombosis. 38 Jun 88

Reversible causes of pulmonary hypertension, such as mitral stenosis or pulmonary embolism, should be corrected causally. The therapy of pulmonary hypertension is difficult in those diseases where the causes or mechanisms are not understood or are unknown. In chronic obstructive lung disease, the primary objective is to improve airflow and alveolar ventilation (theophylline, beta-sympathicomimetics). Long-term oxygen (more than 18 hours a day) should be used in patients with paO2 below 55 mm Hg, since a reduction in pulmonary vascular resistance and a prolonged survival has been demonstrated. The role of vasodilator therapy (hydralazine, nitrates, diazoxide, captopril, calcium-blockers and others) in chronic obstructive lung disease remains uncertain. In primary pulmonary hypertension, a pulmonary vasodilator is recommended after demonstrating (for example with an infusion of prostaglandin I2), that the increased pulmonary vascular resistance is still reversible. The initiation of therapy should be performed cautiously under hemodynamic monitoring.
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PMID:Treatment of pulmonary hypertension. 287 21

We report here a 70-year-old female patient with a history of breast cancer who presented with dyspnea that had lasted for 2 weeks following a long-distance trip by bus. She was at first suspected of having a pulmonary embolism given the typical presentation, elevated D-dimer level, and enlargement of the right-side heart. However, her systemic condition deteriorated despite the initiation of anti-coagulation therapy. Given the absence of a major thrombus in the pulmonary major arteries but multiple low perfusion lesions in the periphery of the lungs, refractoriness to conventional therapy, an increase in tumor markers, and anaplastic cells demonstrated by aspiration cytology from the pulmonary artery, we diagnosed her as pulmonary tumor thrombotic microangiopathy (PTTM). She died on day 23 due to respiratory failure despite administration of inotropes and prostaglandin I2. The patient had an obvious history of malignancy, but we should emphasize that PTTM can develop even in patients with early-stage or completely cured malignancies. Although an early and definite diagnosis of PTTM is currently challenging, an optimal diagnostic and therapeutic strategy is warranted.
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PMID:How to Diagnose and Treat Pulmonary Tumor Thrombotic Microangiopathy. 3217 12