Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bosentan is a nonpeptide, specific, competitive, dual antagonist at both endothelin receptor subtypes (ET(A) and ET(B)). Orally administered bosentan effectively prevents endothelin 1-induced vasoconstriction in pulmonary vessels in patients with pulmonary arterial hypertension. Improvement in exercise capacity from baseline was significantly greater with bosentan than with placebo in two phase III trials in patients with WHO functional class III or IV pulmonary arterial hypertension (primary or associated with connective tissue disease) despite treatment with vasodilators, diuretics, anticoagulants, cardiac glycosides, or supplemental oxygen. The beneficial effects of bosentan on exercise capacity were maintained for at least 20 weeks. Compared with placebo, bosentan led to a significantly greater improvement from pretreatment values in secondary efficacy endpoints such as the Borg dyspnea index, WHO functional class, and cardiopulmonary hemodynamic parameters (cardiac index, pulmonary vascular resistance, pulmonary artery pressure, pulmonary capillary wedge pressure, mean right atrial pressure). Bosentan significantly reduced the incidence, and delayed the onset, of clinical worsening of pulmonary arterial hypertension compared with placebo. In published clinical trials, adverse events that occurred with similar or greater frequency with bosentan 125 mg twice daily than with placebo included headache, syncope, flushing and abnormal hepatic function. Those that occurred less frequently with bosentan 125 mg twice daily than with placebo included dizziness, worsening of symptoms of pulmonary arterial hypertension, cough and dyspnea.
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PMID:Bosentan. 1472 63

Idiopathic pulmonary fibrosis is a disease of unknown cause characterized by cough, progressive dyspnea, restrictive respiratory disorder, a typical honeycomb aspect on the high-resolution CT-scan, and usual interstitial pneumonia at histological examination of the lung biopsy. Most patients die 3 to 8 years after diagnosis. Current treatment is based on a combination of corticosteroids and immunosuppressants, but the efficacy of treatment remains a matter of debate. New therapeutics currently under evaluation in controlled clinical trials include interferon-gamma, pirfenidone, N-acetylcysteine, etanercept (anti-TNFalpha), bosentan (endothelin receptor antagonist), imatinib (tyrosine-kinases inhibitor of the PDGF receptor), etc. At the same time, new compounds showing efficacy in experimental models of fibrosis and the development of new pathophysiological concepts open new perspectives both in terms of concept and clinical practice.
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PMID:[Drug treatments for idiopathic pulmonary fibrosis]. 1614 96

This chapter outlines sex differences in pharmacokinetics and pharmacodynamics of the most frequently used drugs in cardiovascular diseases, e.g., coronary artery disease, hypertension, heart failure. Retrospective analysis of previously published drug trials revealed marked sex differences in efficacy and adverse effects in a number of cardiovascular drugs. This includes a higher mortality among women taking digoxin for heart failure, more torsade de pointes arrhythmia in QT prolonging drugs and more cough with ACE inhibitors. Trends towards a greater benefit for women and/or female animals have been observed in some studies for endothelin receptor antagonists, the calcium channel blocker amlodipine, the ACE-inhibitor ramipril and the aldosterone antagonist eplerenone. However, reproduction of these results in independent studies and solid statistical evidence is still lacking. Some drugs require a particularly careful dose adaptation in women: the beta-blocker metoprolol, the calcium channel blocker verapamil, loop-, and thiazide diuretics. In conclusion, sex differences in pharmacokinetics and pharmacodynamics have to be taken into account for cardiovascular drug therapy in women.
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PMID:Sex and gender differences in cardiovascular drug therapy. 2302 53

High-altitude pulmonary hypertension (HAPH) affects individuals residing at altitudes of 2,500 meters and higher. Numerous pathogenic variables play a role in disease inception and progression and include low oxygen concentration in inspired air, vasculopathy, and metabolic abnormalities. Since HAPH affects only some people living at high altitude genetic factors play a significant role in its pathogenesis. The clinical presentation of HAPH is nonspecific and includes fatigue, shortness of breath, cognitive deficits, cough, and in advanced cases hepatosplenomegaly and overt right-sided heart failure. A thorough history is important and should include a search for additional risk factors for lung disease and pulmonary hypertension (PH) such as smoking, indoor air pollution, left-sided cardiac disease and sleep disordered breathing. Twelve-lead electrocardiogram, chest X-ray and echocardiography can be used as screening tools. A definitive diagnosis should be made with right-sided heart catheterization using a modified mean pulmonary artery pressure of at least 30 mm Hg, differing from the 25 mm Hg used for other types of PH. Treatment of HAPH includes descent to a lower altitude whenever possible, oxygen therapy and the use of medications such as endothelin receptor antagonists, phosphodiesterase 5 blockers, fasudil and acetazolamide. Some recent evidence suggests that iron supplementation may also be beneficial. However, it is important to note that the scientific literature lacks long-term randomized controlled data on the pharmacologic treatment of HAPH. Thus, an individualized approach to treatment and informing the patients regarding the benefits and risks of the selected treatment regimen are essential.
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PMID:High-altitude Pulmonary Hypertension: an Update on Disease Pathogenesis and Management. 2701 74