Abstract
INTRODUCTION: Pulmonary hypertension in sarcoidosis has been attributed to end-stage lung fibrosis with resultant destruction of pulmonary vasculature(1), granulomatous pulmonary angiitis(2), or extrinsic compression of major pulmonary vessels(3). Sarcoidosis-associated pulmonary hypertension (SAPH) has been shown to be responsive to vasodilator therapy with inhaled nitric oxide (iNO)(4), intravenous epoprostenol(5), and corticosteroid therapy(6). Our group has previously reported that SAPH can be treated successfully with endothelin-receptor antagonist bosentan(7), signifying the role of altered endothelium-derived vasoactive mediators in pulmonary vasculature of such patients.
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