Prostaglandin E1 (PGE1) is a naturally occurring substance that is present in a variety of mammalian tissues, including the semen of fertile men. Its use in the diagnosis and treatment of erectile dysfunction has been extensively studied. In doses of 10-20 micrograms, PGE1 produces full erections in 70-80% of patients with erectile dysfunction. In diagnostic use PGE1 is employed as a simple office test and in conjunction with various hemodynamic tests. Self-injection of PGE1, either with the patient or his partner administering the injection, is a minimally invasive and effective treatment for erectile dysfunction in patients with organic or psychogenic erectile dysfunction. Its use is contraindicated in patients with sickle cell anemia, severe coagulopathy, schizophrenia or severe psychiatric disorder, poor manual dexterity, severe venous incompetence, or severe systemic disease. As calculated from data in the published literature, the most frequent side effects are pain at the injection site or during erection (occurring in 16.8% of patients), hematoma/ecchymosis (1.5% of patients), and prolonged erection/priapism (1.3% of patients). The potential for prolonged erection/priapism, the most serious side effect, can be minimized by careful titration of the dose and through patient education. Systemic side effects occur rarely during PGE1 use. During extended use, patients should be monitored for potential long-term side effects, such as fibrosis and angulation.
Our understanding of the biochemistry and biologic actions of AA metabolites has been greatly expanded in recent years. The discoveries of TXA2, PGI2, and LTs have fostered new concepts of the pathophysiology of cerebral ischemia. New approaches to treatment of ischemia include seeking an optimal dose of aspirin, developing drugs that selectively inhibit or antagonize TXA2 or LTs, and administering PGI2 or its analogues. Altering the dietary content of essential fatty acids for prophylaxis is also being studied. Though the results of this thrust are still preliminary, the exploration of these therapeutic strategies in cerebrovascular disorders based on further understanding of the pathophysiologic roles of TXA2, PGI2, LTs and probably other AA metabolites is anticipated with some optimism.
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