enalapril and Erythema

Our pharmacologic armamentarium is expanding at a tremendous pace, and requires that we as clinicians maintain a certain level of knowledge of the drugs that we use, as well as their metabolism, and how they may function, both positively and negatively, in a given patient. Certain drugs, such as the angiotensin-converting enzyme inhibitors, interfere with the natural deactivation of certain vasoactive substances normally present in the body. Since many of these systems are functionally interrelated (eg, angiotensin-converting enzyme and kininase II), we may see cutaneous side effects when these drugs are administered. Enalapril is an angiotensin-converting enzyme inhibitor that promoted a cutaneous eruption in a patient with renal failure secondary to diabetes. We suspect that our patient's vasculitis and maculopapular erythema is included in a large number of polymorphic eruptions that can be seen with angiotensin-converting enzyme inhibitors, and review the operative pathogenetic mechanism. Many of these side effects are dose related, and can be controlled or eliminated by lowering the dosage of angiotensin-converting enzyme inhibitor, depending upon the clinical circumstances.

Topics: Adult; Drug Eruptions; Enalapril; Erythema; Female; Humans; Skin; Vasculitis

Major developments in the use of angiotensin converting enzyme (ACE) inhibition for the treatment of hypertension and congestive heart failure have occurred since the discovery of captopril in June 1975. Early in the past decade, this oral ACE inhibitor was restricted to refractory and severe cases of hypertension. By July 1985, the Food and Drug Administration approved its use not only for all degrees of hypertension but also for the initial treatment of hypertensive patients with uncomplicated disease. New information has confirmed the effectiveness of twice-daily administration (which favorably influences compliance) and the lack of a need to monitor blood or urine levels to assure safety. The renin-mediated and non-renin-mediated mechanisms of action of captopril-induced ACE inhibition have been fully delineated, as has its side effect profile, which does not include various CNS, sympathetic reflex, and metabolic side effects seen with other antihypertensive agents. As the first vasodilator to prove its efficacy in the acute and chronic treatment of congestive heart failure to the FDA, captopril is now widely used throughout the United States. ACE inhibition reduces symptoms, enhances exercise capacity, and favorably affects sodium, water, and potassium homeostasis in patients with heart failure. Also, recent but as yet unconfirmed evidence suggests that ACE inhibition may prolong survival in these patients. The success of captopril, the first oral agent of this class, promises to hold true for other ACE inhibitors (such as enalapril), which have similar activities but differing pharmacokinetic properties and will soon be available for clinical use. Further information on these newer agents is anxiously awaited. In the near future, the clinician will undoubtedly be able to choose from a large selection of ACE inhibitors for the treatment of hypertension and heart failure. Therefore, it is important to learn about any meaningful differences among ACE inhibitors and to contrast this class of agents with older, standard therapies. This learning process is crucial as we assess whether newer agents offer clinical advantages over the old.

Topics: Adrenergic beta-Antagonists; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Captopril; Enalapril; Erythema; Heart Failure; Humans; Hypotension; Neutropenia; Renin-Angiotensin System; Taste