[Chronic pulmonary hypertension of vascular origin, plexogenic pulmonary arteriopathy and the appetite depressant aminorex: addenda to an epidemic].

An epidemic of chronic pulmonary hypertension occurred in Austria, the Federal Republic of Germany, and Switzerland, starting in 1967, peaking in 1968/69, and disappearing after 1972. The mechanism leading to pulmonary hypertension was precapillary vascular obstruction due to plexogenic pulmonary arteriopathy. There was a close geographic and temporal relationship between the epidemic and the marketing and intake of the appetite-depressing drug aminorex fumarate (Menocil). The epidemic was limited to the three above countries where aminorex had been on sale. In the individual patient the symptoms, usually dyspnea, angina pectoris and syncope on exertion, used to follow the beginning of the drug in-take after one year. A similar phase shift could be observed between marketing of the anoretic and the incidence of patients with chronic pulmonary hypertension of vascular origin. The new disease is compared with known forms of pulmonary vascular obstruction. It cannot be distinguished from classical primary pulmonary hypertension or from recurrent silent pulmonary thromboembolism on either clinical or functional grounds; it has plexogenic pulmonary arteriography in common with the former. The prognosis, however, is different: survival is considerably longer in patients with aminorex-associated pulmonary hypertension, and a marked decrease in the pulmonary vascular obstruction after 10 years is no exception. Considering the closeness of the various associations between the event (i.e. the epidemic) and its suspected cause (the anoretic aminorex) from the viewpoint of epidemiological, pharmacological, morphological and prognostic findings and considerations, there is little doubt that aminorex, besides other partly known and partly unknown factors, can in fact favour or cause the development of plexogenic pulmonary arteriography and pulmonary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)