Gurtner H P
Bull Eur Physiopathol Respir. 1979 Sep-Oct;15(5):897-923.
An epidemic of chronic pulmonary hypertension of vascular origin (CPHVO) has occurred in Austria, the Federal Republic of Germany, and Switzerland. The epidemic started in 1967 and reached its peak in 1968 and 1969. Since 1972, the prevalence of patients with CPHVO among individuals investigated by cardiac catheterization is again as low as in the pre-epidemic years. In Bern the prevalence of CPHVO during the peak of the epidemic was 20 times higher than during the 12-year period preceding the epidemic. The clinical, physical, electrocardiographic, radiologic, haemodynamic and respiratory findings of the patients observed in Bern (n = 102) are summarized. There has been a mortality between 12 and 20% at the time of the epidemic. Most patients observed for the first time during the epidemic have remained severely disabled over the years. A minute fraction seems to have recovered. There is a close geographic as well as temporal relation of the epidemic to the marketing and intake of the appetite depressing drug aminorex fumarate (Menocil). Acute administration of aminorex leads to a transient rise of the pulmonary artery pressure and vascular resistance in a number of animal species. It has not been possible to produce sustained precapillary pulmonary hypertension and chronic cor pulmonale vasculare under the conditions of chronic administration of the drug in the species tested. Morphologic examination of lung biopsy and autopsy material of patients who have died from CPHVO after the intake of aminorex reveals the presence of "plexogenic pulmonary arteriopathy". The vascular lesions are identical with those observed in pulmonary hypertension due to large congenital left-to-right shunts. In balancing the pros and cons, it appears that the arguments in favour of a cause-effect relationship between aminorex and pulmonary hypertension, which are derived from epidemiological evidence, outweigh the results of "negative" animal experiments. A "propter" in the title of this paper, therefore, seems to be more appropriate than a post".
在奥地利、德意志联邦共和国和瑞士出现了血管源性慢性肺动脉高压（CPHVO）的流行。该流行始于1967年，在1968年和1969年达到高峰。自1972年以来，通过心导管检查的人群中CPHVO患者的患病率再次降至流行前水平。在伯尔尼，流行高峰期CPHVO的患病率比流行前12年期间高出20倍。总结了在伯尔尼观察到的患者（n = 102）的临床、体格检查、心电图、放射学、血流动力学和呼吸方面的发现。流行期间的死亡率在12%至20%之间。在流行期间首次观察到的大多数患者多年来一直严重残疾。似乎只有极小一部分患者康复。该流行在地理和时间上与食欲抑制药物富马酸氨基苯恶唑（美诺西）的销售和使用密切相关。对许多动物物种急性给予氨基苯恶唑会导致肺动脉压和血管阻力短暂升高。在对受试物种长期给予该药物的情况下，未能产生持续性的毛细血管前肺动脉高压和慢性肺血管病。对摄入氨基苯恶唑后死于CPHVO的患者的肺活检和尸检材料进行形态学检查，发现存在“丛状肺小动脉病”。血管病变与因大型先天性左向右分流导致的肺动脉高压中观察到的病变相同。权衡利弊后，基于流行病学证据支持氨基苯恶唑与肺动脉高压之间存在因果关系的论据似乎比“阴性”动物实验结果更具说服力。因此，本文标题中的“因”似乎比“果”更合适。
