Iproniazid * (1-isonicotinyl-2-isopropyl\x=req-\ hydrazine) was initially introduced to clinical medicine as an antituberculous agent in 1952.1 Although potent in its therapeutic effect, the drug was eventually abandoned in favor of its chemical relative, isoniazid, largely because of its distressing si de\ x=req-\ effects. In addition to its antituberculous activity, early studies with iproniazid clearly indicated a striking nonspecific action in promoting elevation of mood, stimulating appetite, and increasing sense of well-being.In view of these nonspecific effects, the drug has been recently reintroduced as a "psychic energizer" in the management of psychiatric depression, with favorable results.2,3 Furthermore, there are indications that this agent is now being used in a large variety of medical disorders. Reports concerning the use of iproniazid in hypertension,4 rheumatoid arthritis,5 and angina pectoris6 have already appeared in the literature.Of the early-recognized side-effects of iproniazid, those resulting from undesirable actions on the autonomic and central nervous systems are most frequent. These include vertigo, insomnia, hyper-reflexia. muscular twitching, convulsions, paresthe-sias, postural hypotension, dry mouth, de¬ layed micturition, and constipation. Perhaps the most serious, and certainly the least-< documented toxic effect, is jaundice. In an effort to clarify further the status of jaun¬ dice as a significant toxic effect of iproniazid therapy, the following five case reports and review of pertinent literature are pre¬ sented.Case 1.-A 49-year-old white woman was ad¬ mitted to Montefiore Hospital on Jan. 25, 1958, because of jaundice of two weeks' duration. Iproniazid therapy had been instituted two months prior to admission because of depression. After a fourweek period of treatment, during which time she took 150 mg. of iproniazid daily for a total of 4.2 mg., the drug was discontinued. Two weeks after cessation of therapy, the patient first noticed jaundice, dark urine, and light-colored stools. Liverfunction tests three days prior to admission revealed a total serum bilirubin of 8.2 mg. '%, cephalin flocculation of 3+, thymol turbidity of 10.0 units, and alkaline phosphatase of 5.5 Bessy-Lowry units. The patient denied all gastrointestinal symptomatol¬ ogy. Although an oral cholecystogram performed three years previously revealed a single gallbladder calculus, she specifically denied previous jaundice as well as recent fever, abdominal pain, dyspepsia, or vomiting. She did not drink alcoholic beverages and was not exposed to jaundiced persons, injec--< tions, or hepatotoxic agents, excluding iproniazid, for at least six months. Her only other medication during this period was an occasional capsule of secobarbital at bedtime. Physical examination revealed a well-nourished, grossly icteric but alert, middle-aged woman in no acute distress. The temperature was 99 F; thep ulse rate, 72, and the blood pressure, 160/90. There were no significant physical findings except jaundice and a soft,...