LeWitt P A
N Engl J Med. 1980 Jan 10;302(2):73-7. doi: 10.1056/NEJM198001103020202.
Oral ingestion of a new rat poison that antagonizes nicotinamide metabolism, N-3-pyridylmethyl-N'-p-nitrophenyl urea (PNU, Vacor), is known to cause diabetes mellitus. I describe neurologic complications of PNU ingestion in 12 patients 19 to 50 years of age who swallowed between 0.39 and 7.02 g of PNU. One died within a day, and five died of chronic complications 40 to 182 days after taking the poison. Apart from the acute hyperglycemic ketoacidosis, the clinical presentation was variable, but orthostatic hypotension, gastrointestinal hypomotility, peripheral neuropathy, and encephalopathy were typical. The peripheral, autonomic, and central-nervous dysfunction could develop either acutely or other several days. It is possible that nicotinamide, given parenterally within minutes, prevents toxicity, but the cases discussed in this paper indicate that the neurologic deficits may progress despite later nicotinamide administration. Neurologic improvement took many months. Full recovery was uncommon, and the orthostatic, hypotension tended to persist.
口服一种能拮抗烟酰胺代谢的新型鼠药——N-3-吡啶甲基-N'-对硝基苯基脲(PNU,灭鼠优),已知会引发糖尿病。我描述了12名年龄在19至50岁之间的患者,他们摄入了0.39至7.02克PNU后出现的神经并发症。其中1人在一天内死亡,5人在服毒40至182天后死于慢性并发症。除急性高血糖酮症酸中毒外,临床表现各异,但体位性低血压、胃肠道动力不足、周围神经病变和脑病较为典型。周围神经、自主神经和中枢神经功能障碍可急性发作,也可在数天后出现。在数分钟内进行胃肠外注射烟酰胺有可能预防毒性,但本文讨论的病例表明,尽管随后给予烟酰胺,神经功能缺损仍可能进展。神经功能改善需要数月时间。完全康复并不常见,体位性低血压往往持续存在。