Nalin D R, Levine R J, Levine M M, Hoover D, Bergquist E, McLaughlin J, Libonati J, Alam J, Hornick R B
Lancet. 1978 Oct 21;2(8095):856-9. doi: 10.1016/s0140-6736(78)91568-4.
Fasting and postprandial stomach acid production were low in 16 of 37 Bangalees convalescing from cholera or non-vibrio cholera. Gastric juice of hypochlorhydric patients did not kill cholera vibrios in vitro, whereas that from normochlorhydric patients rapidly killed vibrios in concentrations up to 10(10)/ml. To determine whether hypoacidity resulted from cholera or was a common predisposing factor, basal and betazole-hydrochloride-stimulated acid production were measured before and after cholera in a second group of patients consisting of American volunteers participating in a vaccine development programme. Cholera did not alter the stomach acid secretion of American volunteers, but low precholera basal acid production predispose to severe cholera. The results indicate that hypochlorhydria observed in convalescent Bangalee cholera patients is not caused by cholera, and must therefore have preceded it. Idiopathic tropical hypochlorhydria may be a major factor accounting for the high incidence of diarrhoea due to acid-sensitive pathogens in developing countries.
在37名从霍乱或非霍乱弧菌感染中康复的孟加拉人当中，有16人的空腹和餐后胃酸分泌量较低。胃酸过少患者的胃液在体外不能杀死霍乱弧菌，而胃酸正常患者的胃液能迅速杀死浓度高达每毫升10的10次方的霍乱弧菌。为了确定胃酸过少是由霍乱导致的，还是一个常见的诱发因素，在另一组由参与疫苗研发项目的美国志愿者组成的患者中，测量了霍乱前后的基础胃酸分泌量以及倍他唑刺激后的胃酸分泌量。霍乱并未改变美国志愿者的胃酸分泌，但霍乱前基础胃酸分泌量低易导致严重霍乱。结果表明，在康复期的孟加拉霍乱患者中观察到的胃酸过少并非由霍乱引起，因此肯定是先于霍乱出现的。特发性热带胃酸过少可能是发展中国家因酸敏感病原体导致腹泻高发的一个主要因素。
