Kanny G, Moneret-Vautrin D A, Schohn H, Feldman L, Mallie J P, Gueant J L
Service de Médecine D, Immunologie Clinique et Allergologie, Centre Hospitalier Universitaire de Nancy, Hôpital de Brabois, France.
Clin Exp Allergy. 1993 Dec;23(12):1015-20. doi: 10.1111/j.1365-2222.1993.tb00293.x.
Histamine plays a key role in the pathogenesis of chronic urticaria (CU). The authors of this paper have studied the effects of ingested histamine in 25 patients with CU. A 120 mg dose of histamine, well-tolerated in the healthy subject, was instillated into the duodenum. Concomitantly, plasma histamine (H) levels and plasma and urinary methylhistamine (MH) levels were measured. Intraduodenal administration of histamine was responsible for the development of an attack of urticaria in 64% of patients, while control subjects were asymptomatic. Plasma histamine levels were significantly higher after digestive histamine challenge (DHC) in patients with CU compared with controls. An abnormal increase in plasma histamine was observed in 72% of them. Plasma MH exhibited the same kinetic behaviour with a usually delayed time-pattern. Urinary MH concentration was higher in patients presenting with early-onset urticaria during the first hour than in those with the late-onset type between 1 and 12 hr after DHC. The coefficient of methylation (plasma MH/MH+H) was not significantly different in patients presenting with an attack of urticaria following DHC and in other subjects. Urinary excretion of MH and urinary flow increased significantly in patients presenting with an attack of urticaria following DHC which corresponds to increased absorption of histamine during the 5-hr period following DHC and its role on excretion by the kidney via vasodilation which it induces. This study demonstrates the abnormal frequency of disturbances in the metabolism of exogenous histamine in patients with CU. Increased plasma H accounts for the abnormal passage of H across the intestinal barrier which can result either from intestinal hyperpermeability and/or a deficit in the enzymatic catabolism of histamine. The systems of methylation and urinary clearance of MH appear to be effective. It is thus postulated that there is a deficit in diamine oxidase (DAO) in the enterocyte. The lack of correlation between the kinetic behaviour of plasma H and the onset of urticaria draws attention to the extent of individual variability in skin reactivity to histamine.
组胺在慢性荨麻疹（CU）的发病机制中起关键作用。本文作者研究了摄入组胺对25例CU患者的影响。将120mg剂量的组胺（在健康受试者中耐受性良好）注入十二指肠。同时，测量血浆组胺（H）水平以及血浆和尿甲基组胺（MH）水平。十二指肠内给予组胺导致64%的患者出现荨麻疹发作，而对照受试者无症状。与对照组相比，CU患者在消化性组胺激发试验（DHC）后血浆组胺水平显著更高。72%的患者观察到血浆组胺异常升高。血浆MH表现出相同的动力学行为，通常具有延迟的时间模式。在DHC后第1小时出现早发性荨麻疹的患者尿MH浓度高于1至12小时出现迟发性荨麻疹的患者。DHC后出现荨麻疹发作的患者与其他受试者的甲基化系数（血浆MH/MH + H）无显著差异。DHC后出现荨麻疹发作的患者尿MH排泄和尿流量显著增加，这对应于DHC后5小时内组胺吸收增加及其通过诱导血管舒张对肾脏排泄的作用。本研究表明CU患者中外源性组胺代谢紊乱的异常频率。血浆H升高解释了H穿过肠道屏障的异常，这可能是由于肠道通透性增加和/或组胺酶促分解代谢缺陷所致。MH的甲基化和尿清除系统似乎是有效的。因此推测肠细胞中二胺氧化酶（DAO）存在缺陷。血浆H的动力学行为与荨麻疹发作之间缺乏相关性，这引起了人们对皮肤对组胺反应个体变异性程度的关注。
