Procaccini E M, Pandolfi G, Monfrecola G, Rotoli B
Department of Dermatology, 2nd Medical School, University of Naples, Italy.
Photodermatol Photoimmunol Photomed. 1992 Feb;9(1):4-7.
We investigated possible alterations induced by psoralen and ultraviolet A radiation (PUVA) on platelet function both in vitro and in vivo. In vitro, using conventional aggregometry and adenosine diphosphate (ADP), collagen, ristocetin and arachidonic acid as aggregating agents, platelet aggregation was determined on platelet-rich plasma (PRP) from normal subjects at basal conditions and following the addition of increasing concentrations of 8-methoxypsoralen (8-MOP) with and without exposure to ultraviolet A (UVA) light (5 J/cm2) and compared with UVA light exposure alone. At basal conditions and following exposure to UVA light alone, no changes in the normal platelet aggregation patterns were observed. Exposure to UVA light of PRP containing 8-MOP also demonstrated no abnormality in the platelet aggregation patterns at 8-MOP concentrations of 200 ng/ml. However, abnormal platelet aggregation as a response to ADP and collagen was observed at higher concentrations of 8-MOP, which was augmented upon exposure to UVA light. In vivo, platelet aggregometry was performed on PRP from 4 patients submitted to PUVA treatment at basal conditions, 2.5 h after oral ingestion of 8-MOP (0.6-0.8 mg/kg) and after 4 PUVA sessions. No patient showed modification of the platelet aggregation profile after either 8-MOP ingestion or PUVA treatment. Our study shows that 8-MOP at high concentrations in vitro impairs platelet aggregation by ADP and collagen augmented by UVA light exposure, but PUVA therapy causes no detectable abnormality in platelet function in vivo.
我们研究了补骨脂素和紫外线A辐射(PUVA)在体外和体内对血小板功能可能产生的改变。在体外,使用传统的血小板聚集测定法,以二磷酸腺苷(ADP)、胶原蛋白、瑞斯托菌素和花生四烯酸作为聚集剂,在基础条件下以及添加不同浓度的8-甲氧基补骨脂素(8-MOP)后,分别在有或无紫外线A(UVA)照射(5 J/cm2)的情况下,对正常受试者的富血小板血浆(PRP)进行血小板聚集测定,并与单独的UVA照射进行比较。在基础条件下以及单独暴露于UVA后,未观察到正常血小板聚集模式的变化。含有8-MOP的PRP暴露于UVA后,在8-MOP浓度为200 ng/ml时,血小板聚集模式也未显示异常。然而,在较高浓度的8-MOP时,观察到对ADP和胶原蛋白的异常血小板聚集,在暴露于UVA后这种异常加剧。在体内,对4例接受PUVA治疗的患者的PRP进行血小板聚集测定,分别在基础条件下、口服8-MOP(0.6 - 0.8 mg/kg)2.5小时后以及4次PUVA治疗后进行。无论是摄入8-MOP还是接受PUVA治疗后,均未观察到患者血小板聚集情况的改变。我们的研究表明,体外高浓度的8-MOP会损害由UVA照射增强的对ADP和胶原蛋白的血小板聚集,但PUVA疗法在体内未引起可检测到的血小板功能异常。