Fjellner B, Hägermark Ö
Acta Derm Venereol. 1979;59(6):505-12. doi: 10.2340/0001555559505512.
The characteristic temperature-dependent pruritus in polycythemia vera (PV) is described. The triggering factor seems to be a sudden decrease in skin temperature, e.g. after a hot bath or shower. The sudden onset and limited duration of the pruritus might suggest an activation or release of some humoral factor(s). In a controlled study we showed that aspirin alleviates this particular pruritus. Therefore, the possibility of prostaglandin and platelet involvement was considered. It was found that substances such as PGE2 and serotonin, produced and released by platelets, could elicit pruritus in healthy volunteers when injected intradermally and that PGE2 enhanced the cutaneous responses to serotonin. Studies of platelet aggregation did not reveal any abnormalitites in the PV patients but ADP was shown to sensitize platelets to adrenaline-induced aggregation in vitro. Although not proven the following hypothesis is suggested: a combination of ADP, emerging from erythrocytes, and catecholamines released from adrenergic vasoconstrictor nerves when the skin is cooled down, might stimulate platelets to aggregation in skin vessels and to production and release of pruritogenic factors.
描述了真性红细胞增多症（PV）中与温度相关的特征性瘙痒。触发因素似乎是皮肤温度的突然下降，例如在热水浴或淋浴后。瘙痒的突然发作和持续时间有限可能提示某些体液因子的激活或释放。在一项对照研究中，我们表明阿司匹林可缓解这种特殊的瘙痒。因此，考虑了前列腺素和血小板参与的可能性。发现血小板产生和释放的诸如PGE2和5-羟色胺等物质，在皮内注射时可引起健康志愿者的瘙痒，并且PGE2增强了皮肤对5-羟色胺的反应。血小板聚集研究未发现PV患者有任何异常，但ADP在体外显示可使血小板对肾上腺素诱导的聚集敏感。尽管未得到证实，但提出了以下假设：当皮肤冷却时，红细胞产生的ADP与肾上腺素能血管收缩神经释放的儿茶酚胺相结合，可能刺激血小板在皮肤血管中聚集，并产生和释放致痒因子。
