口服钙可以减轻登革热患者的血小板减少症。试点研究报告。

Jorge Isaac Cabrera-Cortina, Emilio Sánchez-Valdéz, Dora Cedas-DeLezama, María Dolores Ramírez-González
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引用次数: 0

摘要

全球气候变化是传染病在人群中流行暴发的策动和促成因素之一。2003年至2005年,墨西哥北部塔毛利帕斯州的坦皮科市反复爆发登革热病毒感染和由此引起的登革热。随着环境温度的升高,DF的标志性症状之一是血小板减少症。由于它是出血表现的标志,血小板减少症是监测感染患者病程的有用标志。细胞外钙(Ca2+ o)在血液凝固中起关键作用;体外与乙二胺四乙酸(EDTA)或柠檬酸盐螯合可防止凝血,而外源性血浆再钙化可缩短凝血时间。在体内,Ca2+ o对血小板功能和免疫反应的调节至关重要。在这项工作中,我们报告了一个显著的增长(p
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oral calcium administration attenuates thrombocytopenia in patients with dengue fever. Report of a pilot study.

Global climate change is one of the instigating and contributing factors for epidemic outbreaks of infectious diseases in human populations. In the years 2003 to 2005 the city of Tampico, in the northern state of Tamaulipas, Mexico, experienced recurrent outbreaks of dengue virus infections (DV) and the resulting dengue fever (DF). One of the hallmark symptoms of DF, which appears to worsen as the environmental temperature increases, is thrombocytopenia. In as much as it is a hallmark for hemorrhagic manifestations, thrombocytopenia is a useful sign to monitor the course of infected patients. Extracellular calcium (Ca2+ o) plays a key role in blood clotting; its chelation in vitro with ethylenediaminetetracetic acid (EDTA) or citrate prevents clotting, while exogenous recalcification of plasma leads to shortening of clotting time. In vivo, Ca2+ o is essential for platelet function and for the regulation of the immune response. In this work we report a significant increase (p<0.05) in the number of blood platelets of patients with clinical signs and symptoms of DF following oral administration of calcium carbonate (CAL, 1.2 to 1.8 g/day; n=10) when compared with a control group (CTL, n=10): 89 (46-132) versus 206 (155-257). Data expressed as mean value (95% confidence interval, C.I.) for x1000 cells/mm3. CAL also improved overall clinical condition and reduced by 36 % the duration of signs and symptoms of DF: 6.7-11.3 days, versus 11.5-16.6 days (95 % C.I., p<0.05) when compared with CTL patients. The possible mechanism of calcium attenuated thrombocytopenia and clinical improvement is discussed.

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