儿科哮喘临床治疗的研究进展

儿童过敏性疾病包括很多种,过去几年其发病率在发达国家有所上升.这类疾病是一些有遗传倾向的儿童受环境因素而诱发,而现在对于这些环境因素仍不完全清楚.异位三合症（atopic triad）通常是指异位性皮炎、过敏性鼻炎和哮喘,患者常同时出现三种疾病的症状,并且一般由最初的异位性皮炎和食物过敏发展到过敏性鼻炎、环境过敏症和哮喘,我们将此过程称之为“遗传性过敏症进行曲”（atopic march）.     

Effects of interleukin-3 and granulocyte-macrophage colony-stimulating factor on thrombopoiesis in congenital amegakaryocytic thrombocytopenia

Amegakaryocytic thrombocytopenia (AMT) is a rare and often fatal disorder of infancy and childhood presenting with isolated thrombocytopenia that progresses to marrow failure. The defect in thrombopoiesis is not well understood nor is the etiology of the progressive marrow failure. No standard modality of treatment exists. Here, we evaluated the capacity of marrow cells isolated from five patients with AMT and progressive marrow failure to generate megakaryocyte progenitor cells (CFU-MK). These in vitro studies demonstrated assayable numbers of CFU-MK from all patient bone marrows that responded in vitro to the addition of interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), or the combination of both. These findings suggest that the defect in AMT might be partially correctable by the administration of these cytokines. A Phase I/II trial of in vivo administration of these same hematopoietins in the identical patients was conducted in which no significant toxicity was observed. IL-3 but not GM-CSF administration resulted in improved platelet counts in two patients and decreased bleeding and transfusion requirement in the remaining three. No clinical benefit was observed when GM-CSF was administered after IL-3 pretreatment. Prolonged IL-3 administration has resulted in platelet increases in an additional two patients. In vitro responsiveness of CFU- MK to either cytokine did not predict the degree of clinical response. Although the optimal dose and schedule of IL-3 either alone or in combination remains to be established, this study suggests that IL-3 may contribute to the treatment of patients with AMT.     

Regulation of hemodynamics and oxygenation in developing intestine: insight into the pathogenesis of necrotizing enterocolitis

The pathogenesis of necrotizing enterocolitis remains unknown, but various factors have been postulated including, but not limited to, mesenteric ischemia, enteral alimentation, and infection. Since an understanding of circulatory physiology in developing intestine may provide insight into the role of mesenteric ischemia in the etiology of necrotizing enterocolitis, this review summarizes what is currently known about the regulation of blood flow and oxygenation in developing intestine and how it differs from that in adult intestine. The discussion is divided into intrinsic versus extrinsic factors. Phenomena which may be used to evaluate the capacity for intrinsic vasoregulation include pressure-flow autoregulation, reactive hyperemia, venous hypertension, arterial hypoxemia, and postprandial hyperemia. Extrinsic factors include neurologic and hormonal influences. Additionally, the susceptibility for tissue hypoxia as a function of age and the correlation with subsequent development of mucosal injury are discussed