Ovarian hyperstimulation syndrome.
Ovarian hyperstimulation syndrome.
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DOI：
10.4103/0974-1208.86080
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发表时间：
2011-05
影响因子：
--
通讯作者：
Kumar M
中科院分区：
文献类型：
--
作者：
Kumar P;Sait SF;Sharma A;Kumar M
卵巢过度刺激综合征（OHSS）是辅助生殖技术的医源性并发症。该综合征的特征是卵巢囊性增大，由于毛细血管通透性增加和卵巢新生血管生成，液体从血管内转移到第三空间。它的发生取决于人绒毛膜促性腺激素（hCG）的施用。β-hCG及其类似物、雌激素、雌二醇、催乳素、组胺和前列腺素都与OHSS有关，但现在人们越来越清楚地认识到卵巢分泌的血管活性物质如白细胞介素、肿瘤坏死因子-α、内皮素-1和血管内皮生长因子（VEGF）与血管通透性增加有关。卵巢肿大会引起腹痛、恶心和呕吐。从卵泡中漏出液体，毛细血管通透性增加导致第三间隔（由于血管活性物质的释放），或卵泡直接破裂都可引起腹水。由于液体通过卵巢内外受损血管渗漏，大量液体从血管内床向第三隔室转移，导致血管内低血容量，并伴有水肿、腹水、胸水和/或心包水。低剂量促性腺激素方案已被实施，以降低多囊卵巢综合征患者生育治疗的风险。预防性给药白蛋白可能通过增加血浆致瘤压力和结合卵巢源介质来阻断OHSS的发展。拮抗剂方案的OHSS明显低于激动剂方案。卡麦角林部分抑制VEGF受体2磷酸化水平和相关的血管通透性，而不影响黄体血管生成，减少OHSS的“早期”发病（hCG后的前9天内）。为防止血栓形成，入院第一天开始皮下注射肝素5000-7500 U/d。这些病人需要一个医院病房，那里的临床情况很好理解，工作人员在治疗和随访方面具有专业知识。当出现严重的OHSS时，必须住进重症监护病房。
Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic complication of assisted reproduction technology. The syndrome is characterized by cystic enlargement of the ovaries and a fluid shift from the intravascular to the third space due to increased capillary permeability and ovarian neoangiogenesis. Its occurrence is dependent on the administration of human chorionic gonadotrophin (hCG). β-hCG and its analogs, estrogen, estradiol, prolactin, histamine and prostaglandins have all been implicated in OHSS but now it is increasingly better understood that the vasoactivesubstances such as interleukins, tumor necrosis factor-α, endothelin-1, and vascular endothelial growth factor (VEGF) secreted by the ovaries have been implicated in increasing vascular permeability. Enlargement of the ovaries causes abdominal pain, nausea and vomiting. Leakage of fluid from follicles, increased capillary permeability leading to third spacing (due to the release of vasoactive substances), or frank rupture of follicles can all cause ascites. Due to leakage of fluid through the impaired blood vessels both within and outside the ovary there is massive fluid-shift from the intra-vescular bed to the third compartment results in intravascular hypovolemia with concomitant development of edema, ascites, hydrothorax and/or hydropericardium. Low-dose gonadotrophin protocols have been implemented to reduce the risks of fertility treatment in polycystic ovary syndrome patients. Prophylactic albumin administration may interrupt the development of OHSS by increasing the plasma oncotic pressure and binding mediators of ovarian origin. OHSS is significantly lower in an antagonist protocol than in an agonist protocol. Cabergoline inhibits partially the VEGF receptor 2 phosphorylation levels and associated vascular permeability without affecting luteal angiogenesis reduces the ‘early’ (within the first 9 days after hCG) onset of OHSS. To prevent thrombosis, subcutaneous heparin 5000-7500 U/d is begun on the first day of admission. These patients need a hospital ward where the clinical picture is well understood and the personnel have expertise in its treatment and follow-up. Admission to an intensive care unit is necessary when critical OHSS develops.