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一、肝细胞性黄疸本型黄疸主要由于先天性缺陷和后天性受损害致肝脏对胆红素的摄取、结合和排泄产生不同程度的障碍,因而使两种胆红素(直接和间接的)均反流入血,但以单葡萄糖醛酸脂为主,间接胆红素和双葡萄糖醛酸脂较少。(一) 病因与机理1.Gilbert’s综合征:是原发性非溶血性非结合胆红素血症。由于正染色体显性遗传,使血浆中非结合胆红素转移到肝内减少(即摄取减少);其次是UDP葡萄糖醛酰转换酶也有所缺少,影响了胆红素结合。血浆胆红素是间接胆红素,一般不太高。仅占5mg%,也有高达18mg%。磺溴肽钠试验正常。多在青少年发病,亦可出生后便发病,本病是良性,非进行性,与活动性肝病或肝硬变无关。长期间歇性轻度黄疸。劳累、饮酒、感染、心衰、甲亢均可使黄疸加重。鉴别诊断应注意代偿性溶血性疾病,门—腔静脉吻合术后、甲亢和高山病。2.新生儿生理性黄疸:正常新生儿出世后3～5天内出现一时性黄疸,血浆非结合胆红素浓度3～10mg%。其机理可能是Y蛋白(Ligandin)和UDP葡萄糖醛酰转换酶延迟发育或发育未至成熟有关。致血
First, hepatocellular jaundice This type of jaundice mainly due to congenital defects and acquired damage to the liver due to the uptake of bilirubin, binding and excretion have varying degrees of obstacles, so that the two bilirubin (direct and indirect) Reflux into the blood, but glucuronide-based, indirect bilirubin and glucuronide less. (A) the etiology and mechanism 1. Gilbert’s syndrome: is a primary non-hemolytic non-conjugated bilirubin. Due to the positive inheritance of the autosomal dominant, the plasma unconjugated bilirubin transferred to the liver decreased (ie, reduced intake); followed by UDP glucuronyl acylase also lacking, affecting bilirubin binding. Plasma bilirubin is indirect bilirubin, generally not too high. Only 5mg%, also up to 18mg%. Sulfasalazine sodium test is normal. More incidence in adolescents, but also after the onset of the disease, the disease is benign, non-progressive, and active liver disease or cirrhosis has nothing to do. Long-term intermittent mild jaundice. Tired, drinking, infection, heart failure, hyperthyroidism can make jaundice increase. Differential diagnosis should pay attention to compensatory hemolytic disease, portal-vena cava anastomosis, hyperthyroidism and mountain sickness. 2. Newborn physiological jaundice: normal newborn 3 to 5 days after the birth of a temporary jaundice, plasma unconjugated bilirubin concentration of 3 ~ 10mg%. The mechanism may be Y protein (Ligandin) and UDP glucuronyl acyltransferase delayed development or development is not mature. Cause blood