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  • 期刊

Risk Factors of Cholestasis in Very Low-Birth-Weight Infants

極低出生體重嬰兒之膽汁鬱積性黃疸:危險因子之分析

摘要


爲了解極低出生體重嬰兒之膽汁鬱汁積性黃疸的發生率、病程以及可能的致病原因,我們回溯性的研究143位出生體重在1500公克以下的嬰兒。我們定義直接膽紅素值高於2mg/dL且持續超過十四天的爲膽汁鬱汁積性黃疸,每個個案所有可能和膽汁鬱汁積性黃疸有關的孌數以及整個前不見古人程均加以登錄,而後用統計方法分析那些變數與膽汁鬱汁積性黃疸的發生及嚴重程度有關?我們的研究中發現卅一例(21.7%)出現膽汁鬱汁積性黃疸,平均發生的年齡是30.3(±15.3)天,或是開始靜脈營養法後的26.0(±15.6)天,平均黃疸持續的時間是77.1(±33.8)天。在發生膽汁鬱汁積性黃疸的個案中有一半即使停止使用靜脈營養法之後,其膽紅素的值依然會持續睦昇一段時間。有一個個案甚至於發生肝硬化的問題而最後死於肝衰竭,有兩例在死前其黃疸的現象持續加重,最後的廿八則最後黃疸消失。在多變數統計分析後我們發現出生體重與禁食的總日數和膽汁鬱汁積性黃疸的發生與否有關,敗血症的發生則與膽汁鬱汁積性黃疸的嚴重程度有關。我們的研究發現膽汁鬱汁積性黃疸在極低出生體重嬰兒是一個常見的併發症,雖然絕大多數的黃疸均會慢慢消失,但是我們並沒有長期的追蹤資料可以證明膽汁鬱汁積性黃疸是絕對無害的。不成熟的肝臓功能、缺乏腸道蠕動的刺激以及賀爾蒙的分泌會使疸汁流下降,而敗血症會破壞膽小管的分泌及加重膽汁鬱汁積性黃疸的程度。

並列摘要


To evaluate the incidence, clinical course, and possible risk factors of cholestasis in very low-birth-weight infants. A retrospective study of 143 very low-birth-weight infants was performed. Cholestasis was defined as direct-reacting bilirubin>2 mg/dL for more than 14 days. The clinical course of cholestasis was described, and perinatal risk factors were evaluated for associations with the development and severity of cholestasis. Cholestasis was present in 31 infants (21.7%). The mean (SD) age of onset was 30.3(15.3) days after birth or 26.0 (15.6) days after receiving parenteral nutrition, and the mean (SD) duration was 77.1 (33.8) days. In half of the cholestatic infants, bilirubin continued to rise after discontinuing parenteral nutrition. One infant developed signs of liver cirrhosis and died, two infants died with progressive cholestasis, while the other 28 patients recovered. Analysis of risk factors revealed that birthweight and duration of fasting significantly correlated with the development of cholestasis, and that sepsis significantly influenced the severity of cholestasis. Cholestasis is a common complication of extreme prematurity. The clinical course seems benign but long-term sequelae are unknown. Immature liver function and absence of stimuli for intestinal motility and hormonal secretion predispose to decreased bile flow, while sepsis further impairs hepatic ductular secretion and aggravates cholestasis.

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