Ohlen J, Richter J
Med Klin. 1976 Feb 13;71(7):292-9.
The isoenzymes of alkaline phosphatase were measured on admission to hospital, and then weekly over a 2 to 3 month period, in 40 patients presenting with uncomplicated acute hepatitis, 12 patients with cholestatic hepatitis, and 10 patients with histologically confirmed chronic persistent hepatitis. In acute uncomplicated hepatitis the increase in total alkaline phosphatase is not due to a cholestatic reaction of the damaged liver, but reflects the impaired catabolic capacity of the liver cells to degrade alkaline phosphatases from intestine and bone, as well as that of hepato-biliary origin. The isoenzyme distribution pattern is the same as found in normal healthy subjects. The increase in total alkaline phosphatase in patients with cholestatic hepatitis results from this impaired catabolic capacity for degradation of all isoenzymes, together with an increase in cholestatic reflux of hepato-biliary enzymes. In patients with chronic persistent hepatitis the raised total alkaline phosphatase activity at each point during the illness is due to this catabolic impairment of degradation of all isoenzymes. A cholestasis is not seen. The isoenzyme distribution pattern remains normal; only the enzyme activity due to the intestinal fraction, when compared with the acute hepatitis, is slightly, but significantly, raised.
对40例单纯性急性肝炎患者、12例胆汁淤积性肝炎患者和10例经组织学确诊的慢性持续性肝炎患者在入院时测定碱性磷酸酶同工酶,然后在2至3个月内每周测定一次。在单纯性急性肝炎中,总碱性磷酸酶升高并非由于受损肝脏的胆汁淤积反应,而是反映肝细胞降解来自肠道和骨骼的碱性磷酸酶以及肝胆源性碱性磷酸酶的分解代谢能力受损。同工酶分布模式与正常健康受试者相同。胆汁淤积性肝炎患者总碱性磷酸酶升高是由于所有同工酶降解的分解代谢能力受损,以及肝胆酶胆汁淤积反流增加。在慢性持续性肝炎患者中,疾病期间各点总碱性磷酸酶活性升高是由于所有同工酶降解的分解代谢受损。未观察到胆汁淤积。同工酶分布模式保持正常;与急性肝炎相比,仅肠道部分的酶活性略有但显著升高。