Griffiths J, Vernocchi A, Simoni E
Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, USA.
Arch Pathol Lab Med. 1995 Sep;119(9):784-9.
To evaluate serum alkaline phosphatase (ALP) isoenzymes, using a sensitive electrofocusing technique, in transient hyperphosphatasemia of infancy and childhood.
Randomized study of infants and children who provided serum samples when an unusual magnitude of total ALP activity was noted.
Reference enzyme laboratories in Gorizia and Bergamo (Italy) and in Charleston, SC (USA).
A total of 135 infants and children noted to have markedly increased total ALP activity.
Recognition of the disease pathogenesis with appropriate treatment instituted.
Three groups of patients were identified: (1) previously healthy patients who showed additional laboratory evidence of viral and protozoal infection, in whom the ALP isoenzyme pattern reflected the primary target organ(s) of the infection; (2) patients with clinical evidence of failure to thrive due to preexisting disease, along with a superimposed infection (the ALP isoenzyme pattern reflected the specific infection and fractions associated with the primary disease); and (3) patients exhibiting failure to thrive (nonorganic or caloric deficit) who did not show evidence of infection. The total ALP in the third group was lower than in the other groups, was of hepatic and bone origin, and decreased when a positive caloric balance was established.
We examined several mechanisms to explain the hyperphosphatasemia. A perplexing question remains: Will a small group of infants and children respond to infection with this magnitude of ALP activity? Conversely, do all children respond, but a small number fortuitously undergo laboratory measurements that include ALP levels?
采用灵敏的电聚焦技术评估婴幼儿期和儿童期短暂性高磷酸酶血症患者的血清碱性磷酸酶(ALP)同工酶。
对总ALP活性异常升高时提供血清样本的婴幼儿和儿童进行随机研究。
意大利戈里齐亚和贝加莫以及美国南卡罗来纳州查尔斯顿的参考酶实验室。
总共135名婴幼儿和儿童,其总ALP活性显著升高。
通过适当治疗确定疾病发病机制。
确定了三组患者:(1)既往健康的患者,有病毒和原生动物感染的其他实验室证据,其ALP同工酶模式反映了感染的主要靶器官;(2)因原有疾病伴发感染而有生长发育迟缓临床证据的患者(ALP同工酶模式反映了特定感染以及与原发疾病相关的组分);(3)表现出生长发育迟缓(非器质性或热量不足)但无感染证据的患者。第三组患者的总ALP低于其他组,来源于肝脏和骨骼,在建立正热量平衡时降低。
我们研究了几种解释高磷酸酶血症的机制。一个令人困惑的问题仍然存在:一小部分婴幼儿和儿童会对感染产生如此程度的ALP活性反应吗?反之,所有儿童都会有反应,但只有少数儿童偶然接受了包括ALP水平在内的实验室检测吗?