del Giglio A, Zukiwski A A, Ali M K, Mavligit G M
Department of Clinical Immunology and Biological Therapy, University of Texas M.D. Anderson Cancer Center, Houston 77030.
Cancer. 1991 May 15;67(10):2459-61. doi: 10.1002/1097-0142(19910515)67:10<2459::aid-cncr2820671011>3.0.co;2-l.
Twenty-two patients with liver metastases received 45 courses of recombinant tumor necrosis factor (rTNF) by hepatic arterial infusion in doses ranging from 12.5 to 175 micrograms/m2/d for 5 days by continuous infusion. The induction of statistically significant, dose-related, severe, albeit transient, hypophosphatemia (less than 1.0 mg/dl) associated with clinically significant, right-sided myocardial dysfunction and severe lassitude was observed. These side effects were promptly reversed after rTNF was stopped and intravenous phosphate supplementation was started. As no significant or consistent increase in urinary phosphate excretion was detected, the rTNF-induced hypophosphatemia probably resulted from an intracellular shift of phosphate. Since tumor regression was clearly associated with the lowest levels of serum phosphate, hypophosphatemia may be important in the antitumor effects of rTNF.
22例肝转移患者通过肝动脉输注接受了45个疗程的重组肿瘤坏死因子（rTNF）治疗，持续输注5天，剂量范围为12.5至175微克/平方米/天。观察到诱导出具有统计学意义的、与剂量相关的、严重的（尽管是短暂的）低磷血症（低于1.0毫克/分升），伴有具有临床意义的右侧心肌功能障碍和严重乏力。在停用rTNF并开始静脉补充磷酸盐后，这些副作用迅速得到逆转。由于未检测到尿磷排泄有显著或持续增加，rTNF诱导的低磷血症可能是由于磷向细胞内转移所致。由于肿瘤消退显然与血清磷酸盐的最低水平相关，低磷血症可能在rTNF的抗肿瘤作用中起重要作用。
