Watts R W, Chalmers R A, Gibbs D A, Lawson A M, Purkiss P, Spellacy E
Q J Med. 1979 Apr;48(190):259-72.
The effects of some putative inhibitors of oxalate production or urinary oxalate excretion have been investigated in the Cynamolgus monkey and in patients with Type I primary hyperoxaluria (hyperoxaluria with glycollic aciduria). Sodium-1-hydroxybutan-sulphonate, D,L-phenyllactate, succinimide and isocarboxazide did not reduce the urinary oxalate excretion in the monkeys. Pyridoxine reduced the excretion of oxalate and glycollate in some patients, and its therapeutic use has been documented over a five-year period. Succinimide, which has been used by other workers for the treatment of non-hyperoxaluric stone formers, did not decrease the excretion of either oxalate or glycollate in three patients in whom it was tried. It did not change the inhibitory activity of the urine with respect to the growth and aggregation of calcium oxalate crystals in any of the three patients, and it did not have any consistent effect on the excretion of calcium oxalate crystals in the one patient who had detectable crystaluria before treatment. We have identified several metabolites of succinimide in the urine of patients taking the drug. These include 2,3-dehydrosuccinamic, 2-hydroxysuccinamic and 3-hydroxysuccinamic acids. Isocarboxazide, cholestyramine and thiamine did not affect the urinary oxalate excretion in the patients. The significance of these observations from the viewpoint of the treatment of primary hyperoxaluria is discussed.
已在食蟹猴和I型原发性高草酸尿症（伴乙醇酸尿症的高草酸尿症）患者中研究了一些假定的草酸生成抑制剂或尿草酸排泄抑制剂的作用。1-羟基丁烷磺酸钠、D,L-苯基乳酸、琥珀酰亚胺和异卡波肼并未降低猴子的尿草酸排泄。吡哆醇可降低部分患者草酸和乙醇酸的排泄，且其治疗用途已有五年的文献记载。其他研究人员曾用琥珀酰亚胺治疗非高草酸尿性结石形成者，但在三名试用该药物的患者中，它并未降低草酸或乙醇酸的排泄。在这三名患者中，它均未改变尿液对草酸钙晶体生长和聚集的抑制活性，且对一名治疗前可检测到结晶尿的患者的草酸钙晶体排泄也没有任何一致的影响。我们已在服用该药物的患者尿液中鉴定出琥珀酰亚胺的几种代谢产物。这些代谢产物包括2,3-脱氢琥珀酰胺酸、2-羟基琥珀酰胺酸和3-羟基琥珀酰胺酸。异卡波肼、考来烯胺和硫胺对患者的尿草酸排泄没有影响。本文讨论了这些观察结果对原发性高草酸尿症治疗的意义。
