[Pyridoxine can normalize oxaluria in idiopathic renal lithiasis].
[Pyridoxine can normalize oxaluria in idiopathic renal lithiasis].
复制标题
[吡哆醇可使特发性肾结石患者的草酸尿正常化]。
作者：
P. Jaeger;L. Portmann;A. Jacquet;P. Burckhardt
原发性I型高草酸尿患者服用吡哆醇（维生素B6），由于刺激乙醛酸盐转化为甘氨酸而不是草酸盐，通常会导致尿中草酸盐排泄减少。然而，目前尚不清楚吡哆醇是否会同样影响其他原因的高草酸血症，例如特发性或肠性。因此，两组患者口服吡哆醇2个月（300 mg/d）。第一组包括10例特发性结石患者，伴有不明原因的轻度高草酸尿。第二组为4例肠分流术后肠内高血氧症患者。平均而言，肠道高草酸尿不受维生素B6的影响，这表明这种疾病是肠道对草酸盐而不是乙醛酸盐过度吸收的结果。相反，特发性高草酸尿受维生素B6的影响：10例患者中有8例草酸尿量减少，7例恢复正常。然而，两名患者对吡哆醇没有反应；两例患者均伴有严重的高尿酸血症（大于1克/24小时），观察结果表明，在这些病例中，高尿酸血症是由饮食引起的。4例在吡啶醇治疗后尿草酸排泄恢复正常的患者在治疗后随访8 ~ 36个月，所有患者草酸排泄均保持正常。草酸尿恢复到正常上限的患者在2年后恢复，尿草酸再次下降。结论：特发性高草酸血症患者给予吡哆醇可以纠正疾病，如原发性I型高草酸血症；这与肠性高血氧症不同。控制这种对维生素B6的敏感性的机制仍有待澄清。
Pyridoxine (vitamin B6), given to patients with primary hyperoxaluria of type I, generally leads to a decrease in urinary excretion of oxalate owing to stimulation of conversion of glyoxylate to glycine instead of oxalate. It is not known, however, whether pyridoxine would equally influence hyperoxalurias of other origins, e.g. idiopathic or enteric. Two groups of patients were therefore given pyridoxine orally for 2 months (300 mg/d). Group 1 consisted of 10 idiopathic stone formers with mild hyperoxaluria of unknown origin. Group 2 consisted of 4 patients with enteric hyperoxaluria after intestinal bypass surgery. As a mean, enteric hyperoxaluria was not influenced by vitamin B6, which suggests that this disorder is the consequence of intestinal hyperabsorption of oxalate rather than of glyoxylate. In contrast, idiopathic hyperoxaluria was influenced by vitamin B6: urinary excretion of oxalate decreased in 8 patients out of 10 and became normal in 7. However, two patients did not respond to pyridoxine; both had concomitant severe hyperuricosuria (greater than 1 g/24 h), an observation suggesting that in these cases hyperoxaluria was of dietary origin. Four of the patients whose urinary excretion of oxalate became normal while on pyridoxine were followed up for 8 to 36 months after treatment: in all of them oxaluria remained normal. One whose oxaluria had returned to the upper normal limit was retreated after 2 years and again displayed a fall in urinary oxalate. It is concluded that pyridoxine given to idiopathic hyperoxalurics may correct the disorder, as in primary hyperoxaluria of type I; this is not the case in enteric hyperoxaluria. The mechanisms governing this sensitivity to vitamin B6 remain to be clarified.