Pak Charles Y, Heller Howard J, Pearle Margaret S, Odvina Clarita V, Poindexter John R, Peterson Roy D
Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, Texas 75390-8885, USA.
J Urol. 2003 Feb;169(2):465-9. doi: 10.1097/01.ju.0000047341.55340.19.
We determined whether dietary restriction of calcium and oxalate, combined with thiazide and potassium citrate treatment, would prevent stone formation and avert bone loss in 18 men and 10 women with type I absorptive hypercalciuria.
Patients were treated with thiazide (20) or indapamide (8) and potassium citrate (average dose 35 mEq. daily) for 1 to 11 years (mean 3.7) while maintained on low calcium oxalate diet. Serum and urinary chemistry studies and bone mineral density were measured at baseline and at the end of treatment. New stones formed were quantitated during 3 years before and during treatment.
During treatment urinary calcium significantly decreased (346 +/- 85 to 248 +/- 79 mg. daily, p <0.001) but urinary oxalate did not change. Urinary pH and citrate significantly increased, and urinary saturation of calcium oxalate significantly decreased by 46%. Stone formation rate decreased significantly from 2.94 to 0.05 per year (p <0.001). L2-L4 bone mineral density increased significantly by 5.7% compared to normal peak value, and by 7.1% compared with normal age and gender matched value. Femoral neck bone mineral density also increased significantly.
Dietary restriction of calcium and oxalate, combined with thiazide and potassium citrate, satisfactorily controlled hypercalciuria, prevented the secondary increase in urinary oxalate, reduced urinary saturation of calcium oxalate, virtually eliminated recurrent stone formation, and increased bone density of the spine and femoral neck. Thus, this dietary pharmacological program controlled stone formation as well as bone loss that often accompany type 1 absorptive hypercalciuria.
我们确定了对于18名男性和10名女性I型吸收性高钙尿症患者，限制钙和草酸盐饮食并联合噻嗪类药物和枸橼酸钾治疗是否能预防结石形成并避免骨质流失。
患者接受噻嗪类药物（20例）或吲达帕胺（8例）及枸橼酸钾（平均每日剂量35 mEq）治疗1至11年（平均3.7年），同时维持低钙草酸盐饮食。在基线和治疗结束时测量血清和尿液化学指标以及骨密度。对治疗前3年和治疗期间形成的新结石进行定量分析。
治疗期间尿钙显著降低（从每日346±85 mg降至248±79 mg，p<0.001），但尿草酸盐未改变。尿pH值和枸橼酸盐显著升高，草酸钙的尿饱和度显著降低46%。结石形成率从每年2.94显著降至0.05（p<0.001）。与正常峰值相比，L2-L4骨密度显著增加5.7%，与正常年龄和性别匹配值相比增加7.1%。股骨颈骨密度也显著增加。
限制钙和草酸盐饮食，联合噻嗪类药物和枸橼酸钾，可令人满意地控制高钙尿症，防止尿草酸盐继发性增加，降低草酸钙的尿饱和度，几乎消除复发性结石形成，并增加脊柱和股骨颈的骨密度。因此，这种饮食药理学方案可控制结石形成以及I型吸收性高钙尿症常伴随的骨质流失。
