Jorde Rolf, Szumlas Kasia, Haug Egil, Sundsfjord Johan
Department of Internal Medicine, University Hospital of North Norway, 9038 Tromsø, Norway.
Eur J Nutr. 2002 Dec;41(6):258-63. doi: 10.1007/s00394-002-0383-1.
In patients with primary hyperparathyroidism (PHPT) a low calcium intake might cause increased bone loss and thus aggravate osteoporosis, and a high intake might increase serum calcium level and the risk of nephrolithiasis.
Generally, guidelines recommend a normal calcium intake, and accordingly, those with a low intake might benefit from a modest calcium supplementation. This hypothesis was tested in the present study.
Thirty-one patients with asymptomatic PHPT were recruited from an epidemiological study (The Tromsø study 1994/95). Those with a daily calcium intake below 450 mg were given calcium supplementation (500 mg Ca(2+)), and those with an intake above 450 mg were followed without supplementation. The study was open and lasted 1 year. Serum levels of calcium, PTH, 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D, urinary calcium excretion, blood pressure, and bone mineral density (BMD) were measured.
Three subjects dropped out without reason, 1 developed abdominal discomfort from the calcium supplementation, and 3 had an increase in serum calcium of more than 0.2 mmol/L and were therefore excluded. The latter three did not differ from the rest of the group at baseline. Of the remaining 24 that completed the study, 17 were given calcium. In this group there was a non-significant increase in serum calcium and urinary calcium excretion, a significant decrease in PTH after 4 weeks (13.2 (6.0) vs 9.4 (3.0) pmol/L, P < 0.05), and a significant increase in BMD at the femoral neck at the end of the study (0.849 (0.139) vs 0.870 (0.153) g/cm(2), P < 0.05). The blood pressure was not significantly affected.
Most patients with mild PHPT and a low calcium intake tolerate a moderate calcium supplement. This may have beneficial effects on the bones, but the patients must be followed carefully.
在原发性甲状旁腺功能亢进症(PHPT)患者中,低钙摄入可能会导致骨质流失增加,从而加重骨质疏松,而高钙摄入可能会提高血清钙水平和肾结石风险。
一般来说,指南推荐正常钙摄入量,因此,钙摄入量低的患者可能会从适度补钙中受益。本研究对这一假设进行了验证。
从一项流行病学研究(1994/95年特罗姆瑟研究)中招募了31例无症状PHPT患者。每日钙摄入量低于450毫克的患者给予补钙(500毫克钙),摄入量高于450毫克的患者不补钙进行随访。该研究为开放性研究,持续1年。测量血清钙、甲状旁腺激素(PTH)、25-羟维生素D3和1,25-二羟维生素D水平、尿钙排泄量、血压和骨密度(BMD)。
3名受试者无故退出,1名因补钙出现腹部不适,3名血清钙升高超过0.2毫摩尔/升,因此被排除。后三名在基线时与组内其他患者无差异。在完成研究的其余24名患者中,17名接受了补钙。该组血清钙和尿钙排泄量有不显著增加,4周后PTH显著降低(13.2(6.0)对9.4(3.0)皮摩尔/升,P<0.05),研究结束时股骨颈骨密度显著增加(0.849(0.139)对0.870(0.153)克/平方厘米,P<0.05)。血压未受到显著影响。
大多数轻度PHPT且钙摄入量低的患者能耐受适度补钙。这可能对骨骼有有益影响,但必须对患者进行密切随访。