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一名青少年男性因慢性低钠血症导致的脆性骨折和可逆性骨质减少。

Fragility fractures and reversible osteopaenia due to chronic hyponatraemia in an adolescent male.

作者信息

Patel Mital, Ayus Juan Carlos, Moritz Michael L

机构信息

Pediatrics, UPMC Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, USA.

Medicine, Renal Consultants of Houston, Houston, Texas, USA.

出版信息

BMJ Case Rep. 2019 Jul 27;12(7):e229875. doi: 10.1136/bcr-2019-229875.

Abstract

Fragility fractures are common in older adults and rare in children. Recent studies have demonstrated that hyponatraemia is a novel risk factor for the development of osteoporosis and hip fractures in older people. Animal studies suggest that hyponatraemia can lead to decreased bone mineral density by stimulating osteoclastic activity in order to mobilise sodium from the bone. Reported is a 16-year-old man with intractable epilepsy and an 11-year history of chronic hyponatraemia (126-135 mEq/L) due to valproic acid induced syndrome of inappropriate antidiuresis who sustained low-impact fragility fractures and had evidence of osteopaenia on both X-ray and dual energy X-ray absorptiometry (DEXA). Hyponatraemia resolved following the discontinuation of valproic acid and bone mineral density normalised on a repeat DEXA 19 months later. This case provides evidence supporting the contention that chronic hyponatraemia contributes to osteopaenia and fragility fractures and that the bone abnormalities are potentially reversible following the correction of hyponatraemia.

摘要

脆性骨折在老年人中很常见,在儿童中则很少见。最近的研究表明,低钠血症是老年人骨质疏松症和髋部骨折发生的一个新的危险因素。动物研究表明,低钠血症可通过刺激破骨细胞活性以从骨骼中动员钠,从而导致骨密度降低。本文报告了一名16岁男性,患有难治性癫痫,因丙戊酸诱发抗利尿激素分泌失调综合征而有11年慢性低钠血症病史(126 - 135 mEq/L),该患者发生了低能量脆性骨折,并且在X线和双能X线吸收法(DEXA)检查中均有骨质减少的证据。停用丙戊酸后低钠血症得到缓解,19个月后复查DEXA时骨密度恢复正常。该病例提供了证据,支持慢性低钠血症导致骨质减少和脆性骨折这一观点,并且低钠血症纠正后骨骼异常可能是可逆的。

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