Abstract

The relationship involving acid-base imbalance, mineral metabolism and bone health status has previously been reported but the efficacy of the alkalizing supplementation in targeting acid overload and preventing bone loss has not yet been fully elucidated. In this randomized, double-blind, placebo-controlled study, the hypothesis that potassium citrate (K citrate) modifies bone turnover in women with postmenopausal osteopenia was tested. Three hundred and ten women were screened; 40 women met the inclusion criteria and were randomly assigned to the treatment or the placebo group. They were treated with K citrate (30 mEq day−1) or a placebo in addition to calcium carbonate (500 mg day−1) and vitamin D (400 IU day−1). At baseline and time points of 3 and 6 months, serum indicators of renal function, electrolytes, calciotropic hormones, serum bone turnover markers (BTMs) (tartrate-resistant acid phosphatase 5b (TRACP5b), carboxy-terminal telopeptide of type I collagen (CTX), bone alkaline phosphatase (BAP), procollagen type 1 N terminal propeptide (PINP)), and urine pH, electrolytes, and citrate were measured. The follow-up was completed by 17/20 patients in the “K citrate” group and 18/20 patients in the “placebo” group. At baseline, 90% of the patients exhibited low potassium excretion in 24 h urine samples, and 85% of cases had at least one urine parameter associated with low-grade acidosis (low pH, low citrate excretion). After treatment, CTX and BAP decreased significantly in both groups, but subjects with evidence of low-grade acidosis gained significant benefits from the treatment compared to the placebo. In patients with low 24h-citrate excretion at baseline, a 30% mean decrease in BAP and CTX was observed at 6 months. A significant reduction was also evident when low citrate (BAP: −25%; CTX: −35%) and a low pH (BAP: −25%; CTX: −30%) were found in fasting-morning urine. In conclusion, our results suggested that K citrate supplementation improved the beneficial effects of calcium and vitamin D in osteopenic women with a documented potassium and citrate deficit, and a metabolic profile consistent with low-grade acidosis.

Highlights

  • Bone mass tends to peak around the third decade of life, after which a continuous decline of0.7% per year is considered to be physiologic

  • It is associated with an increased rate of bone turnover, with an elevated number of active bone remodeling units (BRUs) in which the removal of bone by osteoclasts (OCs) prevails over the formation of bone matrix by osteoblasts (OBs) [3,4]

  • The imbalance between osteogenesis and bone resorption leads first to osteopenia and, subsequently, to osteoporosis, both characterized by decreased bone mineral density (BMD) (T-scores of

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Summary

Introduction

Bone mass tends to peak around the third decade of life, after which a continuous decline of0.7% per year is considered to be physiologic. Bone loss is accelerated and, on average, women lose approximately 5% of trabecular bone and 1.5% of the total bone mass per year [1]. Postmenopausal estrogen deficiency is considered to be the major cause of accelerated bone loss [2]. It is associated with an increased rate of bone turnover, with an elevated number of active bone remodeling units (BRUs) in which the removal of bone by osteoclasts (OCs) prevails over the formation of bone matrix by osteoblasts (OBs) [3,4]. The level of self-sufficiency is significantly decreased in 50% of women with hip fractures, and approximately 20% are candidates for long-term institutionalization [6]

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