Bone histology and hyperparathyroidism.

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Abstract

[Indexed for MEDLINE] 20. Nutrients. 2019 Sep 5;11(9):2111. doi: 10.3390/nu11092111. The Paradoxical Role of Uric Acid in Osteoporosis. Lin KM(1), Lu CL(2), Hung KC(3), Wu PC(4), Pan CF(5), Wu CJ(6), Syu RS(7), Chen JS(8), Hsiao PJ(9)(10)(11), Lu KC(12). Author information: (1)Division of Nephrology, Department of Medicine, Mackay Memorial Hospital, Taipei 10449, Taiwan. icekumo@yahoo.com.tw. (2)Division of Nephrology, Department of Medicine, Fu Jen Catholic University Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 24352 Taiwan. janlin0123@gmail.com. (3)Division of Nephrology, Department of Medicine, Min-Sheng General Hospital, Taoyuan City 33044, Taiwan. corey926@gmail.com. (4)Division of Nephrology, Department of Medicine, Mackay Memorial Hospital, Taipei 10449, Taiwan. ivorie3@gmail.com. (5)Division of Nephrology, Department of Medicine, Mackay Memorial Hospital, Taipei 10449, Taiwan. pan530319@yahoo.com.tw. (6)Division of Nephrology, Department of Medicine, Mackay Memorial Hospital, Taipei 10449, Taiwan. wcjyali@yahoo.com.tw. (7)Division of Nephrology, Department of Medicine, Min-Sheng General Hospital, Taoyuan City 33044, Taiwan. M001324@e-ms.com.tw. (8)Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan. dgschen@vghks.gov.tw. (9)Division of Nephrology, Department of Medicine, Fu Jen Catholic University Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 24352 Taiwan. a2005a660820@yahoo.com.tw. (10)Division of Nephrology, Department of Internal Medicine, Taoyuan Armed Forces General Hospital & Tri-Service General Hospital, National Defense Medical Center, Taipei 32551, Taiwan. a2005a660820@yahoo.com.tw. (11)Department of Life Sciences, National Central University, Taoyuan City 32001, Taiwan. a2005a660820@yahoo.com.tw. (12)Division of Nephrology, Department of Medicine, Fu Jen Catholic University Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 24352 Taiwan. kuochenglu@gmail.com. Because of its high prevalence worldwide, osteoporosis is considered a serious public health concern. Many known risk factors for developing osteoporosis have been identified and are crucial if planning health care needs. Recently, an association between uric acid (UA) and bone fractures had been explored. Extracellular UA exhibits antioxidant properties by effectively scavenging free radicals in human plasma, but this benefit might be disturbed by the hydrophobic lipid layer of the cell membrane. In contrast, intracellular free oxygen radicals are produced during UA degradation, and superoxide is further enhanced by interacting with NADPH oxidase. This intracellular oxidative stress, together with inflammatory cytokines induced by UA, stimulates osteoclast bone resorption and inhibits osteoblast bone formation. UA also inhibits vitamin D production and thereby results in hyper-parathyroidism, which causes less UA excretion in the intestines and renal proximal tubules by inhibiting the urate transporter ATP-binding cassette subfamily G member 2 (ABCG2). At normal or high levels, UA is associated with a reduction in bone mineral density and protects against bone fracture. However, in hyperuricemia or gout arthritis, UA increases bone fracture risk because oxidative stress and inflammatory cytokines can increase bone resorption and decrease bone formation. Vitamin D deficiency, and consequent secondary hyperparathyroidism, can further increase bone resorption and aggravated bone loss in UA-induced osteoporosis. DOI: 10.3390/nu11092111 PMCID: PMC6769742