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Abstract Number: 358

Bone Microstructure Assessed By Hrpqct in Subjects with Hyperuricemia without Arthritis

Roland Kocijan1, Arastoo Nia1, Christian Muschitz2, David Simon3, Corinna Geiger1, Judith Haschka4, Arnd Kleyer3, Sara Bayat5, Juergen Rech5, Annemarie Kocijan6, Larissa Dzirlo7, Monika Graninger7 and Heinrich Resch1, 1Medical Department II, Karl Landsteiner Society for Gastroenterology and Rheumatology, St. Vincent Hospital, Vienna, Austria, 2Medical Department II, St. Vincent Hospital, Vienna, Austria, 3Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany, 4Internal Medicine 3, Rheumatology and Immunology, University of Erlangen-Nuremberg, Erlangen, Germany, 5Department of Internal Medicine 3, Rheumatology & Immunology, University of Erlangen-Nuremberg, Erlangen, Germany, 6Optimal Essen e.U., Vienna, Austria, 7Medical Department III, St. Vincent Hospital, Vienna, Austria

Meeting: 2015 ACR/ARHP Annual Meeting

Date of first publication: September 29, 2015

Keywords: Bone, HR-pQCT, hyperuricemia and osteoporosis

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Session Information

Date: Sunday, November 8, 2015

Title: Osteoporosis and Metabolic Bone Disease - Clinical Aspects and Pathogenesis Poster

Session Type: ACR Poster Session A

Session Time: 9:00AM-11:00AM

Background/Purpose:

Gouty arthritis is a common inflammatory joint disorder and hyperuricemia (HU) is known to be the main risk factor. Beside clinical signs of inflammation such as pain and swelling, gout is associated with local bone loss. Higher serum uric acid concentrations correspond with higher bone mineral density (BMD), a lower prevalence of non-vertebral fractures and a lower bone turnover. Other inflammatory joint disorders such as rheumatoid arthritis (RA) and psoriatic arthritis (PsA) are associated with low BMD, altered bone microstructure and consequently secondary osteoporosis. To date there is no information about the influence of HU on bone microstructure. The objectives were to investigate trabecular and cortical bone microstructure, volumetric BMD (vBMD), bone turnover markers in female and male subjects with HU without signs and symptoms of arthritis and respective controls with low serum uric acid.

Methods:

Otherwise healthy male and female subjects with HU (uric acid>7.5 mg/dl) and respective controls with low serum uric acid (CO, uric acid<6.0 mg/dl) were included. Patients with known gouty arthritis, inflammatory disorders, osteoporosis, liver or kidney diseases were excluded.

Microstructure and vBMD were assessed by HR-pQCT (XtremeCT, SCANCO Medical, Brüttisellen, Switzerland) at the ultra-distal radius (standard non weight bearing bone site) in all subjects.

Total vBMD (Tot.BMD, mgHA/cm3), trabecular vBMD (Trab.BMD, mgHA/cm3) and cortical vBMD (Ct.BMD, mgHA/cm3) were evaluated. Microstructure analyses included the trabecular bone volume fraction (BV/TV), trabecular number (Tb.N, 1/mm), inhomogeneity of the trabecular network (Tb.1/N.SD, mm), trabecular thickness (Tb.Th, mm) and cortical thickness (Ct.Th, mm). Bone turnover markers including Cross Laps (CTX), reflecting osteoclast activity, Procollagen type 1 Amino-terminal Propeptide (P1NP), reflecting osteoblast activity, intact parathyroid hormone (iPTH), 25-hydroxyvitaminD(25-OH vitamin D), calcium and phosphate were measured. 

Results:

29 subjects with HU (57.4±10.1 years) and 15 CO (57.7±11.3) were analyzed. Serum uric acid was 8.9±1.4 mg/dl in HU and 4.4±1.0 mg/dl in CO. Body Mass Index (BMI, 30.0±6.4 vs. 26.9±6.1) was non-significantly different between HU and CO.

Similar results were found for Tot.BMD (p=0.590) and Ct.BMD (p=0.566). Trab.BMD differed by trend in HU (p=0.068) but not BV/TV (p=0.201), Tb.N, (p=0.071), inhomogeneity of trabecular network (p=0.227), Tb.Th (p=0.614) as well as Ct.Th (p=0.271).

Vitamin D levels, CTX, P1NP, calcium or phosphate were similar and within normal range in the two groups. iPTH levels were higher by trend in HU when compared to CO (p=0.053).

Conclusion:

Our results suggest similar volumetric bone mineral density and bone microstructure in subjects with HU and subjects with low serum uric acid levels. Despite the well-known negative effects of uric acid on local bone loss, HU does not seem to be a predictive factor for systemic bone loss. This is in contrast to other inflammatory joint diseases such as RA and PsA where systemic bone loss and changes in microarchitecture start before the onset of clinical disease.


Disclosure: R. Kocijan, None; A. Nia, None; C. Muschitz, None; D. Simon, None; C. Geiger, None; J. Haschka, None; A. Kleyer, None; S. Bayat, None; J. Rech, None; A. Kocijan, None; L. Dzirlo, None; M. Graninger, None; H. Resch, None.

To cite this abstract in AMA style:

Kocijan R, Nia A, Muschitz C, Simon D, Geiger C, Haschka J, Kleyer A, Bayat S, Rech J, Kocijan A, Dzirlo L, Graninger M, Resch H. Bone Microstructure Assessed By Hrpqct in Subjects with Hyperuricemia without Arthritis [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/bone-microstructure-assessed-by-hrpqct-in-subjects-with-hyperuricemia-without-arthritis/. Accessed .
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