Objective Few studies have systematically and quantitatively addressed the impact of urate‐lowering therapy on monosodium urate (MSU) deposits. This study was undertaken to analyze the effect of lifestyle measures and conventional urate‐lowering therapy on MSU deposits in patients with gout. Methods In this prospective study, subjects with gout according to the American College of Rheumatology/European League Against Rheumatism classification criteria and presence of MSU deposits seen on dual‐energy computed tomography (DECT) scans received either lifestyle intervention or conventional urate‐lowering therapy for a mean period of 18 months before a follow‐up DECT scan. Detected MSU deposits were quantified by volumetric measurement and validated by semiquantitative scoring, and baseline and follow‐up measurements were compared. Results Baseline and follow‐up DECT scans were available for all 83 subjects. Six subjects discontinued treatment, and 77 subjects underwent a lifestyle intervention (n = 24) or were treated with allopurinol (n = 29), febuxostat (n = 22), or benzbromarone (n = 2) over the entire observation period. The mean serum uric acid (UA) level decreased from 7.2 to 5.8 mg/dl in the overall population. In patients who discontinued treatment, no change in MSU deposits or serum UA levels was observed. The burden of MSU deposits significantly decreased in patients undergoing lifestyle intervention (MSU volume P = 0.007; MSU score P = 0.001), and in patients treated with allopurinol (MSU volume and score P < 0.001) or febuxostat (MSU volume P < 0.001; MSU score P = 0.001). No significant decline in MSU deposits was noted in patients who discontinued treatment. Conclusion These data show that lifestyle intervention and xanthine oxidase inhibitors significantly decrease the MSU deposit burden. Hence, conventional gout therapy not only lowers serum UA levels, but also reduces pathologic MSU deposits.
Objective. To characterize in detail the structural bone changes associated with the deposition of monosodium urate crystals in the first metatarsophalangeal (MTP1) joint in patients with tophaceous gout. Methods. Twenty patients with tophaceous gout and involvement of the MTP1 joint received both dual-energy computed tomography (DECT) of the feet for the detection of tophi and high-resolution peripheral quantitative computed tomography (HR-pQCT) of the feet for the detection of bone erosions and osteophytes. Demographic and clinical data were collected. Tophi in DECT and erosions and osteophytes in HR-pQCT were overlayed to define their anatomical relation. In addition, the feet of 20 sex-and age-matched healthy controls were scanned to define the normal architecture of the MTP1 joint. Results. Patients with gout had an increased number and extent of bone erosions and osteophytes compared with their healthy counterparts (
Background:Gout is based on the deposition of monosodium urate (MSU) crystals. While it is well established that life-style intervention and/or conventional urate lowering therapy can lead to a decrease in serum urate levels, the impact of such interventions to resolve already existing MSU deposits is very limited.Objectives:In this study we wanted to determine if and to what extent MSU deposits resolve if patients follow structured life-style intervention or continuously conventional urate lowering therapy.Methods:Subjects with diagnosis of gout and the presence of MSU deposits in the feet in baseline dual energy CT (DECT) scan, received either life-style intervention only (N=24) or additional conventional urate lowering therapy (allopurinol: N=29, febuxostat: N=22, benzbromarone N=2) for a mean period of 18 months before receiving a follow-up DECT examination. MSU deposits were quantified by volumetric measurement and semi quantitative scoring at baseline and follow up.Results:Serum uric acid (SUA) level decreased from 7.2±1.7 to 6.7±1.7mg/dl with life-style intervention; from 7.0±1.5 to 5.5±1.8mg/dl with allopurinol and from7.8±3.0 to 5.1 ± 2.5mg/dl with febuxostat. MSU volume significantly decreased in patients undergoing life-style intervention (baseline: 0,07cm3 ± 0,09; follow up: 0,05 ± 0,15cm3; p=0.007), treatment with allopurinol (0,11 ± 0.15 cm3 to follow up: 0.02 ± 0,04 cm3, p<0.001) or febuxostat (MSU volume baseline: 0.99 ± 2.8 to follow up: 0.64 ± 2.09; p=0.001). With respect to conversion from a DECT+ into a DECT- state, baseline MSU deposit burden, but not baseline SUA level or decrease in SUA level, was associated with reaching a DECT- state. Thus patients with smaller deposits were more likely to completely resolve the deposits.Conclusion:We show that both life-style intervention and conventional urate lowering drug therapy reduce the volume of monosodium urate deposits. The size of MSU deposits, but not serum urate level, was the main factor that influenced complete resolution of deposits. This finding reemphasizes that the burden of deposits essentially defines the likelihood and time for complete resolution of gout.References[1] Manger B, Lell M, Wacker J, Schett G, Rech J. Detection of periarticular urate deposits with dual energy CT in patients with acute gouty arthritis. Ann Rheum Dis. 2012;71(3):470-2.[2] Bongartz T, Glazebrook KN, Kavros SJ, Murthy NS, Merry SP, Franz WB, 3rd, et al. Dual-energy CT for the diagnosis of gout: an accuracy and diagnostic yield study. Ann Rheum Dis. 2015;74(6):1072-7.[3] Bayat S, Aati O, Rech J, Sapsford M, Cavallaro A, Lell M, et al. Development of a Dual-Energy Computed Tomography Scoring System for Measurement of Urate Deposition in Gout. Arthritis Care Res (Hoboken). 2016;68(6):769-75.Disclosure of Interests:Sara Bayat: None declared, Hanna Ellmann: None declared, Elizabeth Araujo: None declared, Bernhard Manger: None declared, Melanie Hagen: None declared, Arnd Kleyer Grant/research support from: Lilly, Consultant for: Lilly, Speakers bureau: Abbvie, Ale...
Background:Deposition of uric acid crystals cause an inflammatory reaction, which can lead to structural bone changes, if such deposits form adjacent to cortical bone [1, 2]. Both erosions and bony spurs can form in conjunction with tophus deposition. The exact spatial inter-relation between tophi and structural bone lesions in humans in vivo is not fully characterized.Objectives:To spatially relate structural bone changes (erosions, osteophytes) to the deposition of monosodium urate crystals in the first metatarsophalangeal (MTP1) joint in patients with tophaceous gout.Methods:Tophaceous gout patients with clinically detected tophi at the MTP1 joint underwent simultaneous dual energy computed tomography (DECT) and high-resolution peripheral quantitative computed tomography (HR-pQCT) of the feet. Tophi detected by DECT and erosions and osteophytes detected by HR-pQCT were overlayed to define their exact anatomical relation. Furthermore, feet of sex- and age-matched healthy controls (HC) were scanned to define the normal architecture of the MTP1 joint.Results:Gout patients (N=20) had significantly higher numbers (5 (0–17 vs. 1 (1– 2)) and volumes (45.32 mm3(7.26–550.32) vs. 0.82 mm3(0.15–21.8)) of bone erosions as well as significantly higher numbers (10.5 (0-26) vs. 1 (0-10)) and sizes of osteophytes (4.93 mm (0.77-7.19 mm vs. 0.93 mm (0.05-7.61 mm))than healthy controls (N=20). Erosions were in direct spatial relation to bone erosions, while osteophytic responses were more widespread and affected bone regions on the MTP1, which were not directly adjacent to tophi. Median tophus volume detected by DECT (0.12 mm3(0.01–2.53)) was associated with the total volume of erosions (r=0.597, p=0.005).Conclusion:This study demonstrates that bone changes in gout are substantial and not only include erosions but also widespread architectural bone remodeling associated osteophyte formation. While there is a direct spatial relation between tophi and bone erosions the anabolic bone responses in gout are more widespread.References:[1]Dalbeth, N. et al. Ann Rheum Dis. 2015 Jun;74(6):1030-6.[2]Dalbeth, N. et al. Arthritis Res Ther. 2012; 14(4): R165.Data are based on high-resolution peripheral quantitative computed tomography (HR-pQCT) of metatarsophalangeal joints I in gout patients (grey boxplots) and healthy controls (white boxplots). (A) number of bone erosions, (B) volume of bone erosions, (C) number of osteophytes and (D) size of osteophytes. Data are shown as medians and inter-quartile ranges (boxes).Distribution of (A) tophi based on dual-energy computed tomography (DECT) as well as (B) bone erosions and (C) osteophytes based on high-resolution peripheral quantitative computed tomography (HR-pQCT) of metatarsophalangeal (MTP) I head in gout patients. Data are shown for the different regions of the MTPI head including the plantar, medial, dorsal and lateral region of the metatarsal head, as well as the medial and lateral sesamoid bones. Data indicate percentage of patients with tophi, erosions and osteophytes in respective region.Disclosure of Interests:Sara Bayat Speakers bureau: Novartis, David Simon Grant/research support from: Else Kröner-Memorial Scholarship, Novartis, Consultant of: Novartis, Lilly, Caroline Pecherstorfer: None declared, Hanna Ellmann: None declared, Camille Figueiredo: None declared, Matthias Englbrecht: None declared, Axel Hueber Grant/research support from: Novartis, Lilly, Pfizer, EIT Health, EU-IMI, DFG, Universität Erlangen (EFI), Consultant of: Abbvie, BMS, Celgene, Gilead, GSK, Lilly, Novartis, Speakers bureau: GSK, Lilly, Novartis, Arnd Kleyer Consultant of: Lilly, Gilead, Novartis,Abbvie, Speakers bureau: Novartis, Lilly, Jürgen Rech Consultant of: BMS, Celgene, Novartis, Roche, Chugai, Speakers bureau: AbbVie, Biogen, BMS, Celgene, MSD, Novartis, Roche, Chugai, Pfizer, Lilly, Georg Schett Speakers bureau: AbbVie, BMS, Celgene, Janssen, Eli Lilly, Novartis, Roche and UCB
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