scholarly journals Prominent Inflammatory Features of Monocytes/Macrophages in Acute Calcium Pyrophosphate Crystal Arthritis: a Comparison with Acute Gouty Arthritis

2019 ◽  
Vol 19 (3) ◽  
Author(s):  
Ji Hye Jeong ◽  
Jae Hyung Jung ◽  
Jung Sun Lee ◽  
Ji Seon Oh ◽  
Yong-Gil Kim ◽  
...  
2019 ◽  
Author(s):  
N Lawrence Edwards

The destructive potential of intracellular crystals has been recognized for over a century. The mechanisms by which crystals induce inflammation and bone and cartilage destruction have been elucidated over the past decade. The three most common crystal-induced arthropathies are caused by precipitation of monosodium urate monohydrate, calcium pyrophosphate dihydrate (CPP) and basic calcium phosphate. The definition, epidemiology, pathogenesis and etiology, diagnosis, and treatment of gout and CPP crystal deposition are reviewed, as well as the clinical stages of gout (i.e., acute gouty arthritis, intercritical gout, advanced gout, nonclassic presentations of gout, and other conditions associated with gout). Also reviewed are the clinical manifestations of calcium pyrophosphate dihydrate deposition disease (CPPD), such as asymptomatic CPPD, osteoarthritis with CPPD, acute CPP crystal arthritis, and chronic CPP crystal inflammatory arthritis. Figures illustrate renal transport of urate, monosodium urate crystals, acute gouty flare, advanced gouty arthritis, gouty synovial fluid, radiographic changes of advanced gout, ultrasound appearance of the femoral intercondylar cartilage, pharmacologic management of gout, the effect of gender and age on knee chondrocalcinosis, radiographs of chondrocalcinosis, and compensated polarized microscopy of CPPD. Tables present the major factors responsible for hyperuricemia, characteristics of classic gouty flares, antiinflammatory therapy for gout, and urate-lowering therapy. This chapter contains 90 references. This review contains 11 figures, 12 tables, and 88 references. Keywords: acute gouty arthritis, intercritical gout, advanced gout, asymptomatic CPPD, osteoarthritis with CPPD, acute CPP crystal arthritis, chronic CPP crystal inflammatory arthritis


2019 ◽  
Author(s):  
N Lawrence Edwards

The destructive potential of intracellular crystals has been recognized for over a century. The mechanisms by which crystals induce inflammation and bone and cartilage destruction have been elucidated over the past decade. The three most common crystal-induced arthropathies are caused by precipitation of monosodium urate monohydrate, calcium pyrophosphate dihydrate (CPP) and basic calcium phosphate. The definition, epidemiology, pathogenesis and etiology, diagnosis, and treatment of gout and CPP crystal deposition are reviewed, as well as the clinical stages of gout (i.e., acute gouty arthritis, intercritical gout, advanced gout, nonclassic presentations of gout, and other conditions associated with gout). Also reviewed are the clinical manifestations of calcium pyrophosphate dihydrate deposition disease (CPPD), such as asymptomatic CPPD, osteoarthritis with CPPD, acute CPP crystal arthritis, and chronic CPP crystal inflammatory arthritis. Figures illustrate renal transport of urate, monosodium urate crystals, acute gouty flare, advanced gouty arthritis, gouty synovial fluid, radiographic changes of advanced gout, ultrasound appearance of the femoral intercondylar cartilage, pharmacologic management of gout, the effect of gender and age on knee chondrocalcinosis, radiographs of chondrocalcinosis, and compensated polarized microscopy of CPPD. Tables present the major factors responsible for hyperuricemia, characteristics of classic gouty flares, antiinflammatory therapy for gout, and urate-lowering therapy. This chapter contains 90 references. This review contains 11 figures, 12 tables, and 88 references. Keywords: acute gouty arthritis, intercritical gout, advanced gout, asymptomatic CPPD, osteoarthritis with CPPD, acute CPP crystal arthritis, chronic CPP crystal inflammatory arthritis


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 457.1-457
Author(s):  
A. Sargsyan ◽  
V. Vardanyan ◽  
K. Ginosyan ◽  
S. Vardanyan ◽  
V. Mukuchyan

Background:Gouty arthritis is a common, potentially disabling and increasingly prevalent disease [1]. The main goals of treatment are to treat acute arthritis, decrease uric acid (UA) levels and prevent occurrence of further attacks. According to 2016 updated EULAR evidence-based recommendations for the management of gout, the most common and efficient options include prescription of colchicine (up to 6 mg during the first day) and intra-articular injections of glucocorticoids (GC) [2]. First option often causes diarrhea, the latter is extremely traumatic and painful in this group of patients.Objectives:The aim of this study was to determine the efficacy of sustainability of anti-inflammatory effect of combination of low dose colchicine with sporadic intramuscular injections of betamethasone in the treatment of acute gouty arthritis.Methods:41 treatment naïve patients with acute gouty arthritis (27 male /65,9 %/, 14 female /34,1 %/, mean age 55,9 ± 13,7 years, mean disease duration 5,9 ± 4,4 years) were recruited in the study. On the first visit all the patients were prescribed 1.5 mg of colchicine per day and 2 intramuscular injections of betamethasone preparation (7mg-1ml) with an interval of 4 days. On the second visit (30thday) daily dose of colchicine was decreased to 1.0 mg, urate-lowering therapy (ULT) was begun. 21 patients (51,2%) received febuxostat 80 mg/day, 20 patients (48,8%) – allopurinol 100-150 mg/day.Routine investigation included accurate collection of disease history, objective examination with determining the disease activity (Gout Activity Score /GAS/) and visual analogue scale (VAS patient), CBC, CRP, measurement of serum UA and creatinine level, urinalysis and other examinations [4]. GAS, VAS, CRP and uric acid were measured 3 times: at baseline, on 30thand 60thday of follow-up period.Results:Investigation had shown the following results at baseline: sUA1- 9,2 ± 1,5 mg/dl, CRP1- 24,3 ± 21,5 mg/L, VAS1- 8,3 ± 1,3 cm, GAS16,3 ± 0,7. All enrolled patients completed 60 days of treatment. Preparations were well tolerated, no serious adverse events occurred: mild dyspepsia was observed in 4 (9,8%) patients, mild hypertension – in 7 (17,1%), 10 (24,4%) patients had transient diarrhea. Only in 14 out of 41 patients (34,1 %) there was a necessity to add NSAIDs to the main scheme of treatment.On the second visit (30thday) all investigated measures with exception for UA (sUA2- 8,8 ± 1,9 mg/dl, p>0.05) had shown significantly lower results: CRP2- 4,9±3,5 mg/dl, VAS2– 4,2±1,2 cm, GAS2- 4,9 ± 0,7 (p<0.001).On the third visit (60thday) the following results were obtained: sUA3- 4,7 ± 1,3 mg/dl, CRP3- 3,5±2,0 mg/L, VAS3- 3,3±2,1 cm, GAS3- 3,7±0,9. All the measures were significantly lower than at baseline (p<0,001).During all the follow-up period recurrent attacks of arthritis were observed in 6 patients (14,6%), particularly, only 2 patients experienced arthritis after the prescription of ULT.Conclusion:Low dose colchicine in combination with sporadic (1-2) intramuscular injections of betamethasone can present as an efficient, non-traumatic, safe and cost-effective option for the treatment of acute gouty arthritis. Moreover, according to results of our study, anti-inflammatory effect was stable even after the prescription of ULT.References:[1]Kuo C-F, Grainge MJ, Zhang W, et al. Global epidemiology of gout: prevalence, incidence and risk factors. Nat Rev Rheumatol 2015;11:649–62. doi:10.1038/nrrheum.2015.91[2]Richette P, et al. 2016 updated EULAR evidence-based recommendations for the management of gout Ann Rheum Dis 2017;76:29–42. doi:10.1136/annrheumdis-2016-209707[3]Scirè, Carlo A et al. “Development and First Validation of a Disease Activity Score for Gout.” Arthritis care & research vol. 68,10 (2016): 1530-7. doi:10.1002/acr.22844Disclosure of Interests: :None declared


2015 ◽  
Vol 30 (6) ◽  
pp. 700 ◽  
Author(s):  
Kwang-Hoon Lee ◽  
Sang-Tae Choi ◽  
Soo-Kyung Lee ◽  
Joo-Hyun Lee ◽  
Bo-Young Yoon

2004 ◽  
Vol 14 (4) ◽  
pp. 306-308 ◽  
Author(s):  
Aliye Kapukıran Tosun ◽  
Nadide Torlak Koca ◽  
Gülçin Kaymak Karataş

2021 ◽  
Vol 16 ◽  
Author(s):  
Doaa M. Abdullah ◽  
Soad L. Kabil

Background: Gout is a metabolic disease strictly related to hyperuricemia. The associated intense inflammation and pain are triggered by the deposited monosodium urate crystals (MSU) in joints. The principal therapeutic strategies of gout involve the control of hyperuricemia and anti-inflammatory medications. Objectives: This study aimed to investigate the possible beneficial effects of ozone therapy, a well-known antioxidant, and an immunomodulation, on gouty arthritis and the underlying mechanisms. Methods : Acute gouty arthritis was induced in male albino rats via MSU crystals intra-articular injection in the ankle joint. The gouty arthritic rats received pre-treatment with ozone, colchicine (as a reference drug), or combination. Results : The obtained results of ozone therapy showed obvious reduction in the degree of ankle edematous swelling, pro-inflammatory cytokines, lipid peroxidation, the nucleotide binding oligomerization domain like receptor containing pyrin domain 3 (NLRP3), procaspase-1, caspase-1, interleukin-1β synovial tissue levels with enhancement of antioxidant defense system. Additionally, ozone therapy significantly attenuated the histological derangements in gouty arthritic rats. Conclusion : This study suggests that ozone is able to treat gouty arthritis and reducing synovial injury through an anti-inflammatory effect as well as antioxidant activity.


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