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Gout
Published in Charles Theisler, Adjuvant Medical Care, 2023
Vitamin C may reduce the risk of developing gout in men. One strategy to prevent gout attacks is to reduce the amount of uric acid in the body by promoting its excretion in the urine. One study found that men who had the highest vitamin C intake were up to 45% less likely to develop the painful condition than those who had the lowest.11
Rheumatology
Published in Kristen Davies, Shadaba Ahmed, Core Conditions for Medical and Surgical Finals, 2020
Risk factors for developing gout include obesity, alcohol intake, drugs that increase plasma urate levels (thiazide diuretics, aspirin), hypertension, renal failure/impairment, diabetes mellitus, hyperlipidaemia, vascular disease, lead intoxication and conditions that cause overproduction of uric acid such as malignancy, myeloproliferative disorders and Lesch–Nyhan syndrome.
Obesity
Published in Geoffrey P. Webb, Nutrition, 2019
Weight loss is also an accepted part of the treatment for hypertension and gout. Gout is the painful joint condition caused by crystals of uric acid forming in the joints when blood uric acid levels are elevated.
Appraisal of anti-gout potential of colchicine-loaded chitosan nanoparticle gel in uric acid-induced gout animal model
Published in Archives of Physiology and Biochemistry, 2022
Poonam Parashar, Ifrah Mazhar, Jovita Kanoujia, Abhishek Yadav, Pranesh Kumar, Shubhini A. Saraf, Sudipta Saha
Prehistoric Babylon documented gout as a painful illness. Gout is a metabolic disorder (acute arthritis) which causes joint inflammation (Singh et al.2017). The inflammation is triggered by tiny needle shaped crystals of uric acid that accumulates mostly in joints, which is comprehensively associated with hyperuricaemia (Martinon 2010, Singh et al. 2017). Hyperuricaemia is caused due to metabolic disorder of purine leading to distressing conditions like arthritis, tophi (deposit of uric acid crystals) and kidney stones (Mohamed and Al-Okbi 2008). Affected areas include toe, foot, ankle, knee, wrist, finger and elbow since uric acid tends to crystallise in cooler parts of the body as reported in various literature (Dalbeth 2007, Robinson et al. 2015). Uric acid concentration above 0.42 mmol/L in physiological fluids consequences in super saturation and thus forming uric acid crystals causing gout and related symptoms (Neogi 2011). Prolonged prophylaxis is commonly recommended with the use of serum urate lowering drug like colchicine or NSAIDs, but augmented frequency of gout flares occurs even after treatment due to number of complications associated with anti-gout drug administration (Singh et al. 2010).
The role of NLRP3 inflammasome in the pathogenesis of rheumatic disease
Published in Autoimmunity, 2022
Ruixue Kong, Lulu Sun, Hua Li, Dashan Wang
Gout is an inflammatory joint disorder characterised by acute arthritis and inflammation in the joints. Gout is caused by precipitation of monosodium urate monohydrate (MSU) in the joints in the setting of hyperuricaemia [54]. MSU crystals were identified as the aetiological agent and danger signal of gout for many years. MSU can induce NLRP3 inflammasome activation, leading to the production of active IL-1β and IL-18 [55–57]. A study found that the expression of NLRP3, ASC and caspase-1 in PBMCs, and the levels of IL-1β and IL-18 in the plasma were significantly increased in the hyperuricaemia group and the gouty nephropathy group in comparing to control group [58]. A genetic study found that there was a significant association between rs3806268 in NLRP3 gene and the risk of primary gout [59]. Another research revealed that NLRP3 rs10754558 polymorphism was associated with an increased susceptibility to gout [60].
Case with long-standing gout showing various ultrasonographic features caused by monosodium urate monohydrate crystal deposition
Published in Modern Rheumatology Case Reports, 2020
Michito Murayama, Mutsumi Nishida, Yusuke Kudo, Takahiro Deguchi, Katsuji Marukawa, Yuichiro Fujieda, Nobuya Abe, Masaru Kato, Hitoshi Shibuya, Yoshihiro Matsuno, Tatsuya Atsumi
Gout is a form of inflammatory arthritis resulting from the deposition of monosodium urate monohydrate (MSU) crystals mostly in the soft tissues and joints of the extremities in sustained hyperuricemia [1]. The natural history of gout involves a continuum of four stages: asymptomatic hyperuricemia, acute monophasic gout, recurrent acute attacks with inter-critical periods and chronic gout, which is often tophaceous [2]. In the modern era, advanced cases owing to inadequate treatment are rare. Gout is unlike other rheumatic diseases in that a gold standard assessment is available, i.e. positive MSU crystal findings. Although synovial fluid or nodule aspirates have a high sensitivity (ranging from 58% to 100%), their feasibility and specificity (ranging from 34% to 86%) may be inadequate [3]. Unlike in the easily recognized acute and monoarticular gouty arthritis, diagnosis of the polyarticular chronic form of tophaceous gouty arthritis may be challenging to physicians. Overlapping clinical features contribute to diagnostic confusion between chronic gouty arthritis and rheumatoid arthritis (RA) [4]. Nevertheless, there have been important advances in imaging techniques, assisting in the non-invasive diagnosis and follow-up of patients being treated for gout, in the last decade. Ultrasonography (US) has been thought to have the ability to detect deposition of MSU crystals in patients with gout [5–10]. Herein, we reported an evocative case of long-standing gout for an in-depth discussion of crystal-induced arthritis with various ultrasonographic features, including tendinitis.