尿酸關節痛 | Uric Acid Arthralgia

Store/尿酸關節痛 | Uric Acid Arthralgia

尿酸關節痛

痛風是一種全身性疾病，由尿酸單鈉晶體（MSU）沉積在組織中引起。血清尿酸（SUA）高於特定閾值是形成尿酸晶體的必要條件。儘管高尿酸血症是痛風的主要致病缺陷，但許多高尿酸血症患者並沒有發展成痛風，甚至沒有形成尿酸結晶。事實上，只有5%的高尿酸血症超過9毫克/分昇的人會患痛風。因此，有人認為遺傳傾向等其他因素也參與了痛風的發病。

尿酸單鈉晶體可以沉積在所有組織中，主要是在形成tophi的關節及其周圍。痛風的診斷主要是通過關節液體抽吸或tophi抽吸來鑒別病理性MSU晶體。痛風的早期表現是急性關節炎症，可通過非甾體抗炎藥或秋水仙堿迅速緩解。腎結石和腎結石是晚期表現。通過飲食調整和使用降低血尿酸的藥物來降低SUA水准低於沉積閾值是痛風治療的主要目標。這導致MSU晶體溶解，防止進一步攻擊。

Ref: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC55121...


關於尿酸結晶的部份研究：

  • 減輕尿酸鈉炎症(1)
  • 高尿酸炎症的改善(2)
  • 尿酸肾结石(3)
  • 痛風性關節炎(4)
  • 高尿酸心血管(5)
  • 尿酸結締鈣化(6)
  • 尿酸鈉冠狀動脈鈣化(7)
  • 焦磷酸鈣結晶溶解(8)
  • 溶解草酸鈣結晶(9)


Uric Acid Arthralgia

Gout is a systemic disease that results from the deposition of monosodium urate crystals (MSU) in tissues. Increased serum uric acid (SUA) above a specific threshold is a requirement for the formation of uric acid crystals. Despite the fact that hyperuricemia is the main pathogenic defect in gout, many people with hyperuricemia do not develop gout or even form UA crystals. In fact, only 5% of people with hyperuriceamia above 9 mg/dL develop gout. Accordingly, it is thought that other factors such as genetic predisposition share in the incidence of gout.

Monosodium urate crystals crystals can be deposited in all tissues mainly in and around the joints forming tophi. Gout is mainly diagnosed by identification of the pathognomonic MSU crystals by joint fluid aspiration or in tophi aspirate. Early presentation of gout is an acute joint inflammation that is quickly relieved by NSAIDs or colchicine. Renal stones and tophi are late presentations. Lowering SUA levels below deposition threshold either by dietary modification and using serum uric acid lowering drugs is the main goal in management of gout. This results in dissolution of MSU crystals preventing further attack.

Ref: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC55121...

Some studies on the crystallization of uric acid

  • Reducing inflammation of sodium urate (1)
  • Improvement of hyperuricemia inflammation (2)
  • Uric acid nephrolithiasis (3)
  • Gouty arthritis (4)
  • Hyperuricemia cardiovascular disease (5)
  • Uric acid connective calcification (6)
  • Sodium urate coronary artery calcification (7)
  • Crystal dissolution of calcium pyrophosphate (8)
  • Dissolution and crystallization of calcium oxalate (9)


Refs:

  1. Eric W Orlowsky, Thomas V Stabler, Eulàlia Montell, Josep Vergés, and Virginia Byers Kraus. Monosodium urate crystal induced macrophage inflammation is attenuated by chondroitin sulphate: pre-clinical model for gout prophylaxis. BMC Musculoskelet Disord. 2014; 15: 318. Published online 2014 Sep 27. doi: 10.1186/1471-2474-15-318. PMCID: PMC4189145. PMID: 25261974
  2. Zhao-Qing Meng, Zhao-Hui Tang, Yun-Xia Yan, Chang-Run Guo. Study on the Anti-Gout Activity of Chlorogenic Acid: Improvement on Hyperuricemia and Gouty Inflammation. November 2014, The American Journal of Chinese Medicine 42(06):1-13. DOI: 10.1142/S0192415X1450092X
  3. CHARLES Y. C. PAK, KHASHAYAR SAKHAEE, and CINDY FULLER. Successful management of uric acid nephrolithiasis withpotassium citrate. Section on Mineral Metabolism, Department of Internal Medicine, Southwestern Medical School, University of Texas Health Science Centerat Dallas, TX 75235. Kidney international, Vol. 30 (1986), pp. 422—428
  4. Qi Zhou, Shumin Liu,1 Donghua Yua, and Ning Zhang. Therapeutic Effect of Total Saponins from Dioscorea nipponica Makino on Gouty Arthritis Based on the NF-κB Signal Pathway: An In vitro Study. Journal List. Pharmacogn Mag. v.12(47); Jul-Sep 2016. PMC4989800. Pharmacogn Mag. 2016 Jul-Sep; 12(47): 235–240. doi: 10.4103/0973-1296.186344. PMCID: PMC4989800. PMID: 27601855
  5. Angelo L Gaffo,1 N Lawrence Edwards,2 and Kenneth G Saag. Gout. Hyperuricemia and cardiovascular disease: how strong is the evidence for a causal link? Journal List.Arthritis Res Ther. v.11(4); 2009.PMC2745789. Arthritis Res Ther. 2009; 11(4): 240. Published online 2009 Aug 19. doi: 10.1186/ar2761. PMCID: PMC2745789. PMID: 19725932
  6. W Mohr 1 , E Görz. [Mixed tophi. Calcium pyrophosphate dihydrate crystals in gout tophi]. Z Rheumatol. 2000 Aug;59(4):240-4. doi: 10.1007/s003930070066. PMID: 11013985. DOI: 10.1007/s003930070066
  7. Mariano Andres,1Marıa-Amparo Quintanilla,2Francisca Sivera,2JoseSanchez-Paya,3Eliseo Pascual,4Paloma Vela,4and Juan-Miguel Ruiz-Nodar3. Silent Monosodium Urate Crystal Deposits Are AssociatedWith Severe Coronary Calcification inAsymptomatic Hyperuricemia. An Exploratory Study. ARTHRITIS & RHEUMATOLOGY Vol. 68, No. 6, June 2016, pp 1531–1539DOI 10.1002/art.39581
  8. R Cinia, D Chindamob, M Catenacciob, S Lorenzinib, E Selvib, F Neruccib, M P Picchib, G Bertib, R Marcolongob. Dissolution of calcium pyrophosphate crystals by polyphosphates: an in vitro and ex vivo study. http://dx.doi.org/10.1136/ard.60.10.962
  9. Shouwu Guo, Michael D. Ward, Jeffrey A. Wesson. Direct Visualization of Calcium Oxalate Monohydrate Crystallization and Dissolution with Atomic Force Microscopy and the Role of Polymeric Additives. Langmuir 2002, 18, 11, 4284–4291. Publication Date:May 1, 2002. https://doi.org/10.1021/la011754+
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