Editing Uric acid (section)

====Gout====
{{main|Gout}}
A 2011 survey in the United States indicated that 3.9% of the population had gout, whereas 21.4% had hyperuricemia without having symptoms.<ref name="pmid30485934">{{cite journal | last1=Li |first1=R. |last2=Yu |first2=K. |last3=Li |first3=C. | title=Dietary factors and risk of gout and hyperuricemia: a meta-analysis and systematic review | journal=Asia Pacific Journal of Clinical Nutrition | volume=27 | issue=6 | pages=1344–1356 | year=2018 | doi = 10.6133/apjcn.201811_27(6).0022 | pmid=30485934}}</ref>

Excess blood uric acid (serum urate) can induce [[gout]],<ref name="Heinig M, Johnson RJ 2006 1059–64">{{cite journal |last1=Heinig |first1=M. |last2=Johnson |first2=R. J. |title=Role of uric acid in hypertension, renal disease, and metabolic syndrome |journal=Cleveland Clinic Journal of Medicine |volume=73 |issue=12 |pages=1059–1064 |date=December 2006 |pmid=17190309 |doi=10.3949/ccjm.73.12.1059|doi-broken-date=29 November 2024 |s2cid=45409308 }}</ref> a painful condition resulting from needle-like crystals of uric acid termed ''monosodium urate crystals''<ref name="Abhishek">{{cite journal |last1=Abhishek |first1=A |last2=Roddy |first2=E |last3=Doherty |first3=M |title=Gout - a guide for the general and acute physicians. |journal=Clinical Medicine |date=February 2017 |volume=17 |issue=1 |pages=54–59 |doi=10.7861/clinmedicine.17-1-54 |pmid=28148582|pmc=6297580 }}</ref> precipitating in [[joint]]s, [[Capillary|capillaries]], [[skin]], and other tissues.<ref name=Lancet2010>{{cite journal |last1=Richette |first1=P. |last2=Bardin |first2=T. |title=Gout |journal=Lancet |volume=375 |issue=9711 |pages=318–328 |date=January 2010 |pmid=19692116 |doi=10.1016/S0140-6736(09)60883-7 |s2cid=208793280 }}</ref> Gout can occur where serum uric acid levels are as low as 6&nbsp;mg per 100&nbsp;mL (357&nbsp;μmol/L), but an individual can have serum values as high as 9.6&nbsp;mg per 100&nbsp;mL (565&nbsp;μmol/L) and not have gout.<ref name=hyperuricemia>{{cite journal |last1=Tausche |first1=A. K. |last2=Unger |first2=S. |last3=Richter |first3=K. |display-authors=etal |trans-title=Hyperuricemia and gout: diagnosis and therapy |language=de |journal=Der Internist |volume=47 |issue=5 |pages=509–521 |date=May 2006 |pmid=16586130 |doi=10.1007/s00108-006-1578-y |title=Hyperurikämie und Gicht|s2cid=11480796 }}</ref>

In humans, purines are metabolized into uric acid, which is then excreted in the urine. Consumption of large amounts of some types of purine-rich foods, particularly meat and seafood, increases gout risk.<ref name=Choi>{{cite journal |last1=Choi |first1=H. K. |last2=Atkinson |first2=K. |last3=Karlson |first3=E. W. |last4=Willett |first4=W. |last5=Curhan |first5=G. |title=Purine-rich foods, dairy and protein intake, and the risk of gout in men |journal=The New England Journal of Medicine |volume=350 |issue=11 |pages=1093–1103 |date=March 2004 |pmid=15014182 |doi=10.1056/NEJMoa035700|doi-access=free }}</ref> Purine-rich foods include liver, kidney, and [[Sweetbread|sweetbreads]], and certain types of seafood, including anchovies, herring, sardines, mussels, scallops, trout, haddock, mackerel, and tuna.<ref>{{Cite web|date=July 2, 2020|title=Gout diet: What's allowed, what's not|url=http://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/gout-diet/art-20048524|website=[[Mayo Clinic]]|publisher=|access-date=13 January 2017|archive-date=7 January 2017|archive-url=https://web.archive.org/web/20170107022952/http://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/gout-diet/art-20048524|url-status=live}}</ref> Moderate intake of purine-rich vegetables, however, is not associated with an increased risk of gout.<ref name=Choi/>

One treatment for gout in the 19th century was administration of [[lithium]] salts;<ref>{{cite journal |first= Gerhard N. |last=Schrauzer |journal=Journal of the American College of Nutrition |volume=21 |issue=1 |pages=14–21 |year=2002 |title= Lithium: Occurrence, Dietary Intakes, Nutritional Essentiality |pmid= 11838882 |doi= 10.1080/07315724.2002.10719188|s2cid=25752882 }}</ref> lithium urate is more soluble. Today, inflammation during attacks is more commonly treated with [[NSAID]]s, [[colchicine]], or [[corticosteroid]]s, and urate levels are managed with [[allopurinol]].<ref>{{cite web|title=NHS Clinical Knowledge Summaries |url=http://www.cks.nhs.uk/gout/background_information/causes_and_risk_factors#-291124 |url-status=dead |archive-url=https://web.archive.org/web/20120304060453/http://www.cks.nhs.uk/gout/background_information/causes_and_risk_factors |archive-date=4 March 2012 |publisher=UK [[National Health Service]]}}</ref> Allopurinol, which weakly inhibits xanthine oxidase, is an analog of hypoxanthine that is hydroxylated by [[Xanthine oxidase|xanthine oxidoreductase]] at the 2-position to give oxipurinol.<ref>{{cite journal|pmid=16507884|pmc=2233605|year=2006|last1=Pacher|first1=P.|title=Therapeutic effects of xanthine oxidase inhibitors: Renaissance half a century after the discovery of allopurinol|journal=Pharmacological Reviews|volume=58|issue=1|pages=87–114|last2=Nivorozhkin|first2=A.|last3=Szabó|first3=C.|doi=10.1124/pr.58.1.6}}</ref>