英文條目：https://en.wikipedia.org/wiki/Gout
目前中文條目：https://zh.wikipedia.org/zh-tw/%E7%97%9B%E9%A3%8E
Gout (also known as podagra when it involves the joint at the base of the big toe)[4] is usually characterized by recurrent attacks of inflammatory arthritis—a red, tender, hot, and swollen joint.[5] Pain typically comes on rapidly in less than twelve hours.[6] The joint at the base of the big toe is affected in about half of cases.[7] It may also result in tophi, kidney stones, orurate nephropathy.[6]
’’’痛風’’’（Gout，學名：metabolic arthritis）又稱’’’代謝性關節炎’’’或者’’’富貴病’’’。當涉及到[[跖趾關節]]時也稱為’’’足痛風’’’（Podagra）[4]。經常被描述為週期性發作的[[刺激性關節炎]]，造成關節紅、軟、熱、{{le|關節積液|joint effusion|腫}}等現象[5]。劇烈疼痛通常在十二小時內就發作。大約一半的病例會影響到[[跖趾關節]]。痛風也會導致{{le|tophus|痛風結節|tophi}}（痛風石）、[[腎結石]]，或者{{tsl|en|urate nephropathy|急性尿酸腎病|urate nephropathy}}[6]。
The cause is a combination of diet and genetic factors. It occurs more commonly in those who eat a lot of meat, drink a lot of beer, or are overweight. The underlying mechanisms involves elevated levels of uric acid in the blood. When the uric acid crystallizes, and the crystals deposit in joints, tendons, and surrounding tissues an attack of gout occurs. Diagnosis may be confirmed by seeing the characteristic crystals in joint fluid or tophus. Blood uric acid levels may be normal during an attack.[6]
導致痛風的原因結合了日常飲食和[[遺傳]]因素。痛風通常較容易發生在吃很多肉，喝很多啤酒或[[超重]]的人身上。潛在機制包含[[血液]]中[[尿酸]]水平的升高。當尿酸[[結晶]]後沉澱在關節，[[肌腱]]和周圍[[組織]]，痛風就開始發作了。可以通過在關節液中看見典型的結晶或痛風結節確診。血液中尿酸水平可能在痛風發作時恢復正常[6]。
Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, or colchicine improves symptoms. Once the acute attack subsides, levels of uric acid are usually lowered via lifestyle changes, and in those with frequent attacks, allopurinol orprobenecid provides long-term prevention.[6] Taking vitamin C and eating a diet high in low fat dairy products may be preventative.[8]
治療配合使用[[非類固醇類抗炎藥物]]、[[類固醇]]，或[[秋水仙素]]來改善症狀。通過生活方式的改變使尿酸水平下降能緩解急性痛風發作，而[[別嘌呤醇]]或[[丙磺舒]]為那些頻繁的痛風發作提供長期預防[6]。服用[[維生素C]]和食用低脂乳製品的飲食也可能預防[8]。
Gout affects about 1 to 2% of the Western population at some point in their lives. It has become more common in recent decades which is believed to be due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancy, and changes in diet. Older males are most commonly affected.[6] Gout was historically known as "the disease of kings" or "rich man’s disease".[6][9] It has been recognized at least since the time of the ancient Egyptians.[6]
大約1到2％的[[西方世界|西方人口]]曾經或正在罹患痛風。近幾十年，人們認為由於人群中越來越多的風險因素，例如[[代謝綜合徵]]，較長的[[平均壽命 ]]和飲食上的改變，痛風的影響變得更普遍，其中年齡較長的男性是最普遍受影響的[6]。至少追溯到[[古埃及時代]][6]，痛風在歷史上被公認為「國王病」或「富人病」[6][9]。
Gout presenting in the metatarsal-phalangeal joint of the big toe: Note the slight redness of the skin overlying the joint.
痛風在跖趾關節的症狀：關節上的皮膚輕微發紅。
Gout can present in a number of ways, although the most usual is a recurrent attack of acute inflammatory arthritis(a red, tender, hot, swollen joint).[5] The metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases.[7] Other joints, such as the heels, knees, wrists, and fingers, may also be affected.[7]Joint pain usually begins over 2–4 hours and during the night.[7] This is mainly due to lower body temperature.[4]Other symptoms may rarely occur along with the joint pain, including fatigue and a high fever.[4][7]
痛風會呈現出許多種症狀，最常見的是急劇的[[刺激性關節炎]]（關節紅，軟，熱和浮腫）[5]週期性地發作，而在[[大腳趾]]基部的[[跖趾關節]]最常受影響，占一半的病例[7]。其他關節，例如腳踝，膝蓋，手腕和手指也有可能受影響。[7]關節疼痛通常在夜間發生且持續2到4個小時。[7]這有可能是由於較低的體溫。[4]其他的罕見症狀包含[[疲乏]]和[[高燒]]也有可能伴隨關節疼痛發生。[4][7]
Long-standing elevated uric acid levels (hyperuricemia) may result in other symptomatology, including hard, painless deposits of uric acid crystals known as tophi. Extensive tophi may lead to chronic arthritis due to bone erosion.[10] Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stoneformation and subsequent urate nephropathy.[11]
血液中的[[尿酸]]濃度若[[高尿酸血|長期偏高]]可能導致其他症狀，包含被稱為[[痛風結節]]的硬且無痛的尿酸結晶沉澱。由於骨骼侵蝕，大量的痛風結節可能導致慢性[[關節炎]]。[10]高的尿酸水平也可能引起[[腎臟]]中的晶體沉澱，導致[[腎結石]]以及隨後的[[急性尿酸腎病]]。[11]
The crystallization of uric acid, often related to relatively high levels in the blood, is the underlying cause of gout. This can occur for a number of reasons, including diet, genetic predisposition, or underexcretion of urate, the salts of uric acid.[5] Underexcretion of uric acid by the kidney is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%.[6] About 10% of people with hyperuricemia develop gout at some point in their lifetimes.[12] The risk, however, varies depending on the degree of hyperuricemia. When levels are between 415 and 530 μmol/l (7 and 8.9 mg/dl), the risk is 0.5% per year, while in those with a level greater than 535 μmol/l (9 mg/dL), the risk is 4.5% per year.[4]
[[尿酸]][[結晶]]是痛風的基本成因，而[[結晶]]常常與高水平的血尿酸濃度有關。[[高尿酸血癥]]與許多因素有關，包括飲食習慣、遺傳預先傾向性，以及腎臟[[尿酸鹽]]清除率的下降[5]。在約90％的病例中，腎尿酸鹽清除率的下降是引起[[高血尿酸癥]]的近因，而相比之下，尿酸的過度產生只是不到10％的病例中[[高尿酸血癥]]的成因[6]。大約10％的[[高尿酸血癥]]患者在人生中的某時刻病情進一步發展為[[痛風]][12]。不過，患[[痛風]]的風險與尿酸水平有關。當個體血尿酸濃度在415μmol/L和 530 μmol/L (7mg/dL 和 8.9 mg/dL)之間時，個體每年患痛風的機率為0.5％；而對於血尿酸濃度高於535 μmol/L (9 mg/dL)的個體，每年患痛風的機率為4.5％[4]。
Lifestyle 生活型態
Dietary causes account for about 12% of gout,[5] and include a strong association with the consumption of alcohol, fructose-sweetened drinks, meat, and seafood.[10][13]Other triggers include physical trauma and surgery.[6]
Studies in the early 2000s have found that other dietary factors once believed associated are, in fact, not.[14][15] Specifically, moderate consumption of purine-rich vegetables (e.g. beans, peas, lentils, and spinach) are not associated with the development of gout.[16] Neither is total consumption of protein.[14][16] Alcohol consumption is a factor, with wine presenting somewhat less of a risk than beer and spirits.[17]
飲食習慣因素佔痛風成因的12%[5]，特別是與酒精、[[果糖]]甜化的飲料、肉類和海鮮類的攝入有較強的關係[10][13]，痛風也與[[體外傷]]和外科手術有一定關係[6]。
在21世紀初的研究中研究人員發現其他的一些曾被認為與痛風存在相關性關係的飲食因素實際上與痛風並無關聯[14][15]。尤其是[[嘌呤]]含量高的植物（例如大豆、豌豆、金麥豌（扁豆）、菠菜）的適當攝入與痛風病情的發展並不相關[16]，蛋白質的總攝入量也與痛風無關[14][16]。酒精飲料的攝入是導致痛風的成因之一，特別是啤酒和烈酒比紅酒的致病風險更大[17]。
The consumption of coffee, vitamin C, and dairy products, as well as physical fitness, appear to decrease the risk.[18][19][20] This is believed to be partly due to their effect in reducing insulin resistance.[20]
[[咖啡]]、[[維他命C]]和[[奶製品]]的攝入，以及體格鍛煉有一定的減小致病風險的傾向[18][19][20]，這可能是與[[胰島素抗性]]的減少有一定的關聯[20]。
Genetics 基因型
The occurrence of gout is partly genetic, contributing to about 60% of variability in uric acid level.[6] Three genes called SLC2A9, SLC22A12, and ABCG2 have been found to be commonly associated with gout, and variations in them can approximately double the risk.[21][22] Loss-of-function mutations in SLC2A9 and SLC22A12 cause hereditary hypouricaemia by reducing urate absorption and unopposed urate secretion.[22] A few rare genetic disorders, including familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetase superactivity, and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch-Nyhan syndrome, are complicated by gout.[6]
痛風也與基因有一定的關係，60％的血尿酸濃度變化與基因有關[6]。三對等位[[基因]][[SLC2A9]]、[[SLC22A12]]以及[[ABCG2]]被發現通常與痛風存在關聯，而這三對基因的基因型的變化可將發病機率大致提高一倍[21][22]。SLC2A9 和 SLC22A12兩對等位基因的[[功能喪失型突變]]可通過尿酸鹽吸收量的減小及未遭調控的的尿酸鹽分泌而導致先天性高尿酸血癥[22]。少數罕見遺傳疾患可能是痛風的並發症，包括[[家族性少年高血尿酸癥腎病]]、[[髓質囊腎病]]、[[磷酸核糖焦磷酸合成酶]]的超活性化以及[[莱希－尼亨氏症候群]]中的次黃嘌呤 - 鳥嘌呤磷酸核糖基轉移酶缺陷[6]。
Medical conditions 健康狀況
Gout frequently occurs in combination with other medical problems. Metabolic syndrome, a combination of abdominal obesity, hypertension, insulin resistance, and abnormal lipid levels, occurs in nearly 75% of cases.[7] Other conditions commonly complicated by gout include: polycythemia, lead poisoning, kidney failure, hemolytic anemia, psoriasis, and solid organ transplants.[6][23] A body mass index greater than or equal to 35 increases a male’s risk of gout threefold.[15] Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function.[24] Lesch-Nyhan syndrome is often associated with gouty arthritis.
痛風患者經常同時患上其他疾病。在約75％的病例中，[[腹部肥胖]]、[[高血壓]]、[[胰島素抵抗]]與[[血脂水平異常]]構成的[[代謝症候群]]與痛風同時發生[7]。痛風是[[紅血球過多症]]、[[鉛中毒]]、[[腎衰竭]]、[[溶血性貧血]]、[[牛皮癬]]等疾病，及實體器官移植的常見併發症[6][23]。若男性個體[[身體質量指數]]（BMI）大於或等於35，其患痛風的機率則會增加兩倍[15]。因為鉛對腎功能有不利影響，長期暴露在含鉛環境中及飲用遭鉛污染的的酒也是痛風的致病因素[24]。[[莱希－尼亨氏症候群]]也常與痛風性關節炎有關。
Medication 用藥狀況
Diuretics have been associated with attacks of gout. However, a low dose of hydrochlorothiazide does not seem to increase the risk.[25] Other medicines that increase the risk include niacin and aspirin (acetylsalicylic acid).[10] The immunosuppressive drugs ciclosporin and tacrolimus are also associated with gout,[6] the former more so when used in combination with hydrochlorothiazide.[26]
[[利尿劑]]的使用與痛風發作有關。但是低劑量的[[氫氯苯噻噠嗪]]（降血壓利尿劑）的使用並沒有增加患病風險的傾向[25]。[[菸鹼]]、[[阿司匹林]]（乙醯水楊酸）等其他藥物的使用也會增加痛風的患病機率[10]。[[免疫抑製劑]][[環孢素]]和[[他克莫司]]的使用也與通風的發病有關[6]，而使用環孢素時，若同時使用氫氯苯噻噠嗪，則致病機率更大[26]。
Gout is a disorder of purine metabolism,[6] and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating and forming deposits (tophi) in joints, on tendons, and in the surrounding tissues.[10] Microscopic tophi may be walled off by a ring of proteins, which blocks interaction of the crystals with cells, and therefore avoids inflammation.[27] Naked crystals may break out of walled-off tophi due to minor physical trauma to the joint, medical or surgical stress, or rapid changes in uric acid levels.[27] When they breach the tophi, they trigger a local immune-mediated inflammatory reaction,[10][27] with one of the key proteins in the inflammatory cascade being interleukin 1β.[6] An evolutionary loss of urate oxidase (uricase), which breaks down uric acid, in humans and higher primates has made this condition common.[6]
痛風是一種[[嘌呤代謝]]紊亂癥[6]，發生在嘌呤代謝終產物[[尿酸]]以單鈉尿酸鹽形式結晶，[[沉澱]]並在關節、肌腱與周圍組織中形成沉澱物（即痛風石）時[10]。微小的痛風石可能被一種環蛋白質清除，這些蛋白質可以阻礙晶體和細胞之間的交互作用，從而避免炎症反應的發生[27]。被蛋白質包裹的痛風石可能會因微小的關節外傷、藥物、手術應激或血尿酸水平的劇烈變化而將裸露的單鈉尿酸鹽晶體釋放[27]。痛風石被釋放時，會引發局部[[免疫]]介導的[[炎性反應]][10][27]。在炎症反應中，[[介白素1β]]是一種重要的蛋白質[6]。的在人類和高級[[靈長類]]中，[[尿酸鹽氧化酶]]（尿酸酶，即分解尿酸的酶）的退化是很常見的[6]。
The triggers for precipitation of uric acid are not well understood. While it may crystallize at normal levels, it is more likely to do so as levels increase.[10][28] Other factors believed to be important in triggering an acute episode of arthritis include cool temperatures, rapid changes in uric acid levels, acidosis,[29][30] articular hydration, and extracellular matrix proteins, such as proteoglycans, collagens, and chondroitin sulfate.[6] The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected.[5] Rapid changes in uric acid may occur due to a number of factors, including trauma, surgery, chemotherapy, diuretics, and stopping or starting allopurinol.[4] Calcium channel blockers and losartan are associated with a lower risk of gout compared to other medications for hypertension.[31]
尿酸沉澱形成的誘因尚不完全明確。儘管尿酸也可在血尿酸濃度正常時結晶，但當血尿酸濃度升高時，尿酸結晶的可能性更大[10][28]。引起急性痛風性關節炎發作的其他重要因素包括低溫，以及血尿酸濃度、[[酸鹼度]][29][30]、關節液成份、[[細胞外基質]]成分（例如[[蛋白多醣]]、[[膠原蛋白]]，及[[硫酸軟骨素]]）的急速變化[6]。而尿酸在低溫下的沉澱量增加可以在一定程度上解釋為何痛風更容易發病於足部關節[5]。很多因素可引起尿酸濃度的急速變化，包括體外傷、手術、[[化療]]、使用利尿劑，以及開始服用或停用[[異嘌呤醇]][4]。相對於其他治療[[高血壓]]的藥物，[[鈣離子通道阻斷劑]]及[[氯沙坦鉀氫氯噻嗪]]引起痛風發作的風險更小[31]。
Spiked rods of uric acid crystals from a synovial fluidsample photographed under a microscope withpolarized light. Formation of uric acid crystals in the joints is associated with gout.
痛風伴隨著關節中尿酸結晶的構成，在[[偏振光]]顯微鏡下可從[[關節滑液]]取得的尿酸結晶的圖片。
Gout may be diagnosed and treated without further investigations in someone with hyperuricemia and the classic podagra. Synovial fluid analysis should be done, however, if the diagnosis is in doubt.[4] X-rays, while useful for identifying chronic gout, have little utility in acute attacks.[6]
痛風可能通過高尿酸血和典型的足痛風症狀被確診及治療而無需進一步檢查。但無法以臨床症狀確診時，患者需要進行關節滑液分析[4]。儘管[[X光]]在識別慢性痛風上有一定的臨床意義，但無法識別痛風的急性發作[6]。
Synovial fluid 滑液
A definitive diagnosis of gout is based upon the identification of monosodium urate crystals in synovial fluid or atophus.[7] All synovial fluid samples obtained from undiagnosed inflamed joints by arthrocentesis should be examined for these crystals.[6] Under polarized light microscopy, they have a needle-like morphology and strong negative birefringence. This test is difficult to perform, and often requires a trained observer.[32] The fluid must also be examined relatively quickly after aspiration, as temperature and pH affect their solubility.[6]
痛風明確的診斷基於在[[滑液]]中辨認出[[單鈉尿酸鹽的結晶]]或[[痛風石]]。[7]所有通過[[關節穿刺術]]取自未被確診的發炎關節的滑液樣本需要進行這種結晶的仔細檢查。[6]在[[偏振光]]顯微鏡下，它們的形態為針狀且具有強烈的負性[[雙折射]]。執行這個檢驗有困難且常常需要受訓練過的醫檢師。[32]因溫度和PH值會影響結晶的溶解度，滑液在抽吸出來后也必須被相當快速地檢驗。[6]
Blood tests 血液檢查
Hyperuricemia is a classic feature of gout, but it occurs nearly half of the time without hyperuricemia, and most people with raised uric acid levels never develop gout.[7][33] Thus, the diagnostic utility of measuring uric acid level is limited.[7] Hyperuricemia is defined as a plasma urate level greater than 420 μmol/l (7.0 mg/dl) in males and 360 μmol/l (6.0 mg/dl) in females.[34] Other blood tests commonly performed are white blood cell count, electrolytes,kidney function, and erythrocyte sedimentation rate (ESR). However, both the white blood cells and ESR may be elevated due to gout in the absence of infection.[35][36] A white blood cell count as high as 40.0×109/l (40,000/mm3) has been documented.[4]
[[高尿酸血症]]也是典型的痛風特征，但近一半的痛風發作沒有伴隨高尿酸血症，且大多數人尿酸水平的升高不會發展成痛風。[7][33]因此，測量尿酸水平的診斷功效是有限的。[7]高尿酸血症定義為男性[[血漿]]中尿酸鹽水平高於420 μmol/l (7.0 mg/dl)或女性血漿中尿酸鹽水平高於360 μmol/l (6.0 mg/dl) 。[34]其他血檢通常是[[白細胞計數]]、[[電解質]]、[[腎功能]]及[[紅細胞沉降率]]。然而，白細胞計數和紅細胞沉降率的升高都可能是由於痛風而不是感染。[35][36]曾有記錄因痛風白細胞計數高至40×109／L（40000 /mm3）。[4]
Differential diagnosis 鑑別診斷
The most important differential diagnosis in gout is septic arthritis.[7][6] This should be considered in those with signs of infection or those who do not improve with treatment.[7] To help with diagnosis, a synovial fluid Gram stainand culture may be performed.[7] Other conditions that look similar include pseudogout and rheumatoid arthritis.[7]Gouty tophi, in particular when not located in a joint, can be mistaken for basal cell carcinoma,[37] or otherneoplasms.[38]
醫師在對痛風的[[鑑別診斷]]中，最重要的是將[[敗血病關節炎]]納入考量[7][6]，特別是在患者有感染症狀或治療效果不佳時[7]。為幫助醫師診斷，實驗室需進行滑液的[[革蘭氏染色]]及培養[7]。痛風也與[[假性痛風]]和[[類風濕性關節炎]]症狀相似[7]。痛風石可被誤認為是[[基底細胞癌]]或是其他[[腫瘤]]，特別是當痛風石並不位於關節時[37][38]。
Both lifestyle changes and medications can decrease uric acid levels. Dietary and lifestyle choices that are effective include reducing intake of food such as meat and seafood, consuming adequate vitamin C, limiting alcohol and fructose consumption, and avoiding obesity.[5] A low-calorie diet in obese men decreased uric acid levels by 100 µmol/l (1.7 mg/dl).[25] Vitamin C intake of 1,500 mg per day decreases the risk of gout by 45%.[39] Coffee, but not tea, consumption is associated with a lower risk of gout.[40] Gout may be secondary to sleep apnea via the release of purines from oxygen-starved cells. Treatment of apnea can lessen the occurrence of attacks.[41]
生活型態的改變與用藥皆能降低尿酸濃度。減少肉類與海鮮的攝取量、服用足量[[維生素 C]]、控制[[醇]]類與果糖的攝取量，以及避免[[肥胖症]]都是有效的飲食與生活型態。[5]低卡路里的飲食可以使肥胖男性之尿酸濃度降低100 微升/升(1.7 毫克/分升)。[25]每日攝取1500 毫克的維生素 C可以降低45%的痛風風險。喝咖啡可降低痛風風險，但茶類不行。[40]痛風可能是由於[[睡眠呼吸中止症]]缺乏氧氣的細胞釋放[[嘌呤]]所導致的。對睡眠呼吸中止症的治療可以降低痛風的發生。
The initial aim of treatment is to settle the symptoms of an acute attack.[42] Repeated attacks can be prevented by different drugs used to reduce the serum uric acid levels.[42] Tentative evidence supports the application of ice for 20 to 30 minutes several times a day to decrease pain.[43] Options for acute treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and steroids,[5] while options for prevention include allopurinol, febuxostat, and probenecid. Lowering uric acid levels can cure the disease.[6] Treatment of associated health problems is also important.[6] Lifestyle interventions have been poorly studied.[43][44] It is unclear if dietary supplements have an effect in people with gout.[45]
最初的治療目標為紓解急性痛風的症狀。[42]不同的藥物可以降低血清的尿酸濃度而避免重複發作。[42]初步的證據顯示一天冰敷20至30分鐘數次可以減少疼痛。[43]急性痛風的處方有[[非類固醇消炎止痛藥]]（NSAIDs）、[[秋水仙素]]與[[類固醇]]。[5]預防用藥有[[別嘌醇]]、福避痛(febuxostat暫譯)與丙璜舒（probenecid）。降低尿酸濃度可以治療痛風。[6]對[[合併症]]的治療也十分重要。[6]生活型態的介入方式尚未被明確研究。[43][44]營養品是否對痛風病患有影響也尚未知曉。
NSAIDs 非類固醇消炎止痛藥
NSAIDs are the usual first-line treatment for gout, and no specific agent is significantly more or less effective than any other.[5] Improvement may be seen within four hours, and treatment is recommended for one to two weeks.[5][6] They are not recommended, however, in those with certain other health problems, such asgastrointestinal bleeding, kidney failure, or heart failure.[46] While indometacin has historically been the most commonly used NSAID, an alternative, such as ibuprofen, may be preferred due to its better side effect profile in the absence of superior effectiveness.[25] For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given.[47] There is some evidence that COX-2 inhibitors may work as well as nonselective NSAIDs for acute gout attack with fewer side effects.[48][49]
非類固醇消炎止痛藥是治療痛風的一線藥物，而且不同的非類固醇消炎止痛藥對痛風的治療效果相近[5]。用藥後痛風症狀可在四小時內緩解，不過一般推薦持續用藥一至兩周[5][6]。但對於以下疾病患者不推薦使用非類固醇消炎止痛藥治療痛風：[[消化道出血]]、[[腎功能衰竭]]、[[心衰竭]][46]。儘管歷史上[[吲哚美辛]]是最廣泛使用的非類固醇消炎止痛藥，其他非類固醇消炎止痛藥例如[[伊布洛芬]]，可在並無更好的療效時由於其更小的副作用而被推薦使用[25]。對於可能出現胃部副作用的患者來說，可以在使用非類固醇消炎止痛藥時同時使用[[氫離子幫浦阻斷劑]][47]。有證據顯示用於治療急性痛風發作時，[[環氧化酶-2抑制劑]]能以更少的副作用達到與非選擇性非類固醇消炎止痛藥同樣的治療效果[48][49]。
Colchicine
Colchicine is an alternative for those unable to tolerate NSAIDs.[5] At high doses, side effects (primarily gastrointestinal upset) limit its usage.[50] At lower doses, which are still effective, it is well tolerated.[25][51] Colchicine may interact with other commonly prescribed drugs, such as atorvastatin and erythromycin, among others.[50]
秋水仙素
對於那些不能使用非類固醇消炎止痛藥的人而言，[[秋水仙素]]能成為它的替代藥物。不過秋水仙素在高劑量時產生的副作用（主要為腸胃道不適），限制了它的使用情況[50]。但就低劑量使用而言，它仍然有不錯的效果，而且具備較好的藥物耐受性[25][51]。秋水仙素會與常用的處方藥（如[[阿托伐他汀]]、[[紅黴素]]等）產生交互作用[50]。
Steroids
Glucocorticoids have been found to be as effective as NSAIDs[52][53] and may be used if contraindications exist for NSAIDs.[5] They also lead to improvement wheninjected into the joint; a joint infection must be excluded, however, as steroids worsens this condition.[5]
類固醇
已知[[糖皮質激素]]是和非類固醇消炎止痛藥同樣有效的藥物[52][53]，因此若是患者不適合使用非類固醇消炎止痛類藥物，那麼糖皮質激素將是個好選擇[5]。在必須治療局部的[[關節感染]]時，於[[關節處注射]]類固醇也能有效地改善疼痛及症狀[5]。
Pegloticase
Pegloticase was approved in the USA to treat gout in 2010.[54] It is an option for the 3% of people who are intolerant to other medications.[54] Pegloticase is administered as an intravenous infusion every two weeks,[54] and has been found to reduce uric acid levels in this population.[55] It is likely useful for tophi but has a high rate of side effects.[56]
Pegloticase
於2010年時，[[Pegloticase]]在美國通過核准正式上市[54]。它能用於對傳統治療藥物無效的百分之三患者身上[54]。Pegloticase在使用上是以靜脈注射作為途徑，每兩個星期需施打一次[54]。根據實驗，它不僅能夠溶解痛風石，還被發現能有效降低痛風患者的尿酸[55]。不過Pegloticase雖然有還不錯的療效，但出現副作用的機率卻很高[56]。
Prophylaxis
A number of medications are useful for preventing further episodes of gout, including xanthine oxidase inhibitor (including allopurinol and febuxostat) and uricosurics(including probenecid and sulfinpyrazone). They are not usually started until one to two weeks after an acute flare has resolved, due to theoretical concerns of worsening the attack,[5] and are often used in combination with either an NSAID or colchicine for the first three to six months.[6] They are not recommended until a person has had two attacks of gout,[5] unless destructive joint changes, tophi, or urate nephropathy exist,[11] as medications have not been found to be cost-effective until this point.[5]Urate-lowering measures should be increased until serum uric acid levels are below 300–360 µmol/l (5.0–6.0 mg/dl), and are continued indefinitely.[5][6] If these medications are being used chronically at the time of an attack, discontinuation is recommended.[7] If levels cannot be brought below 6.0 mg/dl and there are recurrent attacks, this is deemed treatment failure or refractory gout.[57] Overall, probenecid appears to be less effective than allopurinol.[5]
預防法
許多藥物對於預防痛風進一步發作是有用的，例如黃嘌呤氧化酶抑制劑（包含異嘌呤醇及福避痛）和促進尿酸排泄藥物（如probenecid、sulfinpyrazone）。由於這些藥物理論上可能會使急診發作的症狀更加惡化，用藥的時間點通常在急性發作症狀緩解之後的一到兩週之後才開始[5]，在開始用藥的頭三到六個月也常搭配治療急性發作的[[非類固醇性止痛藥]]與[[秋水仙素]]使用[6]。一般而言由於成本考量，痛風患者要發生過兩次以上的發作才會建議開始使用預防性用藥[5]，但如果關節已經出現損傷、痛風石、或者是已經發生尿酸性腎病也會考慮投藥[11]。降尿酸藥物的劑量應該要調整到血清尿酸濃度介於300到600微莫耳/升(5.0到6.0毫克/公合)，並終生服藥[5][6]，但若發生急性發作則建議在發作期間暫時停藥[7]。如果血清尿酸濃度無法降到理想範圍且痛風重覆發作，這會被認定為治療失敗或是難治性痛風[57]。整體而言，異嘌呤醇在痛風治療上比probenecid來得有效[5]。
Uricosuric medications are typically preferred if undersecretion of uric acid, as indicated by a 24-hour collection of urine results in a uric acid amount of less than 800 mg, is found.[58] They are, however, not recommended if a person has a history of kidney stones.[58] In a 24-hour urine excretion of more than 800 mg, which indicates overproduction, a xanthine oxidase inhibitor is preferred.[58]
如果檢驗顯示尿酸排除不佳(通常是24小時尿液排除的總尿酸量低於800毫克)，那麼促進尿酸排泄藥物會是比較好的選擇[58]，但若患者有[[腎結石]]病史則不適合使用這類藥物。如果24小時尿液排除的總尿酸量高於800毫克，這通常顯示尿酸排除的功能正常，但生產過多，這種時候黃嘌呤氧化酶抑制劑是較佳的選擇。
Xanthine oxidase inhibitors (including allopurinol and febuxostat) block uric acid production, and long-term therapy is safe and well tolerated, and can be used in people with decreased kidney function or urate stones, although allopurinol has caused hypersensitivity in a small number of individuals.[5] In such cases, the alternative drug, febuxostat, has been recommended.[59]
黃嘌呤氧化酶抑制劑(包含異嘌呤醇及福避痛)會抑制尿酸合成，長期使用這類藥物目前被認為是安全且身體也能容忍長期用藥。腎功能不佳的患者或有尿酸結石的患者都可以使用黃嘌呤氧化酶抑制劑，但少數的人對於異嘌呤醇有過敏反應[5]，這些人則應該使用福避痛做為替代用藥[59]。
Without treatment, an acute attack of gout usually resolves in five to seven days; however, 60% of people have a second attack within one year.[4] Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and kidney and cardiovascular disease, and thus are at increased risk of death.[6][60] This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.[60]
預後
在沒接受治療的狀況下，急性痛風發作一般會在五到七天內緩解，但有六成的患者在一年內會第二次發作[4]。患有痛風的人罹患[[高血壓]]、[[糖尿病]]、[[代謝症候群]]、腎臟及[[心血管疾病|心血管]]疾病的風險也比較高，也因此整體死亡風險相對於常人較高[6][60]。痛風與疾病風險的相關部分可能是因為痛風與胰島素抗性與[[肥胖症]]的關係，但也有部分的風險上升似乎是獨立的[60]。
Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi.[6] These tophi occur in 30% of those who are untreated for five years, often in the helix of the ear, over the olecranon processes, or on the Achilles tendons.[6] With aggressive treatment, they may dissolve. Kidney stones also frequently complicate gout, affecting between 10 and 40% of people, and occur due to low urine pH promoting the precipitation of uric acid.[6]Other forms of chronic kidney dysfunction may occur.[6]
如果不接受治療，急性痛風發作可能會惡化為慢性痛風並造成關節面損傷、關節變形、或是無痛性的痛風石[6]。痛風患者如果在五年內不接受治療，產生痛風石的機會約為三成，通常會出現在耳殼、手肘的尺骨鷹嘴突、或是[[阿基里斯腱]][6]。在接受積極治療後，痛風石可能會消失。[[腎結石]]也是痛風常見的併發症，約有一至四成的患者有這個問題，目前認為是由於尿液的酸鹼值偏酸，因而會促使尿酸在腎臟形成沉澱[6]。其他的慢性腎功能異常也可能出現在痛風患者身上[6]。
Gout affects around 1–2% of the Western population at some point in their lifetimes, and is becoming more common.[5][6] Rates of gout have approximately doubled between 1990 and 2010.[10] This rise is believed to be due to increasing life expectancy, changes in diet, and an increase in diseases associated with gout, such as metabolic syndrome and high blood pressure.[15] A number of factors have been found to influence rates of gout, including age, race, and the season of the year. In men over the age of 30 and women over the age of 50, prevalence is 2%.[46]
流行病學
西方人終其一生有1到2%的人會患上痛風，而且這個比率正在上升[5][6]。從1990到2010年，痛風的發生率上升了將近兩倍[10]，一般認為上升的原因包括壽命延長、飲食改變、以及與痛風相關的疾病的發生率上升（比方說[[代謝症候群]]和[[高血壓]][15]）。有許多因素會影響痛風的發生率，包括年齡、種族、季節。在大於30歲的男性與50歲以上的女性族群中，痛風的盛行率為2%[46]。
In the United States, gout is twice as likely in African American males as it is in European Americans.[61] Rates are high among the peoples of the Pacific Islands and theMāori of New Zealand, but rare in Australian aborigines, despite a higher mean concentration of serum uric acid in the latter group.[62] It has become common in China, Polynesia, and urban sub-Saharan Africa.[6] Some studies have found that attacks of gout occur more frequently in the spring. This has been attributed to seasonal changes in diet, alcohol consumption, physical activity, and temperature.[63]
在美國，非裔美國男性相對於歐裔美國人而言有兩倍的機會患上痛風[61]，太平洋島國居民與紐西蘭的[[毛利人]]的痛風發生率也偏高，而澳洲原住民雖然血中尿酸濃度平均較高，但發生率卻不高。在中國、玻里尼西亞、撒哈拉沙漠以南的都會區，痛風的發生率也都在上升[6]。有些研究指出痛風急性發作好發於春季，這可能是飲食習慣隨季節改變、酒精攝取量、運動量或是氣溫的改變造成的[63]。
Antonie van Leeuwenhoek described the microscopic appearance of uric acid crystals in 1679.[64]
[[安東尼．范．列文虎克]]在1679年初次描述了尿酸結晶在顯微鏡下的結構[64]。
The word "gout" was initially used by Randolphus of Bocking, around 1200 AD. It is derived from the Latin wordgutta, meaning "a drop" (of liquid).[64] According to the Oxford English Dictionary, this is derived from humorism and "the notion of the ’dropping’ of a morbid material from the blood in and around the joints".[65]
「痛風」的英文(gout)則是在西元1200年，由一位名叫Randolphus of Bocking的一名修士發明，它來自於拉丁文的gutta，指的是一滴液體[64]。命名的理由是[[體液學說]]認為痛風是由於血液中的病態物質「滴」到關節內部與周圍造成。
Gout has, however, been known since antiquity. Historically, it has been referred to as "the king of diseases and the disease of kings"[6][66] or "rich man’s disease".[9] The first documentation of the disease is from Egypt in 2,600 BC in a description of arthritis of the big toe. The Greek physician Hippocrates around 400 BC commented on it in his Aphorisms, noting its absence in eunuchs and premenopausal women.[64][67] Aulus Cornelius Celsus (30 AD) described the linkage with alcohol, later onset in women, and associated kidney problems:
痛風自古就已為人所知，它曾被稱作「疾病之王並同時是屬於王者的疾病」[6][66]或「富貴病」[9]。關於痛風的記載最早可追溯到西元前2600年埃及關於大腳趾關節炎的記錄。希臘醫師[[希波克拉底]]在西元前400年所著的[[格言]]中提到痛風不發生在[[更年期]]前的婦女及[[宦官]]身上[64][67]。[[凱爾蘇斯]]在西元30年則描述了痛風與酒精和腎病的關聯，並發現在女性身上痛風會相對晚發作的現象：
Again thick urine, the sediment from which is white, indicates that pain and disease are to be apprehended in the region of joints or viscera... Joint troubles in the hands and feet are very frequent and persistent, such as occur in cases of podagra and cheiragra. These seldom attack eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed... some have obtained lifelong security by refraining from wine, mead and venery.[68]
……濃厚的尿液中有白色的沉澱物顯示疼痛與疾病潛藏在臟器與關節……在手與腳的關節問題很常見並且會持續發生(手部痛風稱為cheiragra，足部則稱為podagra)。這種疾病甚少影響宦官與童子之身的男孩，也不常在女性身上看到，除非他們的月事已經停止……有些患者在戒酒與禁慾後，此病一生不再發作。[68]
In 1683, Thomas Sydenham, an English physician, described its occurrence in the early hours of the morning, and its predilection for older males:
Gouty patients are, generally, either old men, or men who have so worn themselves out in youth as to have brought on a premature old age—of such dissolute habits none being more common than the premature and excessive indulgence in venery, and the like exhausting passions. The victim goes to bed and sleeps in good health. About two o’clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle or instep. The pain is like that of a dislocation, and yet parts feel as if cold water were poured over them. Then follows chills and shivers, and a little fever... The night is passed in torture, sleeplessness, turning the part affected, and perpetual change of posture; the tossing about of body being as incessant as the pain of the tortured joint, and being worse as the fit comes on.[69]
英國醫師湯瑪斯．席登漢在1683年描述痛風容易在清晨發作，並好發於老年男性：
痛風患者一般是老年男性，或是那些過於操勞以致於身體未老先衰的男性（當中最常見的是沉緬於對酒精無限制的慾望中者，或是投身其他令人疲憊的熱情中)。患者通常在良好的狀態下入睡，但在約凌晨兩點就會因為腳拇趾的劇痛而醒來，有時候疼痛也會發生在腳跟、腳踝或是腳背，但較為少見。痛風的疼痛類似脫臼加上冰水淋在患部上，然後緊接而來的是寒顫與低燒……夜晚在折磨與無眠中消磨，不斷翻動著疼痛的部位與改變姿勢，疼痛與身體不斷的翻動都不會停止，並不斷惡化[69]。
The Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679.[64] In 1848, English physician Alfred Baring Garrodidentified excess uric acid in the blood as the cause of gout.[70]
荷蘭科學家[[安東尼．范．列文虎克]]在1679年初次描述了尿酸結晶在顯微鏡下的結構[64]。到了1848年，英國醫師阿弗列德．巴靈．加洛德發現血中過多的尿酸會導致痛風[70]。
Gout is rare in most other animals due to their ability to produce uricase, which breaks down uric acid.[71] Humans and other great apes do not have this ability, thus gout is common.[4][71] Other animals with uricase include fish, amphibians, and most non primate mammals.[72] The Tyrannosaurus rex specimen known as "Sue", however, is believed to have suffered from gout.[73]
其他動物
由於其他動物能合成[[尿酸氧化酶]]來分解尿酸，痛風在其他動物身上並不常見[71]。人類與其他[[人科]]動物無法合成這種酵素，因此在這些生物身上常見到痛風的發生[4][71]。[[魚|魚類]]、[[兩棲動物]]與其他非[[靈長目]]動物能合成尿酸氧化酶[72]。被命名為[[蘇(化石)]]的[[暴龍]]被認為在生前患有痛風[73]。
A number of new medications are under study for treating gout, including anakinra, canakinumab, and rilonacept.[74] Canakinumab may result in better outcomes than a low dose of a steroid but costs five thousand times more.[75] A recombinant uricase enzyme (rasburicase) is available; its use, however, is limited, as it triggers anautoimmune response. Less antigenic versions are in development.[4]
相關研究
目前有數種針對痛風的新藥正在開發中，包括anakinra（[[白細胞介素1族]]受體拮抗劑)）、canakinumab（抗IL-1B抗體）、以及rilonacept（[[白細胞介素1族]]抑制劑）[74]。Canakinumab可能比低劑量的類固醇效果更佳，但價位也高了五千倍[75]。合成[[尿酸氧化酶]]是可以取得的，但它的用途很有限，因為它會誘發自體免疫反應，目前正在開發較不會誘發免疫反應版本的合成尿酸氧化酶[4]。
痛風是一種因嘌呤（一譯「普林」）代謝障礙，使尿酸累積而引起的疾病，屬於關節炎的一種，女性一般在50歲之前不會發生痛風，因為雌激素對尿酸的形成有抑制作用；但是在更年期後會增加發作比率。由於尿酸在人體血液中濃度過高，在軟組織如關節膜或肌腱裡形成針狀結晶，導致身體免疫系統過度反應（敏感）而造成痛苦的炎症。一般發作部位為大拇趾關節（這種情況稱為podagra），踝關節，膝關節等。長期痛風病初期會出現於下肢，繼而會發生於手指關節，或者耳廓的軟組織位置。急性痛風發作部位出現紅、腫、熱、劇烈疼痛，一般多在子夜發作，可使人從睡眠中驚醒。
痛風的歷史
痛風古稱「王者之疾」、「帝王病」、「富貴病」，因為此症好發在達官貴人的身上，如元世祖忽必烈晚年就因飲酒過量而飽受痛風之苦，使他無法走路和騎馬領兵上陣。頗為有趣的一點是在歷史上，患上痛風曾一度被認為是一種社會嚮往的疾病，因為只有達官貴人，有權有勢的上流社會人士才有機會患上痛風（高尿酸飲食多數只有富人才負擔得起）。此外，亦有認為痛風的發作是可預防癱瘓和中風等更嚴重的疾病[1]。
「痛風」一詞最早出現在南北朝時期的醫學典藉裡，因其疼痛來得快如一陣風，故由此命名。古代又稱「痛痹」，明朝虞摶所著醫學正傳云：「夫古之所謂痛痹者，即今之痛風也。諸方書又謂之白虎歷節風，以其走痛於四肢骨節，如虎咬之狀，而以其名名之耳」。
世界其它地方亦有痛風疾病的古代紀錄，如西元前2640年，埃及人的身上已經發現有痛風引至大拇趾關節病變。古希臘名醫希波克拉底稱痛風為「不能步行的病」，並指出痛風是富者的關節炎，而風濕則是貧者的關節炎。在他的《格言》（Aphorisms）中，他對痛風下了以下的結論：「太監不會得到痛風，女人在更年期以後才會得到痛風，痛風的發炎在發生後40天內就會消退，痛風在春秋兩季較會發生。」[2]。
西元三世紀，羅馬醫師蓋倫首次描述痛風石（尿酸鹽）。痛風英文字「gout」是約在西元12世紀由一位名為Randolphus of Bocking的修士。這個字是由拉丁文gutta來，是一滴的意思。以當時中世紀的醫學概念「四體液説」，痛風是被認為關節的部位多了惡毒液體[2]。
引起高尿酸的原因
當血中尿酸濃度長期高於7.8毫克/100C.C，醫學上就稱為「高尿酸血症」。血中尿酸會因為尿酸的產量過多以及排泄減少而上升，引至尿酸的產量過多的原因包括先天性代謝異常、淋巴增生疾病等，這些原因佔高尿酸血症約百份之十。而引至尿酸排泄減少的原因則包括腎功能障礙和藥物引起的不良尿酸排泄。這些藥物包括噻嗪類利尿劑、環孢黴素A、吡嗪醯胺、乙胺丁醇、煙酸和地達諾新[3]。
雖然約三份之二患有高尿酸血症者不會在身上出現任何症狀，但是血中尿酸濃度持續上升，最終會形成一般稱為「尿酸鹽」的「尿酸單鈉」（monosodium urate） 針狀結晶體，積聚於軟組織中，尤其是以下肢足部關節最常見。當白血球來吞噬在關節腔內之晶體時，會釋出發炎物質，進而引起一連串的發炎性反應，造成關節劇痛及關節腫脹和變形。若尿酸鹽沉積在腎臟，則會造成腎結石、尿路結石，引發劇烈腰痛。
高尿酸血症是引起痛風的主因。研究指出在男性身上，血尿酸濃度愈高者，出現痛風症狀的機會愈高，血尿酸濃度超過每公合9毫克者，4.9%會出現痛風[4]。近年的大型流行病學研究發現，痛風與飲酒（尤其是啤酒）、過量的肉類海產（尤其是內臟及帶殼海鮮）攝取有關，近來的研究指出高糖（如碳酸飲料及果糖）會導致痛風。另一方面，維生素C，咖啡和奶製品則可能對阻止痛風的發生有所幫助[5][6]。
酒精引發痛風的原因是因為酒精在肝組織代謝時，大量吸收水份，使血濃度加強，使得原來已經接近飽和的尿酸，加速進入軟組織形成結晶，導致身體免疫系統過度反應（敏感）而造成炎症。一些食品經過代謝後，其中部分衍生物可以引發原來積蓄在軟組織的尿酸結晶重新溶解，這時可誘發並加重關節炎。此外，劇烈運動、肥胖及壓力亦會導致尿酸濃度上升，誘發痛風[7]。
痛風大多在半夜才發作是因為晚上睡覺時，人體的抗炎物質促腎上腺皮質激素在半夜時分泌最少，加上睡眠時酸鹼值因體內累積二氧化碳而偏向酸性，而腳趾的溫度較低，加上腳趾附近的液體會被身體吸收使尿酸濃度增加，因此痛風最易在半夜出現在腳拇趾的部位。
40歲以上者應定期健康檢查，接受血中尿酸值檢查，預防痛風。若患上高尿酸血症，除了在醫師指示下服用降尿酸藥物，將尿酸值控制在正常範圍外，亦必須從生活與飲食杜絕一切痛風的誘因。減少進食動物性的高嘌呤食物（如海鮮、內臟類、非素食的高湯，植物性的高嘌呤食物則不必擔心），也需避免飲用過量酒精飲料，尤其是啤酒是痛風患者的禁忌。以長期來說更有效的飲食是能預防心血管疾病、糖尿病及腎臟病的飲食（低飽和脂肪、低鈉、低升糖指數、低精緻糖、蛋白質不要過多或過少，腎功能損失已經到一定程度的患者鉀及磷也不能過多），這樣也容易維持理想體重，減少肥胖問題。切勿暴飲暴食（包括盡可能的經常飲水、不要到口渴才喝水、用少量多次的飲水來達到充足的飲水）、飢餓過度，運動不足及激烈運動也會增加痛風風險。
若痛風已經發作，則須立即檢測尿酸濃度、腎功能、血壓血糖及接受治療，並開始預防心血管疾病及糖尿病（第一次痛風是要開始預防這些疾病的信號），以免引起心肌梗塞、腦栓塞和痛風性腎病等併發症。
過去的觀念是認為高嘌呤成份食品會增加痛風機率，但最新的流行病學研究 顯示除了啤酒及發酵食品外，幾乎所有的高嘌呤植物性食品，反而可以降低痛風機率；傳統上認為不含嘌呤的果糖，則會造成高尿酸；而且預防及治療痛風就是預防及治療代謝症候群的方法。
需要控制的飲食：
痛風治療[編輯 | 編輯原始碼]減肥[編輯 | 編輯原始碼]
對於過重的痛風患者，健康的減肥也可以降低尿酸。不過過速地減肥減重及乳酸堆積（高強度有氧運動及無氧運動會造成乳酸堆積，但可以用運動後按摩避免，中低強度有氧運動不容易造成乳酸堆積）也會增加尿酸、增加痛風發作的可能性。
健康的減肥也可以讓脂肪肝、心血管疾病及糖尿病變更輕微、輕微患者甚至很有機會不藥而癒。
而減肥的目標是讓腰圍小於身高的一半、安全的減肥速度是一個月小於1~2公斤。
如果能接受素食，改採素食大多可以降低血液尿酸含量，蛋奶素更好；而用植物性蛋白來取代部分動物性蛋白攝取，也是有幫助的；傳統上被認為是高嘌呤的植物性食品，其實會降低痛風機率。只是仍然要避免高精緻糖、高鹽、過高蛋白、高熱量、高飽和脂肪，並且盡可能的排除反式脂肪的攝取。
糖尿病治療及預防
一些研究認為，胰島素抵抗是造成腎臟無法排泄尿酸的原因，而統計學已經指出，高果糖攝取會造成高尿酸；因此對於尚未罹患糖尿病的痛風患者，就當成糖尿病前期患者來處置，尿酸自然會降下來。
控制尿酸的藥物
由於是代謝障礙毛病，如果控制飲食也未見成效，必須要長期用藥物控制。 常用藥物分兩類：
減少尿酸合成
別嘌醇片（Allopurinol 100mg），亦作別嘌呤醇。
增加排出尿酸[編輯 | 編輯原始碼]急性痛風患者在使用此類藥物時，常配合生理食鹽水或葡萄糖的點滴使用，以加速排出尿酸。
尿酸排泄劑的作用機制為抑制腎小管對尿酸的再吸收，增加尿酸從尿液中排出，從而減少血中尿酸的濃度，最終減少尿酸鹽沉積在軟組織裡，減少痛風炎的發生。下列病患不宜使用；泌尿系統結石，血液失衝，化療及癌腫引起的尿酸症。
苯溴馬隆亦名為本補麻隆。苯溴馬隆屬於苯馬並呋喃類衍生物，主要的藥理作用為抑制腎小管對尿酸的重吸收，從而降低血中尿酸濃度。苯溴馬隆於1978年在德國研製並用於臨床試驗，此藥在歐洲應用多年，根據超過十年的治療經驗，苯溴馬隆的耐受性和藥效均要高於別嘌呤醇和丙磺舒。（100mg苯溴馬隆藥效相當於300mg別嘌呤醇，而丙磺舒的副作用較大，患者耐受性較差且療效不如苯溴馬隆）而且苯溴馬隆的半衰期長，一天口服一次，每次50-100mg既能將尿酸控制在安全範圍內。需要注意的是，在服用苯溴馬隆的初期，每天至少飲水2L，將尿液PH值維持在6.0-6.8之間（合用碳酸氫鈉），如關節疼痛，合用非甾體類消炎藥。定期複查肝腎功能。
常用消炎藥物
急性痛風可以服用
在急性痛風期間，不應增加控制嘌呤藥物的份量，否則增加身體免疫系統過度反應。
補充劑
鵝肌肽，又名胺（氨）肌肽（Anserine）是人體二肽組胺酸，在腎臟中代謝，超過90%轉化為三甲基組胺酸（3-Methyl-Histidine）排出體外。可以幫助尿酸排泄。
手術
痛風石是可以手術治療、開刀取的，但一定要根據患者自身病情及醫生指導進行，不能盲目的選擇。[9]
冷敷以及熱敷
在疼痛時熱敷和冷敷都是不適合的做法，可能會使得病情或炎症加重；最佳的方法是臥床休息（側身），將患肢適當地和在感到安全狀況時略微的抬高，並立即服用秋水仙鹼或芬必得等藥物。[10]