剛解釋痛風與尿酸關係. 找不到筆記. 重寫一篇. 先列出以前印象
尿酸異常的人. 90% 一輩子不會發生痛風
急性痛風發作時. 有30% 抽血尿酸正常.
降尿酸的目的是要減少痛風發生頻率
痛風一年發作超過兩次以上考慮給藥治療, 頻繁痛風發作建議將尿酸降到6以下
針對2046名健康男性進行 14.9年追蹤.
尿酸 ≥9 mg/dl 每年有4.9% 發生痛風, 五年後累積有 22% 發生痛風
尿酸 7.0~8.9 mg/dl, 每年有 0.5% 發生痛風
尿酸 < 7 每年有 0.1% 發生痛風
尿酸 ≥9 mg/dl 的民眾發生高血壓機率上升三倍
(有相關性.不代表有因果關係)
為了量化無症狀高尿酸血症的後果,本研究基於30,147人年的前瞻性觀察數據,分析了首次發生痛風性關節炎的發生率。研究納入了「正常老化研究」(Normative Aging Study)中2,046名初始健康的男性,並對其進行了14.9年的隨訪,期間進行了系列檢查並測量了尿酸水平。先前血清尿酸濃度≥9 mg/dl的患者,痛風性關節炎的年發生率為4.9%;尿酸濃度為7.0~8.9 mg/dl的患者,年發生率為0.5%;尿酸濃度<7.0 mg/dl的患者,年發生率為0.1%。尿酸濃度≥9 mg/dl的患者,五年後痛風性關節炎的累積發生率達22%。高血壓患者的發生率是血壓正常患者的三倍(p<0.01)。在比例風險模型中,痛風最強的預測因子是年齡、體重指數、高血壓、膽固醇水平和飲酒量。當血清尿酸濃度納入模型後,這些變數均不再具有獨立的預測能力。在最終檢查時,僅有0.7%的參與者血清肌酸酐濃度≥2.0 mg/dl,且無證據顯示存在高尿酸血症引起的腎功能損害。這些數據支持對無症狀高尿酸血症採取保守治療。
Abstract
To quantify the consequences of asymptomatic hyperuricemia, this study examined rates for a first episode of gouty arthritis based on 30,147 human-years of prospective observation. A cohort of 2,046 initially healthy men in the Normative Aging Study was followed for 14.9 years with serial examinations and measurement of urate levels. With prior serum urate levels of 9 mg/dl or more, the annual incidence rate of gouty arthritis was 4.9 percent, compared with 0.5 percent for urate levels of 7.0 to 8.9 mg/dl and 0.1 percent for urate levels below 7.0 mg/dl. With urate levels of 9 mg/dl or higher, cumulative incidence of gouty arthritis reached 22 percent after five years. Incidence rates were three times higher for hypertensive patients than for normotensive patients (p less than 0.01). The strongest predictors of gout in a proportional hazards model were age, body mass index, hypertension, and cholesterol level, and alcohol intake. When the serum urate level became a factor in the model, none of these variables retained independent predictive power. At the final examination, only 0.7 percent of participants had a serum creatinine level of 2.0 mg/dl or more, with no evidence of renal deterioration attributable to hyperuricemia. These data support conservative management of asymptomatic hyperuricemia.
約略來說,尿酸是身體的物質,而痛風是一種疾病。尿酸並不全然與痛風可以劃上等號。有三大觀念需要澄清[Am J Med. 1987 Mar;82(3):421-6.]:
2022年台灣內科學誌-痛風及高尿酸血症最新各國指引比較
痛風的診斷
目前以 2015 年 ACR/EULAR 分類為標準 23 ,當病患至少有一個周邊關節或滑 囊腫、痛、觸痛時才可進入分類標準,其中痛 風進一步下分成臨床標準、實驗室檢查及影像 學檢查共三個面向。
1. 臨床標準包含影響關節、 症狀、發病時間以及有無其他痛風石共計四個項目;
2. 實驗室標準包含血中尿酸濃度及滑囊液 檢查;
3. 影像標準包含超音波、雙能電腦斷層及 X 光,
上述三個面向分數總和大於或等於 8 分 即可診斷為痛風發作。
Gout-StatPearls.
痛風風險隨血清尿酸濃度單調增加。
血清尿酸濃度高於 9 mg/dL 時,一年內痛風發作的可能性是血清尿酸濃度低於 6 mg/dL 時的 3 倍
痛風診斷標準:
建議使用 2015 ACR/EULAR 診斷標準
1. 若關節內或滑液囊內出現尿酸結晶. 即可確診
Presence of MSU crystals in a symptomatic joint or bursa (i.e., in synovial fluid) or tophus
2. 若無法檢測關節液. 可採用下列選項計算總分. 8分以上可診斷為痛風發作.
Score ≥8 required for classification as gout
. The 2015 ACR/EULAR criteria have a sensitivity of 92% and a specificity of 89%, surpassing the accuracy of all previous definitions and enabling more precise and reliable diagnosis of gout in epidemiological studies.

