第五章 討論
第三節 痛風疼痛發作之相關因子探討
目前尚未有研究針對痛風患者的疼痛發作狀態進行探討。在本研究中，對 於生化檢驗結果與發作狀態之間，經控制干擾因子(性別、年齡與種族)後，曾經 發作組中除尿酸濃度顯著較高外，亦伴隨三酸甘油脂有較高的表現量，這樣相似 的結果，也存在於其他病例對照研究之痛風患者身上6, 77。
本研究發現，原住民與非原住民的平均初次發作年齡 (50.0±1.9 vs. 60.0 ±2.5 歲)有顯著差異，原住民族群明顯早發於非原住民族群。2002 年時，顏氏21於南 投縣信義鄉中所作的研究，也發現以布農族為主的原住民族群，初次發作年齡比 非原住民提早 19.1 年發生。本次研究發現，女性的初次發作年齡相對較男性晚 發生，這也與美國Harrold 79及 De Souza 等人49的研究結果相似。
Choi 與 Curhan78的研究發現，酒類[啤酒、烈酒以及水果酒(葡萄酒)]的攝取 與尿酸濃度有顯著的正相關，有飲酒習慣者也會有較高的勝算罹患痛風6，但在 Lyu 等人的病例對照研究中14以及本研究之結果發現，飲酒的習慣與痛風或痛風 急性疼痛發作皆無顯著的相關，由於體內尿酸的平衡機制受到外因性的環境因素 以及內因性的遺傳因子差異所影響7, 79，遂造成飲酒習慣與痛風疼痛發作狀態之 間的關係不顯著。
除了解與痛風疼痛發作狀態有關的因子外，本研究亦進ㄧ步探討初次疼痛 發作年齡的相關因子。飲酒狀態與種族對於初次疼痛發作年齡所產生之交互作用 發現，飲酒習慣對於非原住民的效應較為明顯(51.5 vs. 68.0 歲)這可能是酒精性飲 料含有過多嘌呤所致 23。至於原住民族群僅有1.4 歲的差距(分別為 48.9 與 50.3 歲)，Lai 等人6認為台灣原住民族群在產生飲酒習慣前就已有尿酸升高的情形，
且其他研究指出與台灣原住民屬相同語系的菲律賓族群80，其高尿酸血症以居住 美國者較高於居住菲律賓地區者，這除了飲食中攝取較高的嘌呤外也有尿酸排泄
不良的情形存在22, 81, 82，因此可推斷原住民痛風的產生受到相同遺傳因子及生活 中的飲食習慣所影響。
第六章、結論
本研究為台灣首次進行 hURAT1 基因與痛風之相關性研究，發現 hURAT1 基因之 C258T 與 C426T 單一核苷酸基因多型性，可作為痛風患病的遺傳指標 (markers)。
男性、原住民和有飲酒的習慣者分別相較於女性、非原住民及未飲酒者皆 使痛風患者初次疼痛發作年齡提早10 年左右。而 hURAT1 基因上帶有 258 T 對 偶基因(258T carrier)及 426C 對偶基因(426 C carrier)者，皆有初次痛風疼痛發作 年齡較晚的趨勢。然而，痛風疼痛發作年齡也會因每個年齡層不同，其痛風發作 的風險而有所差異。
原住民是痛風及痛風疼痛發作的高危險族群，因受遺傳及環境因素共同影 響所致，因此醫療照護及高尿酸血症預防之衛教宣導，可能才是有效改善原住民 高痛風盛行率的根本之道。
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表一、依種族分層探討與痛風相關之人口學資料A
(year) mean±SD 52.9±14.8 51.1±16.2 61.3±14.3 60.3±12.6 56.2±15.0 57.5±14.1
年齡 0.960 0.635 0.320
表二、依種族分層探討與生理生化值相關性A
尿酸 <0.001 <0.001 <0.001
(mg/dL) 9.1±0.3
A values were performed by ‘Least Square MEAN±SE’;
B控制’性別&年齡’條件下的 p-value
C 控制’性別&年齡、種族’的條件下的 p-value`;
註:「種族」狀態未知的對象共五名(痛風組 2 名,對照組 3 名)
表三、依種族分層探討痛風相關之共病症A
表四、依種族分層探討hURAT1 單一核苷酸基因多型性與對偶基因之分布A
表五、利用邏輯斯迴歸探討hURAT1 單一核苷酸基因多型性與痛風發生之關聯性
表五、利用邏輯斯迴歸探討hURAT1 單一核苷酸基因多型性與痛風之關聯性(續)
Model 2-1 Model 3-1 Model 4-1 Model 5-1
OR (95% CI) OR (95% CI) OR (95% CI) OR (95% CI)
性別 男/女 5.38 (2.14-13.53) 5.82 (2.29-14.76) 5.41 (2.16-13.58) 5.32 (2.08-13.64)
種族 原住民 / 非原住民 6.33 (2.53-15.85) 5.83 (2.38-14.29) 6.04 (2.44-14.99) 6.29 (2.49-15.89)
高血壓 有/無 86.93 (9.67-781.50) 77.03 (8.87-669.13) 86.66 (9.70-774.52) 85.11 (9.45-766.53)
C258T
258 T 攜帶者/ 258 CC 0.19 (0.08-0.49)
C426T
426 TT / 426 C 攜帶者 3.85 (1.53-9.68)
兩者SNP 合併
258 T 攜帶者+426 C carrier /其他組合 0.21 (0.08-0.56)
C258T* C426T
258 T 攜帶者 + 426 C 攜帶者(n=51) 1
258 T 攜帶者+ 426 TT(n=4) 0.76 (0.04-13.27)
258 CC + 426 TT(n=94) 5.09 (1.90-13.68)
258 CC + 426 C 攜帶者(n=8) 4.70 (0.58-38.32)
表六、痛風病患疼痛發作狀態之人口學分布A
表六-1、痛風病患疼痛發作狀態與生理生化檢測之相關性#
# values were performed by ‘Least Square MEAN±SE’;
A控制’性別、年齡&種族’條件下的 p-value;
註: 112 名痛風患者中，其中 2 名患者的發作狀態未知
表六-2、痛風病患發作狀態與共病症之關聯性
痛風發作狀態 未曾發作
(n=32)
曾經發作
(n=78) p-valueA
高血壓 0.194
無 18 (56.3) 54 (69.2) 有 14 (43.8) 24 (30.8)
糖尿病 0.225
無 26 (81.3) 70 (89.7) 有 6 (18.8) 8 (10.3)
中風 0.511
無 31 (96.9) 77 (98.7) 有 1 (3.1) 1 (1.3)
肺結核 0.261
無 32 (100.0) 75 (96.2) 有 0 (0.0) 3 (3.9)
肝病 0.636
無 30 (93.8) 71 (91.0) 有 2 (6.3) 7 (9.0)
高血脂症 0.824
無 28 (87.5) 67 (85.9) 有 4 (12.5) 11 (14.1)
腎臟病 0.361
無 32 (100.0) 76 (97.4) 有 0 (0.0) 2 (2.6)
A為卡方檢定的p-value
註: 112 名痛風患者中，其中 2 名患者的發作狀態未知
表六-3、痛風病患疼痛發作狀態之 hURAT1 基因型分布情況
表七、痛風病患初次疼痛發作年齡之存活分析