今日の臨床サポート

痛風(痛風発作/痛風関節炎)

著者: 寺井千尋 自治医科大学、サクラビア・クリニック

監修: 野田光彦 国際医療福祉大学市川病院 糖尿病・代謝・内分泌内科

著者校正/監修レビュー済:2020/10/14
参考ガイドライン:
  1. 日本痛風・尿酸核酸学会:高尿酸血症・痛風の治療ガイドライン 第3版(2019)
患者向け説明資料

概要・推奨   

  1. 痛風発作既往者や痛風結節を有する者は尿酸降下療法の対象となる(推奨度1)(JG)[1]
  1. 急性痛風関節炎(痛風発作)は、臨床経過や重症度、合併症、併用薬を考慮して、NSAIDs、グルココルチコイド、コルヒチンのいずれかか、組み合わせで治療する(推奨度1)(RsJG)[1]
  1. 痛風発作時のコルヒチンは少量投与で十分である(推奨度1)(RJG)[1]
  1. 尿酸値の急激な低下は痛風発作再発リスクを増大させるので、尿酸降下薬は少量から徐々に増量して尿酸値6mg/dl以下を目標とする(推奨度2)(OJ)[1]
  1. 尿酸降下薬開始後の痛風発作再発の予防対策を行う(推奨度2)(OJ)[1]
  1. 尿酸値が高いほどその後の痛風発作発症のリスクが増大するので、無症候性高尿酸血症でも尿酸値9mg/dl以上で生活習慣の改善が無効な患者では、尿酸降下療法を開始する(推奨度2)(OJ)[1]
  1. 痛風の確定診断は関節液中の白血球に貪食された尿酸一ナトリウム結晶の検出による(推奨度2)(JG)[1]
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となり
薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
寺井千尋 : 特に申告事項無し[2021年]
監修:野田光彦 : 特に申告事項無し[2021年]

改訂のポイント:
  1. 高尿酸血症・痛風の治療ガイドライン 第3版に基づき、全体的にアップデートを行った。

病態・疫学・診察

疾患(疫学・病態)のまとめ  
  1. 痛風(痛風発作/痛風関節炎)とは、尿酸一ナトリウム結晶(MSU:monosodium urate)による結晶誘発性関節炎(ないし滑液包炎)であり、その基礎には代謝異常である高尿酸血症がある。痛風発作の大半が母趾基関節、足根部、足首に生じ、90%以上の発作は膝関節より末梢に生じる。
  1. 日本では高尿酸血症は成人男性の25~30%にみられ[2]、痛風はその1/20に発症するが[3]、米国ではもっとも頻度の高い関節炎とされる。日本における女性痛風患者は患者全体の1~1.5%に過ぎない[4]
  1. 肥満、高血圧、糖尿病、高脂血症などのメタボリック症候群を合併することが多く、高尿酸血症が長期持続すると痛風結節を生じ、腎機能障害、尿路結石を来す。
問診・診察のポイント  
  1. 「これまでに同じような急激な関節痛(関節炎)を起こしたことがないか。」痛風発作は初期の発作頻度は1~2年に1回程度で間欠期には全く無症候であり、患者自身が以前の関節痛を無関係と考えていることもある。急性関節炎の既往があり、それが拇趾基関節や足首であれば痛風の確率は高くなる。

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文献 

著者: Tuhina Neogi, Tim L Th A Jansen, Nicola Dalbeth, Jaap Fransen, H Ralph Schumacher, Dianne Berendsen, Melanie Brown, Hyon Choi, N Lawrence Edwards, Hein J E M Janssens, Frédéric Lioté, Raymond P Naden, George Nuki, Alexis Ogdie, Fernando Perez-Ruiz, Kenneth Saag, Jasvinder A Singh, John S Sundy, Anne-Kathrin Tausche, Janitzia Vaquez-Mellado, Steven A Yarows, William J Taylor
雑誌名: Ann Rheum Dis. 2015 Oct;74(10):1789-98. doi: 10.1136/annrheumdis-2015-208237.
Abstract/Text OBJECTIVE: Existing criteria for the classification of gout have suboptimal sensitivity and/or specificity, and were developed at a time when advanced imaging was not available. The current effort was undertaken to develop new classification criteria for gout.
METHODS: An international group of investigators, supported by the American College of Rheumatology and the European League Against Rheumatism, conducted a systematic review of the literature on advanced imaging of gout, a diagnostic study in which the presence of monosodium urate monohydrate (MSU) crystals in synovial fluid or tophus was the gold standard, a ranking exercise of paper patient cases, and a multi-criterion decision analysis exercise. These data formed the basis for developing the classification criteria, which were tested in an independent data set.
RESULTS: The entry criterion for the new classification criteria requires the occurrence of at least one episode of peripheral joint or bursal swelling, pain, or tenderness. The presence of MSU crystals in a symptomatic joint/bursa (ie, synovial fluid) or in a tophus is a sufficient criterion for classification of the subject as having gout, and does not require further scoring. The domains of the new classification criteria include clinical (pattern of joint/bursa involvement, characteristics and time course of symptomatic episodes), laboratory (serum urate, MSU-negative synovial fluid aspirate), and imaging (double-contour sign on ultrasound or urate on dual-energy CT, radiographic gout-related erosion). The sensitivity and specificity of the criteria are high (92% and 89%, respectively).
CONCLUSIONS: The new classification criteria, developed using a data-driven and decision-analytic approach, have excellent performance characteristics and incorporate current state-of-the-art evidence regarding gout.

Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
PMID 26359487  Ann Rheum Dis. 2015 Oct;74(10):1789-98. doi: 10.1136/an・・・
著者: Akira Shoji, Hisashi Yamanaka, Naoyuki Kamatani
雑誌名: Arthritis Rheum. 2004 Jun 15;51(3):321-5. doi: 10.1002/art.20405.
Abstract/Text OBJECTIVE: To evaluate the proposed relationship between persistent reduction of serum urate into the subsaturating range and reduction in the frequency of acute gouty attacks.
METHODS: We retrospectively examined data derived from 267 patients who had experienced at least 1 gouty attack before their first visit to our clinic. Serum urate concentration, history of recurrent gouty attacks, and information about antihyperuricemic drug use were collected on each visit for up to 3 years from the first visit of each patient. Data derived from visits >1 year after study entry were subjected to statistical analysis.
RESULTS: When adjusted for baseline serum urate level and the number of gouty attacks prior to study entry, reduction of followup serum urate concentration and antihyperuricemic drug use were each significantly associated with a reduced risk of gouty attacks (odds ratio [OR] 0.42, 95% confidence interval [95% CI] 0.31-0.57; OR 0.22, 95% CI 0.10-0.47, respectively).
CONCLUSION: The data indicate that reduction of serum urate concentrations to 6 mg/dl or lower will eventually result in a reduced frequency or prevention of future gouty attacks.

PMID 15188314  Arthritis Rheum. 2004 Jun 15;51(3):321-5. doi: 10.1002/・・・
著者: E W Campion, R J Glynn, L O DeLabry
雑誌名: Am J Med. 1987 Mar;82(3):421-6.
Abstract/Text 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.

PMID 3826098  Am J Med. 1987 Mar;82(3):421-6.
著者: Robert A Terkeltaub, Daniel E Furst, Katherine Bennett, Karin A Kook, R S Crockett, Matthew W Davis
雑誌名: Arthritis Rheum. 2010 Apr;62(4):1060-8. doi: 10.1002/art.27327.
Abstract/Text OBJECTIVE: Despite widespread use of colchicine, the evidence basis for oral colchicine therapy and dosing in acute gout remains limited. The aim of this trial was to compare low-dose colchicine (abbreviated at 1 hour) and high-dose colchicine (prolonged over 6 hours) with placebo in gout flare, using regimens producing comparable maximum plasma concentrations in healthy volunteers.
METHODS: This multicenter, randomized, double-blind, placebo-controlled, parallel-group study compared self-administered low-dose colchicine (1.8 mg total over 1 hour) and high-dose colchicine (4.8 mg total over 6 hours) with placebo. The primary end point was > or = 50% pain reduction at 24 hours without rescue medication.
RESULTS: There were 184 patients in the intent-to-treat analysis. Responders included 28 of 74 patients (37.8%) in the low-dose group, 17 of 52 patients (32.7%) in the high-dose group, and 9 of 58 patients (15.5%) in the placebo group (P = 0.005 and P = 0.034, respectively, versus placebo). Rescue medication was taken within the first 24 hours by 23 patients (31.1%) in the low-dose group (P = 0.027 versus placebo), 18 patients (34.6%) in the high-dose group (P = 0.103 versus placebo), and 29 patients (50.0%) in the placebo group. The low-dose group had an adverse event (AE) profile similar to that of the placebo group, with an odds ratio (OR) of 1.5 (95% confidence interval [95% CI] 0.7-3.2). High-dose colchicine was associated with significantly more diarrhea, vomiting, and other AEs compared with low-dose colchicine or placebo. With high-dose colchicine, 40 patients (76.9%) had diarrhea (OR 21.3 [95% CI 7.9-56.9]), 10 (19.2%) had severe diarrhea, and 9 (17.3%) had vomiting. With low-dose colchicine, 23.0% of the patients had diarrhea (OR 1.9 [95% CI 0.8-4.8]), none had severe diarrhea, and none had vomiting.
CONCLUSION: Low-dose colchicine yielded both maximum plasma concentration and early gout flare efficacy comparable with that of high-dose colchicine, with a safety profile indistinguishable from that of placebo.

PMID 20131255  Arthritis Rheum. 2010 Apr;62(4):1060-8. doi: 10.1002/ar・・・
著者: Robert L Wortmann, Patricia A Macdonald, Barbara Hunt, Robert L Jackson
雑誌名: Clin Ther. 2010 Dec;32(14):2386-97. doi: 10.1016/j.clinthera.2011.01.008.
Abstract/Text BACKGROUND: Use of urate-lowering therapy (ULT), such as febuxostat or allopurinol, is recommended for the long-term management of hyperuricemia in patients with gout to reduce the incidence of acute flares. Because of the paradoxical relationship between early use of ULT and the increased incidence of gout flares, prophylaxis with either low-dose colchicine or NSAIDs has been recommended, although there have been concerns about the long-term prophylactic use of these agents.
OBJECTIVES: The present analysis examined flare rates during the 3 Phase III trials of febuxostat based on mean postbaseline serum urate (sUA) concentrations and duration of prophylaxis. Adverse events (AEs) were assessed by prophylaxis with colchicine or naproxen.
METHODS: This investigator-initiated, post hoc reanalysis of data on gout flares from the 3 randomized, placebo-controlled, Phase III trials evaluated the proportion of patients requiring treatment for gout flares at 4-week intervals based on mean postbaseline sUA concentrations <6.0 and ≥ 6.0 mg/dL. The 3 trials enrolled males or females aged 18-85 years who had a diagnosis of gout and a baseline sUA concentration ≥ 8.0 mg/dL. Patients received ULT (febuxostat or allopurinol) or placebo for 6 months or 1 year and flare prophylaxis with colchicine 0.6 mg/d or naproxen 250 mg BID for 8 weeks or 6 months. The prophylactic regimen was chosen at the discretion of the investigator, based on renal function and known intolerance to either drug. Patients with an estimated creatinine clearance <50 mL/min were not to receive naproxen. AEs were summarized based on prophylaxis with colchicine or naproxen.
RESULTS: The 3 trials enrolled a total of 4101 patients with gout. The majority were white (80.1%), male (94.5%), and obese (body mass index ≥ 30 kg/m(2)) (62.8%). The mean duration of gout ranged from 10.9-11.9 years, and the mean baseline sUA concentration ranged from 9.6-9.9 mg/dL. Flare rates increased sharply (up to 40%) at the end of 8 weeks of prophylaxis and then declined gradually, whereas flare rates were consistently low (range, 3%-5%) at the end of 6 months of prophylaxis. Mean postbaseline sUA concentrations were correlated with flare rates; by the end of each study, patients with a mean postbaseline sUA concentration <6.0 mg/dL had fewer flares than did those with a mean postbaseline sUA concentration ≥ 6.0 mg/dL. There were differences in rates of AEs between prophylaxis groups, but the rates did not increase with increased duration of prophylaxis.
CONCLUSION: This analysis of gout flare data from the 3 Phase III trials of febuxostat found that flare prophylaxis for up to 6 months during the initiation of ULT appeared to provide greater benefit than flare prophylaxis for 8 weeks, with no increase in AEs.

Copyright © 2010. Published by EM Inc USA.
PMID 21353107  Clin Ther. 2010 Dec;32(14):2386-97. doi: 10.1016/j.clin・・・
著者: Michael A Becker, H Ralph Schumacher, Robert L Wortmann, Patricia A MacDonald, Denise Eustace, William A Palo, Janet Streit, Nancy Joseph-Ridge
雑誌名: N Engl J Med. 2005 Dec 8;353(23):2450-61. doi: 10.1056/NEJMoa050373.
Abstract/Text BACKGROUND: Febuxostat, a novel nonpurine selective inhibitor of xanthine oxidase, is a potential alternative to allopurinol for patients with hyperuricemia and gout.
METHODS: We randomly assigned 762 patients with gout and with serum urate concentrations of at least 8.0 mg per deciliter (480 micromol per liter) to receive either febuxostat (80 mg or 120 mg) or allopurinol (300 mg) once daily for 52 weeks; 760 received the study drug. Prophylaxis against gout flares with naproxen or colchicine was provided during weeks 1 through 8. The primary end point was a serum urate concentration of less than 6.0 mg per deciliter (360 micromol per liter) at the last three monthly measurements. The secondary end points included reduction in the incidence of gout flares and in tophus area.
RESULTS: The primary end point was reached in 53 percent of patients receiving 80 mg of febuxostat, 62 percent of those receiving 120 mg of febuxostat, and 21 percent of those receiving allopurinol (P<0.001 for the comparison of each febuxostat group with the allopurinol group). Although the incidence of gout flares diminished with continued treatment, the overall incidence during weeks 9 through 52 was similar in all groups: 64 percent of patients receiving 80 mg of febuxostat, 70 percent of those receiving 120 mg of febuxostat, and 64 percent of those receiving allopurinol (P=0.99 for 80 mg of febuxostat vs. allopurinol; P=0.23 for 120 mg of febuxostat vs. allopurinol). The median reduction in tophus area was 83 percent in patients receiving 80 mg of febuxostat and 66 percent in those receiving 120 mg of febuxostat, as compared with 50 percent in those receiving allopurinol (P=0.08 for 80 mg of febuxostat vs. allopurinol; P=0.16 for 120 mg of febuxostat vs. allopurinol). More patients in the high-dose febuxostat group than in the allopurinol group (P=0.003) or the low-dose febuxostat group discontinued the study. Four of the 507 patients in the two febuxostat groups (0.8 percent) and none of the 253 patients in the allopurinol group died; all deaths were from causes that the investigators (while still blinded to treatment) judged to be unrelated to the study drugs (P=0.31 for the comparison between the combined febuxostat groups and the allopurinol group).
CONCLUSIONS: Febuxostat, at a daily dose of 80 mg or 120 mg, was more effective than allopurinol at the commonly used fixed daily dose of 300 mg in lowering serum urate. Similar reductions in gout flares and tophus area occurred in all treatment groups.

Copyright 2005 Massachusetts Medical Society.
PMID 16339094  N Engl J Med. 2005 Dec 8;353(23):2450-61. doi: 10.1056/・・・
著者: H Ralph Schumacher, Michael A Becker, Robert L Wortmann, Patricia A Macdonald, Barbara Hunt, Janet Streit, Christopher Lademacher, Nancy Joseph-Ridge
雑誌名: Arthritis Rheum. 2008 Nov 15;59(11):1540-8. doi: 10.1002/art.24209.
Abstract/Text OBJECTIVE: To compare the urate-lowering efficacy and safety of febuxostat, allopurinol, and placebo in a large group of subjects with hyperuricemia and gout, including persons with impaired renal function.
METHODS: Subjects (n = 1,072) with hyperuricemia (serum urate level > or = 8.0 mg/dl) and gout with normal or impaired (serum creatinine level >1.5 to < or = 2.0 mg/dl) renal function were randomized to receive once-daily febuxostat (80 mg, 120 mg, or 240 mg), allopurinol (300 or 100 mg, based on renal function), or placebo for 28 weeks.
RESULTS: Significantly (P < or = 0.05) higher percentages of subjects treated with febuxostat 80 mg (48%), 120 mg (65%), and 240 mg (69%) attained the primary end point of last 3 monthly serum urate levels <6.0 mg/dl compared with allopurinol (22%) and placebo (0%). A significantly (P < 0.05) higher percentage of subjects with impaired renal function treated with febuxostat 80 mg (4 [44%] of 9), 120 mg (5 [45%] of 11), and 240 mg (3 [60%] of 5) achieved the primary end point compared with those treated with 100 mg of allopurinol (0 [0%] of 10). Proportions of subjects experiencing any adverse event or serious adverse event were similar across groups, although diarrhea and dizziness were more frequent in the febuxostat 240 mg group. The primary reasons for withdrawal were similar across groups except for gout flares, which were more frequent with febuxostat than with allopurinol.
CONCLUSION: At all doses studied, febuxostat more effectively lowered and maintained serum urate levels <6.0 mg/dl than did allopurinol (300 or 100 mg) or placebo in subjects with hyperuricemia and gout, including those with mild to moderately impaired renal function.

PMID 18975369  Arthritis Rheum. 2008 Nov 15;59(11):1540-8. doi: 10.100・・・
著者: Hisashi Yamanaka, Shigenori Tamaki, Yumiko Ide, Hyeteko Kim, Kouichi Inoue, Masayuki Sugimoto, Yuji Hidaka, Atsuo Taniguchi, Shin Fujimori, Tetsuya Yamamoto
雑誌名: Ann Rheum Dis. 2018 Feb;77(2):270-276. doi: 10.1136/annrheumdis-2017-211574. Epub 2017 Nov 4.
Abstract/Text OBJECTIVES: To determine whether febuxostat with stepwise dose increase is as useful as colchicine prophylaxis in reducing gout flares during the initial introduction of urate-lowering therapy in patients with gout in comparison with febuxostat with no dose titration.
METHODS: In this prospective, multicentre, randomised open-label comparative study, patients were randomised to group A (stepwise dose increase of febuxostat from 10 to 40 mg/day), group B (fixed-dose febuxostat 40 mg/day plus colchicine 0.5 mg/day) or group C (fixed-dose febuxostat 40 mg/day) and observed for 12 weeks. Gout flare was defined as non-steroidal anti-inflammatory drug use for gout symptoms.
RESULTS: A total of 255 patients were randomised, and 241 patients were treated. Among the treated patients, gout flares were experienced by 20/96 (20.8%) in group A, 18/95 (18.9%) in group B and 18/50 (36.0%) in group C. The incidence of flare was significantly lower in groups A and B than that in group C (P=0.047 and P=0.024, respectively), although the differences were not significant after correction for multiple comparisons. No significant difference was noted between the incidence of gout flare in groups A and B.
CONCLUSIONS: Our data suggested that stepwise dose increase of febuxostat and low-dose colchicine prophylaxis effectively reduced gout flares in comparison with fixed-dose febuxostat alone. Stepwise dose increase of febuxostat may be an effective alternative to low-dose colchicine prophylaxis during the introduction of urate-lowering therapy.
TRIAL REGISTRATION NUMBER: UMIN 000008414.

© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.
PMID 29102957  Ann Rheum Dis. 2018 Feb;77(2):270-276. doi: 10.1136/ann・・・
著者: Hyon K Choi, Karen Atkinson, Elizabeth W Karlson, Walter Willett, Gary Curhan
雑誌名: N Engl J Med. 2004 Mar 11;350(11):1093-103. doi: 10.1056/NEJMoa035700.
Abstract/Text BACKGROUND: Various purine-rich foods and high protein intake have long been thought to be risk factors for gout. Similarly, the possibility that the consumption of dairy products has a role in protecting against gout has been raised by metabolic studies. We prospectively investigated the association of these dietary factors with new cases of gout.
METHODS: Over a 12-year period, we prospectively examined the relationship between purported dietary risk factors and new cases of gout among 47,150 men who had no history of gout at base line. We used a supplementary questionnaire to ascertain whether participants met the American College of Rheumatology survey criteria for gout. Diet was assessed every four years by means of a food-frequency questionnaire.
RESULTS: During the 12 years of the study, we documented 730 confirmed new cases of gout. The multivariate relative risk of gout among men in the highest quintile of meat intake, as compared with those in the lowest quintile, was 1.41 (95 percent confidence interval, 1.07 to 1.86; P for trend = 0.02), and the corresponding relative risk associated with seafood intake was 1.51 (95 percent confidence interval, 1.17 to 1.95; P for trend = 0.02). In contrast, the incidence of gout decreased with increasing intake of dairy products; the multivariate relative risk among men in the highest quintile, as compared with those in the lowest quintile, was 0.56 (95 percent confidence interval, 0.42 to 0.74; P for trend <0.001). The level of consumption of purine-rich vegetables and the total protein intake were not associated with an increased risk of gout.
CONCLUSIONS: Higher levels of meat and seafood consumption are associated with an increased risk of gout, whereas a higher level of consumption of dairy products is associated with a decreased risk. Moderate intake of purine-rich vegetables or protein is not associated with an increased risk of gout.

Copyright 2004 Massachusetts Medical Society
PMID 15014182  N Engl J Med. 2004 Mar 11;350(11):1093-103. doi: 10.105・・・
著者: Hyon K Choi, Simin Liu, Gary Curhan
雑誌名: Arthritis Rheum. 2005 Jan;52(1):283-9. doi: 10.1002/art.20761.
Abstract/Text OBJECTIVE: Various commonly consumed foods have long been suspected of affecting the serum uric acid level, but few data are available to support or refute this impression. Our objective was to evaluate the relationship between dietary factors and serum uric acid levels in a nationally representative sample of men and women in the US.
METHODS: Using data from 14,809 participants (6,932 men and 7,877 women) ages 20 years and older in the Third National Health and Nutrition Examination Survey (for the years 1988-1994), we examined the relationship between the intake of purine-rich foods, protein, and dairy products and serum levels of uric acid. Diet was assessed with a food-frequency questionnaire. We used multivariate linear regression to adjust for age, sex, total energy intake, body mass index, use of diuretics, beta-blockers, allopurinol, and uricosuric agents, self-reported hypertension and gout, serum creatinine level, and intake of alcohol.
RESULTS: The serum uric acid level increased with increasing total meat or seafood intake and decreased with increasing dairy intake. After adjusting for age, the differences in uric acid levels between the extreme quintiles of intake were 0.48 mg/dl for total meat (95% confidence interval [95% CI] 0.34, 0.61; P < 0.001 for trend), 0.16 mg/dl for seafood (95% CI 0.06, 0.27; P = 0.005 for trend), and -0.21 mg/dl for total dairy intake (95% CI -0.37, -0.04; P = 0.02 for trend). After adjusting for other covariates, the differences between the extreme quintiles were attenuated but remained significant (P < 0.05 for all comparisons). The total protein intake was not associated with the serum uric acid level in multivariate analyses (P = 0.74 for trend). Those who consumed milk 1 or more times per day had a lower serum uric acid level than did those who did not drink milk (multivariate difference -0.25 [95% CI -0.40, -0.09]; P < 0.001 for trend). Similarly, those who consumed yogurt at least once every other day had a lower serum uric acid level than did those who did not consume yogurt (multivariate difference -0.26 [95% CI -0.41, -0.12]; P < 0.001 for trend).
CONCLUSION: These findings from a nationally representative sample of adults in the US suggest that higher levels of meat and seafood consumption are associated with higher serum levels of uric acid but that total protein intake is not. Dairy consumption was inversely associated with the serum uric acid level.

PMID 15641075  Arthritis Rheum. 2005 Jan;52(1):283-9. doi: 10.1002/art・・・
著者: Hyon K Choi, Walter Willett, Gary Curhan
雑誌名: Arthritis Rheum. 2007 Jun;56(6):2049-55. doi: 10.1002/art.22712.
Abstract/Text OBJECTIVE: Coffee is one of the most widely consumed beverages in the world and may affect the risk of gout via various mechanisms. We prospectively evaluated the relationship between coffee intake and the risk of incident gout in a large cohort of men.
METHODS: Over a 12-year period, we studied 45,869 men with no history of gout at baseline. Intake of coffee, decaffeinated coffee, tea, and total caffeine was assessed every 4 years through validated questionnaires. We used a supplementary questionnaire to ascertain whether participants met the American College of Rheumatology survey criteria for gout.
RESULTS: We documented 757 confirmed incident cases of gout. Increasing coffee intake was inversely associated with the risk of gout. The multivariate relative risks (RRs) for incident gout according to coffee consumption categories (0, <1, 1-3, 4-5, and > or = 6 cups per day) were 1.00, 0.97, 0.92, 0.60 (95% confidence interval [95% CI] 0.41-0.87), and 0.41 (95% CI 0.19-0.88), respectively (P for trend = 0.009). For decaffeinated coffee, the multivariate RRs according to consumption categories (0, <1, 1-3, and > or = 4 cups per day) were 1.00, 0.83, 0.67 (95% CI 0.54-0.82), and 0.73 (95% CI 0.46-1.17), respectively (P for trend = 0.002). Total caffeine from all sources and tea intake were not associated with the risk of gout.
CONCLUSION: These prospective data suggest that long-term coffee consumption is associated with a lower risk of incident gout.

PMID 17530645  Arthritis Rheum. 2007 Jun;56(6):2049-55. doi: 10.1002/a・・・
著者: Hyon K Choi, Gary Curhan
雑誌名: BMJ. 2008 Feb 9;336(7639):309-12. doi: 10.1136/bmj.39449.819271.BE. Epub 2008 Jan 31.
Abstract/Text OBJECTIVE: To examine the relation between intake of sugar sweetened soft drinks and fructose and the risk of incident gout in men.
DESIGN: Prospective cohort over 12 years.
SETTING: Health professionals follow-up study.
PARTICIPANTS: 46 393 men with no history of gout at baseline who provided information on intake of soft drinks and fructose through validated food frequency questionnaires.
MAIN OUTCOME MEASURE: Incident cases of gout meeting the American College of Rheumatology survey criteria for gout.
RESULTS: During the 12 years of follow-up 755 confirmed incident cases of gout were reported. Increasing intake of sugar sweetened soft drinks was associated with an increasing risk of gout. Compared with consumption of less than one serving of sugar sweetened soft drinks a month the multivariate relative risk of gout for 5-6 servings a week was 1.29 (95% confidence interval 1.00 to 1.68), for one serving a day was 1.45 (1.02 to 2.08), and for two or more servings a day was 1.85 (1.08 to 3.16; P for trend=0.002). Diet soft drinks were not associated with risk of gout (P for trend=0.99). The multivariate relative risk of gout according to increasing fifths of fructose intake were 1.00, 1.29, 1.41, 1.84, and 2.02 (1.49 to 2.75; P for trend <0.001). Other major contributors to fructose intake such as total fruit juice or fructose rich fruits (apples and oranges) were also associated with a higher risk of gout (P values for trend <0.05).
CONCLUSIONS: Prospective data suggest that consumption of sugar sweetened soft drinks and fructose is strongly associated with an increased risk of gout in men. Furthermore, fructose rich fruits and fruit juices may also increase the risk. Diet soft drinks were not associated with the risk of gout.

PMID 18244959  BMJ. 2008 Feb 9;336(7639):309-12. doi: 10.1136/bmj.3944・・・
著者: K C Lin, H Y Lin, P Chou
雑誌名: J Rheumatol. 2000 Jun;27(6):1501-5.
Abstract/Text OBJECTIVE: To investigate the incidence of gout and the interaction between uric acid level and other risk factors in the development of gout.
METHODS: Two hundred twenty-three asymptomatic hyperuricemic men initially studied in 1991-92 were reassessed in 1996-97. Gout was clinically diagnosed by a senior rheumatologist based on history and physical according to the clinical criteria of Wallace. Basic demographic and lifestyle variables as well as biochemical data were collected in both baseline and followup periods. Both the stability analysis and the analysis of repeated relationships were applied.
RESULTS: The 5-year cumulative incidence of gout was 18.83% (42/223). The risk factors for gout based on the analysis of repeated relationships were uric acid level, alcohol consumption, use of diuretics, and obesity. The only predictor of gout at baseline was uric acid level. After adjusting for baseline uric acid level, followup uric acid increase, persistent alcohol consumption, use of diuretics in the followup period, and body mass index increase were independent predictors for gout among asymptomatic hyperuricemic men. Excessive alcohol consumption, particularly if occasional, was the most important factor in the development of gout, even when the concentration of uric acid level was below 8 mg/dl.
CONCLUSION: Uric acid level is the key factor for prevention of gout and needs constant monitoring. Other contributing or possible etiologic factors such as alcohol consumption, diuretics use, and excess weight gain carry an increased risk of gout attack among patients with hyperuricemia.

PMID 10852278  J Rheumatol. 2000 Jun;27(6):1501-5.

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