Chattopadhyay Aheli, Ye Morgan, Chiang Brenda, Halezeroglu Yagmur, Van Blarigan Erin L, Liao Wilson, Bhutani Tina, Abuabara Katrina
Department of Dermatology, University of California San Francisco, San Francisco, California, USA.
Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California, USA.
J Eur Acad Dermatol Venereol. 2025 Sep;39(9):1622-1630. doi: 10.1111/jdv.20540. Epub 2025 Jan 28.
Sodium is stored in skin and may trigger or perpetuate autoimmune diseases including psoriasis. One previous study found skin sodium was elevated in a small group of patients with severe psoriasis compared to healthy controls, but the relationship between sodium intake and psoriasis within a population has not been investigated.
To identify whether dietary sodium intake is associated with psoriasis and whether there are subgroups of individuals more likely to have salt-sensitive psoriasis.
This cross-sectional, population-based study evaluated a UK Biobank cohort of nearly 500,000 participants in the 2006-2010 period and a US-based National Health and Nutrition Examination Survey (NHANES) validation cohort of 2393 participants in the 2003-2004 period. Dietary sodium intake, the exposure, was estimated using urine biomarkers and the previously validated INTERSALT equation. Psoriasis outcome was assessed by the presence of ICD-10 code L40.
In the UK Biobank, of the 468,913 included participants, 54% were female and mean (standard deviation) age at recruitment was 57 (8) years. Multivariable logistic regression models revealed that every 1 g increase in estimated 24-h urine sodium was associated with an 18% increase in odds of psoriasis (OR 1.18, 95% CI: 1.14-1.21) after adjustment for sex, age, race/ethnicity, education and socioeconomic status. There was no consistent evidence of large effect modification by age, sex, race/ethnicity, polygenic risk score for psoriasis or those with a history of hypertension, chronic renal failure or type 2 diabetes mellitus. In NHANES, each additional gram of self-reported dietary sodium intake was also associated with increased odds of examination-confirmed psoriasis (OR: 1.47, 95% CI: 1.19-1.83).
Increased sodium intake was associated with psoriasis in two population-based cohorts; future clinical trials could investigate whether decreasing sodium intake improves psoriasis.
钠储存于皮肤中，可能引发或使包括银屑病在内的自身免疫性疾病持续存在。此前一项研究发现，与健康对照相比，一小部分重度银屑病患者的皮肤钠含量升高，但尚未对人群中钠摄入量与银屑病之间的关系进行研究。
确定饮食钠摄入量是否与银屑病相关，以及是否存在更易患盐敏感性银屑病的亚组人群。
这项基于人群的横断面研究评估了英国生物银行2006 - 2010年期间近50万名参与者的队列，以及美国国家健康与营养检查调查（NHANES）2003 - 2004年期间2393名参与者的验证队列。使用尿液生物标志物和先前验证的INTERSALT方程估算饮食钠摄入量（暴露因素）。通过国际疾病分类第十版（ICD - 10）编码L40的存在情况评估银屑病结局。
在英国生物银行纳入的468,913名参与者中，54%为女性，招募时的平均（标准差）年龄为57（8）岁。多变量逻辑回归模型显示，在调整性别、年龄、种族/民族、教育程度和社会经济地位后，估计的24小时尿钠每增加1克，银屑病患病几率增加18%（比值比1.18，95%置信区间：1.14 - 1.21）。没有一致的证据表明年龄、性别、种族/民族、银屑病多基因风险评分或有高血压、慢性肾衰竭或2型糖尿病病史的人群存在显著的效应修正。在NHANES中，自我报告的饮食钠摄入量每增加1克，经检查确诊的银屑病患病几率也会增加（比值比：1.47，95%置信区间：1.19 - 1.83）。
在两个基于人群的队列中，钠摄入量增加与银屑病相关；未来的临床试验可以研究减少钠摄入量是否能改善银屑病。
