Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe and life-threatening mucocutaneous disorders, primarily triggered by medications. Despite the frequent need for antipyretic and analgesic therapy, the impact of nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen on clinical outcomes in patients with SJS/TEN remains unclear. This study aimed to compare the effects of NSAIDs and acetaminophen use on in-hospital mortality, infection-related events, and renal outcomes, with particular attention to the presence or absence of chronic kidney disease (CKD). We conducted a retrospective analysis using a nationwide administrative database of over 1200 acute care hospitals in Japan between July 2010 and March 2022. Adult patients diagnosed with SJS or TEN who received either NSAIDs or acetaminophen within the first 5 days of hospitalization were included. Patients who received both drugs or neither were excluded. Among 8301 eligible patients, 2484 met inclusion criteria. Overall mortality did not differ significantly between groups (4.1% vs. 4.6%; risk difference [RD], −0.6%; 95% confidence interval [CI], −2.5% to 1.4%). In patients without CKD, NSAID use was associated with lower mortality (2.6% vs. 4.3%; RD, −1.7%; 95% CI, −3.4% to 0.0%). Conversely, in patients with CKD, acetaminophen use was associated with lower mortality (12.0% vs. 38.2%; RD, 26.2%; 95% CI, 5.0% to 47.4%). In conclusion, NSAID use may be associated with relatively improved survival compared with acetaminophen in patients without CKD, while acetaminophen appears safer in those with CKD, suggesting that renal function may inform the selection of antipyretic or analgesic therapy when such treatment is unavoidable. As both drugs are known causative agents of SJS/TEN, these results should be interpreted with caution. Further studies are warranted to validate these observational findings.
Atherosclerosis is now considered to reflect systemic inflammation involving the elevation of multiple proinflammatory cytokines, sharing common underlying pathophysiological mechanisms with psoriasis. There has been increasing interest in whether anti-inflammatory treatment of psoriasis can prevent or halt the progression of atherosclerosis. Here, we conducted a cross-sectional observational clinical study in psoriasis patients with at least one traditional cardiovascular risk factor, such as diabetes, hypertension, or dyslipidemia, and who were being treated with systemic anti-inflammatory drugs. To assess CAD risk, we performed coronary computed tomography angiography (CCTA). We assessed 27 psoriasis patients (14 males/13 females), whose median PASI score was 0 [range, 0–2.3] at the time of CCTA. They had sustained well-controlled psoriasis for a median of 44 months [range, 1–144]. Coronary plaques of varying degrees were detected in 20 patients (74%) by CCTA. Four patients were diagnosed with silent myocardial ischemia (SMI) by invasive coronary angiography (CAG), revealing severe coronary stenosis in major arteries. The severity of coronary plaque burden was significantly associated with male sex, hypertension, and carotid ultrasound abnormalities. Furthermore, notably, we detected a significant positive correlation between the duration of biologic treatment and calcified plaque burden among patients treated with biologic agents for over 6 months. Our study highlights the importance of tight disease control and screening for CAD even in well-controlled psoriasis patients. Further accumulation of studies may lead to better management of CAD risks in this population.
Systemic sclerosis is an autoimmune disease characterized by vasculopathy, fibrosis, and immune dysregulation. Anti-SS-A antibodies (anti-SSA) have been reported to confer severe clinical manifestations in some Western and Japanese cohorts. We aimed to determine whether anti-SSA seropositivity affects clinical outcomes in Japanese patients. We retrospectively analyzed 307 Japanese patients with systemic sclerosis who underwent initial evaluation between January 2011 and March 2020 in our clinic. “Isolated” anti-SSA seropositivity was defined as positivity for anti-SSA in the absence of anti-topoisomerase I, anti-centromere, anti-RNA polymerase III, and anti-U1 ribonucleoprotein antibodies. Overall survival was defined as time to all-cause mortality, and progression-free survival was defined as time to disease progression necessitating intensified therapy. Cox proportional hazards models were employed to estimate hazard ratios and 95% confidence intervals. For patients with “isolated” anti-SSA seropositivity, further investigation for SSc-related autoantibodies was conducted utilizing Autoantibody Array Assay (A-Cube). Anti-SSA were detected in 31.3% of patients. Although anti-SSA seropositivity overall correlated with interstitial lung disease, it was not independently associated with overall survival or progression-free survival. In contrast, “isolated” anti-SSA seropositivity emerged as an independent risk factor for both shorter overall survival (hazard ratio 21.7, 95% confidence interval 5.57–84.8) and progression-free survival (hazard ratio 4.18, 95% confidence interval 1.05–16.7). Expanded serologic testing revealed additional autoantibodies implicated in severe SSc phenotypes. These findings underscore the importance of routinely assessing anti-SSA and highlight the need for autoantibody screening in depth in this subpopulation.
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：