Growing evidence suggests that inflammation may pose an atypical risk factor for pulmonary embolism (PE), as it drives venous thrombosis via several pathways. The increased risk of PE in several autoimmune diseases has lent weight to this concept. However, the relative risk of PE among patients with pemphigus has not yet been established. We aimed to examine the risk of PE in patients with pemphigus. A large-scale population-based longitudinal cohort study was conducted to evaluate the relative risk (RR) of PE among 1,985 patients with pemphigus relative to 9,874 age-, sex-, and ethnicity-matched control subjects. A multivariate Cox regression model was utilized. The incidence of PE was 3.0 (95% CI, 2.2–4.0) and 1.2 (95% CI, 1.0–1.5) per 1,000 person-years among patients with pemphigus and controls, respectively. The period prevalence of PE corresponding to the study period was 2.2% (95% CI, 1.6–2.9%) among cases and 0.9% (95% CI, 0.7–1.1%) among controls. Patients with pemphigus were twice as likely to develop PE as compared to control subjects (adjusted RR, 1.98; 95% confidence interval [CI], 1.29–3.04). The highest PE risk was observed during the 1st year following the diagnosis of pemphigus (adjusted RR, 3.55; 95% CI, 1.78–7.09) and decreased over time. The increased risk was robust to a sensitivity analysis that included only cases managed by pemphigus-related systemic medications (adjusted RR, 1.82; 95% CI, 1.11–2.98). In conclusion, pemphigus is associated with an increased risk of PE, particularly during the 1st year of the disease. An awareness of this risk should be increased, additional precipitating factors for PE should be avoided, and thromboprophylaxis may be evaluated in high-risk patients. Further research is required to establish this risk.
The coexistence of pyoderma gangrenosum (PG) and gout has been reported in individual patients; however, the association between these conditions has not been investigated. We aimed to assess the association between PG and gout and to examine whether the presence of gout predisposes to the development of PG. A population-based case-control study was conducted comparing PG patients (n = 302) with age-, sex-, and ethnicity-matched control subjects (n = 1497) with respect to the presence of preceding gout. Logistic regression models were utilized for univariate and multivariate analyses. The prevalence of preceding gout was greater in patients with PG than in control subjects (3.7% vs. 0.7%, respectively; p < 0.001). Gout was associated with a more than fivefold increase in the risk of PG (OR, 5.15; 95% CI, 2.21–11.98). After adjusting for confounding factors, gout emerged as a significant independent predictor of PG (adjusted OR, 4.08; 95% CI, 1.69–9.80). Gout preceded the diagnosis of PG by a median latency of 4.6 years. Patients with gout-associated PG were older, predominantly male, and had a higher prevalence of metabolic syndrome than other patients with PG. In conclusion, gout increases the risk of developing PG by more than fivefold. Physicians managing patients with gout and PG should be aware of this emerging association.
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