There is a high comorbidity between attention-deficit/hyperactivity disorder (ADHD) and asthma, and inflammation has been proposed as a potential pathophysiological mechanism behind this association. Most studies conducted so far have used a cross-sectional design, and none has evaluated the prevalence of asthma symptoms in patients with ADHD followed from childhood to adulthood. We relied on data from the 1993 Pelotas birth cohort to evaluate the association between ADHD and asthma in patients with distinct patterns of incidence, persistence and remission, and to explore the potential role of inflammatory markers in the comorbidity. We analyzed data from 3281 individuals from the 1993 Pelotas birth cohort collected at birth (1993), 11 years (2004), 18 years (2011), and 22 years (2015). Subjects were first classified according to their ADHD and asthma status as early-onset (EO) persistent (positive screening for ADHD at 11 and diagnosis of ADHD according to DSM-5, except criterion E, at either 18 or 22 years), EO-remittent (positive screening for ADHD at 11 years only), late-onset (diagnosis of ADHD according to DSM-5, except criterion E, at 18 or 22 years only), or healthy subjects (negative for both conditions in all evaluation). After controlling for confounders, significant associations were observed between EO-remittent ADHD and EO-remittent asthma (OR 1.68, 95% CI 1.11-2.55), EO-persistent ADHD and EO-persistent asthma (OR 4.33, 95% CI 1.65-11.34), and between late-onset ADHD and late-onset asthma (OR 1.86, 95% CI 1.28-2.70), suggesting a state-dependent association. Serum interleukin-6 (IL-6) and C-reactive protein (CRP) were measured at the 18- and 22-year evaluations and compared between subjects positive for ADHD, asthma, and subjects with both or none conditions, regardless of the previously defined trajectories. Subjects with comorbid ADHD and asthma presented higher levels of IL-6 at the 18- and 22-year evaluations when compared to subjects negative for both conditions. Our results demonstrate a state-dependent association between ADHD and asthma despite underlying trajectories. Higher levels of serum IL-6 in patients with both conditions suggest that a pro-inflammatory environment might have a role in the pathophysiological mechanisms underlying the comorbidity.

注意缺陷/多动障碍 (ADHD) 和哮喘之间存在高度共病，炎症被认为是这种关联背后的潜在病理生理机制。迄今为止进行的大多数研究都使用了横断面设计，但没有一项研究评估了 ADHD 患者从儿童期到成年期哮喘症状的患病率。我们依靠来自 1993 年 Pelotas 出生队列的数据来评估 ADHD 与哮喘在不同发病率、持续性和缓解模式的患者中的关联，并探索炎症标志物在合并症中的潜在作用。我们分析了来自 1993 年 Pelotas 出生队列的 3281 个人的数据，这些人在出生时（1993 年）、11 年（2004 年）、18 年（2011 年）和 22 年（2015 年）收集。首先根据他们的 ADHD 和哮喘状态将受试者分类为早发性 (EO) 持续性（11 岁时 ADHD 筛查呈阳性，根据 DSM-5 诊断为 ADHD，除了标准 E，18 或 22 岁时）、EO-缓和（仅在 11 岁时筛查 ADHD 呈阳性）、迟发性（根据 DSM-5 诊断 ADHD，标准 E 除外，仅在 18 或 22 岁时）或健康受试者（在所有评估中两种情况均为阴性）。控制混杂因素后，观察到 EO 缓解型 ADHD 和 EO 缓解型哮喘（OR 1.68，95% CI 1.11-2.55）、EO 持续性 ADHD 和 EO 持续性哮喘（OR 4.33，95% CI 1.65-11.34）之间存在显着关联)，以及迟发性 ADHD 和迟发性哮喘之间 (OR 1.86, 95% CI 1.28-2.70)，表明存在状态依赖性关联。在 18 年和 22 年的评估中测量血清白细胞介素 6 (IL-6) 和 C 反应蛋白 (CRP)，并在多动症、哮喘阳性受试者和两种或两种情况都没有的受试者之间进行比较，无论以前的情况如何定义的轨迹。与两种情况均呈阴性的受试者相比，患有 ADHD 和哮喘的受试者在 18 年和 22 年的评估中表现出更高水平的 IL-6。我们的结果表明，尽管存在潜在的轨迹，但 ADHD 和哮喘之间存在状态依赖性关联。两种疾病患者血清 IL-6 水平较高表明促炎环境可能在共病的病理生理机制中起作用。无论先前定义的轨迹如何，都具有或没有条件的受试者。与两种情况均呈阴性的受试者相比，患有 ADHD 和哮喘的受试者在 18 年和 22 年的评估中表现出更高水平的 IL-6。我们的结果表明，尽管存在潜在的轨迹，但 ADHD 和哮喘之间存在状态依赖性关联。两种疾病患者血清 IL-6 水平较高表明促炎环境可能在共病的病理生理机制中起作用。和有两个条件或没有条件的对象，无论先前定义的轨迹如何。与两种情况均呈阴性的受试者相比，患有 ADHD 和哮喘的受试者在 18 年和 22 年的评估中表现出更高水平的 IL-6。我们的结果表明，尽管存在潜在的轨迹，但 ADHD 和哮喘之间存在状态依赖性关联。两种疾病患者血清 IL-6 水平较高表明促炎环境可能在共病的病理生理机制中起作用。我们的结果表明，尽管存在潜在的轨迹，但 ADHD 和哮喘之间存在状态依赖性关联。两种疾病患者血清 IL-6 水平较高表明促炎环境可能在共病的病理生理机制中起作用。我们的结果表明，尽管存在潜在的轨迹，但 ADHD 和哮喘之间存在状态依赖性关联。两种疾病患者血清 IL-6 水平较高表明促炎环境可能在共病的病理生理机制中起作用。