Abstract Uterine leiomyomas are benign smooth-muscle tumors responsive to estrogen and progesterone. While influence of sex hormones on asthma control has long been recognized, the relationship between gynecologic pathology such as uterine leiomyomata and airway reactivity remains poorly characterized.A 45-year-old woman with severe persistent asthma had well-controlled childhood asthma until two years prior, when she developed worsening dyspnea and chest tightness, which she described as typical previous asthma symptoms. Around the same time, she began experiencing vaginal spotting and heavy menstrual cycles. Despite escalation from inhaled corticosteroid (ICS)/long-acting β-agonist (LABA) therapy to ICS/LABA/long-acting muscarinic antagonist, leukotriene receptor antagonist, intranasal corticosteroids, antihistamines, and proton-pump inhibitors, asthma remained poorly controlled. She continued to require frequent courses of systemic corticosteroids. Her allergy testing revealed sensitization to dust and cockroach , peripheral eosinophilia (290/µL), and a total IgE of 71.7 IU/mL. Mepolizumab was initiated with minimal clinical improvement.During this period evaluation of her uterine bleeding revealed two large uterine fibroids. She underwent total abdominal hysterectomy with bilateral salpingectomy. Pathology confirmed benign leiomyomas. Following surgery, she noticed significant improvement in her symptoms. Over the subsequent 4-6 months, Mepolizumab and triple inhaler therapy were successfully de-escalated. She remained well controlled on fluticasone/salmeterol, and montelukast. Sex hormones play a key role in modulating airway inflammation and asthma severity. Estrogen promotes Th2 cytokine (IL-4, IL-13) signaling, leading to eosinophilic inflammation, mucus hypersecretion, and airway hyperreactivity, while enhancing ILC2 activity that may blunt corticosteroid responsiveness. Progesterone, conversely, may increase airway smooth muscle reactivity, but attenuate inflammation through macrophage modulation. Although catamenial asthma and pulmonary benign metastasizing leiomyoma illustrate hormone-mediated airway pathology, a direct relationship between uterine fibroids and asthma control is rarely reported. Giamarchi et al. found bronchial hyperreactivity in 28% of women with fibroids but without asthma, and Toaff et al. documented asthma improvement post-myomectomy, implicating hormonal or mechanical influences. Our case similarly suggests that large uterine leiomyomata may exacerbate asthma via hormonal modulation, mechanical diaphragmatic restriction, or systemic inflammation. Our case also demonstrated significant improvement in asthma symptoms following hysterectomy. In contrast, a NHANES analysis (1999-2016) found hysterectomy associated with increased the odds of asthma (aOR 1.26, 95 % CI 1.11-1.48) but not with active disease severity. Despite such conflicting data, this case calls for further studies exploring hormonal-gynecologic influences on asthma phenotypes in women. The resolution of severe refractory asthma in our patients following hysterectomy for leiomyomas suggests a potential line between fibroid burden and asthma control. This abstract is funded by: none
Bista et al. (Fri,) studied this question.