Keswani, S

Abstract Rationale Asthma, a chronic inflammatory airway disease, can be influenced by hormonal fluctuations that affect immune function and airway responsiveness. During in-vitro fertilization (IVF), women undergo sequential hormonal treatments—including gonadotropin administration to stimulate follicle development and induce ovulation, and progesterone and estrogen to support implantation and early pregnancy. These precisely timed hormonal changes may affect asthma symptoms and increase the risk of exacerbations. This study evaluates the hypothesis that undergoing IVF increases the risk of asthma exacerbations prior to, but not during or after pregnancy. Methods Data were extracted from the Mayo Clinic electronic health records. Women were included if their pregnancy was recorded in the Mayo Clinic obstetric delivery dataset. Asthma was defined as the presence of an ICD code J45.xx in combination with a prescription for any asthma medication. For women with multiple pregnancies, only the first pregnancy was analyzed. An asthma exacerbation was defined as a course of oral corticosteroids lasting ≤28 days or a corticosteroid injection. Multivariable logistic regression was used to assess exacerbation risk, adjusting for age, body mass index (BMI), and prior history of diabetes mellitus. Results Among 3,623 pregnant women, 112 underwent IVF treatment. Compared with non-IVF patients, women undergoing IVF were older (mean ± SD: 34.16 ± 5.24 vs. 29.11 ± 5.55, p < 0.001), had lower parity (1.44 ± 0.79 vs. 1.83 ± 1.20, p = 0.001), and fewer full-term deliveries (1.31 ± 0.79 vs. 1.68 ± 1.11, p = 0.001) (Table 1). There were no differences in pre-pregnancy BMI, racial distribution, ethnicity, or prior history of diabetes mellitus. Adjusted analysis indicated that IVF was associated with an increased risk of asthma exacerbation in the year before pregnancy (adjusted OR [95% CI]: 1.097 [1.025-1.173]), but not during (adjusted OR [95% CI]: 1.044 [0.973-1.121]) or after pregnancy (adjusted OR [95% CI]: 1.026 [0.963-1.094]). Conclusion These findings suggest that the preconception hormonal changes associated with IVF may temporarily worsen asthma control. Further studies are warranted to replicate these results, clarify the underlying mechanisms, and guide asthma management in women undergoing fertility treatment. This abstract is funded by: NIH

Abstract Rationale Asthma is a chronic inflammatory airway disorder influenced by pulmonary and systemic factors. Epidemiologic and experimental data suggest associations between asthma, anemia, and reduced iron stores. Sex may modify this relationship: females, with lower baseline iron reserves, menstrual blood loss, and hormone-mediated immune effects, may exhibit greater susceptibility, whereas males, with higher iron stores and androgen-related anti-inflammatory influences, appear less affected. This study tested the hypothesis that diminished iron stores, rather than anemia itself, are associated with asthma, and that this relationship differs by sex. Methods Data were analyzed from nine consecutive NHANES 2-year cycles (1999-2018), a nationally representative U.S. dataset. Lifetime asthma was defined as a prior physician diagnosis and active asthma as “Do you still have asthma?”. Anemia was defined by WHO criteria (hemoglobin <12 g/dL in females and <13 g/dL in males), and iron deficiency as ferritin <30 ng/mL. Accordingly, iron status was categorized as normal, iron deficiency anemia (IDA), iron deficiency without anemia (IDWA), and anemia without iron deficiency (AWID). Analyses followed NHANES guidelines and were conducted with the SURVEY package in R. Results Female participants were older and had lower eosinophil counts, ferritin, and hemoglobin levels, with a higher prevalence of anemia, lifetime asthma, and current asthma. Similar trends were observed among participants with available ferritin data (Table 1). In unadjusted analyses, ferritin levels were inversely associated with lifetime (β = -0.19; p <0.001) and active asthma (β = -0.35; p <0.001), but these associations were not significant after adjustment for sex, age, BMI, race, and log10-transformed eosinophil count (lifetime: β = 0.03; p = 0.61; active: β = -0.08; p = 0.40). In contrast, anemia was associated with increased odds of lifetime (adjusted OR [95% CI], 1.52 [1.21-1.92]) and active (1.50 [1.13-1.99]) asthma in males, but not in females (0.98 [0.86-1.12] and 0.98 [0.83-1.15], respectively). Among males, AWID was associated with active asthma (2.07 [1.08-3.96]), whereas IDA and IDWA were not. No associations were observed among females. Conclusion The relationship between anemia and asthma may be primarily driven by inflammation related to asthma rather than true iron deficiency. After adjustment, ferritin was not independently associated with asthma, whereas anemia—particularly AWID—remained associated among males. These findings suggest that asthma-associated systemic inflammation contributes to anemia of chronic disease, underscoring the need to distinguish inflammatory anemia from nutritional iron deficiency in research and clinical management. This abstract is funded by: NIH