Geertje M de Boer1, Gerdien A Tramper-Stranders2, Laura Houweling3, Cathelijne M van Zelst1, Nadine Pouw4, Gert T Verhoeven5, Bianca M Boxma-de Klerk6, Johannes C C M In 't Veen1, Elisabeth F C van Rossum7, Rudi W Hendriks8, Gert-Jan Braunstahl9. 1. Department of Pulmonary Medicine, Franciscus Gasthuis & Vlietland, Rotterdam, the Netherlands; Department of Pulmonary Medicine, Erasmus MC, Rotterdam, the Netherlands. 2. Department of Pediatrics, Franciscus Gasthuis & Vlietland, Rotterdam, the Netherlands. 3. Department of Pulmonary Medicine, Franciscus Gasthuis & Vlietland, Rotterdam, the Netherlands. 4. Department of Clinical Chemistry, Franciscus Gasthuis & Vlietland, Rotterdam, the Netherlands. 5. Department of Pulmonary Medicine, Maasstad Hospital, Rotterdam, the Netherlands. 6. Department of Statistics and Education, Franciscus Gasthuis & Vlietland, Rotterdam, the Netherlands. 7. Department of Internal Medicine, Division of Endocrinology and Obesity Centre CGG, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands. 8. Department of Pulmonary Medicine, Erasmus MC, Rotterdam, the Netherlands. 9. Department of Pulmonary Medicine, Franciscus Gasthuis & Vlietland, Rotterdam, the Netherlands; Department of Pulmonary Medicine, Erasmus MC, Rotterdam, the Netherlands. Electronic address: gm.vandijk.deboer@gmail.com.
Abstract
INTRODUCTION: Adult-onset asthma (AOA) is usually more severe compared to childhood onset asthma (CoA). Given the increasing evidence that AoA is associated with obesity, we investigated the relationship of other related metabolic comorbid conditions with AoA compared to CoA. STUDY DESIGN AND METHODS: This cross-sectional study compared the metabolic syndrome and lipid derived inflammatory markers in patients with AoA, CoA and age- and sex-matched control subjects without asthma. Participants were asthma patients visiting the outpatient clinic of two teaching hospitals in Rotterdam, The Netherlands. All participants underwent lung function tests, blood tests and physical activity tracking. AoA was defined as asthma age of onset after the age of 18 years. Metabolic syndrome was defined according to the international joint interim statement criteria. RESULTS: Eighty-one participants were included (27 AoA, 25 CoA, 29 controls). AoA was associated with the metabolic syndrome (Odds Ratio = 3.64 95% CI (1.16-11.42) p = 0.03, Nagelkerke R2 = 0.26), adjusted for age, sex, body mass index and smoking habits. AoA patients had higher median serum IL-6 and leptin-adiponectin (LA) ratio compared to controls (IL-6 (pg/mL): 3.10 [1.11-4.30] vs. 1.13 [0.72-1.58], p = 0.002 and LA ratio (pg/mL): 6.21 [2.45-14.11] vs. 2.24 [0.67-4.71], p = 0.0390). This was not observed in CoA and controls. CONCLUSION: AoA was associated with the metabolic syndrome and its related pro-inflammatory endocrine and cytokine status. This may suggest adipose tissue derived inflammatory markers play a role in the pathophysiology of AoA.
INTRODUCTION: Adult-onset asthma (AOA) is usually more severe compared to childhood onset asthma (CoA). Given the increasing evidence that AoA is associated with obesity, we investigated the relationship of other related metabolic comorbid conditions with AoA compared to CoA. STUDY DESIGN AND METHODS: This cross-sectional study compared the metabolic syndrome and lipid derived inflammatory markers in patients with AoA, CoA and age- and sex-matched control subjects without asthma. Participants were asthma patients visiting the outpatient clinic of two teaching hospitals in Rotterdam, The Netherlands. All participants underwent lung function tests, blood tests and physical activity tracking. AoA was defined as asthma age of onset after the age of 18 years. Metabolic syndrome was defined according to the international joint interim statement criteria. RESULTS: Eighty-one participants were included (27 AoA, 25 CoA, 29 controls). AoA was associated with the metabolic syndrome (Odds Ratio = 3.64 95% CI (1.16-11.42) p = 0.03, Nagelkerke R2 = 0.26), adjusted for age, sex, body mass index and smoking habits. AoA patients had higher median serum IL-6 and leptin-adiponectin (LA) ratio compared to controls (IL-6 (pg/mL): 3.10 [1.11-4.30] vs. 1.13 [0.72-1.58], p = 0.002 and LA ratio (pg/mL): 6.21 [2.45-14.11] vs. 2.24 [0.67-4.71], p = 0.0390). This was not observed in CoA and controls. CONCLUSION: AoA was associated with the metabolic syndrome and its related pro-inflammatory endocrine and cytokine status. This may suggest adipose tissue derived inflammatory markers play a role in the pathophysiology of AoA.