C58-10 Tirzepatide Improves Lung Function in Obese Patient With Hypersensitivity Pneumonitis

Abstract Introduction Hypersensitivity pneumonitis (HP) is a heterogenous diffuse parenchymal lung disease caused by an inflammatory reaction to an inhaled antigen. HP is a progressive disease in which early biopsies are characterized by cellular inflammation. As the disease becomes chronic the inflammation is replaced by fibrosis. The mainstay of treatment for HP involves immune suppression prior to progression to fibrosis along with antigen avoidance; however there are currently no medications approved for treatment of HP alone. We report a case of a patient with HP on immune suppression whose symptoms and PFT improved significantly after introduction of a glucagon-like peptide-1 receptor antagonist (GLP-1RA) medication. Case Presentation A 67 year old obese male (BMI 32 kg/m2) with type 2 diabetes mellitus and progressive interstitial lung disease was treated in pulmonary clinic. The patient’s lung biopsy showed characteristics of chronic HP, and despite treatment with prednisone and mycophenolate his pulmonary function showed no improvement. The patient was started on Tirzepatide by his endocrinologist for improved glycemic control. He achieved weight loss of 41 pounds (26.7% total body weight). The patient’s total lung capacity (TLC), vital capacity (VC), functional residual capacity (FRC), and diffusion capacity (DLCO) improved 24%, 14%, 70% and 9% respectively after GLP1-RA use. His hypoxemia on exertion and pulmonary symptoms also improved. Discussion of importance of case HP is a condition without definitive treatment. GLP-1RA have pleiomorphic effects which, while not entirely understood, provide significant impact on morbidity and mortality for patients. There is limited data regarding the use of GLP-1RA in pulmonary disease, though weight loss is known to have a beneficial effect on pulmonary function. One study of 11 obese patients with ILD showed that weight loss lead to an improvement in forced vital capacity, FRC, and DLCO. While much of our patient’s improvement in respiratory status can be attributed to his weight loss, the changes are out of proportion to those expected with weight loss alone. Current data suggests that GLP-1RA likely have an anti-inflammatory effect and GLP-1R activation has been shown to inhibit pulmonary fibrosis in a mouse model. To date, there is no published data regarding the impact of GLP-1RA on pulmonary function of patients with HP, but our patient’s dramatic improvement suggests that this area may benefit from continued research. This abstract is funded by: None