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Proteolytic action of NSPs is controlled endogenously by the serpin (serine proteinase inhibitor) superfamily of proteins (e.g., alpha1-antitrypsin (AAT), alpha1antichymotrypsin, monocyte NE inhibitor) and the chelonianin family of canonical inhibitors (elafin, secretory leukocyte protease inhibitor) ( 3.1 Inflammatory respiratory diseases NSPs are released in the airways of patients with multiple types of chronic pulmonary diseases such as COPD, AATD, bronchiectasis, and CF, and have been implicated as key mediators of chronic inflammation and disease progression ( 3.1.1 Chronic obstructive pulmonary disease COPD is characterized by persistent neutrophilic inflammation of the airway lumen and destruction of the lung parenchyma, leading to progressive deterioration of lung function ( Multiple lines of evidence point to NSPs as primary mediators of COPD-associated pulmonary tissue damage and clinical decline ( NE has generally been regarded as the principal NSP contributing to the pathophysiology of COPD, but more recent data indicate that PR3 and CatG also have significant roles ( 3.1.2 Alpha-1 antitrypsin deficiency AAT is the archetypal member of the serpin superfamily ( AATD is an underrecognized genetic condition characterized by low circulating AAT levels that may lead to lung and liver disease

The standard of care here is aggressive for a reason

Brezinova, Anna

By week 30, only 28% of people on placebo had an HbA1c (the average blood sugar levels over the last three months) less than 7%, whereas as much as 70% or more of people on any dose of Ozempic achieved an A1C of less than 7%

Document any alternative medications that the patient has received or attempted, including any yes/no responses and dates