VITAMIN D METABOLISM DISORDERS IN PATIENTS WITH CHRONIC PANCREATITIS WITH CONCOMITANT CHRONIC OBSTRUCTIVE PULMONARY DISEASE
DOI:
https://doi.org/10.32689/2786-7161-2026-2-2Ключові слова:
chronic pancreatitis, chronic obstructive pulmonary disease, vitamin D, calcium, systemic inflammationАнотація
Background. The comorbid progression of chronic pancreatitis (CP) and chronic obstructive pulmonary disease (COPD) is characterized by chronic systemic inflammation, oxidative stress, and the advancement of structural and functional impairments. These factors can adversely affect vitamin D and calcium homeostasis. Vitamin D deficiency is considered a contributing factor to heightened inflammatory responses, disruptions in mineral metabolism, and the progression of exocrine pancreatic insufficiency. Objective. To investigate the characteristics of vitamin D homeostasis in cases of comorbid CP and COPD compared to the isolated progression of these diseases. Materials and Methods. A total of 145 patients were examined, including 35 with COPD, 35 with CP, and 75 with combined CP and COPD. Study Results. The most significant disruptions in vitamin D and calcium homeostasis were observed in patients with comorbid CP and COPD. The concentration of 25(OH)D was lower than the levels in practically healthy individuals by 24.8% in COPD, 54.4% in CP, and 75.2% with combined CP and COPD (p<0.05). Total and ionized calcium content was also lowest in the comorbid group by 13.3% and 14.3%, respectively (p<0.05). The highest intensity of systemic inflammation was seen in patients with both CP and COPD, as indicated by 21.5 times increase in C-reactive protein levels compared to healthy individuals (p<0.05). Exocrine pancreatic insufficiency was more pronounced in patients with the combined progression of the diseases, evidenced by a twofold reduction in fecal elastase-1 levels (p<0.05). A strong inverse correlation was found between 25(OH)D concentration and C-reactive protein levels (r=-0.68; p<0.05), and a strong direct correlation between 25(OH)D levels and fecal elastase-1 (r=0.79; p<0.05). Conclusions. The comorbid progression of CP and COPD is associated with the most pronounced vitamin D deficiency and disruption of calcium homeostasis, accompanied by increased systemic inflammation and advancement of exocrine pancreatic insufficiency. The identified correlations suggest the utility of measuring 25(OH)D levels as an additional laboratory marker for systemic inflammation activity and pancreatic functional status, emphasizing the need for routine monitoring of vitamin D sufficiency and calcium metabolism indicators in patients with comorbid CP and COPD.
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