Cytokine profile in combination with chronic pancreatitis with hypothyroidism

Objective — to analize cytokine profile indicators and cytokine ratios in patients with chronic pancreatitis (CP) depending on the presence of concomitant hypothyroidism. Materials and methods. The study group consisted of 74 patients with CP combined with hypothyroidism, the comparison group — 44 patients with isolated CP, and the control group — 20 practically healthy individuals comparable in age and gender ratio. The inclusion criteria for the study were verified CP, the presence of subclinical hypothyroidism, and mild and moderate hypothyroidism. The level of pro‑inflammatory cytokines (tumour necrosis factor (TNF‑α), interleukin‑1β (ІL‑1β_, ІL‑2, and ІL‑6) and anti‑inflammatory cytokines (ІL‑4) in blood serum were determined by enzyme‑linked immunosorbent assay using ELISA Kits on the STAT FAX 303/plus analyzer. The ratio of pro‑inflammatory and anti‑inflammatory cytokines (TNF‑α/ІL‑4, ІL‑1β/ІL‑4, ІL‑2/ІL‑4, ІL‑6/ІL‑4) were determined with statistical processing of the results using Microsoft Excel spreadsheets and Statistica for Windows 10 (Stat Soft Inc). Results. In the group of patients, significantly higher levels of TNF‑α, ІL‑1β, ІL‑2, and ІL‑6 in the blood serum and decreased levels of ІL‑4 in comparison with the control group (p<0.05) were found. The severity of pathological changes in patients with CP was higher in the presence of thyroid pathology (hypothyroidism). Significantly higher levels of pro‑inflammatory cytokine activity were found in patients with CP with concomitant hypothyroidism compared to that in isolated CP (TNF‑α — by 22.1%, ІL‑1β — by 23.6%, ІL‑2 — by 23.6%) and a lower level of the anti‑inflammatory cytokine ІL‑4 — by 22.2% and pro‑inflammatory ІL‑6 — by 18.4% (p<0.05). It was also found that the TNF‑α /ІL‑4 ratio was 1.68 times higher, ІL‑1β/ІL‑4—1.66 times higher and ІL‑2/ІL‑4—1.62 times higher compared to similar ratios in patients with isolated CP (p<0.05), which indicated a more significant predominance of the pro‑inflammatory pool in comorbidity compared to isolated CP. This motivates us to take into account the obtained data when developing a comprehensive treatment for comorbidity of CP with hypothyroidism. Conclusions. It has been proven that the presence of comorbid hypothyroidism enhances the imbalance between pro‑ and anti‑inflammatory cytokines, which is also established in isolated chronic pancreatitis, which proves the mutually aggravating effect of the combined course of these pathologies. Significant deviations were found in the ratios of pro‑ and anti‑inflammatory cytokines with a significant predominance of pro‑inflammatory cytokines in patients with CP compared to those in the control group, especially in the case of comorbidity with hypothyroidism (p<0.05).