Physiological responses of individuals with idiopathic chilblains during cold exposure and rewarming: a non-randomized clinical trial

Idiopathic chilblains (IC) is a localized inflammatory disorder affecting acral areas, with unclear pathophysiology and pathogenesis. This study aimed to investigate the vasomotor, autonomic, and inflammatory responses of adults with (HIC+) and without (HIC-) a history of IC during cold exposure and rewarming. Sixteen healthy adults (eight HIC+, eight HIC-; both sexes, aged 19-60 years) underwent a controlled environmental protocol involving progressive cooling (22°C to 10°C) followed by rewarming (22°C). Skin blood flow (SkBF), finger and toe temperatures (Tf and Tt), mean skin temperature (Tsk), and microvascular oxygenation parameters Tissue Saturation Index (TSI), oxyhemoglobin (O₂Hb), and deoxyhemoglobin (HHb) and total blood volume (tHb) were recorded throughout. Serum cortisol, ferritin, vitamin D3, and antibodies (ANAs), and scleroderma antibody (SCL-70) were also assessed. Compared to HIC- participants, the HIC+ group showed significantly lower SkBF (| d| =0.43-0.56; p<0.05), Tf and Tt (| d|=0.07-0.75) during cold exposure, along with reduced O₂Hb (| d|=0.33 at 10°C) and increased HHb (| d|=0.43-0.46 at 14°C and 10°C), suggesting impaired oxygen delivery. No between-group differences were observed in TSI. During rewarming, SkBF (47.06±54.94 vs 22.69±21.48 PU) and HHb levels (5.53±3.64 vs 3.07±2.84 μM) in the right finger were higher in the HIC+ than the HIC- group (| d|=0.35-0.54). No significant differences were observed in serum cortisol, or thermal perception. No participants developed chilblains or acral symptoms during the eight-week follow-up. These findings indicate that individuals with a history of IC exhibit heightened cold-induced vasoconstriction and peripheral microvascular hypoxia, which may underlie susceptibility to chilblains and non-freezing cold injuries.