Alopecia areata coexisting with Hashimoto’s thyroiditis and Sjögren’s syndrome: case report of hair regrowth and selected laboratory changes during combination treatment including tofacitinib

Background Alopecia areata (AA) is an autoimmune disorder characterized by transient, non-scarring hair loss and preservation of the hair follicle. Hashimoto’s thyroiditis (HT) and Sjögren’s syndrome (SS) are common systemic autoimmune disorders that may share genetic and immunological predispositions with AA. Co-occurrence of all three conditions is rarely reported. Case presentation We report a 36-year-old female who presented with a 1-year history of progressive hair loss involving the occipital scalp margins, with a Severity of Alopecia Tool (SALT) score of 30 at treatment initiation (retrospectively revised to 15 on unblinded image review). She had a 10-year history of HT on stable levothyroxine replacement and a 6-month history of SS. Laboratory evaluation revealed elevated TSH (6.299 uIU/mL), markedly elevated TPO-Ab (922.7 IU/mL), positive anti-SSA antibodies. The patient received tofacitinib 5 mg twice daily, together with intralesional compound betamethasone, topical clobetasol propionate, and topical minoxidil. At 6 months, SALT score was 0; TPO-Ab was 255 IU/mL and Tg-Ab was 430 IU/mL; anti-SSA antibodies were negative; and TSH was 2.760 uIU/mL during continued levothyroxine replacement. Baseline and follow-up thyroid assays used different platforms (CLIA vs ECLIA), and the 6-month Tg-Ab value (430 IU/mL) was numerically higher than baseline (307.52 IU/mL); therefore, neither a biological increase nor decrease in thyroid autoantibodies can be confidently inferred from these numbers alone. Hair regrowth occurred under combination treatment and cannot be attributed to tofacitinib alone. No adverse events were reported during the available follow-up (6 months in clinic; 9 months by telephone). Conclusion This case describes hair regrowth and selected laboratory changes observed during combination treatment including tofacitinib in a patient with AA and comorbid HT/SS. The observations are hypothesis-generating and temporal association does not establish treatment causation.