Currently, topical glucocorticoids are still the first-line treatment of chronic hand eczema, while systemic treatment is required for moderate to severe chronic hand eczema with no response to topical corticosteroids. Traditional treatments include glucocorticoids, antihistamines, retinoids, immunosuppressants, etc. In recent years, some progress has been made in the treatment of chronic hand eczema with Janus kinase inhibitors, phosphodiesterase 4 inhibitors, biological agents, statins, timolol, daylight photodynamic therapy, etc. This review summarizes recent advances in the treatment of chronic hand eczema, including basic therapy, topical treatment, physical therapy and systemic therapy.

Currently, topical glucocorticoids are still the first-line treatment of chronic hand eczema, while systemic treatment is required for moderate to severe chronic hand eczema with no response to topical corticosteroids. Traditional treatments include glucocorticoids, antihistamines, retinoids, immunosuppressants, etc. In recent years, some progress has been made in the treatment of chronic hand eczema with Janus kinase inhibitors, phosphodiesterase 4 inhibitors, biological agents, statins, timolol, daylight photodynamic therapy, etc. This review summarizes recent advances in the treatment of chronic hand eczema, including basic therapy, topical treatment, physical therapy and systemic therapy.

Objective: To explore the functions of DNA-PKcs in cellular low dose hyper-radiosensitivity. Methods: Colony-formation assay was used to detect the survival fractions of M059K and M059J cell lines treated by X-ray irradiation. Micronucleus assay and γ-H2AX foci assay were used to measure the radiation-induced DNA damage. Western blot was used to detect the relative expression levels of phospho-Chk1, total Chk1, phospho-Chk2 and total Chk2 of M059K and M059J cells. Results: The hyper-radiosensitivity was observed in M059K cells irradiated with X-ray of doses lower than 1 Gy. DNA damage levels did not show HRS/IRR in the cell lines we used. pChk1/Chk1 in M059K cells was significantly increased during 20 min to 60 min after 0.2 Gy X-ray irradiation (t=14.157, 13.661, 14.177, 11.317, 14.512, P<0.05); pChk2/Chk2 in M059K cells was markedly increased during 20 min to 50 min after 0.2 Gy X-ray irradiation (t=13.182, 13.868, 14.155, 14.477, P<0.05). Conclusions M059K cells show the phenomenon of low dose hyper-radiosensitivity, which may be related to activation of proteins in G₂/M phase checkpoints regulated by DNA-PKcs.