Several possibilities may explain the differences of the low

Several possibilities may explain the differences of the lower PASI 75 response in the present study. Firstly, the stringent reimbursement criteria of biologics may select a subgroup of high-need patients. Secondly, human leukocyte antigen (HLA) polymorphism in Taiwan compared to Western countries may also play a role. HLA-Cw6 was reported to be associated with a more favorable response to ustekinumab, but HLA-Cw6 is underrepresented in Taiwanese patients with psoriasis, especially in the moderate-to-severe group. Thirdly, 40% of patients in our study had a history of erythrodermic psoriasis. Biological drug survival rate and efficacy in patients with erythrodermic psoriasis appears to be lower than in patients with plaque type psoriasis treated with either TNF-α or IL-12/23 blockers. Fourthly, 70% of patients had psoriatic arthritis which was shown to adversely affect the ustekinumab efficacy. Fifthly, patients who failed biological agents were more likely to have poor response, as shown in a phase III study of ustekinumab, where 36% PASI 75 responders at Week 28 were previously treated with biological agents. However, our subgroup analysis did not show statistically significant differences of PASI response regarding the number of switchers, and history of erythrodermic psoriasis and psoriatic arthritis, which could be due to low patient number. With regards to the safety of ustekinumab, no serious adverse events were apparent in our study. One recent study reported that early clinical response of ixekizumab, an IL17A monoclonal antibody, could be served as a predictor of subsequent response to treatment. Our analysis by a similar method showed that patients not achieving PASI 30 at Week 4 were less likely to achieve PASI 50 at Week 16 based on YI analyses. However, our result is limited by the small sample sizes. In our daily clinical practice, washout periods of systemic therapies are required to maintain optimal disease control in high-need psoriasis patients. Previous studies reported that about 30–40% of psoriasis patients received concurrent biologics and traditional systemic agents in clinical practice. In the current study, 46% of patients received systemic combination therapy, which may complicate the interpretation of the results. However, 55% of them did not reach PASI 50 response during the study period, revealing their demand for concomitant therapies to control the intractable disease.
Conclusion
Introduction Fibrotic diseases in humans, including lung fibrosis, liver cirrhosis, scleroderma, and keloid, occur as a result of deposition of collagen in tissues or purchase Teneligliptin hydrobromide due to an imbalance of fibrogenesis and fibrolysis. No effective cure is available to treat these fibrotic diseases. Immunosuppressive agents are usually recommended but they may have significant adverse effects. For skin fibrosing diseases, a safer and effective treatment is UV irradiation. UV-A light is an electromagnetic radiation with a wavelength of 320–400 nm. Phototherapy with UV-A to treat different skin diseases is usually accompanied by a systemic or topical photosensitizer to enhance the efficacy of the irradiation. The development of a lamp emitting radiation predominantly in the long-wavelength UV-A1 (340–400 nm), was described in 1981. High-dose-UV-A1 irradiation without photosensitizer emerged a decade later to treat atopic dermatitis. Hypertrophic scars and keloid result from excessive extracellular matrix deposition in the dermis after wound healing. Hypertrophic scars are limited to the wound area and usually resolve spontaneously with time. Keloid is defined as scar tissues growing beyond original wounds and is challenging to treat. Large scars may cause disfiguration and loss of function due to scar contracture. Both scars may be complicated with pruritus and pain. Traditional scar treatments include pressure garments, silicone gel sheeting, silicone cream and gel, local steroid injection, and excision and repair with/without skin graft and/or radiation. Pressure garments are inconvenient and uncomfortable especially in tropical and subtropical countries due to humid and hot weather. Surgical removal of keloid, although temporarily rewarding, is almost invariably followed by even more aggressive regrowth of scar tissue. The combination of radiation and surgery provides a higher success rate to cure keloid. However, long-term safety has not been established and invasive tumor may develop after this regimen. Intralesional steroid injections are probably the most common therapy clinically. Many patients are reluctant to undergo this painful therapy, especially for children and patients with large keloid. Recently, UV-A1 has been used in treating localized and generalized scleroderma with encouraging results. UV-A1 irradiation has been shown to stimulate collagenase production by human fibroblasts in vitro. Asawanonda et al demonstrated that UV-A1 with a cumulative dose of 2860 J/cm2 was helpful in treating keloid in a 37-year-old man. The results were not supported in a subsequent study in which three keloid patients showed no response after receiving UV-A1 irradiation with cumulative doses of 1500–1800 J/cm2. Moreover, the application of UV-A1 therapy is limited to a few centers because of the large size and high cost of the machines.