Background and Objectives Treatment of melasma with lasers remains a challenge due to its limited clinical efficacy in addition to high rates of recurrence and side effects. Recently, picosecond lasers have shown favorable results in treatment of benign pigmented lesions. To compare the efficacy and safety of using a 755‐nm picosecond laser for the treatment of melasma in a split‐face manner, having one side treated with a fractionated beam (diffractive lens array [DLA] coupling) and with a full‐beam (flat optics) on the other side. Study Design/Materials and Methods Eighteen subjects presenting with mixed‐type melasma were enrolled. Each patient was randomly treated with a 755‐nm picosecond laser coupled with DLA on one side of the face and without DLA (flat optics) on the other side. The laser was delivered through an 8‐mm spot size with an average fluence of 0.4 J/cm2 at 2.5 Hz for a total of two passes without pulse overlapping. All subjects received five monthly treatments. Subjective (clinical evaluation) and objective (color readings) assessments on the degree of pigment clearance and adverse effects were obtained at 1‐, 3‐, and 6‐month after the final treatment. Results At 6 months after the last treatment, physician‐rating scores were 1.50 ± 0.76 and 1.50 ± 0.65 of the DLA and flat‐optics sides, respectively. Pigment clearance significantly improved from 1 to 6 months after the treatment on each side (P = 0.019 on DLA and P = 0.023 on flat‐optics sides). No statistically significant differences in physician‐rating scores between the two treatment techniques were observed at all follow‐up visits. Objective assessments of melasma clearance corresponded to the clinical evaluation. However, the full‐beam (flat optics) provided lower incidence of pos‐tinflammatory hyperpigmentation than the fractioned one. Conclusions A 755‐nm picosecond laser is safe and effective for the treatment of melasma in dark‐skinned individuals. The use of DLA does not provide additional benefit over the flat optics in clearing pigmentation. Lasers Surg. Med. © 2020 Wiley Periodicals LLC

Background and Objective Fractional 1064‐nm picosecond‐domain laser has recently been utilized for the treatment of atrophic acne scars and showed promising results. However, data on the safety and efficacy of this procedure in dark‐skinned patients are limited. This prospective, self‐controlled study was conducted to objectively evaluate the safety and efficacy of a 1064‐nm picosecond laser coupled with a microlens array (MLA) for the treatment of atrophic acne scars on Asian skin. Study Design/Materials and Methods Twenty‐six subjects of Fitzpatrick skin types (FSTs) III and IV with atrophic acne scars were enrolled. All subjects were treated with a 1064‐nm picosecond laser (spot size of 8 mm, fluence of 1.0 J/cm2, a repetition rate of 10 Hz) in combination with the MLA handpiece for an average of three passes, for 6 monthly sessions. Objective (measurement of scar volume using three‐dimensional (3D) photography and skin roughness analysis using ultraviolet A‐light video camera) and subjective (clinical evaluation by two blinded dermatologists) assessments were obtained at baseline and at 1, 3, and 6 months after the final treatment. Results Statistically significant reduction of the scar volume from baseline at 1, 3, and 6 months after the final treatment were observed by 3D photography and ultraviolet A‐light video camera. At the 6‐month follow‐up, 50% (13 of 26) of the subjects were rated as having at least 50% improvement of the scars. The rate of improvement significantly increased from the 1‐month follow‐up to the 6‐month follow‐up (P = 0.013). Similarly, at the 6‐month follow‐up, the scar volume (P = 0.024) and skin roughness (P = 0.001) also significantly improved, in comparison with the baseline. Mild postinflammatory hyperpigmentation (PIH) was observed to develop in approximately 18% of all the treatment sessions. All cases of PIH were temporary and resolved within 4 weeks on average. Conclusions The 1064‐nm picosecond laser with MLA is a safe therapeutic alternative for the treatment of atrophic acne scars in dark‐skinned individuals. Lasers Surg. Med. © 2020 Wiley Periodicals LLC

Introduction Botulinum toxin A (BoT/A) treatment failure (BTF) affects patients subjected to repeated BoT/A exposure for cosmetic indications. BoT/A’s general formulation contains core BoT/A and complexing proteins. BTF may be caused by antibody-induced treatment failure. Antibodies against core BoT/A can occur; however, anti-complexing protein antibodies have never been demonstrated, and tools for anti-complexing protein antibody detection have not been developed. The aim of this study was to evaluate immune involvement in BoT/A-nonresponsive patients. Methods Patients suspected of nonresponsiveness to BoT/A for cosmetic indications were recruited. All volunteers were categorized as BoT/A-responsive or BoT/A-tolerant according to frontalis testing with onabotulinumtoxinA (onaA). Twenty-two BoT/A-tolerant volunteers were recruited separately for frontalis testing with incobotulinumtoxinA (incoA). Anti-BoT/A and anti-complexing protein antibodies were quantified by special ELISA using sera from blood sampled before and after frontalis testing. Results Significantly higher levels of IgG against complexing protein were detected in onaA-tolerant sera but not in onaA-responders, leading to proposals that anti-complexing protein antibodies could cause onaA unresponsiveness. Some onaA-tolerant patients according to frontalis test with incoA were responsive to incoA. Newly developed absorption ELISA confirmed that incoA-responsive sera predominantly contained IgG against complexing proteins, whereas incoA-tolerant sera contained significant levels of IgG against core BoT/A. The presence of anti-complexing protein antibodies higher than 90.75% in sera of onaA-tolerant patients could respond to incoA. The ELISA technique might be employed as a tool to predict incoA responsiveness. Our frontalis testing after incoA treatment showed that anti-incoA IgG levels were not increased by incoA. Conclusions BoT/A-exposed patients may develop antibodies against core botulinum toxin and complexing proteins. Our study is the first to demonstrate that anti-complexing protein antibodies cause BTF. High levels of antibodies against complexing proteins can cause onaA unresponsiveness, although some patients were still incoA-responsive. Our developed ELISA to detect anti-complexing protein antibodies can determine whether onaA-tolerant patients respond to incoA without incoA frontalis testing.