Context The high prevalence of acne vulgaris and its significant morbidity underscore the need for convenient, low-risk, and efficacious therapy. Treatment with various lasers has been reported to improve acne. Objective To evaluate the clinical efficacy of pulsed dye laser therapy in the treatment of acne. Design, Setting, and Patients Randomized, single-blind, controlled, split-face clinical trial of a volunteer sample of 40 patients aged 13 years or older with facial acne conducted at an academic referral center from August 2002 to September 2003. Intervention One or 2 nonpurpuric pulsed dye laser treatments to half of the face (fluence of 3 J/cm 2), serial blinded clinical assessments (lesion counts), and grading of acne severity using standardized bilateral serial photographs. Main Outcome Measures Comparison of the changes in lesion counts from baseline to 12 weeks between treated and untreated sides of the face and changes in photographic evidence of acne severity as graded by a panel of dermatologists blinded to treatment assignment. Results After 12 weeks, using intent-to-treat analysis with last observation carried forward, there were no significant differences between laser-treated and untreated skin for changes in mean papule counts (−4.2 vs −2.2; P=.08), mean pustule counts (0 vs −1.0; P=.12), or mean comedone counts (2.9 vs 1.6; P=.63). Grading of serial photographs confirmed the clinical assessments, showing no significant mean (SE) differences in Leeds scores (range, 1-12) for treated skin (3.98 [0.32] at baseline and 3.94 [0.27] at week 12) compared with untreated skin (3.83 [0.32] at baseline and 3.79 [0.28] at week 12) (PϾ.99). Conclusions In this study, the nonpurpuric pulsed dye laser therapy did not result in significant improvement of facial acne. More research is needed before this laser therapy may be recommended as an acne treatment.

The study population comprised 36 elderly subjects (mean age, 87 years), residing in 2 senior citizen facilities.Intervention: Topical 0.4% retinol lotion or its vehicle was applied at each visit by study personnel to either the right or the left arm, up to 3 times a week for 24 weeks.Main Outcome Measures: Clinical assessment using a semiquantitative scale (0, none; 9, most severe) and biochemical measurements from skin biopsy specimens obtained from treated areas.Results: After 24 weeks, an intent-to-treat analysis using the last-observation-carried-forward method revealed that there were significant differences between retinoltreated and vehicle-treated skin for changes in fine wrinkling scores (−1.64 [95% CI, −2.06 to −1.22] vs −0.08 [95% CI, −0.17 to 0.01]; PϽ.001). As measured in a subgroup, retinol treatment significantly increased glycosaminoglycan expression (P =.02 [n=6]) and procollagen I immunostaining (P=.049 [n=4]) compared with vehicle.Conclusions: Topical retinol improves fine wrinkles associated with natural aging. Significant induction of glycosaminoglycan, which is known to retain substantial water, and increased collagen production are most likely responsible for wrinkle effacement. With greater skin matrix synthesis, retinol-treated aged skin is more likely to withstand skin injury and ulcer formation along with improved appearance.

Summary Background Pseudoxanthoma elasticum (PXE) manifests with cutaneous lesions consisting of yellowish papules coalescing into plaques of inelastic skin. Histopathology demonstrates accumulation of pleiomorphic elastic structures with progressive mineralization. The classic form of PXE is caused by mutations in the ABCC6 gene. Objectives A 2-year old patient with PXE of the neck, inguinal folds and lower abdomen, and with extensive tissue mineralization was evaluated for the underlying mutations in candidate genes known to be involved in ectopic mineralization disorders. Methods The patient’s genotype was studied by sequencing ABCC6, MGP and ENPP1 genes, encoding proteins which harbor mutations in ectopic mineralization disorders. Results No pathogenetic mutations were found in the ABCC6 or MGP genes. Sequencing of ENPP1 disclosed a homozygous missense mutation, p.Y513C, associated with generalized arterial calcification of infancy. Conclusions This study demonstrates the presence of the cutaneous features of PXE in a genetically distinct disease, generalized arterial calcification of infancy, and thus expands the spectrum of PXE-related disorders.

A range of spinal anomalies is associated with cutaneous lumbosacral infantile hemangiomas and MRI can be used to characterize these abnormalities.