Shah, Monica

Treating actinic keratosis (AK) and photodamaged skin is critical to reduce the risk of progression to skin cancer. Laser resurfacing for AK treatment is available as either lesion-directed or field therapy. Laser resurfacing removes the superficial epidermis and dermis containing actinic damage, promoting re-epithelialization of healthy skin. Although laser resurfacing has been explored as a modality for AK treatment in the literature, studies summarizing its efficacy in the treatment of AK are lacking. This review summarizes existing research on laser resurfacing as a monotherapy for AK treatment, highlighting the various laser resurfacing modalities available for AK treatment as well as their complications and efficacy in comparison to other therapies. Despite longer healing time, fully ablative laser resurfacing, including carbon dioxide and erbium-doped yttrium aluminum garnet were found to be more effective for AK treatment than fractional ablative techniques. Although some studies suggest laser resurfacing monotherapy as less efficacious than photodynamic therapy, and equally effective to 5-fluorouracil and 30% trichloroacetic acid, clinical trials of larger sample size are required to establish stronger evidence-based conclusions. Moreover, laser resurfacing used as lesion-directed therapy, as opposed to the usual field-therapy, requires further investigation.

Background— Oxidative stress may contribute to heart failure (HF) progression. Inhibiting xanthine oxidase in hyperuricemic HF patients may improve outcomes. Methods and Results— We randomly assigned 253 patients with symptomatic HF, left ventricular ejection fraction ≤40%, and serum uric acid levels ≥9.5 mg/dL to receive allopurinol (target dose, 600 mg daily) or placebo in a double-blind, multicenter trial. The primary composite end point at 24 weeks was based on survival, worsening HF, and patient global assessment. Secondary end points included change in quality of life, submaximal exercise capacity, and left ventricular ejection fraction. Uric acid levels were significantly reduced with allopurinol in comparison with placebo (treatment difference, –4.2 [–4.9, –3.5] mg/dL and –3.5 [–4.2, –2.7] mg/dL at 12 and 24 weeks, respectively, both P <0.0001). At 24 weeks, there was no significant difference in clinical status between the allopurinol- and placebo-treated patients (worsened 45% versus 46%, unchanged 42% versus 34%, improved 13% versus 19%, respectively; P =0.68). At 12 and 24 weeks, there was no significant difference in change in Kansas City Cardiomyopathy Questionnaire scores or 6-minute walk distances between the 2 groups. At 24 weeks, left ventricular ejection fraction did not change in either group or between groups. Rash occurred more frequently with allopurinol (10% versus 2%, P =0.01), but there was no difference in serious adverse event rates between the groups (20% versus 15%, P =0.36). Conclusions— In high-risk HF patients with reduced ejection fraction and elevated uric acid levels, xanthine oxidase inhibition with allopurinol failed to improve clinical status, exercise capacity, quality of life, or left ventricular ejection fraction at 24 weeks. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00987415.