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ObjectiveTo evaluate the efficacy, adverse effects, and recurrence of oral propranolol for treatment of infantile hemangioma.MethodsParticipants were treated with oral propranolol three times daily, with inpatient monitoring of adverse effects. The starting dosage was 2 mg/kg per day, which had been for the remaining duration of treatment. Therapy duration was planned for 4–6 months; if there was significant relapse, the period of treatment was extended. A photograph based severity scoring assessment was performed by three observers to evaluate efficacy by visual analog scale (VAS).ResultsSixty-one infants [median age 3.3 (1.2–8.1) months] were included in the study. The median follow-up-time was 15 (6–20) months and 53 patients completed treatment at a median age of 10.3 (8.4–18.1) months, after a duration of 8.5 (4.5–14) months. In all patients, there was significant fading of color [with a VAS of −9 (−6 to −9) after 6 months] and significant decrease in size of the infantile hemangiomas [with a VAS of −8 (−3 to −10) after 6 months]. We did not observe any life-threatening adverse effects. The therapy was interrupted due to temporary aggravation of pre-existing bronchial asthma in one child. Four cases presented partial recurrences.ConclusionsOral propranolol 2 mg/kg per day was a well-tolerated and effective treatment, mild adverse effects, and low recurrence for infantile hemangiomas. Propranolol should now be used as a first-line treatment in hemangiomas when intervention is required. Also, prospective studies should be needed in determining the most effective treatment dosage, optimum treatment duration, and exact mechanism of action of propranolol in future.

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Impaired wound healing is a major diabetes-related complication. Keratinocytes play an important role in wound healing. Multiple factors have been proposed that can induce dysfunction in keratinocytes. The focus of present research is at a more specific molecular level. We investigated the role of advanced oxidative protein products (AOPPs) in inducing human immortalized keratinocyte (HaCaT) cell apoptosis and the cellular mechanism underlying the proapoptotic effect of AOPPs. HaCaT cells were treated with increasing concentrations of AOPP-human serum albumin or for increasing time durations. The cell viability was measured using the thiazolyl blue tetrazolium bromide method, and flow cytometry was used to assess the rate of cell apoptosis. A loss of mitochondrial membrane potential (MMP) and an increase in intracellular reactive oxygen species (ROS) were observed through a confocal laser scanning microscope system, and the level of ROS generation was determined using a microplate reader. Nicotinamide adenine dinucleotide phosphate oxidase (NOX)4, extracellular signal-regulated kinase (ERK)1/2, p38 mitogen-activated protein kinase (MAPK), and apoptosis-related downstream protein interactions were investigated using the Western blot analysis. We found that AOPPs triggered HaCaT cell apoptosis and MMP loss. After AOPP treatment, intracellular ROS generation increased in a time- and dose-dependent manner. Proapoptotic proteins, such as Bax, caspase 9/caspase 3, and poly(ADP-ribose) polymerase (PARP)-1 were activated, whereas anti-apoptotic Bcl-2 protein was downregulated. AOPPs also increased NOX4, ERK1/2, and p38 MAPK expression. Taken together, these findings suggest that extracellular AOPP accumulation triggered NOX-dependent ROS production, which activated ERK1/2 and p38 MAPK, and induced HaCaT cell apoptosis by activating caspase 3 and PARP-1.

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