Background: Loxoscelism is an important public health problem in Chile and South America, due to the higher rate of cutaneous-visceral involvement. The diagnosis of loxoscelism is mostly clinical without established diagnostic criteria. There is little evidence to support any treatment used in this condition. Aim: To characterize the clinical features and epidemiology of loxoscelism among patients consulting at the Emergency and Dermatology Services of a clinical hospital between 2013 and 2017. Material and Methods: Review of medical records of patients registered in the electronic clinical record system with a confirmed diagnosis of loxoscelism. Epidemiological, clinical, laboratory tests and treatment variables were analyzed. Results: We reviewed data from 200 patients. Ninety-four percent presented cutaneous loxoscelism and 5.5% cutaneous-visceral loxoscelism. Systemic symptoms were present in 73% of patients with cutaneous-visceral loxoscelism. Patients who developed systemic symptoms had an 18 times higher risk of developing cutaneous-visceral loxoscelism. Laboratory abnormalities were more common in patients with cutaneous-visceral loxoscelism. Not all patients with hematuria had cutaneous-visceral loxoscelism. Most patients required analgesia. Anti-loxosceles serum was not used in any patient. Conclusions: Many questions remain to be answered regarding the diagnosis and treatment of the disease. Studies are required to validate diagnostic criteria for loxoscelism, predictors for visceral involvement and response to treatment.

Background: Plasma high density lipoproteins (HDL) are involved in reverse cholesterol transport mediated by the scavenger receptor class B type I (SR-BI). Nicotinic acid increases HDL cholesterol levels, even though its specific impact on SR-BI dependent-cellular cholesterol transport remains unknown. Aim: To determine the effect of nicotinic acid on HDL particle functionality in cholesterol efflux and uptake mediated by SR-BI in cultured cells in hypoalphalipoproteinemic patients. Material and Methods: In a pilot study, eight patients with low HDL (≤ 40 mg/dL) were treated with extended release nicotinic acid. HDL cholesterol and phospholipid levels, HDL2 and HDL3 fractions and HDL particle sizes were measured at baseline and post-therapy. Before and after nicotinic acid treatment, HDL particles were used for cholesterol transport studies in cells transfected with SR-BI. Results: Nicotinic acid treatment raised total HDL cholesterol and phospholipids, HDL2 levels as well as HDL particle size. Nicotinic acid significantly increased HDL cholesterol efflux and uptake capacity mediated by SR-BI in cultured cells. Conclusions: Nicotinic acid therapy increases SR-BI-dependent HDL cholesterol transport in cultured cells, establishing a new cellular mechanism by which this lipid-lowering drug appears to modulate HDL metabolism in patients with hypoalphalipoproteinemia.