Introduction Malignant triton tumor (MTT) is an extremely rare variant of the malignant peripheral nerve sheath tumors (MPNSTs) with rhabdomyosarcomatous differentiation, which was first described in 1932 by Mason. MTT affects, in most cases, patients under 35 years of age, and it is usually manifested as a mass that may or not be painful. However, the incidence in pediatric patients is atypical. This tumor presents an aggressive course and limited survival rate, and the prognosis is different between individuals with or without a concomitant diagnosis of neurofibromatosis type 1 (NF1). Currently, the recommended treatment is surgical resection, and adjuvant chemotherapy and radiotherapy, but its efficacy is not yet clear. Presentation of the case A 13-year-old female patient was referred to the pediatric oncology service due to the presence of an abdominal mass and weight loss, initially diagnosed with Wilms' tumor. After extensive investigation, surgical resection, and immunohistopathological evaluation, the diagnosis of malignant triton tumor was confirmed. The patient also underwent cycles of chemotherapy after resection, and is currently awaiting immunotherapy. Discussion and conclusion Malignant triton tumor is extremely rare and difficult to diagnose, especially in children or young people, age groups in which the incidence of the disease is even lower. This may be the reason it is rarely suspected, and it was a great challenge for the clinical care team. It is essential to consider and investigate this possibility of differential diagnosis, as patients diagnosed with this malignant tumor have a low survival rate and poor prognosis.

Cardiovascular (CV) disease is the main cause of death in nonalcoholic fatty liver disease (NAFLD), a clinical condition without any approved pharmacological therapy. Thus, we investigated the effects of ornithine aspartate (LOLA) and/or Vitamin E (VitE) on CV parameters in a steatohepatitis experimental model. Adult Sprague Dawley rats were randomly assigned (10 animals each) and treated from 16 to 28 weeks with gavage as follows: controls (standard diet plus distilled water (DW)), NAFLD (high-fat choline-deficient diet (HFCD) plus DW), NAFLD+LOLA (HFCD plus LOLA (200 mg/kg/day)), NAFLD+VitE (HFCD plus VitE (150 mg twice a week)) or NAFLD+LOLA+VitE in the same doses. Atherogenic ratios were higher in NAFLD when compared with NAFLD+LOLA+VitE and controls (p < 0.05). Serum concentration of IL-1β, IL-6, TNF-α, MCP-1, e-selectin, ICAM-1, and PAI-1 were not different in intervention groups and controls (p > 0.05). NAFLD+LOLA decreased miR-122, miR-33a, and miR-186 (p < 0.05, for all) in relation to NAFLD. NAFLD+LOLA+VitE decreased miR-122, miR-33a and miR-186, and increased miR-126 (p < 0.05, for all) in comparison to NAFLD and NAFLD+VitE. NAFLD+LOLA and NAFLD+LOLA+VitE prevented liver collagen deposition (p = 0.006) in comparison to NAFLD. Normal cardiac fibers (size and shape) were lower in NAFLD in relation to the others; and the inverse was reported for the percentage of regular hypertrophic cardiomyocytes. NAFLD+LOLA+VitE promoted a significant improvement in atherogenic dyslipidemia, liver fibrosis, and paracrine signaling of lipid metabolism and endothelial dysfunction. This association should be further explored in the treatment of NAFLD-associated CV risk factors.