Miliary metastasis to the central nervous system (CNS) is a rare presentation of metastasis mainly found in primary adenocarcinoma of the lung. Its association with breast cancer is even less frequent. We present the case of a 50-year-old female patient diagnosed in 2010 with stage IIA infiltrating ductal breast cancer RE (-), RP (+), HER 2 (-), HER2 NEU (+). She was treated with modified radical left breast mastectomy, radiation therapy, and chemotherapy. Her condition began presenting oppressive frontal headache without irradiation, predominantly in the evening, intensity 8/10, which decreased when sleeping and was exacerbated with stressful situations, in addition to progressive cognitive deterioration. Simple and contrasted computed tomography (CT) of the skull and thoracoabdominal were requested, showing multiple micronodular lesions with calcium density in the brain parenchyma, left pleural effusion, hypo and hyperdense lesions in the liver parenchyma, as well as osteoblastic lesions in the lumbar spine. Simple and contrasted magnetic resonance imaging (MRI) of the skull showed multiple supra and infratentorial intra-axial lesions. The most frequent associated symptom with miliary metastasis is cognitive impairment. Miliary metastasis, confirmed by imaging studies and histopathology, requires the ruling out of other causes of this calcification pattern, such as neurocysticercosis, due to specific treatment for each pathology.

The advance of technology has made possible the use of new techniques within medicine for the treatment of diseases; monoclonal antibodies are a clear example of this. Keloid scars are one of the most difficult pathologies to treat due to the high percentage of recidivism, formed by the growth of a scar with benign fibrous tissue in genetically predisposed individuals, resulting from a process of inflammation and abnormal scarring. Monoclonal antibodies, being a line of treatment that has increased over the years, can show a new frontier in the treatment of them by focusing on the signaling that causes it. We review the literature on the signaling mechanisms of keloid scars and the possible monoclonal approach.

No abstract