RESUMO
Antineoplastic treatments can negatively affect body composition, leading to metabolic derangements and worse clinical outcomes in breast cancer patients. This scoping review assesses body adiposity changes during breast cancer therapy. We included clinical and observational studies, published until the last search date in any language, with women aged >18 years, after breast cancer diagnosis, at any clinical stage and with any history of breast cancer treatment, who had body adiposity quantified by imaging tools at least twice during follow-up. In total, 17 studies were included (n = 1,009 individuals), six of which found a significant increase in body adiposity during treatment, two found a significant decrease, one presented divergent findings according to the imaging method and the analyzed body adiposity depots, and eight studies found no significant change in the outcome. Selective estrogen receptor modulators were associated with increased body adiposity, whereas aromatase inhibitors were associated with its decrease (n = 3). Chemotherapy was associated with increased body adiposity (n = 1), and monoclonal antibody with reduced brown adipose tissue activity (n = 1). Breast cancer treatment may have different effects on body adiposity, according to its mechanisms and protocols. Further studies are necessary to better elucidate this scenario.
Assuntos
Antineoplásicos , Neoplasias da Mama , Adiposidade , Antineoplásicos/farmacologia , Composição Corporal , Neoplasias da Mama/tratamento farmacológico , Neoplasias da Mama/metabolismo , Feminino , Humanos , Obesidade/complicações , Obesidade/tratamento farmacológicoRESUMO
Investigation of hyperferritinemia in metabolic syndrome patients represents a diagnostic challenge, but it is essential for the identification of individuals with iron overload. Hepcidin negatively regulates iron absorption and release. An increase in hepcidin occurs when iron levels are sufficient or in inflammatory states, conditions often associated with hyperferritinemia. Hemochromatosis causes hyperferritinemia due to iron overload, but frequently has low hepcidin levels. Our aim was to evaluate biochemical and molecular parameters related to iron metabolism in patients with metabolic syndrome. We evaluated 94 patients with metabolic syndrome according to the International Diabetes Federation criteria in a cross-sectional study. Anthropometric data and diagnostic criteria for metabolic syndrome, iron dosage, ferritin, transferrin saturation, hepcidin, and the C282Y and H63D mutations in the HFE hemochromatosis gene were evaluated. Prevalence of hyperferritinemia in the study population was 27.7% and was higher in males (46.2%) than in females (14.5%). Increase in transferrin saturation correlated with mutations in the hemochromatosis gene. Hyperferritinemia was associated to transferrin saturation and hepcidin after logistic regression analysis. In conclusion, hyperferritinemia is a frequent finding in metabolic syndrome patients, most frequently in men; and hepcidin assessment can be useful for the investigation of ferritin increase in those subjects.