RESUMO
The cancer invasion of the large intestine, a destructive process that begins within the mucous membrane, causes cancer cells to gradually erode specific layers of the intestinal wall. The normal tissues of the intestine are progressively replaced by a tumour mass, leading to the impairment of the large intestine's proper morphology and function. At the ultrastructural level, the disintegration of the extracellular matrix (ECM) by cancer cells triggers the activation of inflammatory cells (macrophages) and connective tissue cells (myofibroblasts) in this area. This accumulation and the functional interactions between these cells form the tumour microenvironment (TM). The constant modulation of cancer cells and cancer-associated fibroblasts (CAFs) creates a specific milieu akin to non-healing wounds, which induces colon cancer cell proliferation and promotes their survival. This review focuses on the processes occurring at the "front of cancer invasion", with a particular focus on the role of the desmoplastic reaction in neoplasm development. It then correlates the findings from the microscopic observation of the cancer's ultrastructure with the potential of modern radiological imaging, such as computer tomography (CT) and magnetic resonance imaging (MRI), which visualizes the tumour, its boundaries, and the tissue reactions in the large intestine.
Assuntos
Neoplasias Colorretais , Imageamento por Ressonância Magnética , Invasividade Neoplásica , Tomografia Computadorizada por Raios X , Microambiente Tumoral , Humanos , Neoplasias Colorretais/patologia , Neoplasias Colorretais/diagnóstico por imagem , Imageamento por Ressonância Magnética/métodos , Tomografia Computadorizada por Raios X/métodos , Matriz Extracelular/ultraestrutura , AnimaisRESUMO
INTRODUCTION: Liver transplantation (LTx) is the only successful treatment for end-stage liver disease. The results of liver transplantation depend not only on graft survival but may be also affected by superimposed cardiovascular morbidities. The aim of this retrospective study was to assess the prevalence of lipid disorders as one of the important cardiovascular risk factors in patients before and after successful LTx. MATERIAL AND METHODS: One hundred eleven patients who underwent liver transplantation because of liver cirrhosis and survived at least 2 years with functioning graft between November 2005 and May 2014 were included in this retrospective analysis. The mean age of the patients at the time of liver transplantation was 49.7±12.2 years. The prevalence of dyslipidemia was assessed before and two years after liver transplantation. This was analyzed in relation to the etiology of liver disease, including alcohol toxicity, viral or autoimmune diseases. RESULTS: The prevalence of hypertriglyceridemia before and after LTx was 13.5% and 40.5%, respectively (P<0.001). Similarly, hypercholesterolemia was noted in 17.1% and 51.4% respectively (P<0.001). The annual incidence of hypertriglyceridemia and hypercholesterolemia during the first two years after LTx was 16.2% and 20.7%, respectively. The prevalence of hypertriglyceridemia (18.5% vs 66.7%, P<0.001) and hypercholesterolemia (29.6% vs 70.0%, P=0.002) was significantly lower in patients with the autoimmune cause of liver cirrhosis in comparison to patients with the alcoholic liver disease. CONCLUSIONS: The prevalence of dyslipidemia is increased after liver transplantation. The prevalence of dyslipidemia may be related to the cause of liver injury before LTx.
Assuntos
Hipercolesterolemia , Hipertrigliceridemia , Transplante de Fígado , Humanos , Adulto , Pessoa de Meia-Idade , Transplante de Fígado/efeitos adversos , Estudos Retrospectivos , Hipercolesterolemia/etiologia , Cirrose Hepática/epidemiologia , Cirrose Hepática/cirurgia , Hipertrigliceridemia/etiologia , LipídeosRESUMO
BACKGROUND Liver transplantation (LTx) is useful in the treatment of end-stage liver disease. Outcomes of transplantation are dependent upon graft survival and can also be affected by superimposed cardiovascular morbidities. The present retrospective study was performed to assess the prevalence of cardiovascular risk factors before and after LTx. MATERIAL AND METHODS A retrospective review of 130 patients undergoing liver transplantation between October 2005 and April 2014 was completed. The mean age of the patients was 49.3±11.9 years. The prevalence of cardiovascular risk factors was assessed before and 2 years after transplantation. The prevalence of cardiovascular risk factors was assessed using a comparison based upon the etiologies of liver disease resulting in transplantation including alcohol, viral, and autoimmune processes using a chi-square analysis. RESULTS The prevalence of diabetes mellitus before and 2 years after liver transplantation (LTx) were 18% and 48% (P<0.001). Hypertension was documented in 24% of patients at baseline and 70% after 2 years of follow-up (P<0.001). The prevalence rates of diabetes mellitus before and 2 years after LTx were 18% and 48% (P<0.001). The prevalence of hypertriglyceridemia before and after LTx was 15% and 38%, respectively (P<0.001). Hypercholesterolemia was noted in 16% and 46%, respectively (P<0.001). Thirteen percent of patients before LTx and 18% after were obese (body mass index higher than 30 kg/m²). The annual incidence of diabetes mellitus, hypertension, hypertriglyceridemia, hypercholesterolemia, and obesity during the first 2 years after LTx was 15%, 23.5%, 15%, 18.5%, and 6%, respectively. Twenty-four percent of patients before and 10% after LTx admitted to tobacco use (P<0.001). The prevalence of diabetes (38% vs 67%, P=0.02), hypertriglyceridemia (19% vs 63%, P<0.001), hypercholesterolemia (28% vs 67%, P=0.002), and obesity (9% vs 33%, P=0.02) was lower in patients with an autoimmune cause of liver cirrhosis in comparison to patients with alcoholic disease. CONCLUSIONS The prevalence of hypertension and glucose and lipid metabolism abnormalities may increase in patients after liver transplantation. The prevalence of cardiovascular risk factors in patients after LTx may be related to the cause of liver injury before LTx.