RESUMO
Autoimmune pancreatitis is a form of pancreatitis with autoimmune stigmata that may present as either focal or diffuse gland involvement. In focal forms, autoimmune pancreatitis shares demographic, clinical, biochemical and imaging features with pancreatic cancer. Since autoimmune pancreatitis is a benign disease and steroid therapy can rapidly resolve symptoms, improve radiological findings and avoid unnecessary surgery, the current clinical challenge is how to differentiate autoimmune pancreatitis from pancreatic neoplasia. Even though definitive diagnosis of the disease is difficult, several diagnostic criteria have been proposed and progress has been made in imaging studies. The management of this unique form of pancreatitis should, therefore, be handled in centres with knowledge of all aspects of the disease. This article briefly reviews clinical aspects of autoimmune pancreatitis with a focus on its diagnostic imaging and management.
Assuntos
Doenças Autoimunes/diagnóstico por imagem , Pancreatite/diagnóstico por imagem , Tomografia Computadorizada por Raios X , Doenças Autoimunes/patologia , Biópsia , Colangiopancreatografia Retrógrada Endoscópica , Meios de Contraste , Fluordesoxiglucose F18 , Humanos , Imageamento por Ressonância Magnética , Pancreatite/imunologia , Pancreatite/parasitologia , Tomografia por Emissão de PósitronsRESUMO
AIMS: To assess whether host metabolic factors influence the degree of hepatic steatosis and fibrosis in patients infected with hepatitis C virus, and to evaluate the impact of anti-viral therapy on insulin resistance and serum levels of adipocytokines. METHODS: Clinical and biochemical features, anthropometrical characteristics, and levels of fasting insulin, leptin, adiponectin and resistin were measured in 'naïve' patients with chronic hepatitis C, before, during and after therapy with Peg-Interferon-alpha 2a plus Ribavirin. RESULTS: Forty-eight patients were included (M/F 28/20; mean age 50.0 +/- 12.6 years; 62.5% genotype-1). Body mass index was 26.4 +/- 4.0 kg/m(2), and visceral obesity was present in 24 patients. At multivariate analysis (RR; 95% CI), steatosis was associated to older age (1.08; 1-1.18), necroinflammatory activity (17.67; 1.6-194.46), and raised insulin levels (1.39; 1.1-1.77). Fibrosis was related to necroinflammatory activity (25.73; 2.54-261.11), and steatosis (6.47; 1.09-38.29). Sustained viral response was achieved by 62.5% of patients and was associated with younger age (0.92; 0.85-0.99), genotype non-1 (10.61; 1.52-73.76) and absence of visceral obesity (13.78; 2.36-80.29). At the end of follow-up, insulin and the homeostasis model assessment for insulin resistance were reduced and adiponectin increased when compared with baseline, all unrelated to the outcome of treatment. CONCLUSIONS: Visceral obesity correlates with the degree of steatosis and fibrosis, and it negatively affects treatment response. Significant changes of insulin resistance and adipocytokines occur under treatment, irrespective of virological outcome.