Overweight persons who achieve significant reductions in body weight through 12 months of physical activity and low caloric diet can decrease liver fat, VAT and SAT. Even in those with minimal weight loss ALT levels, steatosis, adipokines and cardiovascular risk factors improved.

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We present the case of a 76 year old female patient admitted in the Department of Cardiology for physical asthenia, profuse sweating and dyspnea with orthopnea for about one month. Clinical and paraclinical assessments performed at admission confirmed the diagnosis of cardiac tamponade. Surgical intervention was performed and 400 mL of clear effusion were drained. Post-operative evolution was marked by recurrence of symptoms, requiring after 3 weeks a new drainage of 600 mL of clear effusion, and biopsy of the pericardium was performed. Pathological exam described serous pericarditis with chronic inflammatory infiltrate, xanthogranulomatous reaction intricated in the pericardium and mesothelial hyperplasia. The patient was subsequently transferred to the Department of Internal Medicine for further investigations. Physical examination showed a patient with altered general status, pallor, vesicular murmur absent in both bases, presenting cutaneous hyperpigmentation at the level of the right hemi-abdomen and hip with posterior extension, and a peripheral indurated erythematous plaque. The patient presented nodular masses of 3 cm in the right latero-cervical and bilateral axillary regions, non-adherent to the superficial structures, as well as adenopathic blocks in both inguinal regions. CT scan of the thorax and abdomen showed moderate bilateral pleuresia, minimal pericardial effusion (15 mm) and multiple adenopathies on both sides of the diaphragm. Skin biopsy was performed, as well as bone marrow aspirate and excision of a right axillary lymph node. Pathological exams and immunohistochemistry tests confirmed the diagnosis of Plasma Cells Castleman disease.

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Chronic metabolic inflammation, maintained by numerous proinflammatory mediators, links the metabolic syndrome to NASH. Epigeal changes that accelerate the synthesis of proinflammatory mediators in response to nutritional factors and life style are not fully known. Numerous proinflammatory transcription pathways have been described where nuclear factor kappa B plays a critical role in stimulating proinflammatory gene promoter region interdependent with epigenetic machinery. Of the many cytokines, adipokines, myokines involved in the evolution of NAFLD from simple steatosis to NASH and cirrhosis, the most important is the balance between proinflammatory cytokines TNFα and IL 6 on one hand and adiponectin on the other hand, these factors being produced by Kupffer cells, hepatic stellate cells and inflammatory hepatocytes. Starting from the classical "two hit" theory of the pathogenesis of NAFLD, recent studies have revealed the important role of free cholesterol, diacylglycerols and ceramides in the induction of insulin resistance by stimulating sterol-element-binding protein 1c and thus stimulating de novo lipogenesis. The important roles of mitochondrial dysfunction, oxidative stress endoplasmic reticulum, inflammasomes, hepatocyte apoptosis and necrosis have also been highlighted.