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Metabolic Syndrome Consequent to Endocrine Disorders


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Direct effect of IGF-1 on stimulation of NO synthesis in the endothelial cells was demonstrated. Increased levels of asymmetrical dimethyl arginine, an endogenous inhibitor of endothelial NO synthase involved in the pathogenesis of endothelial dysfunction, have also been reported in these patients, as well as, reduction during GHRT along with improved endothelial function [59, 60]. Higher levels of pregnancy-associated plasma protein A were found in GHD patients compared to controls [47]. Pregnancy-associated plasma protein A is proposed as a marker of increased atherothrombotic risk, which is highly expressed in eroded and ruptured atherosclerotic plaques in acute coronary syndrome and ischemic stroke. It is produced by smooth muscle cells in the arterial wall.

      Available data support the evidence of beneficial direct GHRT effects on vasculature, endothelial function, proinflammatory molecules, adhesion markers, and fibrinolytic function in adult GHD patients with hypopituitarism. Data regarding autonomic nervous system dysfunction are scarce. Reported reduction and normalization of cardiovascular mortality rates and death from myocardial infarction further support these findings [14].

      Cardiac Function and Morphology

      Anabolic effects of GHRT on LV mass seem to be short-lasting (1–2 years of GHRT) and disappear soon after discontinuation of treatment or return to normal after 2 years of long-term (10 years) GHRT. However, decrease in diastolic BP and improvement of diastolic filling seem to persist during long-term (7 years) GHRT [32].

      MetS and Fatty Liver Disease in Patients with GHD and Hypopituitarism

      Recently, several reports have suggested that hepatic impairment and hepatic steatosis may be particularly related to MetS in GHD. Non-alcoholic fatty liver disease (NAFLD) can be diagnosed using imaging techniques while diagnosis of non-alcoholic steato-hepatitis (NASH) is based on histological finding obtained by liver biopsy. NASH is progressive disease characterized by steatosis, inflammatory infiltration, hepatocyte injury, and fibrosis, which can lead to hepatic cirrhosis [3, 81].