Annals of medicine
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During sepsis or acute respiratory distress syndrome, the hypothalamic pituitary adrenal axis is rapidly activated through a systemic pathway, i.e. by circulating pro-inflammatory cytokines and through the vagus nerve. Subsequently, the adrenal glands release cortisol, a hormone which will likely counteract the inflammatory process and restore cardiovascular homeostasis. Both experimental models and studies in humans suggest that inadequate hypothalamic pituitary adrenal axis response to stress accounts, at least partly, for the genesis of shock and organ dysfunction in sepsis and acute respiratory distress syndrome. ⋯ These trials showed consistently that, in these patients, the use of low dose of corticosteroids alleviated inflammation, restored cardiovascular homeostasis, reduced organ dysfunction, improved survival and was safe. Further studies are ongoing to better identify the target population. In the meantime, cortisol replacement (i.e. 200 to 300 mg daily of hydrocortisone or equivalent) should be considered as standard care for these patients.
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Glucose transport, the rate limiting step in glucose metabolism in skeletal muscle, is mediated by insulin-sensitive glucose transporter 4 (GLUT4) and can be activated in skeletal muscle by two separate and distinct signalling pathways: one stimulated by insulin and the second by muscle contractions. Skeletal muscle is the principal tissue responsible for insulin-stimulated glucose disposal and thus the major site of peripheral insulin resistance. Impaired glucose transport in skeletal muscle leads to impaired whole body glucose uptake, and contributes to the pathogenesis of Type 2 diabetes mellitus. ⋯ Intense efforts are underway to define the molecular mechanisms that regulate glucose metabolism in insulin sensitive tissues. This review will present our current understanding of mechanisms regulating glucose transport in skeletal muscle in humans. Elucidation of the pathways involved in the regulation of glucose homeostasis will offer insight into the pathogenesis of insulin resistance and Type 2 diabetes mellitus and may lead to the identification of biochemical entry points for drug intervention to improve glucose homeostasis.
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Meta Analysis
Effects of thyroid hormone suppression therapy on adverse clinical outcomes in thyroid cancer.
Long-term thyroid hormone (TH) therapy aiming at the suppression of serum thyrotropin (TSH) has been traditionally used in the management of well differentiated thyroid cancer (ThyrCa). However, formal validation of the effects of thyroid hormone suppression therapy (THST) through randomized controlled trials is lacking. Additionally, the role - if any - of TSH effect at low ambient concentrations upon human thyroid tumorigenesis remains unclear. ⋯ THST appears justified in ThyrCa patients following initial therapy. As most primary studies were imperfect, future research will better define the effect of THST upon ThyrCa clinical outcomes.