The systemic inflammatory response syndrome (SIRS) is characterized by a hypercatabolic state induced by inflammatory mediators.
Two years later, she presented with a hypercatabolic state, with progressive hepato-splenomegaly and constitutional features.
The systemic inflammatory response syndrome (SIRS) is an inflammatory state affecting the whole body just characterized by a hypercatabolic state induced by inflammatory mediators [ 1– 6].
Because of acute systemic inflammation response syndrome, AP always triggers a hypercatabolic state, resulting in increased energy requirements and protein catabolism [ 23].
The results showed that muscle protein metabolism of the unaffected side was prevalently in a hypercatabolic state (MH) due to excess of protein catabolism over protein synthesis indicated by muscle release of phenyl-.
Patients with MF develop a hypercatabolic state with progressively debilitating symptoms, including constitutional (fever, night sweats, weight loss) and general (fatigue and lethargy) symptoms, and organ-localized complaints [ 3– 5].
The systemic inflammation associated with RA causes a hypercatabolic state, which, together with a sedentary lifestyle, results in a loss of muscle bulk and an increased tendency to gain fat in the presence of stable or even slightly decreased weight, often referred to as rheumatoid cachexia [ 45].
Our speculation is that peritonitis may disrupt aquaporin-mediated water removal, reduce Na+ intake due to poor appetite, and, probably most important, lead to a hypercatabolic state, in which intracellular osmoles, such as protein, nucleic acids, phosphates, are degraded and thus move intracellular water into extracellular space.
This produces a mildly hypercatabolic state, increases resting energy expenditure, and causes chronic oxidative stress [ 39].
Hypermetabolism also leads to futile protein use, resulting in induction of a dynamic hypercatabolic state [ 15- 18].
