The article by Scivoletto et al, Spinal Cord 2004; 42: 473–476, points out the inflammatory nature of pressure sores, noting the consequent anemia and hypoalbuminemia as well as other indicators of chronic inflammation.1 The explanation for the hypoalbuminemia offered was an inhibition of hepatic synthesis. However, the cited reference that addressed this issue showed a turnover of albumin during infectious and toxic diseases no different from that of controls.2 Furthermore, the normally rapid elimination rate of albumin in spinal cord-injured patients is accentuated during inflammatory states, suggesting increased microvascular permeability to albumin tracers.3, 4 Even during parenteral nutrition albumin levels remain low and disappearance from the intravascular space high with sepsis.5 Direct evidence for depressed liver synthesis of albumin during an inflammatory state such as a pressure sore is lacking, but a leak to the extravascular space is a likely factor in the hypoalbuminemia of inflammatory states.