The mechanism of hypoalbuminemia in AP may be driven by (1) a reduced intake of protein due to fasting and a high catabolism state in acute pancreatitis, (2) the fact that albumin is synthesized in the liver, and the excessive release of inflammatory cytokines such as IL-1, IL-6, and TNFα in SAP results in decreased liver synthesis, and (3) the increased vascular permeability increases the transcapillary loss of albumin in the progress of the stress response [26, 27, 34, 35]. Here, TNF is linked to acute pancreatitis.