Acquired antithrombin III (AT III) deficiency is based on either decreased activity or synthesis, increased loss or increased consumption. The activity of AT III is decreased in metabolic acidosis, hyperlipoproteinemias and by lipid peroxides. Chronic liver diseases especially liver cirrhosis are associated with very low levels of AT III due to insufficient hepatic synthesis, reduced transcapillary flux ratios, diffuse intravascular coagulation and loss in the ascites. Gastrointestinal loss of AT III may occur in patients with active inflammatory bowel diseases. AT III deficiency is observed in nephrotic syndrome when urinary loss of protein exceeds 5 g/d. During hemodialysis we have not found low AT III levels. Disseminated intravascular coagulation is characterized by activation of the coagulation system and increased consumption of AT III. AT III complexes with activated coagulation factors are subsequently cleared by the reticuloendothelial system.