There are two main types of protein<unk>  assays, activity and antigen (immunoassays).<unk> ommercially available activity assays are based on<unk> hromogenic assays that use activation by snake venom in an activating reagent, or<unk> lotting and enzyme-linked immunosorbant assays. Repeated testing for protein<unk>  functional activity allows differentiation between transient and<unk> ongenital deficiency of protein<unk> . Initially, a protein<unk>  activity (functional) assay<unk> an be performed, and if the result is low, a protein<unk>  antigen assay<unk> an be<unk> onsidered to determine the deficiency subtype (Type I or Type II). In type I deficiencies, normally functioning protein<unk>  molecules are made in reduced quantity. In type II deficiencies normal amounts of dysfunctional protein<unk>  are synthesized. Antigen assays are immunoassays designed to measure the quantity of protein<unk>  regardless of its function. Type I deficiencies are therefore<unk> haracterized by a decrease in both activity and antigen protein<unk>  assays whereas type II deficiencies exhibit normal protein<unk>  antigen levels with decreased activity levels. The human protein<unk>  gene (PROC)<unk> omprises 9 exons, and<unk>  has been linked to over 160 mutations to date. Therefore, DNA testing for<unk>  is generally not available outside of specialized research laboratories. Manifestation of purpura fulminans as it is usually associated with reduced protein<unk>  plasma<unk> oncentrations of <5 mg IU/dL. The normal<unk> oncentration of plasma protein<unk>  is 70 nM (4 µg/mL) with a half live of approximately 8 hours. Healthy term neonates, however, have lower (and more variable) physiological levels of protein<unk>  (ranging between 15-55 IU/dL) than older<unk> hildren or adults, and these<unk> oncentrations progressively increase throughout the first 6 months of life. Protein<unk>  levels may be <10 IU/dL in preterm or twin neonates or those with respiratory distress without manifesting either purpura fulminans or disseminated intravascular<unk> oagulation.
Protein C deficiency
Activated protein C resistance
Factor VII deficiency
Protein S deficiency
COAT platelet defect
Factor XIII deficiency
Factor XII deficiency
Antithrombin III deficiency