Des-γ-carboxy Prothrombin (DCP)

Serum, frozen

0.5 mL

0.25 mL (Note: This volume does not allow for repeat testing.)

Red-top tube or gel-barrier tube

No special preparations are necessary.

DCP is intended for use as an aid in the risk assessment of patients with chronic liver disease for progression to hepatocellular carcinoma in conjunction with other laboratory findings, imaging studies, and clinical assessment.¹

It is recommended that this assay be used in conjunction with imaging studies for clinical diagnosis.

Liquid-phase binding assay (LiBaSys)

0.0−7.5 ng/mL

Hepatocellular carcinoma (HCC) is a highly fatal cancer that results in approximately 10,000 deaths in the United States each year.^2,3 The objective of the HCC screening programs is to find small lesions when potential curative treatment options are available.^3,4 The tests commonly employed for screening are imaging of the liver by ultrasound and measurement of serum α-fetoprotein (AFP) levels.^2,5 This arsenal has recently been enhanced through the addition of the AFP-L3% test.⁶

Des-γ-carboxy prothrombin (DCP), also referred to as protein induced by vitamin K absence (PIVKA-II), is a nonfunctional precursor of prothrombin.⁷ Prothrombin, produced by the liver, serves a critical role in normal hemostasis. Functional prothrombin contains several γ-carboxy-glutamic acid (Gla) residues that are produced as result of post-translational modification of glutamic acid residues mediated by vitamin K-dependent γ-glutamyl carboxylase. The formation of Gla residues can be impaired in patients with vitamin K deficiency or in patients receiving oral anticoagulant therapy. DCP lacks thrombotic activity and has been shown in multiple studies to be present in the serum of patients with HCC.^7-13

Patients who test positive for DCP often exhibit clinical features of HCC that are different from those who test postive for AFP-L3.^9-15 Published studies have indicated that DCP elevation reflects the progression of the disease and tumor diameter.^9-15 Increased DCP levels have been associated with the development of portal vein invasion (PVI), a strongly negative prognostic indicator.⁹ Patients with elevated DCP and normal AFP tend to have more advanced HCC.^10-14 Volk and coworkers showed that DCP can be particularly useful in the assessment of HCC risk in high-risk patients.¹⁶

The combined use of the three biomarkers, AFP, AFP-L3%, and DCP can support the discrimination between benign and malignant conditions related to primary liver disease.^10,11,14,15 DCP and AFP-L3% are considered complementary assays for assessing the risk of developing HCC.¹ When used in combination, a greater number of patients at risk of developing HCC can be identified resulting in more treatment options for a larger number of patients.¹

DCP/PIVKA-II has also been used for the assessment of the vitamin K status of newborns.¹⁷ Vitamin K deficiency may cause unexpected bleeding during the first week of life in previously healthy-appearing neonates.^17,18 This condition has been referred to as early vitamin K deficiency bleeding (VKDB) of the newborn or classic hemorrhagic disease of the newborn. Vitamin K prophylaxis (oral or parenteral) has been found to be effective in the prevention of this condition.¹⁸ Late VKDB, defined as unexpected bleeding attributable to severe vitamin K deficiency in infants 2 to 12 weeks of age, can occur in exclusively breast-fed infants who have received inadequate neonatal vitamin K prophylaxis.^17,18 Infants with intestinal malabsorption defects (cholestatic jaundice, cystic fibrosis, etc) may also have late VKDB.^17,18