Des-gamma carboxyprothrombin
Des-gamma carboxyprothrombin (DCP), also known as protein induced by vitamin K absence/antagonist-II (PIVKA-II), is an abnormal form of the coagulation protein, prothrombin. Normally, the prothrombin precursor undergoes post-translational carboxylation (addition of a carboxylic acid group) by gamma-glutamyl carboxylase in the liver prior to secretion into plasma. DCP/PIVKA-II may be detected in people with deficiency of vitamin K (due to poor nutrition or malabsorption) and in those taking warfarin or other medication that inhibits the action of vitamin K.
Diagnostic use
=Hepatocellular carcinoma=
A 1984 study first described the use of DCP as a marker of hepatocellular carcinoma (HCC); it was present in 91% of HCC patients, while not being detectable in other liver diseases. The DCP level did not change with the administration of vitamin K, suggesting a defect in gamma-carboxylation activity rather than vitamin K deficiency.{{cite journal |vauthors=Liebman HA, Furie BC, Tong MJ |title=Des-gamma-carboxy (abnormal) prothrombin as a serum marker of primary hepatocellular carcinoma |journal=N. Engl. J. Med. |volume=310 |issue=22 |pages=1427–31 |year=1984 |pmid=6201741 |doi=10.1056/NEJM198405313102204|display-authors=etal}} A number of subsequent studies have since confirmed this phenomenon.{{cite journal |vauthors=Tsai SL, Huang GT, Yang PM, Sheu JC, Sung JL, Chen DS |author6-link=Ding-Shinn Chen |title=Plasma des-gamma-carboxyprothrombin in the early stage of hepatocellular carcinoma |journal=Hepatology |volume=11 |issue=3 |pages=481–8 |year=1990 |pmid=2155866 |doi=10.1002/hep.1840110321}}{{cite journal |vauthors=Cui R, Wang B, Ding H, Shen H, Li Y, Chen X |title=Usefulness of determining a protein induced by vitamin K absence in detection of hepatocellular carcinoma |journal=Chin. Med. J. |volume=115 |issue=1 |pages=42–5 |year=2002 |pmid=11930656 }}{{cite journal |vauthors=Marrero JA, Su GL, Wei W |title=Des-gamma carboxyprothrombin can differentiate hepatocellular carcinoma from nonmalignant chronic liver disease in American patients |journal=Hepatology |volume=37 |issue=5 |pages=1114–21 |year=2003 |pmid=12717392 |doi=10.1053/jhep.2003.50195|display-authors=etal|doi-access=free }}
A 2007 comparison of various HCC tumor markers found DCP the least sensitive to risk factors for HCC (such as cirrhosis), and hence the most useful in predicting HCC.{{cite journal |vauthors=Volk ML, Hernandez JC, Su GL, Lok AS, Marrero JA |title=Risk factors for hepatocellular carcinoma may impair the performance of biomarkers: a comparison of AFP, DCP, and AFP-L3 |journal=Cancer Biomark |volume=3 |issue=2 |pages=79–87 |year=2007 |doi=10.3233/cbm-2007-3202 |pmid=17522429 }} It differentiates HCC from non-malignant liver diseases.{{cite journal |vauthors=Lamerz R, Runge M, Stieber P, Meissner E |title=Use of serum PIVKA-II (DCP) determination for differentiation between benign and malignant liver diseases |journal=Anticancer Res. |volume=19 |issue=4A |pages=2489–93 |year=1999 |pmid=10470180 }} Moreover, it has been demonstrated that a combined analysis of DCP and Alpha-fetoprotein (AFP) can lead to a better prediction in early stages of HCC.{{cite journal|last1=Ertle|first1=JM|last2=Heider|first2=D|last3=Wichert|first3=M|last4=Keller|first4=B|last5=Kueper|first5=R|last6=Hilgard|first6=P|last7=Gerken|first7=G|last8=Schlaak|first8=JF|title=A combination of α-fetoprotein and des-γ-carboxy prothrombin is superior in detection of hepatocellular carcinoma.|journal=Digestion|date=2013|volume=87|issue=2|pages=121–31|pmid=23406785|doi=10.1159/000346080}}
Despite many years of use in Japan, only did a 2003 American study reevaluate its use in an American patient series. It also identified HCC at an earlier stage.
=Anticoagulant intoxication=
A 1987 report described the use of DCP determination in the detection of intoxication with acenocoumarol, a vitamin K antagonist.{{cite journal |vauthors=Lefrere JJ, Gozin D |title=Use of des-gamma-carboxyprothrombin in retrospective diagnosis of hidden intoxication of anticoagulants |journal=J. Clin. Pathol. |volume=40 |issue=5 |pages=589 |year=1987 |pmid=3584512 |doi=10.1136/jcp.40.5.589-b |pmc=1141034}}