An elevation of des-gamma-carboxyprothrombin (DCP) has been observed in about 70 % of cases of hepatocellular carcinoma (HCC). Howewer, an increased DCP is not specific of HCC. Oral anticoagulant therapy increases the DCP level by preventing the gamma-carboxylation of prothrombin : thereafter an increased DCP can not be used as an HCC marker before three weeks have elapsed after stopping anti vitamin K therapy. Furthermore, since vitamin K is necessary for the gamma-carboxylation of vitamin K dependent factors, a vitamin K deficiency increases the DCP level long before the modification of the prothrombin time. It is thus imperative to eliminate an underlying vitamin K deficiency before attributing an increased DCP to a HCC. We used a method of DCP assay using staphylocoagulase. We studied the effect of an intravenous injection of 20 mg of vitamin K1 on DCP level in 7 patients with histologically proven HCC and in 10 patients with various disorders (5 alcoholic cirrhosis, 1 chronic hepatitis, 4 pancreatic cancer). All these 17 patients had increased DCP before vitamin K injection. In a second sampling obtained 15 days or more after injection, only the 7 patients with HCC kept increased DCP level. In patients of both categories in whom we obtained intermediary samplings, we observed that the DCP level decreased In all cases. The normalisation of the DCP level was lasting only in those patients without HCC, confirming the hypothesis of an underlying vitamin K deficiency ; this decrease was very transitory in those patients with HCC, suggesting that the elevated DCP came from a yet unexplained (but not linked to a vitamin K deficiency) mechanism. We may conclude that an increased DCP level 15 days after vitamin K injection may constitute a specific marker of HCC.
Persistent Elevation of Serum Prothrombin Induced by Vitamin K Deficiency or Antagonist Despite Discontinuation of Warfarin Administration in Alcoholic Cirrhosis in The Absence of Hepatocellular Carcinoma: A Case Report