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Treatment of patients with acquired inhibitors

i.e. the father, mother and a sibling in the heterozygous state. This deletion led to the frame-shift with a stop codon at 207. At diagnosis of homozygous protein C deficiency, fresh frozen plasma was infused immediately at a rate of 30 mL kg day. Skin lesions apparently improved. Warfarin (1 mg day) was started on the 10th hospital day jointly with fresh frozen plasma, which was continued for 21 days. The infant was discharged on the 27th day on warfarin treatment (1 mg day). This case report adds a new frame-shift deletion mutation, occurring in the exon 8 involving catalytic domain, which introduces a stop codon, thereby generating a prematurely truncated protein. Genetic analysis of Japanese protein C deficiency has revealed that five recurrent defects (Phe139Val, Arg169Trp, Val297Met, and Met364Ile substitutions, and a G8857 deletion) can explain half of the protein C deficiency found in Japanese patients [7]. Mutations identified in Korean subjects also include Arg169Trp and Val297Met [8,9]. It is interesting that G8857 deletions were found in 33 Japanese families, accounting for 49% of Japanese families with protein C deficiency [7]. The G8857 deletion seems to be identified solely in Japanese families; it has not been identified in Korean families yet. A genetic study in this case suggests that a new deletion mutation of 10 base pairs may be a unique genetic defect based on ethnic bias. As the parents are not consanguineous, we suppose that there could be some asymptomatic heterozygotes for this new mutation as a feature of autosomal recessive inheritance in the Korean population. Further studies by screening undetermined patients with protein C deficiency as well as the general population would reveal the impact of this new mutation in Korea. Because homozygous protein C deficiency is fatal if untreated, the timely identification of such patients may be lifesaving and permit therapeutic intervention. Although there are some diagnostic limitations because of its rarity, lack of symptoms in the parents, and physiological low level of protein C in newborn infants, the purpura fulminans in this case was successfully controlled shortly after birth by infusions of fresh frozen plasma and anticoagulation. The treatment options include fresh frozen plasma and protein C concentrate in the acute phase [10]. In conclusion, we have identified a novel deletion mutation in exon 8 of the PROC gene that leads to severe protein C deficiency which causes severe neonatal purpura fulminans.