Wenjie Liu1, Min Xuan1, Feng Xue1, Renchi Yang1. 1. State Key Laboratory of Experimental Hematology, Institute of Hematology & Blood Diseases Hospital, CAMS & PUMC, Tianjin 300020, China.
Abstract
OBJECTIVE: To deepen the understanding of acquired coagulation factor X (F X) deficiency. METHODS: The clinical data of 3 patients were analyzed and related literature were reviewed. RESULTS: Case 1, a 57-year-old male, secondary to multiple myeloma and amyloidosis, was presented with spontaneous mucous hemorrhage with the level of FX:C 1.8%, which kept unchanged after chemotherapy with melphalan, glucocorticoid, and thalidomide, and died of primary disease progression. Case 2, a 41-year-old male with psoriasis, was presented with cerebral and retinal hemorrhage with the level of FX:C 26.8%. The signs of hemorrhage were alleviated after the supplement of folic acid, vitamin B12, and vitamin K, and transfusion with red blood cells, platelets, and fresh frozen plasma. Case 3, a 63-year-old female, associated with high level of lupus anticoagulant, was presented with repeated ecchymosis and haemarthrosis with the level of FX:C 6.1%, which was refractory to prothrombin complex concentrate, methyprednisolone, azathioprine, and rituximab. CONCLUSION: Acquired FX deficiency is a rare disorder with variable symptoms. The diagnosis relies on history of disease and laboratory test. Currently, there is no standardized treatment. The prognosis of acquired FX deficiency is mainly related to the underlying disease.
OBJECTIVE: To deepen the understanding of acquired coagulation factor X (F X) deficiency. METHODS: The clinical data of 3 patients were analyzed and related literature were reviewed. RESULTS: Case 1, a 57-year-old male, secondary to multiple myeloma and amyloidosis, was presented with spontaneous mucous hemorrhage with the level of FX:C 1.8%, which kept unchanged after chemotherapy with melphalan, glucocorticoid, and thalidomide, and died of primary disease progression. Case 2, a 41-year-old male with psoriasis, was presented with cerebral and retinal hemorrhage with the level of FX:C 26.8%. The signs of hemorrhage were alleviated after the supplement of folic acid, vitamin B12, and vitamin K, and transfusion with red blood cells, platelets, and fresh frozen plasma. Case 3, a 63-year-old female, associated with high level of lupus anticoagulant, was presented with repeated ecchymosis and haemarthrosis with the level of FX:C 6.1%, which was refractory to prothrombin complex concentrate, methyprednisolone, azathioprine, and rituximab. CONCLUSION: Acquired FX deficiency is a rare disorder with variable symptoms. The diagnosis relies on history of disease and laboratory test. Currently, there is no standardized treatment. The prognosis of acquired FX deficiency is mainly related to the underlying disease.