BACKGROUND: Pancreas graft thrombosis remains the leading non-immunologic cause of graft loss after pancreas transplantation. We studied the role of hypercoagulable states (HCS) in pancreas graft thrombosis (pthx). METHODS: Between January 1, 1994, and January 1, 2003, 131 pancreas transplant recipients experienced a pthx (n = 67) or other thrombotic events. Fifty-six recipients consented to have their blood drawn and tested for the HCS. These results were compared with a control group of pancreas transplant recipients who did not experience a thrombotic event. Fisher's exact test was used to compare the groups. RESULTS: We found 18% of the recipients with pancreas thrombosis to have a HCS. Factor V Leiden (FVL) was found in 15% vs. 4% in the control group (p = ns) vs. 3-5% in the general white population. We found 3% of the pancreas thrombosis patients to have a prothrombin gene mutation (PGM) vs. 0% in the control group (p = ns) vs. 1-2% in the general white population. CONCLUSIONS: Of pancreas transplant recipients with thrombosis, 18% had one or more of the most common factors associated with a HCS (FVL or PGM). This can be compared with 4% in a control group and 4-7% in the general white population, respectively. Although the differences are not statistically significant due to small numbers, we feel that the findings may be clinically relevant. While this is only a pilot study, it may be reasonable to screen select pancreas transplant candidates for HCS, especially FVL and PGM, until more data become available.
BACKGROUND:Pancreas graft thrombosis remains the leading non-immunologic cause of graft loss after pancreas transplantation. We studied the role of hypercoagulable states (HCS) in pancreas graft thrombosis (pthx). METHODS: Between January 1, 1994, and January 1, 2003, 131 pancreas transplant recipients experienced a pthx (n = 67) or other thrombotic events. Fifty-six recipients consented to have their blood drawn and tested for the HCS. These results were compared with a control group of pancreas transplant recipients who did not experience a thrombotic event. Fisher's exact test was used to compare the groups. RESULTS: We found 18% of the recipients with pancreas thrombosis to have a HCS. Factor V Leiden (FVL) was found in 15% vs. 4% in the control group (p = ns) vs. 3-5% in the general white population. We found 3% of the pancreas thrombosispatients to have a prothrombin gene mutation (PGM) vs. 0% in the control group (p = ns) vs. 1-2% in the general white population. CONCLUSIONS: Of pancreas transplant recipients with thrombosis, 18% had one or more of the most common factors associated with a HCS (FVL or PGM). This can be compared with 4% in a control group and 4-7% in the general white population, respectively. Although the differences are not statistically significant due to small numbers, we feel that the findings may be clinically relevant. While this is only a pilot study, it may be reasonable to screen select pancreas transplant candidates for HCS, especially FVL and PGM, until more data become available.