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  1. A. Lobrano*,
  2. K. Blanchard*,
  3. T. Abell*,
  4. A. Minocha*,
  5. W. Rock
  1. *University of Mississippi Medical Center, Jackson
  2. Helsinki University Hospital


Introduction Patients with severe gastrointestinal motility disorders often are found to have intravenous access clots or deep venous thrombosis, which can especially be difficult to manage, particularly if the patients require sustained intravenous access (IVA). We have previously reported that many patients who have IVA thrombosis have concomitant coagulation disorders. In this study, our goal was to determine the underlying prevalence of hypercoagulability in a series of patients with documented severe gastroparesis.

Methods We studied 63 consecutive patients (10 male, 53 female, mean age 42 years) who had both symptoms of gastroparesis and documented disorders of gastric emptying in order to assess the prevalence of inherited and acquired coagulopathies in this group. All patients were being evaluated for a gastric neural stimulation device or had one placed previously. Patients underwent a hematologic interview and previously standardized measures of coagulation. Laboratory studies performed included measuring acquired defects of factor VII, factor VIII, fibrinogen, lupus anticoagulant panel, antiphospholipid antibody panel, homocysteine (in the setting of kidney disease), and activated protein resistance. The congenital defects measured were antithrombin III, protein C, protein S (total and free), factor II mutation, factor V Leiden, methylenetetrahydrofolate resistance (MTHFR), and homocysteine.

Results Of the 63 patients, all but 7 (89%) were found to have detectable coagulation abnormalities. Twenty-five of the 63 (40%) patients had a documented history of abnormal clotting, including deep venous thrombosis, intravenous access thrombosis, and pulmonary embolism. All of the patients with a previous history of thrombosis were found to have detectable clotting abnormalities. No abnormalities in antithrombin III, protein C, or factor V Leiden were detected in this study group.

Conclusion We conclude that there is a high prevalence of both acquired and congenital hypercoagulable defects in patients with gastroparesis that may predispose them to thrombosis. This unique finding warrants consideration of a coagulation evaluation in patients with severe gastroparesis, especially when those patients found to have underlying clotting abnormalities are placed in thrombophilic situations.

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