NEW ORLEANS — Patients with gastroparesis often have a coagulopathy that causes hypercoaguability, based on an analysis of 63 patients with gastroparesis, Amy Lobrano, M.D., reported at the southern regional meeting of the American Federation for Medical Research.
Prior reports have linked inflammatory bowel disease with a high prevalence of coagulopathies, but a similar association had not been reported previously for patients with gastroparesis, Dr. Lobrano said while presenting a poster.
“We believe that an autoimmune etiology may connect [gastroparesis and coagulopathy],” she told this newspaper. An autoimmune dysfunction, perhaps triggered by an infection or by a genetic cause, may bring on both of the disorders, said Dr. Lobrano, a gastroenterologist at the University of Mississippi, Jackson.
The take-home message is that physicians should carefully assess patients diagnosed with gastroparesis for the full panel of possible coagulopathies. In addition, physicians should be alert to the increased risk of thrombosis in patients with gastroparesis, as well as their possible need for anticoagulation therapy.
Dr. Lobrano and her associates assessed 63 consecutive patients diagnosed with gastroparesis who presented to the University of Mississippi Medical Center.
A comprehensive workup for 13 different acquired or congenital coagulopathies showed that 56 patients (87%) had one or more hypercoaguability defects. Of these 56 patients, 31 had not previously been diagnosed with a coagulopathy.
Many of the patients were affected by two or more different coagulopathies, and one patient was diagnosed with five different coagulation defects. The high prevalence of multiple coagulopathies was further evidence that a single trigger in each patient caused an autoimmune state that led to both the coagulopathies and the gastroparesis.
The most common coagulopathy diagnosed was factor VIII deficiency, in 39 patients, followed by activated protein C resistance, in 23 patients, and a deficiency in methylenetetrahydrofolate reductase, also in 23 patients. In contrast, none of the patients had abnormalities in antithrombin III, factor V Leiden, or protein C.