By Faith Reidenbach
NEW YORK (Reuters Health) – In Greek patients with Crohn's disease, serum levels of lipoprotein (a) and other apolipoproteins differ from those in ulcerative colitis patients and controls, according to researchers from University Hospital Heraklion in Crete. They suggest that the differences, especially an elevated level of lipoprotein (a), contribute to the increased risk of thromboembolic disease in Crohn's disease.
Dr. Ioannis E. Koutroubakis and colleagues evaluated 66 consecutive patients with ulcerative colitis, 63 patients with Crohn's disease and 66 controls. "Elevated levels of lipoprotein (a) >30 mg/dL is the limit considered as a risk factor for the development of occlusive vascular disease," Dr. Koutroubakis told Reuters Health. "In our study increased levels were found in 46% of Crohn's disease patients" and 23% of ulcerative colitis patients.
In Crohn's disease patients the mean lipoprotein (a) level was significantly higher than in controls (p = 0.005), and mean levels of apolipoprotein A-1 (apoA-1) and apoB-100 were significantly lower (p = 0.005 and p = 0.001, respectively). The differences in lipoprotein (a) and apoA-1 were more pronounced in Crohn's disease patients with active disease than in those with inactive disease.
In ulcerative colitis patients the mean level of apoB-100 was significantly lower than in controls (p = 0.005), although lipoprotein (a) and apoA-1 levels were not significantly different. The data are presented in detail in the December issue of the European Journal of Gastroenterology and Hepatology.
Of the five inflammatory bowel disease patients with a history of thrombosis, only one, an ulcerative colitis patient, had a lipoprotein (a) level >30 mg/dL. This supports the view that thrombosis in inflammatory bowel disease patients is multifactorial, the researchers note.
Still, Dr. Koutroubakis said, "prothrombic effects of lipoprotein (a) are presumably mediated via interference with activation of plasminogen, with binding of tissue-type plasminogen activator to fibrin, and probably also with stimulation of plasminogen activator inhibitor-1 synthesis, all well-established factors leading to thrombosis."
In an editorial, Drs. Ad A. van Bodegraven and Stephan G. M. Meuwissen of Free University Medical Centre in Amsterdam point out that this hypothesis–that elevated lipoprotein (a) concentrations inhibit fibrinolytic capacity–still needs to be tested by measuring markers of coagulation and fibrinolysis.
They add that inflammatory bowel disease patients in Crete may not be representative of inflammatory bowel disease patients in general because of the low fat content of the Mediterranean diet, which affects levels of apoA-1 and apoB-100, although not the level of lipoprotein (a).