Abstract BACKGROUND: Accelerated progression of atherosclerosis and increased cardiovascular risk have been described in immune-mediated disorders, but few data are available in coeliac disease. AIM: To evaluate instrumental and biochemical signs of atherosclerosis risk in 20 adults at first diagnosis of coeliac disease and after 6-8 months of gluten-free diet with mucosal recovery. METHODS: We analysed total, high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol, triglycerides, homocysteine, C-reactive protein, folate and vitamin B12; ultrasound measurement of carotid intima-media thickness (IMT) and endothelium-dependent dilatation were both carried on at diagnosis and after gluten withdrawal. Twenty-two healthy members of the hospital staff served as matched controls for vascular examinations. RESULTS: At baseline, mean total and HDL-cholesterol (HDL-C) were both within normal range, while mean LDL-cholesterol concentration was slightly increased; diet was associated with an increment in total and HDL-C (68.2 ± 17.4 vs. 51.4 ± 18.6 mg/dL; P < 0.001) and a significant improvement in total/HDL-C ratio (3.05 ± 0.71 vs. 3.77 ± 0.92; P < 0.02). Mean plasma homocysteine was elevated and not influenced by diet. C-reactive protein significantly decreased with diet (1.073 ± 0.51 vs. 1.92 ± 1.38 mg/dL; P < 0.05). At baseline, in coeliacs, IMT was increased (0.082 ± 0.011 vs. 0.058 ± 0.012 cm; P < 0.005), while endothelium-dependent dilatation was decreased (9.3 ± 1.3 vs. 11.2 ± 1.2%; P < 0.05). Both parameters improved after gluten abstinence. CONCLUSIONS: Adults with coeliac disease seem to be at potentially increased risk of early atherosclerosis as suggested by vascular impairment and unfavourable biochemical risk pattern. Chronic inflammation might play a determining role. Gluten abstinence with mucosal normalisation reverts to normal the observed alterations.

Young adults with coeliac disease may be at increased risk of early atherosclerosis.

DE MARCHI, Sergio;CHIARIONI, GIUSEPPE;PRIOR, MANLIO;AROSIO, Enrico
2013

Abstract

Abstract BACKGROUND: Accelerated progression of atherosclerosis and increased cardiovascular risk have been described in immune-mediated disorders, but few data are available in coeliac disease. AIM: To evaluate instrumental and biochemical signs of atherosclerosis risk in 20 adults at first diagnosis of coeliac disease and after 6-8 months of gluten-free diet with mucosal recovery. METHODS: We analysed total, high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol, triglycerides, homocysteine, C-reactive protein, folate and vitamin B12; ultrasound measurement of carotid intima-media thickness (IMT) and endothelium-dependent dilatation were both carried on at diagnosis and after gluten withdrawal. Twenty-two healthy members of the hospital staff served as matched controls for vascular examinations. RESULTS: At baseline, mean total and HDL-cholesterol (HDL-C) were both within normal range, while mean LDL-cholesterol concentration was slightly increased; diet was associated with an increment in total and HDL-C (68.2 ± 17.4 vs. 51.4 ± 18.6 mg/dL; P < 0.001) and a significant improvement in total/HDL-C ratio (3.05 ± 0.71 vs. 3.77 ± 0.92; P < 0.02). Mean plasma homocysteine was elevated and not influenced by diet. C-reactive protein significantly decreased with diet (1.073 ± 0.51 vs. 1.92 ± 1.38 mg/dL; P < 0.05). At baseline, in coeliacs, IMT was increased (0.082 ± 0.011 vs. 0.058 ± 0.012 cm; P < 0.005), while endothelium-dependent dilatation was decreased (9.3 ± 1.3 vs. 11.2 ± 1.2%; P < 0.05). Both parameters improved after gluten abstinence. CONCLUSIONS: Adults with coeliac disease seem to be at potentially increased risk of early atherosclerosis as suggested by vascular impairment and unfavourable biochemical risk pattern. Chronic inflammation might play a determining role. Gluten abstinence with mucosal normalisation reverts to normal the observed alterations.
coeliac disease; endothelium; atherosclerosis; Ultrasound
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11562/583550
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