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AB0507 Cobalamin (VITAMIN B12) status in patients with antiphospholipid syndrome (APS), its association with atherosclerotic vascular lesions
  1. I Segeda1,
  2. S Shevchuk1,
  3. I Kuvikova1,
  4. O Shevchuk2,
  5. I Segeda3,
  6. S Shevchuk3,
  7. I Kuvikova3,
  8. O Shevchuk3
  1. 1Rheumatology, Institute of Invalid Rehabilitation
  2. 2Rheumatology, Vinnitsya National Medical University, Vinnitsya, Ukraine
  3. 3Affiliation not provided


Background Cobalamin (vitamin B12) insufficienty is associated with the development of many diseases. It is known that the growth of clinical and subclinical manifestations of atherosclerotic vascular lesions are often associated with low cobalamin level. Cobalamin status is unknown in patients with antiphospholipid syndrome (APS). There are no data about the role of folic acid in the development of atherosclerotic vascular lesions in patients with APS

Objectives To evaluate vitamin B12 status in patients with APS and to explore its relationship with atherosclerotic vascular lesion.

Methods We observed 82 patients with APS and 37 healthy individuals. Content of cobalamin (vitamin B12) in serum were determined by immunochemical detection (ECLIA). Cobalamin level above 200 pg/ml was considered as normal within 200–300 pg/mL - both extremely low, below 200 pg/ml - insufficienty. All patients were underwent detection of endothelial dysfunction - dilatation of brachial artery endothelium, investigation of “intima-media” thickness of common carotid artery (IMT) and the presence of atherosclerotic plaques (AP).

Results In patients with APS we recorded a significant reduction of cobalamin in the serum (351±14,3 pg/mL (95% CI: 148–562 pg/mL) compared to control group (445±18,1 pg/mL (95% CI: 272–622 pg/mL). Indicators of cobalamin status in patients with secondary APS were significantly worse than patients with primary APS. Thus, in patients with secondary APS cobalamin content was on 26.7% lower (95% CI: 140–559 pg/ml) than in the control group. In patients with primary APS cobalamin content was on 13.0% lower (95% CI: 202–565 pg/ml) than in controls, but 18.7% higher than in patients with secondary APS. Cobalamin (vitamin B12) insufficienty is accompanied by significant thickening of the walls of the common carotid artery. Thus, in patients with cobalamin deficiency IMT was on 17% higher than that in patients with optimal levels of the vitamin. Cobalamin deficiency is also associated with endothelial dysfunction. Thus, in patients with vitamin deficiency dilatation of brachial artery was significantly, by 48.6% less than in people with normal vitamin B12 status. The share of people with the presence of atherosclerotic plaques, transient ischemic attack (TIA), stroke, myocardial infarction (MI) and angina in patients with cobalamin deficiency was also higher.

Conclusions Thus, in patients with APS low cobalamin status is associated with subclinical manifestations of atherosclerotic vascular lesions.

Disclosure of Interest None declared

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