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Mediators of Inflammation
Volume 2017 (2017), Article ID 6412531, 8 pages
Research Article

Vitamin D Deficiency Is Associated with Increased Osteocalcin Levels in Acute Aortic Dissection: A Pilot Study on Elderly Patients

1Department of Biomedical Sciences for Health, Università degli Studi di Milano, Via L. Mangiagalli 31, 20133 Milan, Italy
2Laboratory of Molecular Pathology, I.R.C.C.S. Policlinico San Donato, Via R. Morandi 30, San Donato Milanese, 20097 Milan, Italy
3Department of Health Sciences, Università degli Studi di Milano, Via A. Di Rudinì 8, 20142 Milan, Italy
4Randox Laboratories Ltd., R&D, 55 Diamond Road, Crumlin, Antrim, Belfast BT29 4QY, UK
5Thoracic Aortic Research Center, I.R.C.C.S. Policlinico San Donato, Piazza E. Malan 1, San Donato Milanese, 20097 Milan, Italy
6Laboratory Medicine Operative Unit-1, Clinical Pathology, I.R.C.C.S. Policlinico San Donato, Piazza E. Malan 1, San Donato Milanese, 20097 Milan, Italy

Correspondence should be addressed to Elena Vianello

Received 27 April 2017; Accepted 6 June 2017; Published 2 July 2017

Academic Editor: Carmela R. Balistreri

Copyright © 2017 Elena Vianello et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


An imbalance between degradation and reconstruction of the aortic wall is one of the leading causes of acute aortic dissection (AAD). Vitamin D seems an intriguing molecule to explore in the field of AAD since it improves endothelial function and protects smooth muscle cells from inflammation-induced remodeling, calcification, and loss of function, all events which are strongly related to the aging process. We quantified 25-hydroxy vitamin D, calcium, parathormone, bone alkaline phosphatase, and osteocalcin levels in 24 elderly AAD patients to identify a potential pathological implication of these molecules in AAD. Median 25-hydroxy vitamin D (10.75 ng/mL, 25th–75th percentiles: 6.86–19.23 ng/mL) and calcium levels (8.70 mg/dL, 25th–75th percentiles: 7.30–8.80 mg/dL) suggested hypovitaminosis D and a moderate hypocalcemia. Thirty-eight percent of AAD patients had severe (<10 ng/mL), 38% moderate (10–20 ng/mL), and 24% mild 25-hydroxy vitamin D deficiency (20–30 ng/mL). A significant inverse correlation was observed between 25OHD and osteocalcin levels. All the other molecules were unchanged. A condition of hypovitaminosis D associated to an increase in osteocalcin levels is present in AAD patients. The identification of these molecules as new factors involved in AAD may be helpful to identify individuals at high risk as well to study preventing strategies.