ORIGINAL RESEARCH PAPER Midkine in vitamin D deficiency and its association with anti- Saccharomyces cerevisiae antibodies F. B. Serinkan Cinemre 1 • Hakan Cinemre 2 • Cengiz Karacaer 2 • Birsen Aydemir 3 • Ahmet Nalbant 2 • Tezcan Kaya 2 • Ali Tamer 2 Received: 7 August 2015 / Revised: 30 October 2015 / Accepted: 2 November 2015 Ó Springer Basel 2015 Abstract Objectives and design The growth factor midkine (MK) is a protein that is involved in cancer, inflammation, immunity. Vitamin D is a potent immunomodulator. Anti- Saccharomyces cerevisiae antibody (ASCA) is reported in autoimmune disorders, some of which are among the causes of vitamin D deficiency. The objective of this study was to investigate a possible association of MK and ASCA with vitamin D deficiency. Materials and methods 208 adults presented to internal medicine outpatient clinic for history and physical exami- nation has been studied. Serum biochemistry, vitamin D, MK, ASCA-IgG and -IgA, IL-1b, IL-6, IL-8, TNF-a, PDGF, VEGF were obtained. Results Vitamin D deficiency was 74.2 %. Serum MK level was significantly higher in vitamin D-deficient com- pared to vitamin D-sufficient individuals (1138.1 ± 262.8 vs 958.6 ± 189 pg/mL, respectively; P \ 0.009). Serum MK levels were also significantly higher in both ASCA- IgG and -IgA positives compared to negatives (1318.5 ± 160.3 vs 1065.5 ± 256.1, P = 0.008 and 1347.7 ± 229.7 vs 1070.1 ± 250.9 pg/mL, P = 0.011, respectively). Vitamin D was significantly lower in ASCA positives (P = 0.044).Vitamin D showed positive correla- tion with IL-1b (r 0.338, P \ 0.009) and negative correlation with VEGF (r -0.366, P \ 0.004). Conclusions MK was significantly elevated in vitamin D deficiency and associated with ASCA positivity which was significantly increased in vitamin D deficiency. These findings suggested that molecular mechanism of vitamin D deficiency may be related with some inflammatory processes. Keywords Midkine Á Vitamin D Á Anti-Saccharomyces cerevisiae antibodies Á Cytokine Á Interleukin Á Angiogenic factor Introduction Midkine (MK) together with pleiotrophin constitutes a separate family of heparin-binding growth factors first discovered as a highly expressed gene (Mdk) during mouse embryogenesis [1]. Nowadays, MK gene expression has been detected at variety of sites, including the gastroin- testinal tract, kidney, spleen, lungs and thyroid in healthy adult [2, 3]. It plays critical roles in a variety of biological phenomena such as inflammation and angiogenesis, immunity, pathogenesis of cancer and some other diseases that were extensively reviewed recently [4–7]. The growth factor MK plays a key role in bone remodeling; it is expressed during bone formation and fracture repair [8]. Several investigators have reported that the migration of various cell types, including macrophages and osteoblastic cells, is stimulated by MK [9]. Recent studies provided evidence for a new role for MK in acute and chronic inflammatory processes by promoting the Responsible Editor: John Di Battista. & F. B. Serinkan Cinemre fcinemre@sakarya.edu.tr 1 Department of Biochemistry, Sakarya U ¨ niversitesi Tıp Faku ¨ltesi Dekanlıg ˘ ı, Sakarya University School of Medicine, Korucuk Kampu ¨su ¨, Konuralp Bulvarı No:81/1, 54187 Sakarya, Turkey 2 Department of Internal Medicine, Sakarya University School of Medicine, Sakarya, Turkey 3 Department of Biophysics, Sakarya University School of Medicine, Sakarya, Turkey Inflamm. Res. DOI 10.1007/s00011-015-0898-6 Inflammation Research 123