INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY

Vol. 26, no. I, 1-13 (2013)

EDITORIAL

ROLE OF VITAMIN D IN CHILDREN WITH RESPIRATORY TRACT INFECTION S. ESPOSITO, E. BAGGI, S. BIANCHINI, P. MARCHISIO and N. PRINCIPI

Pediatric Clinic 1, Department ofPathophysiology and Transplantation, Universita degli Studi di Milano, Fondazione IReCS Ca'Uranda Ospedale Maggiore Polic/inico, Milan, Italy Received July 16, 2012 - Accepted December 10, 2012 It has recently been shown that vitamin D (VitD) plays an important role in host defences, inflammation and immunity. We reviewed PubMed and selected all of the studies published over the last 15 years concerning vun deficiency and VitD supplementation in children with respiratory tract infections. Our analysis showed that VitD seems to be very important because of its part in the complexity of the immune system. However, there are few pediatric studies and most have various limitations. First of all, the literature mainly refers to studies concerning the prevalence of VitD insufficiency and deficiency in specific pathologies. Secondly, it is extremely difficult to identify a common specific range of normal, insufficient and deficient VitD levels. Thirdly, the available studies of VitD supplementation often combined VitD with the use of other micronutrients, thus obscuring the role of VitD itself. Finally, different doses have been used for VitD supplementation. These observations clearly highlight the fact that further studies are needed to evaluate the impact ofVitD deficiency and insufficiency in terms ofthe epidemiology and outcomes of pediatric respiratory tract infection, and whether VitD supplementation favours a positive outcome.

tubule and involves the mitochondrial cytochrome P450 enzyme 25-hydroxyvitamin-D-Ia-hydroxylase (1). Most ofthe final product ofVitD is transported in the blood by albumin and vitamin binding proteins, and thus reaches the numerous target tissues with VitD receptors (VitDRs) found throughout the human body. Once it has performed its function, VitD is inactivated by means of 25 (OH)D-24-hydroxylasis into the inactive 24,25-hydroxyvitamin D (1). VitD is essential for the correct development of mineralised bone (1). In the case of a calciumpoor diet, calcitriols interact with the VitDRs on osteoblasts to induce the expression of the RANK cytokine which, by means of various intracellular messages stimulates maturation of osteoclasts and

Vitamin D (VitD) is a fat-soluble vitamin that has long been known to play a role in calcium homeostasis and bone metabolism (1). The chemical structure ofthe lateral chains ofthe two natural forms of VitD (D2 derived from plants, and D3 derived from humans and animals) are slightly different, and this causes them to bind differently to their carrier proteins. However, the biological activity of their active metabolic products is very similar. Both can be obtained from diet or from sunlight conversion of skin 7-dehydrocholesterol (1). In order to become active, VitD undergoes two different hydroxylations: the first (in position 25) mainly takes place in the liver and involves the mitochondrial 25-hydroxylase enzyme; the second takes place in the proximal kidney

Key words: children, community-acquiredpneumonia, respiratory tract infection, tuberculosis, vitamin D, vitamin D supplementation Mailing address: Prof. Susanna Esposito, Pediatric Clinic I, Department of Pathophysiology and Transplantation, Universita degli Studi di Milano, Fondazione IRCCS, Ca' Granda Ospedale Maggiore Polic1inico, Via Commenda 9, 20122 Milano, Italy Tel.: +39 02 55032498 Fax: +39 02 50320206 e-mail: [email protected]

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DISCLOSURE: ALL AUTHORS REPORT NO CONFLICTS OF INTEREST RELEVANT TO THIS ARTICLE.

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S. ESPOSITO ET AL.

leads to calcium and phosphate absorption (l). Several studies have shown the worldwide increasing prevalence of VitD deficiency/insufficiency especially in recent years (l, 2). However, a more recent and detailed analysis of the ways in which VitD becomes available to the body has led to the conclusion that the old methods of assessing VitD status were grossly inaccurate because factors such as limited ambient ultraviolet radiation, inadequate sun exposure and host factors could significantly influence the final results and lead to a wrong cutoff value (2). Data collected in studies evaluating the correlation between plasma 25(OH)D levels and a series of biomarkers (intestinal calcium absorption, maximal parathyroid hormone suppression, bone fracture prevention, and optimal bone turnover) clearly indicate that only concentrations significantly higher than 10 ng/mL can permit an adequate bone metabolism (2). However, there is no definite consensus about the minimum normal 25(OH)D value for healthy humans of different ages. Several experts consider suboptimal all the 25(OH)D serum values lower than 30 ng/mL and distinguish deficiency when the 25(OH)D is 12 years, including adults (9). Recent URTIs were reported by 24% ofthe participants with 25(OH)D levels of