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bs_bs_banner Pain Medicine 2012; 13: 735–736 Wiley Periodicals, Inc. Hypovitaminosis D and Pain in Cystic Fibrosis Reprint requests to: Luca Mascitelli, MD, Comando Brigata alpina “Julia,” Medical Service, 8 Via S. Agostino, Udine 33100, Italy. Tel: +390432584044; Fax: +390432584053; E-mail: [email protected]. Conflict of Interest: WBG receives funding from the UV Foundation (McLean, VA), the Sunlight Research Forum (Veldhoven), Bio-Tech-Pharmacal (Fayetteville, AR), the Vitamin D Council (San Luis Obispo, CA), and the Vitamin D Society (Canada). Drs. Mascitelli and Goldstein have no conflicts of interest to disclose. To the Editor, Cystic fibrosis (CF) is the most common life-shortening genetic disease in whites. It principally affects the lungs, pancreas and gastrointestinal tract [1]. Advances in the treatment have improved the life expectancy of people with CF [2]. The increased longevity of adults with CF is accompanied by a rising prevalence of secondary complications including pain [3], which can be associated with the diagnosis and treatment of the disease, and the disease itself [4]. A recent study [5] found that 82% of patients reported pain within the past month, the most common sites being the head, sinuses, back, and chest. Pain frequently interfered with general activities (41.9%), mood (56.8%), and work (47.3%). Symptoms of depression and anxiety, as well as lower quality-of-life scores, were associated with the presence of pain. Furthermore, it was also found that pain increased the risk of severe pulmonary exacerbations and death [5]. Factors associated with pain in patients with CF are poorly understood. We suggest that hypovitaminosis D may partially explain this association. Decreased bone mineral density and increased risk of fracture are common complications in CF. It has been reported that 50–75% of adults with CF have low bone density, with approximately 20–25% having osteoporosis and 40% having osteopenia [6]. Multiple factors contribute to this increased risk of osteoporosis and osteopenia, and, among them, hypovitaminosis D represents an important factor. Vitamin D insufficiency is significantly more prevalent among individuals with CF compared with healthy control subjects, most likely secondary to low exposure to sunlight, poor nutrition, and malabsorption of fat-soluble vitamins resulting from pancreatic insufficiency [6]. On the other hand, it is well known that a clinical feature of osteomalacia, a disorder of bone mineralization caused by pme_1372 735..736 severe vitamin D deficiency, is generalized bone pain. Indeed, severe vitamin deficiency is not asymptomatic, and, before the clinical presentation of osteomalaciarelated bone pain, severe hypovitaminosis D results in a syndrome of persistent, nonspecific musculoskeletal pain, which has been well documented: up to 93% of patients with persistent pain have been reported to have hypovitaminosis D [7]. Because vitamin D deficiency and decreased bone density are important complications in individuals with CF, consensus guidelines for optimizing CF bone health have, therefore, been developed, recommending that individuals with CF receive vitamin D supplementation to maintain their 25-hydroxyvitamin D [25(OH)D] level ⱖ30 ng/mL [8]. However, this recommendation was based on the relationship between 25(OH)D and parathyroid hormone (PTH) levels in individuals without CF. In fact, it has recently been demonstrated in patients with CF that correction to ⱖ35 ng/mL resulted in a greater likelihood of suppressing PTH levels below those associated with increased bone loss [6]. In addition to its action on bone, there is increasing evidence of extraskeletal health benefits of vitamin D. 1,25Dihydroxyvitamin D, the biologically active form of vitamin D, is involved in the regulation of immune responses. Interestingly, one hypothesis for the cause of chronic widespread pain is the activation of inflammatory cytokine responses after infection; cytokines having been shown to modulate pain perception both peripherally and centrally [9]. Therefore, although the threshold for optimum vitamin D status is known to be considerably higher than that required to prevent osteomalacia, it is still important to establish the risk of pain across a broader range of 25(OH)D concentrations. This may be particularly important for pain individuals with CF who are at high risk of vitamin D deficiency. For these patients, also for the management of pain, we recommend close monitoring of vitamin D status and adequate supplementation in order to reach and maintain 25(OH)D levels ⱖ35 ng/mL. LUCA MASCITELLI, MD Comando Brigata Alpina “Julia,” Medical Service Udine, Italy MARK R. GOLDSTEIN, MD, FACP NCH Healthcare Group Naples, Florida, USA WILLIAM B. GRANT, PhD Sunlight, Nutrition, and Health Research Center San Francisco, California, USA 735 Mascitelli et al. References 1 Kerem E, Conway S, Elborn S, Heijerman H; Consensus Committee. Standards of care for patients with cystic fibrosis: A European consensus. J Cyst Fibros 2005;4:7–26. 2 Dodge JA, Lewis PA, Stanton M, Wilsher J. Cystic fibrosis mortality and survival in the UK: 1947–2003. Eur Respir J 2007;29:522–6. 3 Kelemen L, Lee AL, Button BM, et al. Pain impacts on quality of life and interferes with treatment in adults with cystic fibrosis. Physiother Res Int 2011 doi: 10.1002/ pri.524 [Epub ahead of print]. 4 Hubbard PA, Broome ME, Antia LA. Pain, coping, and disability in adolescents and young adults with cystic fibrosis: A Web-based study. Pediatr Nurs 2005;31: 82–6. 736 5 Hayes M, Yaster M, Haythornthwaite JA, et al. Pain is a common problem affecting clinical outcomes in adults with cystic fibrosis. Chest 2011;140:1598– 603. 6 West NE, Lechtzin N, Merlo CA, et al. Appropriate goal level for 25-hydroxyvitamin D in cystic fibrosis. Chest 2011;140:469–74. 7 Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc 2003;78:1463– 70. 8 Aris RM, Merkel PA, Bachrach LK, et al. Guide to bone health and disease in cystic fibrosis. J Clin Endocrinol Metab 2005;90:1888–96. 9 Staud R. Fibromyalgia pain: Do we know the source? Curr Opin Rheumatol 2004;16:157–63.