The Journal of Emergency Medicine, Vol. -, No. -, pp. 1–4, 2014 Copyright Ó 2014 Published by Elsevier Inc. Printed in the USA 0736-4679/$ - see front matter
http://dx.doi.org/10.1016/j.jemermed.2014.02.005
Clinical Communications: Adults HYPOVITAMINOSIS D PRESENTING AS DIFFUSE MYALGIA IN A 22-YEAR-OLD WOMAN: A CASE REPORT Deshon Moore, MD,* Robert Wahl, MD,* and Phillip Levy, MD, MPH*† *Department of Emergency Medicine, Wayne State University School of Medicine, Detroit, Michigan and †The Cardiovascular Research Institute, Wayne State University, Detroit, Michigan Reprint Address: Deshon Moore, MD, Department of Emergency Medicine, Wayne State University School of Medicine, 4201 St. Antoine, Detroit, MI 48201
, Abstract—Background: Caused predominantly by insufficient conversion of vitamin D precursors by sunlight, hypovitaminosis D is an issue of increasing importance worldwide. Although it has been associated with a range of diseases, musculoskeletal effects dominate the clinical picture and can lead to significant physical debility, whether acute or chronic. Although diagnosis of vitamin D deficiency typically occurs in the outpatient setting, it is an easily treatable condition, and timely intervention can dramatically improve one’s quality of life. As highlighted by this case report, hypovitaminosis D may be an important but underappreciated etiology of undifferentiated myalgia that, when present, warrants initiation of vitamin D repletion therapy even from the emergency department (ED). Case Report: A 22-year-old African-American female presented to our ED with diffuse myalgia for 4 months. She reported significant debility from these symptoms with difficulty ambulating and performing activities of daily living. There had been no upper respiratory infection symptoms. The patient had discussed all of this with her primary care physician who, despite an extensive laboratory work-up, had not identified a definitive etiology. Why Should an Emergency Physician Be Aware of This?: Chronic pain has stricken the ED patient population across the board. Studies demonstrate that the myalgia caused by hypovitaminosis D can have a profound and negative impact on an individual’s lifestyle. Our patient was found to have hypovitaminosis D and had substantial improvement with her myalgia and quality of life after treatment. The purpose of this report is to help
the emergency physician appreciate this disease and consider it when clinically appropriate. Ó 2014 Published by Elsevier Inc. , Keywords—hypovitaminosis D; myalgia; chronic pain; vitamin D deficiency
INTRODUCTION Chronic pain affects between 9% and 20% of adults in the United States (US) and is a common reason for patients to visit the emergency department (ED) (1). Such encounters present a vexing problem for emergency physicians, as the differential diagnosis is wide and appropriate case management is highly variable. Regardless of the cause, nearly 89% of those who experience chronic pain have some degree of disability, whether long or short term, and almost all have reduced health-related quality of life (2–5). Although much attention has been directed toward the relationship between vitamin D deficiency and cardiovascular disease, hypovitaminosis D can present as persistent, nonspecific musculoskeletal pain, especially when the deficiency is prolonged and severe (3,5). Identifying chronic nonspecific musculoskeletal pain as a consequence of hypovitaminosis D, especially in those
RECEIVED: 8 July 2013; FINAL SUBMISSION RECEIVED: 21 January 2014; ACCEPTED: 9 February 2014 1
2
D. Moore et al.
presumed to be sufficient, could greatly improve quality of life, as vitamin D supplementation is largely curative. The prevalence of hypovitaminosis D is unexpectedly high in nonelderly, non-house bound patients with persistent nonspecific musculoskeletal pain, especially those younger than 30 years of age (3). African Americans are at particular risk for vitamin D deficiency, with a 10-fold increase in the prevalence (defined as a 25hydroxvitamin D level < 15 ng/mL) compared with Caucasians (32% vs. 3%) (6). CASE REPORT A 22-year-old African-American female with a history of asthma presented to our ED complaining of persistent chest, back, and leg pain along with diffuse muscle discomfort for 4 months. The patient also noted weakness in her upper and lower extremities during the same period. She reported significant debility from these symptoms, with difficulty ambulating and performing activities of daily living. During the preceding few weeks, she experienced increasing limitations in her energy level and had been spending much of her time in bed. The patient had discussed all of this with her primary care physician who, despite an extensive laboratory work-up, had not identified a definitive etiology. She denied respiratory or gastrointestinal symptoms, fever, headache, recent illness, travel, or excessive physical exertion and, other than ibuprofen, was not taking any medications. Her vital signs on presentation to the ED showed blood pressure of 119/69 mm Hg, heart rate of 97 beats/min, respiratory rate of 18 breaths/min, temperature of 36.2 C, and pulse oximetry of 100% on room air. Physical examination was notable for diffuse, reproducible pain with palpation or manipulation of her extremities (both upper and lower) without evidence of joint effusion or redness. The remainder of her examination, including cardiac, respiratory, gastrointestinal, neurologic, and psychiatric assessment, was normal. A chest x-ray study was obtained to evaluate for signs of sarcoidosis, but returned negative. Laboratory studies including complete blood count, comprehensive metabolic profile, and urinalysis also showed no abnormalities. To assess the diffuse myalgia, a creatine phosphokinase (CPK) level was obtained and found to be significantly elevated (5680 mg/L). Initial ED management included aggressive i.v. hydration with normal saline and i.v. morphine sulfate for pain control. Concurrently, a more extensive review of the patient’s electronic medical record was undertaken. Four months before our ED visit, her primary care physician performed extensive laboratory testing that revealed a markedly low vitamin D level of 5 ng/mL and normal rheumatoid factor, thyroid-stimulating hormone level, and vitamin B-12 level. The patient had apparently not
been informed of her hypovitaminosis D and no treatment had been initiated. We determined that her diffuse myalgia and weakness were likely secondary to untreated vitamin D deficiency. The patient was feeling better after normal saline hydration, however, despite our recommendation to hospitalize for, among other things, serial measurement of her CPK, she wanted to go home. We arranged followup with her primary care physician within the next 48 72 h and gave her a 50,000-U dose of cholecalciferol (vitamin D-3) before discharge from the ED. She was given a prescription for the same medication with instructions to take one tablet weekly for the next 8 weeks. The patient was contacted 2 weeks after discharge from the ED. She had followed up with her primary care physician who scheduled continued vitamin D therapy (via intramuscular injection rather than ingestion) in the office. She was feeling much better and, on medical record review, her CPK levels were decreasing. The patient was contacted at 6 months and again at 1 year from ED discharge, by which time she had made a full recovery and was able to resume normal daily activities. Although her vitamin D levels had risen, she remained on oral vitamin D supplemental therapy and had no further visits to the ED for pain. DISCUSSION Severe hypovitaminosis D is often associated with nonspecific musculoskeletal complaints, but the connection between this condition and its clinical effect is often overlooked. Early recognition is important, as vitamin D deficiency can contribute significantly to short-term and long-term disability (7). In addition, when untreated, it can lead to osteomalacia with severe bone pain and, especially in the elderly, an increased risk of fracture. Untreated hypovitaminosis D has been associated with elevated blood levels of creatine kinase (CK) in patients who develop osteomalacia, myositis, and those on statin therapy among others, as seen with our patient (8). Studies have shown, using electromicroscopy, that even in mild cases of statin-induced myositis there is a breakdown of the T-tubular system and subsarcolemmal rupture (9). In addition, an upregulation in expression of the ryanodine receptor 3, indicating an intracellular leak, is associated with vitamin D deficiency (10). This process causes an elevation in CK levels, which can cause further muscle damage and complicate physical symptoms. Our patient presented with muscle pain and weakness that has caused her to struggle with her day-to-day activities. After identifying her hypovitaminosis D and starting treatment, she was found to have significant improvement of her symptoms. As evident by our case, a simple replacement regimen can dramatically improve one’s physical status
Hypovitaminosis D Presenting as Diffuse Myalgia
3
Table 1. Common Causes of Hypovitaminosis D Causes Limited sunlight exposure Low consumption of recommended vitamin D levels over time Decreased skin synthesis Decreased conversion to active form Inability to absorb through the gastrointestinal tract Increased body loss
Examples Homebound or institutionalized, live in northern latitudes, wear long robes or head coverings, occupation that requires prolonged stays indoors Strict vegetarian diet (most of the natural sources are animal-based, including fish and fish oils, egg yolks, cheese, fortified milk, and beef liver) Dark skin pigmentation, advanced age, long-term sunscreen use, post-skin graft Chronic liver disease (reduction in 25-hydroxyvitamin D), chronic kidney disease (reduction in 1,25-hydroxyvitamin D) Crohn’s disease, cystic fibrosis, and celiac disease Nephrotic syndrome, antiviral, anticonvulsant, or immunosuppressive medication use
and essentially cure hypovitaminosis D. Vitamin D assays might not result for up to 3 days, therefore, routine vitamin D testing in patients who present to the ED with chronic pain is not usual practice (11). An earlier study has shown that 93% of individuals with nonspecific musculoskeletal pain have laboratory evidence of vitamin D deficiency, however, it is important to recognize when an underlying cause of such debility is present and act on the information accordingly (3). Vitamin D comes primarily from three sources: exposure to sunlight, routine dietary intake, and dietary supplements. However, the majority (> 80%) of vitamin D in humans originates when solar ultraviolet B radiation (wavelength, 290–315 nm) is absorbed through the skin, converting 7-dehydrocholesterol to previtamin D-3, a prohormone that is further metabolized in a series of enzymatic steps to its active form, 1,25-dihydroxyvitamin D. Although there are many reasons to be deficient in vitamin D (Table 1), the primary cause of hypovitaminosis D worldwide is insufficient skin synthesis. African Americans, especially those with dark skin pigmentation, are particularly prone to vitamin D deficiency, as are individuals who lack sufficient access or exposure to sunlight (i.e., people with excessive sunscreen use, a religious aversion to public display of uncovered skin, and those who are institutionalized long term or reside at increasing distances from the equator). Not surprisingly, the most holistic treatment for hypovitaminosis D is increased sunlight. One minimal erythematic dose of sunlight (i.e., exposure that causes a slight pinkness to the skin) is equivalent to ingesting 20,000 IU of vitamin D (4,7). However for some, this is simply not achievable and dietary supplementation will be needed. Although fortified milk is a reasonable dietary source of vitamin D, the per capita milk consumption in the US provides < 25% of the recommended daily intake of vitamin D, which, according to the Institute of Medicine, should be 600 IU/day for those younger than 70 years of age and 800 IU/day for those 70 years or older (3,4,12). For individuals who are vitamin D
deficient, higher initial doses will be needed to achieve repletion, perhaps as much as 4000 IU/day. Such patients can be given an oral or intramuscular dose of 50,000 IU of vitamin D once a week for 8–12 weeks. Subsequent, long-term prevention of vitamin D deficiency can be achieved by giving 50,000 IU of vitamin D once or twice a month (13). We present a case of diffuse myalgia in a young woman with underlying hypovitaminosis D. Our patient improved significantly with vitamin D therapy, highlighting the importance of vitamin D deficiency as a cause of nonspecific musculoskeletal pain and the relevance of this disorder to the ED setting. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS? Chronic pain has stricken the ED patient population across the board (14). Studies have shown that hypovitaminosis D has been manifested as nonspecific myalgias and has had a profound effect on patient lifestyle. Our patient was found to have hypovitaminosis D and had substantial improvement with her myalgia and quality of life after treatment. The purpose of this report is to help the emergency physician appreciate this disease and consider it when clinically appropriate. REFERENCES 1. Crook J, Rideout E, Brown G. The prevalence of pain complaints in a general population. Pain 1984;18:299–314. 2. Nesby-O’Dell S, Scanlon KS, Cogswell ME, et al. Hypovitaminosis D prevalence and determinants 4 among African American and white women of reproductive age: Third National Health and Nutrition Examination Survey, 1988-1994. Am J Clin Nutr 2002; 76:187–92. 3. Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc 2003;78:1463–70. 4. Malabanan A, Veronikis IE, Holick MF. Redefining vitamin D insufficiency [letter]. Lancet 1998;351:805–6. 5. Adams JS, Kantorovich V, Wu C, Javanbakht M, Hollis BW. Resolution of vitamin D insufficiency in osteopenic patients results in
4
6. 7.
8. 9.
D. Moore et al. rapid recovery of bone mineral density. J Clin Endocrinol Metab 1999;84:2729–30. Looker AC, Johnson CL, Lacher DA, et al. Vitamin D status: United States, 2001 2006. NCHS data brief, no 59. Hyattsville, MD: National Center for Health Statistics; 2011. Holick MF. Vitamin D: photobiology, metabolism, mechanism of action, and clinical applications. In: Favus MJ, ed. Primer on the metabolic bone diseases and disorders of mineral metabolism. 5th ed. Washington, DC: American Society for Bone and Mineral Research; 2003:129–37. Ahmed W, Khan N, Glueck CJ, et al. Low serum 25 (OH) vitamin D levels (< 32 ng/ml) are associated with reversible myositis-myalgia in statin-treated patients. Transl Res 2009. 153L11 6. Draeger A, Monastyrskaya K, Mohaupt M, et al. Statin therapy induces ultrastructural damage in skeletal muscle in patients without myalgia. J Pathol 2006;210:94–102.
10. Mohaupt MG, Karas RH, Babiychuk EB, et al. Association between statin-associated myopathy and skeletal muscle damage. CMAJ 2009;181:E11–8. 11. Binkley N, Krueger D, Cowgill CS, et al. Assay variation confounds the diagnosis of hypovitaminosis D: a call for standardization. J Clin Endocrinol Metab 2004;89:3152–7. 12. Ross AC, Manson JE, Abrams SA, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab 2011;96:53–8. 13. Glerup H, Eriksen EF. Vitamin D deficiency: easy to diagnose, often overlooked [in Danish]. Ugeskr Laeger 1999;161: 2515–21. 14. Croft P, Rigby AS, Boswell R, Schollum J, Silman A. The prevalence of chronic widespread pain in the general population. J Rheumatol 1993;20:710–3.
http://dx.doi.org/10.1016/j.jemermed.2014.02.005
Clinical Communications: Adults HYPOVITAMINOSIS D PRESENTING AS DIFFUSE MYALGIA IN A 22-YEAR-OLD WOMAN: A CASE REPORT Deshon Moore, MD,* Robert Wahl, MD,* and Phillip Levy, MD, MPH*† *Department of Emergency Medicine, Wayne State University School of Medicine, Detroit, Michigan and †The Cardiovascular Research Institute, Wayne State University, Detroit, Michigan Reprint Address: Deshon Moore, MD, Department of Emergency Medicine, Wayne State University School of Medicine, 4201 St. Antoine, Detroit, MI 48201
, Abstract—Background: Caused predominantly by insufficient conversion of vitamin D precursors by sunlight, hypovitaminosis D is an issue of increasing importance worldwide. Although it has been associated with a range of diseases, musculoskeletal effects dominate the clinical picture and can lead to significant physical debility, whether acute or chronic. Although diagnosis of vitamin D deficiency typically occurs in the outpatient setting, it is an easily treatable condition, and timely intervention can dramatically improve one’s quality of life. As highlighted by this case report, hypovitaminosis D may be an important but underappreciated etiology of undifferentiated myalgia that, when present, warrants initiation of vitamin D repletion therapy even from the emergency department (ED). Case Report: A 22-year-old African-American female presented to our ED with diffuse myalgia for 4 months. She reported significant debility from these symptoms with difficulty ambulating and performing activities of daily living. There had been no upper respiratory infection symptoms. The patient had discussed all of this with her primary care physician who, despite an extensive laboratory work-up, had not identified a definitive etiology. Why Should an Emergency Physician Be Aware of This?: Chronic pain has stricken the ED patient population across the board. Studies demonstrate that the myalgia caused by hypovitaminosis D can have a profound and negative impact on an individual’s lifestyle. Our patient was found to have hypovitaminosis D and had substantial improvement with her myalgia and quality of life after treatment. The purpose of this report is to help
the emergency physician appreciate this disease and consider it when clinically appropriate. Ó 2014 Published by Elsevier Inc. , Keywords—hypovitaminosis D; myalgia; chronic pain; vitamin D deficiency
INTRODUCTION Chronic pain affects between 9% and 20% of adults in the United States (US) and is a common reason for patients to visit the emergency department (ED) (1). Such encounters present a vexing problem for emergency physicians, as the differential diagnosis is wide and appropriate case management is highly variable. Regardless of the cause, nearly 89% of those who experience chronic pain have some degree of disability, whether long or short term, and almost all have reduced health-related quality of life (2–5). Although much attention has been directed toward the relationship between vitamin D deficiency and cardiovascular disease, hypovitaminosis D can present as persistent, nonspecific musculoskeletal pain, especially when the deficiency is prolonged and severe (3,5). Identifying chronic nonspecific musculoskeletal pain as a consequence of hypovitaminosis D, especially in those
RECEIVED: 8 July 2013; FINAL SUBMISSION RECEIVED: 21 January 2014; ACCEPTED: 9 February 2014 1
2
D. Moore et al.
presumed to be sufficient, could greatly improve quality of life, as vitamin D supplementation is largely curative. The prevalence of hypovitaminosis D is unexpectedly high in nonelderly, non-house bound patients with persistent nonspecific musculoskeletal pain, especially those younger than 30 years of age (3). African Americans are at particular risk for vitamin D deficiency, with a 10-fold increase in the prevalence (defined as a 25hydroxvitamin D level < 15 ng/mL) compared with Caucasians (32% vs. 3%) (6). CASE REPORT A 22-year-old African-American female with a history of asthma presented to our ED complaining of persistent chest, back, and leg pain along with diffuse muscle discomfort for 4 months. The patient also noted weakness in her upper and lower extremities during the same period. She reported significant debility from these symptoms, with difficulty ambulating and performing activities of daily living. During the preceding few weeks, she experienced increasing limitations in her energy level and had been spending much of her time in bed. The patient had discussed all of this with her primary care physician who, despite an extensive laboratory work-up, had not identified a definitive etiology. She denied respiratory or gastrointestinal symptoms, fever, headache, recent illness, travel, or excessive physical exertion and, other than ibuprofen, was not taking any medications. Her vital signs on presentation to the ED showed blood pressure of 119/69 mm Hg, heart rate of 97 beats/min, respiratory rate of 18 breaths/min, temperature of 36.2 C, and pulse oximetry of 100% on room air. Physical examination was notable for diffuse, reproducible pain with palpation or manipulation of her extremities (both upper and lower) without evidence of joint effusion or redness. The remainder of her examination, including cardiac, respiratory, gastrointestinal, neurologic, and psychiatric assessment, was normal. A chest x-ray study was obtained to evaluate for signs of sarcoidosis, but returned negative. Laboratory studies including complete blood count, comprehensive metabolic profile, and urinalysis also showed no abnormalities. To assess the diffuse myalgia, a creatine phosphokinase (CPK) level was obtained and found to be significantly elevated (5680 mg/L). Initial ED management included aggressive i.v. hydration with normal saline and i.v. morphine sulfate for pain control. Concurrently, a more extensive review of the patient’s electronic medical record was undertaken. Four months before our ED visit, her primary care physician performed extensive laboratory testing that revealed a markedly low vitamin D level of 5 ng/mL and normal rheumatoid factor, thyroid-stimulating hormone level, and vitamin B-12 level. The patient had apparently not
been informed of her hypovitaminosis D and no treatment had been initiated. We determined that her diffuse myalgia and weakness were likely secondary to untreated vitamin D deficiency. The patient was feeling better after normal saline hydration, however, despite our recommendation to hospitalize for, among other things, serial measurement of her CPK, she wanted to go home. We arranged followup with her primary care physician within the next 48 72 h and gave her a 50,000-U dose of cholecalciferol (vitamin D-3) before discharge from the ED. She was given a prescription for the same medication with instructions to take one tablet weekly for the next 8 weeks. The patient was contacted 2 weeks after discharge from the ED. She had followed up with her primary care physician who scheduled continued vitamin D therapy (via intramuscular injection rather than ingestion) in the office. She was feeling much better and, on medical record review, her CPK levels were decreasing. The patient was contacted at 6 months and again at 1 year from ED discharge, by which time she had made a full recovery and was able to resume normal daily activities. Although her vitamin D levels had risen, she remained on oral vitamin D supplemental therapy and had no further visits to the ED for pain. DISCUSSION Severe hypovitaminosis D is often associated with nonspecific musculoskeletal complaints, but the connection between this condition and its clinical effect is often overlooked. Early recognition is important, as vitamin D deficiency can contribute significantly to short-term and long-term disability (7). In addition, when untreated, it can lead to osteomalacia with severe bone pain and, especially in the elderly, an increased risk of fracture. Untreated hypovitaminosis D has been associated with elevated blood levels of creatine kinase (CK) in patients who develop osteomalacia, myositis, and those on statin therapy among others, as seen with our patient (8). Studies have shown, using electromicroscopy, that even in mild cases of statin-induced myositis there is a breakdown of the T-tubular system and subsarcolemmal rupture (9). In addition, an upregulation in expression of the ryanodine receptor 3, indicating an intracellular leak, is associated with vitamin D deficiency (10). This process causes an elevation in CK levels, which can cause further muscle damage and complicate physical symptoms. Our patient presented with muscle pain and weakness that has caused her to struggle with her day-to-day activities. After identifying her hypovitaminosis D and starting treatment, she was found to have significant improvement of her symptoms. As evident by our case, a simple replacement regimen can dramatically improve one’s physical status
Hypovitaminosis D Presenting as Diffuse Myalgia
3
Table 1. Common Causes of Hypovitaminosis D Causes Limited sunlight exposure Low consumption of recommended vitamin D levels over time Decreased skin synthesis Decreased conversion to active form Inability to absorb through the gastrointestinal tract Increased body loss
Examples Homebound or institutionalized, live in northern latitudes, wear long robes or head coverings, occupation that requires prolonged stays indoors Strict vegetarian diet (most of the natural sources are animal-based, including fish and fish oils, egg yolks, cheese, fortified milk, and beef liver) Dark skin pigmentation, advanced age, long-term sunscreen use, post-skin graft Chronic liver disease (reduction in 25-hydroxyvitamin D), chronic kidney disease (reduction in 1,25-hydroxyvitamin D) Crohn’s disease, cystic fibrosis, and celiac disease Nephrotic syndrome, antiviral, anticonvulsant, or immunosuppressive medication use
and essentially cure hypovitaminosis D. Vitamin D assays might not result for up to 3 days, therefore, routine vitamin D testing in patients who present to the ED with chronic pain is not usual practice (11). An earlier study has shown that 93% of individuals with nonspecific musculoskeletal pain have laboratory evidence of vitamin D deficiency, however, it is important to recognize when an underlying cause of such debility is present and act on the information accordingly (3). Vitamin D comes primarily from three sources: exposure to sunlight, routine dietary intake, and dietary supplements. However, the majority (> 80%) of vitamin D in humans originates when solar ultraviolet B radiation (wavelength, 290–315 nm) is absorbed through the skin, converting 7-dehydrocholesterol to previtamin D-3, a prohormone that is further metabolized in a series of enzymatic steps to its active form, 1,25-dihydroxyvitamin D. Although there are many reasons to be deficient in vitamin D (Table 1), the primary cause of hypovitaminosis D worldwide is insufficient skin synthesis. African Americans, especially those with dark skin pigmentation, are particularly prone to vitamin D deficiency, as are individuals who lack sufficient access or exposure to sunlight (i.e., people with excessive sunscreen use, a religious aversion to public display of uncovered skin, and those who are institutionalized long term or reside at increasing distances from the equator). Not surprisingly, the most holistic treatment for hypovitaminosis D is increased sunlight. One minimal erythematic dose of sunlight (i.e., exposure that causes a slight pinkness to the skin) is equivalent to ingesting 20,000 IU of vitamin D (4,7). However for some, this is simply not achievable and dietary supplementation will be needed. Although fortified milk is a reasonable dietary source of vitamin D, the per capita milk consumption in the US provides < 25% of the recommended daily intake of vitamin D, which, according to the Institute of Medicine, should be 600 IU/day for those younger than 70 years of age and 800 IU/day for those 70 years or older (3,4,12). For individuals who are vitamin D
deficient, higher initial doses will be needed to achieve repletion, perhaps as much as 4000 IU/day. Such patients can be given an oral or intramuscular dose of 50,000 IU of vitamin D once a week for 8–12 weeks. Subsequent, long-term prevention of vitamin D deficiency can be achieved by giving 50,000 IU of vitamin D once or twice a month (13). We present a case of diffuse myalgia in a young woman with underlying hypovitaminosis D. Our patient improved significantly with vitamin D therapy, highlighting the importance of vitamin D deficiency as a cause of nonspecific musculoskeletal pain and the relevance of this disorder to the ED setting. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS? Chronic pain has stricken the ED patient population across the board (14). Studies have shown that hypovitaminosis D has been manifested as nonspecific myalgias and has had a profound effect on patient lifestyle. Our patient was found to have hypovitaminosis D and had substantial improvement with her myalgia and quality of life after treatment. The purpose of this report is to help the emergency physician appreciate this disease and consider it when clinically appropriate. REFERENCES 1. Crook J, Rideout E, Brown G. The prevalence of pain complaints in a general population. Pain 1984;18:299–314. 2. Nesby-O’Dell S, Scanlon KS, Cogswell ME, et al. Hypovitaminosis D prevalence and determinants 4 among African American and white women of reproductive age: Third National Health and Nutrition Examination Survey, 1988-1994. Am J Clin Nutr 2002; 76:187–92. 3. Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc 2003;78:1463–70. 4. Malabanan A, Veronikis IE, Holick MF. Redefining vitamin D insufficiency [letter]. Lancet 1998;351:805–6. 5. Adams JS, Kantorovich V, Wu C, Javanbakht M, Hollis BW. Resolution of vitamin D insufficiency in osteopenic patients results in
4
6. 7.
8. 9.
D. Moore et al. rapid recovery of bone mineral density. J Clin Endocrinol Metab 1999;84:2729–30. Looker AC, Johnson CL, Lacher DA, et al. Vitamin D status: United States, 2001 2006. NCHS data brief, no 59. Hyattsville, MD: National Center for Health Statistics; 2011. Holick MF. Vitamin D: photobiology, metabolism, mechanism of action, and clinical applications. In: Favus MJ, ed. Primer on the metabolic bone diseases and disorders of mineral metabolism. 5th ed. Washington, DC: American Society for Bone and Mineral Research; 2003:129–37. Ahmed W, Khan N, Glueck CJ, et al. Low serum 25 (OH) vitamin D levels (< 32 ng/ml) are associated with reversible myositis-myalgia in statin-treated patients. Transl Res 2009. 153L11 6. Draeger A, Monastyrskaya K, Mohaupt M, et al. Statin therapy induces ultrastructural damage in skeletal muscle in patients without myalgia. J Pathol 2006;210:94–102.
10. Mohaupt MG, Karas RH, Babiychuk EB, et al. Association between statin-associated myopathy and skeletal muscle damage. CMAJ 2009;181:E11–8. 11. Binkley N, Krueger D, Cowgill CS, et al. Assay variation confounds the diagnosis of hypovitaminosis D: a call for standardization. J Clin Endocrinol Metab 2004;89:3152–7. 12. Ross AC, Manson JE, Abrams SA, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab 2011;96:53–8. 13. Glerup H, Eriksen EF. Vitamin D deficiency: easy to diagnose, often overlooked [in Danish]. Ugeskr Laeger 1999;161: 2515–21. 14. Croft P, Rigby AS, Boswell R, Schollum J, Silman A. The prevalence of chronic widespread pain in the general population. J Rheumatol 1993;20:710–3.
