http://informahealthcare.com/rnf ISSN: 0886-022X (print), 1525-6049 (electronic) Ren Fail, 2014; 36(7): 1145–1147 ! 2014 Informa Healthcare USA, Inc. DOI: 10.3109/0886022X.2014.917765
CASE REPORT
Central venous catheter infection-induced Henoch-Scho¨nlein purpura in a patient on hemodialysis Jian Jun Gao, Jia Mei Wei, Yue Hua Gao, Shuang Li, and Yu Na Department of Nephrology, the 306th Hospital of Chinese PLA, Beijing, China
Abstract
Keywords
A 69-year-old man, who had been dialyzed using a permanent central venous catheter for 2 years, presented with Henoch-Scho¨nlein purpura and positive perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA). He was diagnosed with catheter-related infection by Staphylococcus aureus. After administration of antibiotic and steroid therapy, purpura disappeared and p-ANCA gradually became negative. This case supports the conclusion that infection can be pathogenesis of the vasculitis, including ANCA-positive HSP. Additionally, impregnation of catheters with antibiotics can be an effective treatment for catheter infections.
Anti-neutrophil cytoplasmic antibody, central venous catheter infection, diabetic nephropathy, hemodialysis, Henoch-Scho¨nlein purpura
Introduction Henoch-Scho¨nlein purpura (HSP) is a vasculitis typically found in childhood and rarely in adults.1 This disease is characterized by vasculitis associated with IgA immune complex deposition affecting multiple organs, including the skin, gastrointestinal tract, joints and frequently the kidneys. Anti-neutrophil cytoplasmic antibody (ANCA) is commonly found in a variety of vasculitides. Two patterns of ANCA, namely, cytoplasmic (c-ANCA) and perinuclear (p-ANCA), can be used to diagnose Wegener’s granulomatosis, microscopic polyangiitis and Churg-Strauss syndrome. However, ANCA-positive HSP was rarely reported. Adult-onset HSP with positive ANCA in combination with diabetes is rarely reported.2 In this report, we describe a diabetic nephropathy patient undergoing maintenance hemodialysis that developed ANCA-positive HSP.
Case report The patient was a 69-year-old male with type 2 DM for 20 years and diabetic nephrology for 10 years. The patient started dialysis 2 years ago and was admitted to the hospital for a fever. Upon admission, vital signs showed a body temperature of 37.4 C, pulse rate of 89/min, respiratory rate of 19/min, and blood pressure of 160/80 mmHg. Physical examination did not reveal moist rales in the bilateral lower
Address correspondence to Yu Na, Department of Nephrology, the 306th Hospital of Chinese PLA, 9 AnXiangBeiLi Road, Beijing 100101, China. Tel: +86 1066935462; Fax: +86 1068130297; E-mail: [email protected]
History Received 25 January 2014 Revised 27 February 2014 Accepted 11 April 2014 Published online 19 May 2014
lung fields or bilateral leg edema. Neurologic, cardiac and abdominal examinations were unremarkable. The laboratory test results showed moderate anaemia and thrombocytopenia with a hemoglobin level of 78.2 g/L, platelet count of 64,000/ mL, and normal white blood cell count of 4000 mL with 76% segments. C-reactive protein level was 15.9 mg/L. Electrocardiograms and chest X-rays were unremarkable. The patient was initially diagnosed with catheter-related infection because he had been dialyzed using a permanent central venous catheter for 2 years twice per week. Blood obtained from the catheter was cultured. The patient was treated with meropenem (500 mg) every 12 h, and was administrated amlodipine besylate tablets, olmesartan and metoprolol for hypertension control. On the fifth admission day, purpuric lesions appeared on both legs. The accompanying symptoms included abdominal pain and hematuria. Laboratory data revealed serum IgA levels of 4.88 g/L (normal 0.72–4.29 g/L), with high IgG levels of 19.62 g/L (normal 8–17 g/L). IgM levels were normal and C3 was low (normal 0.78–2.14 g/L). IIFA showed positive p-ANCA and negative c-ANCA. C-reactive protein was high (15.9 mg/L, normal 0–4 mg/L) and rheumatoid factors (RF) were negative. Skin biopsy was performed and histology revealed leukocytoclastic vasculitis with perivascular infiltration of neutrophils (Figure 1). Blood culture revealed Staphylococcus aureus. The patient was treated with prednisolone (40 mg/d) and received treatment for the central vein catheter infection with heparin and meropenem impregnation of the catheter. Two weeks later, cutaneous lesions improved, and IgA (14.48 g/L), IgG (3.87 g/L), IgM (0.40 g/L) and C3 (0.80 g/L) levels returned to
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Figure 1. Histology study of skin biopsy. Neutrophil infiltration in perivascular area and in the vascular walls (magnification 400).
normal. Treatment with meropenem was stopped and prednisolone was gradually reduced. p-ANCA was negative over 3 months.
Discussion HSP is the most common systemic vasculitis, but it is rare in adults. The classic clinical symptoms include purpuric rash, abdominal pain, arthralgias, and hematuria. Few case reports have described HSP in patients with hemodialysis.3,4 Here, we report a patient on maintenance hemodialysis that developed purpura, abdominal pain and hematuria. HSP has pathologically been regarded as a specific immune-mediated entity induced by multiple factors, including infection, cancer, allergic reaction to some allergens, and drug-induced hypersensitivity reactions.5 Ciprofloxacin, angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers (ARB), vancomycin and minocycline are possible causes of HSP.6,7 In this case, the patient was treated with amlodipine besylate tablets, olmesartan and metoprolol to control hypertension. There are no reports of HSP in association with amlodipine besylate tablets and metoprolol administration. Olmesartan, a type of ARB, was administered to this patient throughout the entire hospital admission. Thus, olmesartan did not induce HSP in this patient. Infection is a major cause of HSP, and cases of S. aureus-induced HSP have been documented in several reports.8 A case of HSP due to S. aureus bacteriemia from central venous catheterization was reported in 2008.9 S. aureus induces HSP by producing enterotoxins that act as superantigen. Superantigen can stimulate resting T cells to produce cytokines that promote polyclonal B-cell activation, which increases immunoglobulin production and immunocomplex formation. Clinical manifestations could be characterized by elevated immunoglobulin and decreased serum complement. Hemodialysis patients have a high incidence of infectious diseases. A total of 48–89% of bacteremias in hemodialysis patients are related to a vascular access.10 The incidence of catheter infections is 10–30-fold higher than native fistulas.11 S. aureus infection is responsible for 27–39% of all
Ren Fail, 2014; 36(7): 1145–1147
bacteriemias in dialysis patients.12 Hemodialysis patients have an 8.1–8.6% chance of developing S. aureus bacteriemia during their dialysis career.13 Based on the US dialysis surveillance network of October 1999 through May 2001, S. aureus accounted for 32% of the vascular access-related bacteriemia in catheters.14 Here, we report that a diabetic nephropathy patient developed HSP during hemodialysis. The patient showed two risk factors for S. aureus bacteriemia, namely hemodialysis and diabetes. However, HSP in chronic hemodialysis patients has been reported only rarely. ANCA is an auto-antibody found in peripheral blood, and has been detected in a variety of vasculitic disorders. HSP is a common systemic vasculitis; however, ANCA-positive HSP has been reported rarely. The association between ANCA and HSP is not clear. Some reports suggested that ANCA plays a role in HSP pathogenesis.15 ANCA can affect the function of neutrophils and monocytes, and can also stimulate an oxidative burst and release reactive oxygen intermediates that may directly damage target tissues, especially vessels.16 ANCA and many auto-antibodies, including anti-cardiolipin antibodies, ANA, and cryoglobulins may be produced during bacterial and viral infections.17 Some ANCA-positive cases induced by S. aureus infection have been documented previously.18,19 HSP with positive ANCA in our patient improved after treatment with meropenem and prednisolone. In conclusion, infection can be associated with multiple forms of vasculitis, including ANCA-positive HSP. Additionally, antibiotics and prednisolone are an effective method of treating infection induced-HSP, and impregnation of catheters with antibiotics can be used to treat patients with catheter infections.
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.
References 1. Hunder GG, Arend WP, Bloch DA, Calabrese LH, Fauci AS. The American College of Rheumatology 1990 criteria for the classification of vasculitis. Introduction. Arthritis Rheum. 1990;33: 1065–1067. 2. Cavarape A, Quinkenstein E, Pizzolitto S, Soardo G, Sechi L. Henoch-Schonlein purpura in a patient with diabetic nephropathy and vascular complications. Nephrol Dial Transplant. 2005;20: 1514–1515. 3. Esposito C, Fasoli G, Cornacchia F, Foschi A, Mazzullo T. Henoch-Schonlein purpura in a chronic hemodialysis patient. J Nephrol. 1999;12:197–200. 4. Yoshino J, Sasamura H, Konishi K, Tsuji M, Suda N. A case of Henoch-Schonlein purpura in a patient on hemodialysis. Nihon Jinzo Gakkai Shi. 2007;49:49–53. 5. Yang YH, Chuang YH, Wang LC, Huang HY, Gershwin ME. The immunobiology of Henoch-Schonlein purpura. Autoimmun Rev. 2008;7:179–184. 6. Davin JC, Weening JJ. Henoch-Schonlein purpura nephritis: an update. Eur J Pediatr. 2001;160:689–695. 7. Davin JC, Ten Berge IJ, Weening JJ. What is the difference between IgA nephropathy and Henoch-Schonlein purpura nephritis? Kidney Int. 2001;59:823–834. 8. Hirayama K, Kobayashi M, Kondoh M, Muro K, Iwabuchi S. Henoch-Schonlein purpura nephritis associated with methicillinresistant Staphylococcus aureus infection. Nephrol Dial Transplant. 1998;13:2703–2704.
DOI: 10.3109/0886022X.2014.917765
9. Uggeri S, Fabbian F, Catizone L. Henoch-Schonlein purpura due to methicillin-sensitive Staphylococcus aureus bacteremia from central venous catheterization. Clin Exp Nephrol. 2008;12:219–223. 10. Vandecasteele SJ, Boelaert JR, De Vriese AS. Staphylococcus aureus infections in hemodialysis: what a nephrologist should know. Clin J Am Soc Nephrol. 2009;4:1388–1400. 11. Taylor G, Gravel D, Johnston L, Embil J, Holton D. Prospective surveillance for primary bloodstream infections occurring in Canadian hemodialysis units. Infect Control Hosp Epidemiol. 2002;23:716–720. 12. Danese MD, Griffiths RI, Dylan M, Yu HT, Dubois R. Mortality differences among organisms causing septicemia in hemodialysis patients. Hemodial Int. 2006;10:56–62. 13. Fluck R, Rao R, van Schalkwyk D, Ansell D, Feest T. The UK Vascular Access Survey–follow-up data and repeat survey (chapter 5). Nephrol Dial Transplant. 2007;22:vii51–vii57. 14. Tokars JI, Miller ER, Stein G. New national surveillance system for hemodialysis-associated infections: initial results. Am J Infect Control. 2002;30:288–295.
Catheter infection-induced Henoch-Scho¨nlein purpura
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15. Esnault VL, Ronda N, Jayne DR, Lockwood CM. Association of ANCA isotype and affinity with disease expression. J Autoimmun. 1993;6:197–205. 16. Weidner S, Neupert W, Goppelt-Struebe M, Rupprecht HD. Antineutrophil cytoplasmic antibodies induce human monocytes to produce oxygen radicals in vitro. Arthritis Rheum. 2001;44: 1698–1706. 17. Bonaci-Nikolic B, Andrejevic S, Pavlovic M, Dimcic Z, Ivanovic B. Prolonged infections associated with antineutrophil cytoplasmic antibodies specific to proteinase 3 and myeloperoxidase: diagnostic and therapeutic challenge. Clin Rheumatol. 2010; 29:893–904. 18. Riding AM, D’Cruz DP. A case of mistaken identity: subacute bacterial endocarditis associated with p-antineutrophil cytoplasmic antibody. BMJ Case Rep. 2010;2010. doi: 10.1136/bcr.09.2010. 3299. 19. Miranda-Filloy JA, Veiga JA, Juarez Y, Gonzalez-Juanatey C, Gonzalez-Gay MA. Microscopic polyangiitis following recurrent Staphylococcus aureus bacteremia and infectious endocarditis. Clin Exp Rheumatol. 2006;24:705–706.
Copyright of Renal Failure is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
CASE REPORT
Central venous catheter infection-induced Henoch-Scho¨nlein purpura in a patient on hemodialysis Jian Jun Gao, Jia Mei Wei, Yue Hua Gao, Shuang Li, and Yu Na Department of Nephrology, the 306th Hospital of Chinese PLA, Beijing, China
Abstract
Keywords
A 69-year-old man, who had been dialyzed using a permanent central venous catheter for 2 years, presented with Henoch-Scho¨nlein purpura and positive perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA). He was diagnosed with catheter-related infection by Staphylococcus aureus. After administration of antibiotic and steroid therapy, purpura disappeared and p-ANCA gradually became negative. This case supports the conclusion that infection can be pathogenesis of the vasculitis, including ANCA-positive HSP. Additionally, impregnation of catheters with antibiotics can be an effective treatment for catheter infections.
Anti-neutrophil cytoplasmic antibody, central venous catheter infection, diabetic nephropathy, hemodialysis, Henoch-Scho¨nlein purpura
Introduction Henoch-Scho¨nlein purpura (HSP) is a vasculitis typically found in childhood and rarely in adults.1 This disease is characterized by vasculitis associated with IgA immune complex deposition affecting multiple organs, including the skin, gastrointestinal tract, joints and frequently the kidneys. Anti-neutrophil cytoplasmic antibody (ANCA) is commonly found in a variety of vasculitides. Two patterns of ANCA, namely, cytoplasmic (c-ANCA) and perinuclear (p-ANCA), can be used to diagnose Wegener’s granulomatosis, microscopic polyangiitis and Churg-Strauss syndrome. However, ANCA-positive HSP was rarely reported. Adult-onset HSP with positive ANCA in combination with diabetes is rarely reported.2 In this report, we describe a diabetic nephropathy patient undergoing maintenance hemodialysis that developed ANCA-positive HSP.
Case report The patient was a 69-year-old male with type 2 DM for 20 years and diabetic nephrology for 10 years. The patient started dialysis 2 years ago and was admitted to the hospital for a fever. Upon admission, vital signs showed a body temperature of 37.4 C, pulse rate of 89/min, respiratory rate of 19/min, and blood pressure of 160/80 mmHg. Physical examination did not reveal moist rales in the bilateral lower
Address correspondence to Yu Na, Department of Nephrology, the 306th Hospital of Chinese PLA, 9 AnXiangBeiLi Road, Beijing 100101, China. Tel: +86 1066935462; Fax: +86 1068130297; E-mail: [email protected]
History Received 25 January 2014 Revised 27 February 2014 Accepted 11 April 2014 Published online 19 May 2014
lung fields or bilateral leg edema. Neurologic, cardiac and abdominal examinations were unremarkable. The laboratory test results showed moderate anaemia and thrombocytopenia with a hemoglobin level of 78.2 g/L, platelet count of 64,000/ mL, and normal white blood cell count of 4000 mL with 76% segments. C-reactive protein level was 15.9 mg/L. Electrocardiograms and chest X-rays were unremarkable. The patient was initially diagnosed with catheter-related infection because he had been dialyzed using a permanent central venous catheter for 2 years twice per week. Blood obtained from the catheter was cultured. The patient was treated with meropenem (500 mg) every 12 h, and was administrated amlodipine besylate tablets, olmesartan and metoprolol for hypertension control. On the fifth admission day, purpuric lesions appeared on both legs. The accompanying symptoms included abdominal pain and hematuria. Laboratory data revealed serum IgA levels of 4.88 g/L (normal 0.72–4.29 g/L), with high IgG levels of 19.62 g/L (normal 8–17 g/L). IgM levels were normal and C3 was low (normal 0.78–2.14 g/L). IIFA showed positive p-ANCA and negative c-ANCA. C-reactive protein was high (15.9 mg/L, normal 0–4 mg/L) and rheumatoid factors (RF) were negative. Skin biopsy was performed and histology revealed leukocytoclastic vasculitis with perivascular infiltration of neutrophils (Figure 1). Blood culture revealed Staphylococcus aureus. The patient was treated with prednisolone (40 mg/d) and received treatment for the central vein catheter infection with heparin and meropenem impregnation of the catheter. Two weeks later, cutaneous lesions improved, and IgA (14.48 g/L), IgG (3.87 g/L), IgM (0.40 g/L) and C3 (0.80 g/L) levels returned to
1146
J.J. Gao et al.
Figure 1. Histology study of skin biopsy. Neutrophil infiltration in perivascular area and in the vascular walls (magnification 400).
normal. Treatment with meropenem was stopped and prednisolone was gradually reduced. p-ANCA was negative over 3 months.
Discussion HSP is the most common systemic vasculitis, but it is rare in adults. The classic clinical symptoms include purpuric rash, abdominal pain, arthralgias, and hematuria. Few case reports have described HSP in patients with hemodialysis.3,4 Here, we report a patient on maintenance hemodialysis that developed purpura, abdominal pain and hematuria. HSP has pathologically been regarded as a specific immune-mediated entity induced by multiple factors, including infection, cancer, allergic reaction to some allergens, and drug-induced hypersensitivity reactions.5 Ciprofloxacin, angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers (ARB), vancomycin and minocycline are possible causes of HSP.6,7 In this case, the patient was treated with amlodipine besylate tablets, olmesartan and metoprolol to control hypertension. There are no reports of HSP in association with amlodipine besylate tablets and metoprolol administration. Olmesartan, a type of ARB, was administered to this patient throughout the entire hospital admission. Thus, olmesartan did not induce HSP in this patient. Infection is a major cause of HSP, and cases of S. aureus-induced HSP have been documented in several reports.8 A case of HSP due to S. aureus bacteriemia from central venous catheterization was reported in 2008.9 S. aureus induces HSP by producing enterotoxins that act as superantigen. Superantigen can stimulate resting T cells to produce cytokines that promote polyclonal B-cell activation, which increases immunoglobulin production and immunocomplex formation. Clinical manifestations could be characterized by elevated immunoglobulin and decreased serum complement. Hemodialysis patients have a high incidence of infectious diseases. A total of 48–89% of bacteremias in hemodialysis patients are related to a vascular access.10 The incidence of catheter infections is 10–30-fold higher than native fistulas.11 S. aureus infection is responsible for 27–39% of all
Ren Fail, 2014; 36(7): 1145–1147
bacteriemias in dialysis patients.12 Hemodialysis patients have an 8.1–8.6% chance of developing S. aureus bacteriemia during their dialysis career.13 Based on the US dialysis surveillance network of October 1999 through May 2001, S. aureus accounted for 32% of the vascular access-related bacteriemia in catheters.14 Here, we report that a diabetic nephropathy patient developed HSP during hemodialysis. The patient showed two risk factors for S. aureus bacteriemia, namely hemodialysis and diabetes. However, HSP in chronic hemodialysis patients has been reported only rarely. ANCA is an auto-antibody found in peripheral blood, and has been detected in a variety of vasculitic disorders. HSP is a common systemic vasculitis; however, ANCA-positive HSP has been reported rarely. The association between ANCA and HSP is not clear. Some reports suggested that ANCA plays a role in HSP pathogenesis.15 ANCA can affect the function of neutrophils and monocytes, and can also stimulate an oxidative burst and release reactive oxygen intermediates that may directly damage target tissues, especially vessels.16 ANCA and many auto-antibodies, including anti-cardiolipin antibodies, ANA, and cryoglobulins may be produced during bacterial and viral infections.17 Some ANCA-positive cases induced by S. aureus infection have been documented previously.18,19 HSP with positive ANCA in our patient improved after treatment with meropenem and prednisolone. In conclusion, infection can be associated with multiple forms of vasculitis, including ANCA-positive HSP. Additionally, antibiotics and prednisolone are an effective method of treating infection induced-HSP, and impregnation of catheters with antibiotics can be used to treat patients with catheter infections.
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.
References 1. Hunder GG, Arend WP, Bloch DA, Calabrese LH, Fauci AS. The American College of Rheumatology 1990 criteria for the classification of vasculitis. Introduction. Arthritis Rheum. 1990;33: 1065–1067. 2. Cavarape A, Quinkenstein E, Pizzolitto S, Soardo G, Sechi L. Henoch-Schonlein purpura in a patient with diabetic nephropathy and vascular complications. Nephrol Dial Transplant. 2005;20: 1514–1515. 3. Esposito C, Fasoli G, Cornacchia F, Foschi A, Mazzullo T. Henoch-Schonlein purpura in a chronic hemodialysis patient. J Nephrol. 1999;12:197–200. 4. Yoshino J, Sasamura H, Konishi K, Tsuji M, Suda N. A case of Henoch-Schonlein purpura in a patient on hemodialysis. Nihon Jinzo Gakkai Shi. 2007;49:49–53. 5. Yang YH, Chuang YH, Wang LC, Huang HY, Gershwin ME. The immunobiology of Henoch-Schonlein purpura. Autoimmun Rev. 2008;7:179–184. 6. Davin JC, Weening JJ. Henoch-Schonlein purpura nephritis: an update. Eur J Pediatr. 2001;160:689–695. 7. Davin JC, Ten Berge IJ, Weening JJ. What is the difference between IgA nephropathy and Henoch-Schonlein purpura nephritis? Kidney Int. 2001;59:823–834. 8. Hirayama K, Kobayashi M, Kondoh M, Muro K, Iwabuchi S. Henoch-Schonlein purpura nephritis associated with methicillinresistant Staphylococcus aureus infection. Nephrol Dial Transplant. 1998;13:2703–2704.
DOI: 10.3109/0886022X.2014.917765
9. Uggeri S, Fabbian F, Catizone L. Henoch-Schonlein purpura due to methicillin-sensitive Staphylococcus aureus bacteremia from central venous catheterization. Clin Exp Nephrol. 2008;12:219–223. 10. Vandecasteele SJ, Boelaert JR, De Vriese AS. Staphylococcus aureus infections in hemodialysis: what a nephrologist should know. Clin J Am Soc Nephrol. 2009;4:1388–1400. 11. Taylor G, Gravel D, Johnston L, Embil J, Holton D. Prospective surveillance for primary bloodstream infections occurring in Canadian hemodialysis units. Infect Control Hosp Epidemiol. 2002;23:716–720. 12. Danese MD, Griffiths RI, Dylan M, Yu HT, Dubois R. Mortality differences among organisms causing septicemia in hemodialysis patients. Hemodial Int. 2006;10:56–62. 13. Fluck R, Rao R, van Schalkwyk D, Ansell D, Feest T. The UK Vascular Access Survey–follow-up data and repeat survey (chapter 5). Nephrol Dial Transplant. 2007;22:vii51–vii57. 14. Tokars JI, Miller ER, Stein G. New national surveillance system for hemodialysis-associated infections: initial results. Am J Infect Control. 2002;30:288–295.
Catheter infection-induced Henoch-Scho¨nlein purpura
1147
15. Esnault VL, Ronda N, Jayne DR, Lockwood CM. Association of ANCA isotype and affinity with disease expression. J Autoimmun. 1993;6:197–205. 16. Weidner S, Neupert W, Goppelt-Struebe M, Rupprecht HD. Antineutrophil cytoplasmic antibodies induce human monocytes to produce oxygen radicals in vitro. Arthritis Rheum. 2001;44: 1698–1706. 17. Bonaci-Nikolic B, Andrejevic S, Pavlovic M, Dimcic Z, Ivanovic B. Prolonged infections associated with antineutrophil cytoplasmic antibodies specific to proteinase 3 and myeloperoxidase: diagnostic and therapeutic challenge. Clin Rheumatol. 2010; 29:893–904. 18. Riding AM, D’Cruz DP. A case of mistaken identity: subacute bacterial endocarditis associated with p-antineutrophil cytoplasmic antibody. BMJ Case Rep. 2010;2010. doi: 10.1136/bcr.09.2010. 3299. 19. Miranda-Filloy JA, Veiga JA, Juarez Y, Gonzalez-Juanatey C, Gonzalez-Gay MA. Microscopic polyangiitis following recurrent Staphylococcus aureus bacteremia and infectious endocarditis. Clin Exp Rheumatol. 2006;24:705–706.
Copyright of Renal Failure is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
