Parvovirus B19
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《新英格兰医药杂志》
To the Editor: We would like to add some information to Young and Brown's review (Feb. 5 issue)1 of parvovirus B19 infection and myocarditis. We studied myocardial tissue from five patients with fulminant parvovirus B19–associated myocarditis by in situ hybridization and showed that parvovirus B19 is present exclusively in endothelial cells of the smaller intramyocardial vessels (Figure 1A), not in cardiac myocytes.2 Additional immunohistochemical investigation revealed marked expression of E-selectin by endothelial cells of parvovirus B19–infected hearts, a finding indicative of endothelial dysfunction, and massive margination and adhesion of T lymphocytes in the venular compartment (Figure 1B). These processes may lead to disturbances in the coronary microcirculation, followed by an increase in coronary resistance with secondary myofibrillar degeneration (Figure 1B) and myocyte necrosis — lesions that are similar to the morphologic lesions seen in ischemic heart disease.3,4 These findings would explain the observation that many patients with parvovirus B19–associated myocarditis present with the clinical signs that are typical of ischemic heart disease.5
Figure 1. Myocardial Tissue from Patients with Parvovirus B19–Associated Myocarditis.
Panel A shows the detection of parvovirus B19 genomes in endothelial cells of a small intramyocardial artery in tissue from a patient with acute myocarditis (radioactive in situ hybridization, x100). Panel B shows myofibrillar degeneration, contraction bands, myocyte necrosis, and inflammation (arrow) in parvovirus B19–associated myocarditis (Luxol fast blue, x80).
Burkhard D. Bültmann, M.D.
Karl Sotlar, M.D.
Karin Klingel, M.D.
University Hospital Tübingen
72076 Tübingen, Germany
karin.klingel@med.uni-tuebingen.de
References
Young NS, Brown KE. Parvovirus B19. N Engl J Med 2004;350:586-597.
Bültmann B, Klingel K, Sotlar K, et al. Fatal parvovirus B19-associated myocarditis clinically mimicking ischemic heart disease: an endothelial cell-mediated disease. Hum Pathol 2003;34:92-95.
Baroldi G. Myocardial cell death, including ischemic heart disease and its complications. In: Silver MD, Gotlieb AI, Schoen FJ, eds. Cardiovascular pathology. 3rd ed. New York: Churchill Livingstone, 2001:198-255.
Arnold G, Kaiser C, Fischer R. Myofibrillar degeneration -- a common type of myocardial lesion and its selective identification by a modified Luxol Fast Blue stain. Pathol Res Pract 1985;180:405-415.
Kühl U, Pauschinger M, Bock T, et al. Parvovirus B19 infection mimicking acute myocardial infarction. Circulation 2003;108:945-950.
To the Editor: In their review of parvovirus B19, Young and Brown do not mention associations between this virus and renal diseases. They acknowledge an association with Henoch–Sch?nlein purpura, but recent reports have shown that this virus also has a role in some cases of collapsing focal segmental glomerulosclerosis1 and acute proliferative glomerulonephritis with hypocomplementemia.2 The patients in these cases were otherwise healthy or were renal-transplant recipients. Renal epithelial-cell infections may lead to collapsing focal segmental glomerulosclerosis, whereas parvovirus immune complexes trapped in the subendothelial or mesangial areas of the nephron may lead to proliferative glomerulonephritis. Finally, because of its effects on erythroid progenitors, parvovirus B19 infection should be considered among the possible diagnoses in certain patients with end-stage renal disease who have anemia that does not respond to erythropoietin.3
Paul H. Pronovost, M.D.
Waterbury Hospital
Waterbury, CT 06708
ppronovost@sbcglobal.net
References
Moudgil A, Nast CC, Bagga A, et al. Association of parvovirus B19 infection with idiopathic collapsing glomerulopathy. Kidney Int 2001;59:2126-2133.
Iwafuchi Y, Morita T, Kamimura A, Kunisada K, Ito K, Miyazaki S. Acute endocapillary proliferative glomerulonephritis associated with human parvovirus B19 infection. Clin Nephrol 2002;57:246-250.
Duranay M, Bali M, Sahin M, Yakinci G, Vurgun N, Dilmen U. Parvovirus B19 infection and unresponsiveness to erythropoietin therapy in haemodialysis patients. Nephrol Dial Transplant 1998;13:779-780.
The authors reply: Space constraints prevented us from describing in full detail the potential role of parvovirus B19 in diverse syndromes; such discussions can be found elsewhere.1 As we did mention, parvovirus B19 has been implicated in cardiac disease, although most pathological studies, especially of fetal myocarditis, have suggested that there is direct infection of myocardiocytes.2 Perhaps endothelial involvement represents vasculitis.
As for kidney disease, a number of reports have described the detection of parvovirus B19 in renal tissue.3,4 Tanawattanacharoen and colleagues have also implicated parvovirus B19 in focal segmental glomerulosclerosis,5 although they also were able to detect B19 DNA in two of four patients who had undergone nephrectomy for malignant disease. As with heart disease, the role of B19 is unclear, and vascular infection may be an underlying mechanism in both organs.
Neal S. Young, M.D.
Kevin E. Brown, M.D.
National Heart, Lung, and Blood Institute
Bethesda, MD 20892
youngn@nhlbi.nih.gov
References
T?r?k TJ. Unusual clinical manifestations reported in patients with parvovirus B19 infection. In: Anderson LJ, Young NS, eds. Human parvovirus B19. Vol. 20 of Monographs in virology. Basel, Switzerland: Karger, 1997:61-92.
Porter HJ, Quantrill AM, Fleming KA. B19 parvovirus infection of myocardial cells. Lancet 1988;1:535-536.
Mori Y, Yamashita H, Umeda Y, et al. Association of parvovirus B19 infection with acute glomerulonephritis in healthy adults: case report and review of the literature. Clin Nephrol 2002;57:69-73.
Wierenga KJ, Pattison JR, Brink N, et al. Glomerulonephritis after human parvovirus infection in homozygous sickle-cell disease. Lancet 1995;346:475-476.
Tanawattanacharoen S, Falk RJ, Jennette C, Kopp JB. Parvovirus B19 DNA in kidney tissue of patients with focal segmental glomerulosclerosis. Am J Kidney Dis 2000;35:1166-1174.
Figure 1. Myocardial Tissue from Patients with Parvovirus B19–Associated Myocarditis.
Panel A shows the detection of parvovirus B19 genomes in endothelial cells of a small intramyocardial artery in tissue from a patient with acute myocarditis (radioactive in situ hybridization, x100). Panel B shows myofibrillar degeneration, contraction bands, myocyte necrosis, and inflammation (arrow) in parvovirus B19–associated myocarditis (Luxol fast blue, x80).
Burkhard D. Bültmann, M.D.
Karl Sotlar, M.D.
Karin Klingel, M.D.
University Hospital Tübingen
72076 Tübingen, Germany
karin.klingel@med.uni-tuebingen.de
References
Young NS, Brown KE. Parvovirus B19. N Engl J Med 2004;350:586-597.
Bültmann B, Klingel K, Sotlar K, et al. Fatal parvovirus B19-associated myocarditis clinically mimicking ischemic heart disease: an endothelial cell-mediated disease. Hum Pathol 2003;34:92-95.
Baroldi G. Myocardial cell death, including ischemic heart disease and its complications. In: Silver MD, Gotlieb AI, Schoen FJ, eds. Cardiovascular pathology. 3rd ed. New York: Churchill Livingstone, 2001:198-255.
Arnold G, Kaiser C, Fischer R. Myofibrillar degeneration -- a common type of myocardial lesion and its selective identification by a modified Luxol Fast Blue stain. Pathol Res Pract 1985;180:405-415.
Kühl U, Pauschinger M, Bock T, et al. Parvovirus B19 infection mimicking acute myocardial infarction. Circulation 2003;108:945-950.
To the Editor: In their review of parvovirus B19, Young and Brown do not mention associations between this virus and renal diseases. They acknowledge an association with Henoch–Sch?nlein purpura, but recent reports have shown that this virus also has a role in some cases of collapsing focal segmental glomerulosclerosis1 and acute proliferative glomerulonephritis with hypocomplementemia.2 The patients in these cases were otherwise healthy or were renal-transplant recipients. Renal epithelial-cell infections may lead to collapsing focal segmental glomerulosclerosis, whereas parvovirus immune complexes trapped in the subendothelial or mesangial areas of the nephron may lead to proliferative glomerulonephritis. Finally, because of its effects on erythroid progenitors, parvovirus B19 infection should be considered among the possible diagnoses in certain patients with end-stage renal disease who have anemia that does not respond to erythropoietin.3
Paul H. Pronovost, M.D.
Waterbury Hospital
Waterbury, CT 06708
ppronovost@sbcglobal.net
References
Moudgil A, Nast CC, Bagga A, et al. Association of parvovirus B19 infection with idiopathic collapsing glomerulopathy. Kidney Int 2001;59:2126-2133.
Iwafuchi Y, Morita T, Kamimura A, Kunisada K, Ito K, Miyazaki S. Acute endocapillary proliferative glomerulonephritis associated with human parvovirus B19 infection. Clin Nephrol 2002;57:246-250.
Duranay M, Bali M, Sahin M, Yakinci G, Vurgun N, Dilmen U. Parvovirus B19 infection and unresponsiveness to erythropoietin therapy in haemodialysis patients. Nephrol Dial Transplant 1998;13:779-780.
The authors reply: Space constraints prevented us from describing in full detail the potential role of parvovirus B19 in diverse syndromes; such discussions can be found elsewhere.1 As we did mention, parvovirus B19 has been implicated in cardiac disease, although most pathological studies, especially of fetal myocarditis, have suggested that there is direct infection of myocardiocytes.2 Perhaps endothelial involvement represents vasculitis.
As for kidney disease, a number of reports have described the detection of parvovirus B19 in renal tissue.3,4 Tanawattanacharoen and colleagues have also implicated parvovirus B19 in focal segmental glomerulosclerosis,5 although they also were able to detect B19 DNA in two of four patients who had undergone nephrectomy for malignant disease. As with heart disease, the role of B19 is unclear, and vascular infection may be an underlying mechanism in both organs.
Neal S. Young, M.D.
Kevin E. Brown, M.D.
National Heart, Lung, and Blood Institute
Bethesda, MD 20892
youngn@nhlbi.nih.gov
References
T?r?k TJ. Unusual clinical manifestations reported in patients with parvovirus B19 infection. In: Anderson LJ, Young NS, eds. Human parvovirus B19. Vol. 20 of Monographs in virology. Basel, Switzerland: Karger, 1997:61-92.
Porter HJ, Quantrill AM, Fleming KA. B19 parvovirus infection of myocardial cells. Lancet 1988;1:535-536.
Mori Y, Yamashita H, Umeda Y, et al. Association of parvovirus B19 infection with acute glomerulonephritis in healthy adults: case report and review of the literature. Clin Nephrol 2002;57:69-73.
Wierenga KJ, Pattison JR, Brink N, et al. Glomerulonephritis after human parvovirus infection in homozygous sickle-cell disease. Lancet 1995;346:475-476.
Tanawattanacharoen S, Falk RJ, Jennette C, Kopp JB. Parvovirus B19 DNA in kidney tissue of patients with focal segmental glomerulosclerosis. Am J Kidney Dis 2000;35:1166-1174.