Molecular Assessment Of Epstein–Barr Virus In Patients With Macular Amyloidosis
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Abstract
An eosinophilic hyaline precipitate and special staining features are symptomatic of amyloidosis. Macular amyloidosis, which occurs only on the skin, is a result of several different factors. Considering that Epstein-Barr virus (EBV) was detected in this lesion, it seems likely that it could factor into the pathogenesis of this disease. The purpose. The EBV DNA was detected with PCR in 30 samples from patients with macular amyloidosis and 31 healthy samples taken from the margins of melanocytic nevi removed from patients. Results. Twenty-three patients tested positive for the BLLF1 gene of EBV in the control and eight in the case groups. A significant difference in EBV DNA levels was not observed between macular amyloidosis or control groups (P<0.08). Based on the findings of this study, EBV does not cause macular amyloidosis.
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References
Fernandez-Flores, “Cutaneous amyloidosis: a concept review,” The American Journal of Dermatopathology, 34(1), 2012, 1–14,.
J. T. Al-Ratrout and M. B. Satti, et al. “Primary localized cutaneous amyloidosis: a clinicopathologic study from Saudi Arabia,” International Journal of Dermatology, 36(6), 1997, 428–434,
Bandhlish, A. Aggarwal, and R. Koranne, et al., “A clinico- epidemiological study of macular amyloidosis from North India,” Indian Journal of Dermatology, 57(4), 2012, 269– 274.
Y. Horiguchi, J.-D. Fine, I. M. Leigh, T. Yoshiki, M. Ueda, and S. Imamura, et al., “Lamina densa malformation involved in histoge- nesis of primary localized cutaneous amyloidosis,” Journal of Investigative Dermatology, 99(1), 1992, 12–18,.
H. Kobayashi and K. Hashimoto, “Amyloidogenesis in organ- limited cutaneous amyloidosis: an antigenic identity between epidermal keratin and skin amyloid,” Journal of Investigative Dermatology, 80(1), 1983, 66–72.
D. M. Touart and P. Sau, et al., “Cutaneous deposition diseases: part I,” Journal of the American Academy of Dermatology, vol. 39(2), 1998, 149–171,
W.-J. Wang, C.-Y. Huang, Y.-T. Chang, and C.-K. Wong, et al., “Anosacral cutaneous amyloidosis: a study of 10 Chinese cases,” British Journal of Dermatology, 143(6), 2000, 1266–1269,
V. Eswaramoorthy, I. Kaur, A. Das, and B. Kumar, et al., “Macular amyloidosis: etiological factors,” The Journal of Dermatology, 26(5), 1999, 305–310,
A.-G. Kibbi, N. G. Rubeiz, S. T. Zaynoun, and A. K. Kurban, et al., “Primary localized cutaneous amyloidosis,” International Journal of Dermatology, 31(2), 1992, 95–98,
Y. T. Chang, C. K. Wong, K. C. Chow, and C. H. Tsai, et al., “Apoptosis in primary cutaneous amyloidosis,” British Journal of Dermatology, 140(2), 1999, 210–215,
Rasi, A. Khatami, and S. M. Javaheri, et al., “Macular amyloidosis: an assessment of prevalence, sex, and age,” International Journal of Dermatology, 43(12), 2004, 898–899,
V. K. Somani, H. Shailaja, V. N. V. L. Sita, and F. Razvi, et al., “Nylon friction dermatitis: a distinct subset of macular amyloidosis,” Indian Journal of Dermatology, Venereology and Leprology, 61(3), 1995, 145–147,
L. Onuma, M. Vega, R. Arenas, and L. Dominguez, et al.,“Friction amyloidosis,” International Journal of Dermatology, 33(1), 1994, 74,
M. Siragusa, R. Ferri, V. Cavallari, and C. Schepis, et al., “Friction melanosis, friction amyloidosis, macular amyloidosis, towel melanosis: many names for the same clinical entity,” European Journal of Dermatology, 11(6), 2001, 545–548,
D. D. Lee, C. K. Huang, P. C. Ko, Y. T. Chang, W. Z. Sun, and Y. J. et al., Oyang, “Association of primary cutaneous amyloidosis with atopic dermatitis: a nationwide population-based study in Taiwan,” British Journal of Dermatology, 164(1), 2011, 148– 153,
Tanaka, K. Arita, J. E. Lai-Cheong, F. Palisson, M. Hide, and J. A. McGrath, et al., “New insight into mechanisms of pruritus from molecular studies on familial primary localized cutaneous amyloidosis,” British Journal of Dermatology, 161(6), 2009, 1217–1224,
M. J. Dahdah, M. Kurban, A.-G. Kibbi, and S. Ghosn, et al., “Primary localized cutaneous amyloidosis: a sign of immune dysregula- tion?” International Journal of Dermatology, 48(4), 2009, 419–421,
F. Drago, E. Ranieri, A. Pasturino, S. Casazza, F. Crovato, and A. Rebora, (1996). “Epstein-Barr virus-related primary cutaneous amy- loidosis. Successful treatment with acyclovir and interferon- alpha,” British Journal of Dermatology, 134(1), 170– 174.
Y. T. Chang, H. N. Liu, C. K. Wong, K. C. Chow, and K. Y. Chen, et al., “Detection of Epstein-Barr virus in primary cutaneous amyloidosis,” British Journal of Dermatology, 136(6), 1997, 823–826,.
N. Suh, H. Liapis, J. Misdraji, E. M. Brunt, and H. L. Wang, et al., “Epstein-Barr virus hepatitis: diagnostic value of in situ hybridization, polymerase chain reaction, and immunohisto- chemistry on liver biopsy from immunocompetent patients,” American Journal of Surgical Pathology, 31(9), 2007, 1403– 1409.
Z.-L. Qi, X.-Q. Han, J. Hu et al., “Comparison of three methods for the detection of Epstein-Barr virus in Hodgkin’s lymphoma in paraffin-embedded tissues,” Molecular Medicine Reports, 7, 189–92,
Janz, M. Oezel, C. Kurzeder, et al., “Infectious Epstein-Barr virus lacking major glycoprotein BLLF1 (gp350/220) demon- strates the existence of additional viral ligands,” Journal of Virology, 74(21), 2000, 10142–10152,