High prevalence of hepatitis C antibody and RNA in patients with Sjögren's syndrome
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CORRESPONDENCE High Prevalence of Hepatitis C Antibody and RNA in Patients With Sji~gren's Syndrome Dear Sir: I read with great interest the editorial by Juan- Manuel Anaya and Norman Talal (June 1999, pp 355-359) (1). The authors did not mention the high prevalence of hepatitis C antibody and RNA in patients with Sjtgren's syndrome (SS). Reliable diagnostic assays for hepatitis C virus (HCV) infection were developed in early 1990. Since then, several studies have shown an association between hepatitis C with various extrahepatic manifestations and immunologic disorders: Sjtgren's syndrome, sialad- enitis, membranoproliferative glomemlonephritis, rheu- matoid arthritis, cryoglobulinemia, autoimmune thy- roiditis, lichen planus (LP), uveitis, and markers of autoimmunity, although not autoimmune hepatitis (2, 3). Moreover, HCV, which is detectable in saliva and lymph nodes of patients with chronic hepatitis C, has been associated with squamous cell carcinoma of the head and neck and non-Hodgkin's lymphoma (4, 5). It is unclear, however, whether the co-occurrence of HCV infection is of etiologic significance. Nagao et al (6) reported an issue of great interest: persistence and replication of HCV in oral LP lesions. Neoplastic transformation of lichen plauns is rare, but there is some evidence to suggest that HCV-associated oral LP may have clinically significant premalignant potential (6). These studies have shown the presence of impor- tant immune dysregulation in chronic HCV infec- tion and suggest that cells in the oral region are continuously exposed to HCV virus, which in turn may increase their risk of genetic instability. In SS associated with chronic HCV infection, very in- tense stimulation by antigenic drive may lead to a greater risk of activated B cell transition from polyclonal to oligoclonal and then to lymphoma. I suggest the need for periodic oral cavity and salivary gland examination in patients with HCV, and patients with SS should be monitored through- out for malignant transformation. EDOARD0 CERVONI, MD Genova, Italy REFERENCES 1. Anaya JM, Talal N. Sjogren's syndrome comes of age. Semin Arthritis Rheum 1999;28:355-9. 2. Pawlotsky JM, Yahia MB, Andre C, et al. Immunological disorders in C virus chronic active hepatitis. Hepatology 1994; 19:841-8. 3. Yosida M, Nagao Y, Sata M, et al. Multiple primary neoplasms and HCV infection in oral cancer patients. Hepatol Res 1997;8:173-7. 4. Ferri C, Civita LL, Monti L, et al. Can type C hepatitis infection be complicated by malignant lymphoma? Lancet 1995;346:1426-7. 5. Komiyama K, Moro I, Mastuda Y. HCV in saliva of chronic hepatitis patients having dental treatment. Lancet 1991; 338:572-3. 6. Nagao Y, Kameyama T, Sata M. Hepatitis C virus RNA detection in oral lichen planus tissue. Am J Gastroenterol 1998;93:850. 266 Seminars in Arthritis and Rheumatism, Vo129, No 4 (February), 2000: p 266
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Transcript of High prevalence of hepatitis C antibody and RNA in patients with Sjögren's syndrome
CORRESPONDENCE
High Prevalence of Hepatitis C Antibody and RNA in Patients
With Sji~gren's Syndrome Dear Sir:
I read with great interest the editorial by Juan- Manuel Anaya and Norman Talal (June 1999, pp 355-359) (1). The authors did not mention the high prevalence of hepatitis C antibody and RNA in patients with Sjtgren's syndrome (SS). Reliable diagnostic assays for hepatitis C virus (HCV) infection were developed in early 1990. Since then, several studies have shown an association between hepatitis C with various extrahepatic manifestations and immunologic disorders: Sjtgren's syndrome, sialad- enitis, membranoproliferative glomemlonephritis, rheu- matoid arthritis, cryoglobulinemia, autoimmune thy- roiditis, lichen planus (LP), uveitis, and markers of autoimmunity, although not autoimmune hepatitis (2, 3). Moreover, HCV, which is detectable in saliva and lymph nodes of patients with chronic hepatitis C, has been associated with squamous cell carcinoma of the head and neck and non-Hodgkin's lymphoma (4, 5). It is unclear, however, whether the co-occurrence of HCV infection is of etiologic significance. Nagao et al (6) reported an issue of great interest: persistence and replication of HCV in oral LP lesions. Neoplastic transformation of lichen plauns is rare, but there is some evidence to suggest that HCV-associated oral LP may have clinically significant premalignant potential (6).
These studies have shown the presence of impor-
tant immune dysregulation in chronic HCV infec- tion and suggest that cells in the oral region are continuously exposed to HCV virus, which in turn may increase their risk of genetic instability. In SS associated with chronic HCV infection, very in- tense stimulation by antigenic drive may lead to a greater risk of activated B cell transition from polyclonal to oligoclonal and then to lymphoma. I suggest the need for periodic oral cavity and salivary gland examination in patients with HCV, and patients with SS should be monitored through- out for malignant transformation.
EDOARD0 CERVONI, MD Genova, Italy
REFERENCES
1. Anaya JM, Talal N. Sjogren's syndrome comes of age. Semin Arthritis Rheum 1999;28:355-9.
2. Pawlotsky JM, Yahia MB, Andre C, et al. Immunological disorders in C virus chronic active hepatitis. Hepatology 1994; 19:841-8.
3. Yosida M, Nagao Y, Sata M, et al. Multiple primary neoplasms and HCV infection in oral cancer patients. Hepatol Res 1997;8:173-7.
4. Ferri C, Civita LL, Monti L, et al. Can type C hepatitis infection be complicated by malignant lymphoma? Lancet 1995;346:1426-7.
5. Komiyama K, Moro I, Mastuda Y. HCV in saliva of chronic hepatitis patients having dental treatment. Lancet 1991; 338:572-3.
6. Nagao Y, Kameyama T, Sata M. Hepatitis C virus RNA detection in oral lichen planus tissue. Am J Gastroenterol 1998;93:850.
266 Seminars in Arthrit is and Rheumatism, Vo129, No 4 (February), 2000: p 266
