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Hepatitis C and Cancer
- Mark A. Marinella, MD; and
- Richard H. Moseley, MD
- Wright State University School of Medicine, Dayton, OH 45429 Veterans Affairs Medical Center, Ann Arbor, MI 48109
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
TO THE EDITOR:
We read with interest the recent review article by Sharara and coworkers [1]. The authors mention the role of hepatitis C virus (HCV) in the pathogenesis of hepatocellular carcinoma and note that HCV does not integrate into the host genome. Chronic HCV infection has also been implicated in various autoimmune phenomenon, including essential mixed cryoglobulinemia, membranoproliferative glomerulonephritis, porphyria cutanea tarda, and autoimmune thyroiditis [2]. Hepatitis C virus is a lymphotrophic virus that supports the association between chronic HCV infection and the clonal B-cell proliferation that occurs with mixed cryoglobulinemia [3]. Recently, HCV was reported to be a risk factor for the development of non-Hodgkin B-cell lymphoma, notably low-grade lymphoma [3, 4]. Ferri and colleagues [3] have detected markers to HCV in as many as 33% of unselected patients with non-Hodgkin B-cell lymphoma.
We recently described a patient with chronic HCV infection who developed chronic lymphocytic leukemia, a malignancy of mature CD5-positive B lymphocytes [5]. Because chronic lymphocytic leukemia is occasionally associated with autoimmune disorders, such as systemic lupus erythematosus and rheumatoid arthritis, it is plausible that chronic HCV infection may trigger antigen-driven proliferation of CD5 B lymphocytes, eventually culminating in chronic lymphocytic leukemia. Because a substantial portion of the U.S. population is infected with HCV, lymphoreticular malignant conditions, including chronic lymphocytic leukemia, may become more evident in the future.
Mark A. Marinella, MD
Wright State University School of Medicine; Dayton, OH 45429
Richard H. Moseley, MD
Veterans Affairs Medical Center; Ann Arbor, MI 48109
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
