Letters To The Editor Open Access
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World J Gastroenterol. Feb 21, 2010; 16(7): 914-914
Published online Feb 21, 2010. doi: 10.3748/wjg.v16.i7.914
Monocyte chemotactic protein-1 gene polymorphism and spontaneous bacterial peritonitis
Levent Filik, Gastroenterology Division, Ankara Research Hospital, Ankara, TR06600, Turkey
Author contributions: Filik L wrote the paper.
Correspondence to: Dr. Levent Filik, Associate Professor, Gastroenterology Division, Ankara Research Hospital, Ankara, TR06600, Turkey. leventfilik@yahoo.co.uk
Telephone: +90-505-2653075 Fax: +90-312-5954272
Received: December 4, 2009
Revised: December 15, 2009
Accepted: December 22, 2009
Published online: February 21, 2010

Abstract

I read with great interest the article by Gäbele et al published in issue 44 of World J Gastroenterol 2009. The results of their study indicate that -2518 Monocyte chemotactic protein-1 (MCP-1) genotype AA is a risk factor for spontaneous bacterial peritonitis in patients with alcoholic cirrhosis. However, there are some items that need to be discussed.

Key Words: Spontaneous bacterial peritonitis, Monocyte chemotactic protein-1, Polymorphism



TO THE EDITOR

I read with great interest the article by Gäbele et al[1] published in issue 44 of World J Gastroenterol 2009. The article provides important data. The results of their study indicate that the -2518 Monocyte chemotactic protein-1 (MCP-1) genotype AA is a risk factor for spontaneous bacterial peritonitis (SBP) in patients with alcoholic cirrhosis. The authors suggested that the reduced MCP-1 ascites level may a cause for patients with SBP compared to those with G allele. However, there are some items that need to be discussed. It is debatable to get this conclusion unless ascites MCP-1 levels are measured before and after the treatment of SBP. It has been reported that the MCP-1 level in both sera and ascites is higher in SBP than in non-SBP patients, and decreases after treatment[2]. Infection other than SBP data is also missed in that article. For example, urinary tract infection and even asymptomatic bacteriuria may precede SBP. It is not easy to decide if MCP-1 polymorphism causes urinary tract infection and subsequently SBP, because MCP-1 plays a role even in asymptomatic bacteriuria[3]. Another issue of my concern is the number of SBP episodes. No data in relation with repeated SBP were provided in the article. Did the authors observe repeated SBP episodes in the patients with genotype AA over a 6-year period between 2001-2007? Did the patients respond to the antibiotic therapy well in a similar time interval?

Footnotes

Peer reviewers: Dr. Sang Geon Kim, PhD, MS, BS, Professor, Chairman, College of Pharmacy, Seoul National University, Sillim-dong, Kwanak-gu, Seoul 151-742, South Korea; Robert Flisiak, PhD, Department of Infectious Diseases, Medical University of Bialystok, 15-540 Bialystok, Zurawia Str., 14, Poland

S- Editor Wang YR L- Editor Wang XL E- Editor Lin YP

References
1.  Gäbele E, Mühlbauer M, Paulo H, Johann M, Meltzer C, Leidl F, Wodarz N, Wiest R, Schölmerich J, Hellerbrand C. Analysis of monocyte chemotactic protein-1 gene polymorphism in patients with spontaneous bacterial peritonitis. World J Gastroenterol. 2009;15:5558-5562.  [PubMed]  [DOI]  [Cited in This Article: ]
2.  Kim JK, Chon CY, Kim JH, Kim YJ, Cho JH, Bang SM, Ahn SH, Han KH, Moon YM. Changes in serum and ascitic monocyte chemotactic protein-1 (MCP-1) and IL-10 levels in cirrhotic patients with spontaneous bacterial peritonitis. J Interferon Cytokine Res. 2007;27:227-230.  [PubMed]  [DOI]  [Cited in This Article: ]
3.  Reyes L, Reinhard M, Brown MB. Different inflammatory responses are associated with Ureaplasma parvum-induced UTI and urolith formation. BMC Infect Dis. 2009;9:9.  [PubMed]  [DOI]  [Cited in This Article: ]