Objective. Helicobacter pylori provokes a host of immune alterations upon colonizing the gastric mucosa. Design. We report 22 individuals with confirmed Helicobacter pylori infection who were also managed for the concurrent elevation of immunoglobulin free light chain (kappa and lambda) levels. Result. Of the 22 patients, 15 patients (68.2%) had elevated free light chain levels: 6 patients (40%) had only kappa chain elevation, 2 patients (13.3%) had only lambda chain elevation, and 7 patients (46.7%) had both kappa and lambda chain elevation. Twenty out of the 22 patients (90.9%) were microbiologically confirmed cured with 3 patients being lost to follow-up for repeat levels. Of the 3 patients who were lost to follow-up, 1 patient had only kappa chain elevation, 1 patient had only lambda chain elevation, and 1 patient had both kappa and lambda chain elevation. For those who were cured (19 patients), 5 patients with kappa elevation had normalized values, 4 patients with lambda elevation had normalized values, and 2 patients with combined kappa and lambda elevation had normalized values. For 6 out of the 19 patients, the light chain levels remained elevated. Conclusion. We speculate that the Helicobacter pylori infection disrupts the immunoglobulin system with potential implications being discussed below. 1. Introduction Helicobacter pylori is one of the most pervasive bacterial pathogens worldwide and is associated with an increased risk of gastritis, gastric and duodenal ulcers, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma [1, 2]. Indeed, it has been nearly three decades since the Australian physicians Warren and Marshall first isolated the pathogen and elucidated its association with gastric and duodenal ulcers as well as gastritis, leading to significant research towards the treatment of these gastrointestinal disorders [3]. While the incidence of the H. pylori infection varies largely by socioeconomic status, geographic region, age, and race, approximately one-half of the world’s population has been estimated to be infected, with the prevalence ranging from 30 to 40 percent in the United States [4, 5]. In fact, in the United States, the prevalence increases from less than 20% at 20 years of age to nearly 50% at 50 years of age [6]. Today, with the advent of the newer concomitant quadruple therapy, the eradication of H. pylori has experienced success rates greater than 90 percent [7, 8]. In a patient with light chain deposition disease, a transient increase in light chain levels was observed upon H. pylori
References
[1]
W. D. Chey and B. C. Y. Wong, “American College of Gastroenterology guideline on the management of Helicobacter pylori infection,” American Journal of Gastroenterology, vol. 102, no. 8, pp. 1808–1825, 2007.
[2]
T. L. Cover and M. J. Blaser, “Helicobacter pylori in health and disease,” Gastroenterology, vol. 136, no. 6, pp. 1863–1873, 2009.
[3]
B. J. Marshall and J. R. Warren, “Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration,” The Lancet, vol. 1, no. 8390, pp. 1311–1315, 1984.
[4]
R. Menon, A. Riera, and A. Ahmad, “A global perspective on gastrointestinal diseases,” Gastroenterology Clinics of North America, vol. 40, no. 2, pp. 427–439, 2011.
[5]
J. G. Smith, W. Li, and R. S. Rosson, “Prevalence, clinical and endoscopic predictors of Helicobacter pylori infection in an urban population,” Connecticut Medicine, vol. 73, no. 3, pp. 133–137, 2009.
[6]
C. P. Dooley, H. Cohen, P. L. Fitzgibbons et al., “Prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic persons,” The New England Journal of Medicine, vol. 321, no. 23, pp. 1562–1566, 1989.
[7]
D. C. Wu, P. I. Hsu, et al., “Sequential and concomitant therapy with four drugs is equally effective for eradication of H. pylori infection,” Clinical Gastroenterology and Hepatology, vol. 8, no. 1, pp. 36.e1–41.e1, 2010.
[8]
A. Zullo, V. De Francesco, C. Hassan, S. Morini, and D. Vaira, “The sequential therapy regimen for Helicobacter pylori eradication: a pooled-data analysis,” Gut, vol. 56, no. 10, pp. 1353–1357, 2007.
[9]
J. P. Gisbert and J. M. Pajares, “Stool antigen test for the diagnosis of Helicobacter pylori infection: a systematic review,” Helicobacter, vol. 9, no. 4, pp. 347–368, 2004.
[10]
T. Azuma, J. Konishi, Y. Tanaka et al., “Contribution of HLA-DQA gene to host's response against Helicobacter pylori,” The Lancet, vol. 343, no. 8896, pp. 542–543, 1994.
[11]
C. K. Lee, R. Weltzin, W. D. Thomas Jr. et al., “Oral immunization with recombinant Helicobacter pylori urease induces secretory IgA antibodies and protects mice from challenge with Helicobacter felis,” Journal of Infectious Diseases, vol. 172, no. 1, pp. 161–172, 1995.
[12]
M. Marchetti, B. Arico, D. Burroni, N. Figura, R. Rappuoli, and P. Ghiara, “Development of a mouse model of Helicobacter pylori infection that mimics human disease,” Science, vol. 267, no. 5204, pp. 1655–1658, 1995.
[13]
M. M. D'Elios, M. Manghetti, F. Almerigogna et al., “Different cytokine profile and antigen-specificity repertoire in Helicobacter pylori-specific T cell clones from the antrum of chronic gastritis patients with or without peptic ulcer,” European Journal of Immunology, vol. 27, no. 7, pp. 1751–1755, 1997.
[14]
S. Licci, P. Sette, F. Del Normo, S. Ciarletti, A. Antlnort, and L. Morellt, “Russell body gastritis associated with Helicobacter pylori Infection in an HIV-positive patient: case report and review of the literature,” Zeitschrift fur Gastroenterologie, vol. 47, no. 4, pp. 357–360, 2009.
[15]
S. Paik, S.-H. Kim, J.-H. Kim, W. I. Yang, and Y. C. Lee, “Russell body gastritis associated with Helicobacter pylori infection: a case report,” Journal of Clinical Pathology, vol. 59, no. 12, pp. 1316–1319, 2006.
[16]
A. Ensari, B. Savas, A. O. Heper, I. Kuzu, and R. Idilman, “An unusual presentation of Helicobacter pylori infection: so-called ‘Russell body gastritis’,” Virchows Archiv, vol. 446, no. 4, pp. 463–466, 2005.
[17]
Y. Leal-Herrera, J. Torres, G. Perez-Perez et al., “Serologic IgG response to urease in Helicobacter pylori-infected persons from Mexico,” American Journal of Tropical Medicine and Hygiene, vol. 60, no. 4, pp. 587–592, 1999.
[18]
M. J. Blaser, “Role of vacA and the cagA locus of Helicobacter pylori in human disease,” Alimentary Pharmacology and Therapeutics, Supplement, vol. 10, supplement 1, pp. 73–77, 1996.
[19]
S. J. Spechler, L. Fischbach, and M. Feldman, “Clinical aspects of genetic variability in Helicobacter pylori,” Journal of the American Medical Association, vol. 283, no. 10, pp. 1264–1266, 2000.
[20]
Z. Xiang, S. Censini, P. F. Bayeli et al., “Analysis of expression of CagA and VacA virulence factors in 43 strains of Helicobacter pylori reveals that clinical isolates can be divided into two major types and that CagA is not necessary for expression of the vacuolating cytotoxin,” Infection and Immunity, vol. 63, no. 1, pp. 94–98, 1995.
[21]
T. Wiedemann, E. Loell, S. Mueller et al., “Helicobacter pylori cag-pathogenicity island-dependent early immunological response triggers later precancerous gastric changes in Mongolian gerbils,” PLoS ONE, vol. 4, no. 3, Article ID e4754, 2009.
[22]
P. Olbermann, C. Josenhans, Y. Moodley et al., “A global overview of the genetic and functional diversity in the Helicobacter pylori cag pathogenicity island,” PLoS Genetics, vol. 6, no. 8, Article ID e1001069, 2010.
[23]
M. Hatakeyama, “SagA of CagA in Helicobacter pylori pathogenesis,” Current Opinion in Microbiology, vol. 11, no. 1, pp. 30–37, 2008.
[24]
J. Wei, T. A. Nagy, A. Vilgelm et al., “Regulation of p53 tumor suppressor by Helicobacter pylori in gastric epithelial cells,” Gastroenterology, vol. 139, no. 4, pp. 1333–1343, 2010.
[25]
J. P. Thiery, “Epithelial-mesenchymal transitions in tumor progression,” Nature Reviews Cancer, vol. 2, no. 6, pp. 442–454, 2002.
[26]
J. Kountouras, C. Zavos, D. Chatzopoulos, and P. Katsinelos, “New aspects of Helicobacter pylori infection involvement in gastric oncogenesis,” Journal of Surgical Research, vol. 146, no. 1, pp. 149–158, 2008.
[27]
J. Lan, Y. Xiong, Y. Lin et al., “Helicobacter pylori infection generated gastric cancer through p53-Rb tumor-suppressor system mutation and telomerase reactivation,” World Journal of Gastroenterology, vol. 9, no. 1, pp. 54–58, 2003.
[28]
F. Shanahan, “Gut microbes: from bugs to drugs,” American Journal of Gastroenterology, vol. 105, no. 2, pp. 275–279, 2010.
[29]
B. Terrier, D. Sène, D. Saadoun et al., “Serum-free light chain assessment in hepatitis C virus-related lymphoproliferative disorders,” Annals of the Rheumatic Diseases, vol. 68, no. 1, pp. 89–93, 2009.
