Potential immunological consequences of pharmacological suppression of gastric acid production in patients with multiple sclerosis
dc.contributor.author | Biswas, Sangita | |
dc.contributor.author | Benedict, Stephen H. | |
dc.contributor.author | Lynch, Sharon G. | |
dc.contributor.author | LeVine, Steven M. | |
dc.date.accessioned | 2014-04-18T14:49:28Z | |
dc.date.available | 2014-04-18T14:49:28Z | |
dc.date.issued | 2012-06-07 | |
dc.identifier.citation | Biswas, Sangita, Stephen H Benedict, Sharon G Lynch, and Steven M LeVine. 2012. “Potential Immunological Consequences of Pharmacological Suppression of Gastric Acid Production in Patients with Multiple Sclerosis.” BMC Medicine 10 . http://dx.doi.org/10.1186/1741-7015-10-57 | |
dc.identifier.uri | http://hdl.handle.net/1808/13557 | |
dc.description.abstract | Corticosteroids are standard treatment for patients with multiple sclerosis experiencing acute relapse. Because dyspeptic pain is a common side effect of this intervention, patients can be given a histamine receptor-2 antagonist, proton pump inhibitor or antacid to prevent or ameliorate this disturbance. Additionally, patients with multiple sclerosis may be taking these medications independent of corticosteroid treatment. Interventions for gastric disturbances can influence the activation state of the immune system, a principal mediator of pathology in multiple sclerosis. Although histamine release promotes inflammation, activation of the histamine receptor-2 can suppress a proinflammatory immune response, and blocking histamine receptor-2 with an antagonist could shift the balance more towards immune stimulation. Studies utilizing an animal model of multiple sclerosis indicate that histamine receptor-2 antagonists potentially augment disease activity in patients with multiple sclerosis. In contrast, proton pump inhibitors appear to favor immune suppression, but have not been studied in models of multiple sclerosis. Antacids, histamine receptor-2 antagonists and proton pump inhibitors also could alter the intestinal microflora, which may indirectly lead to immune stimulation. Additionally, elevated gastric pH can promote the vitamin B12 deficiency that patients with multiple sclerosis are at risk of developing. Here, we review possible roles of gastric acid inhibitors on immunopathogenic mechanisms associated with multiple sclerosis. | |
dc.publisher | BioMed Central | |
dc.rights | This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. | |
dc.rights.uri | http://creativecommons.org/licenses/by/2.0 | |
dc.subject | Antacid | |
dc.subject | autoimmune | |
dc.subject | Dyspepsia | |
dc.subject | Experimental autoimmune encephalomyelitis | |
dc.subject | GERD | |
dc.subject | Histamine receptor 2 antagonists | |
dc.subject | multiple sclerosis | |
dc.subject | Proton pump inhibitor | |
dc.title | Potential immunological consequences of pharmacological suppression of gastric acid production in patients with multiple sclerosis | |
dc.type | Article | |
kusw.kuauthor | Benedict, Stephen H. | |
kusw.kudepartment | Molecular Biosciences | |
kusw.oastatus | fullparticipation | |
dc.identifier.doi | 10.1186/1741-7015-10-57 | |
kusw.oaversion | Scholarly/refereed, publisher version | |
kusw.oapolicy | This item meets KU Open Access policy criteria. | |
dc.rights.accessrights | openAccess |
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Except where otherwise noted, this item's license is described as: This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.