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Clavulanic Acid in the Scope of Helicobacter pylori Treatment: A Literature Review and Beyond.
Current Clinical Pharmacology 2020 July 3
BACKGROUND: Helicobacter pylori (H.pylori) infection is the most common cause of peptic ulcer disease and it can be associated with many complications including malignancies. In clinical practice, some clinicians may use clavulanic acid (CA) in combination with amoxicillin or other beta-lactams as an addition to the standard treatment regimens. This practice may be made by habitual mistake, non-evidence based hypothetical assumptions, or by prescribing it as an alternative treatment. This review aims to expose the effect of CA against H.pylori infection and to review the possible mechanisms that may contribute to that effect.
METHODS: A PubMed and Google Scholar literature search was obtained on both pre-clinical and clinical studies related to CA and H.pylori infection.
RESULTS: Available clinical studies showed improvement in the eradication of H. pylori by about 10-20% when CA was added to the treatment regimens. This effect for CA could be related to several mechanisms including inhibition of H. pylori growth by binding to penicillin-binding proteins (PBPs), the transformation of H. pylori from the active filamentous form into coccoidal form, induction of the release of dopamine, modulation of immunological response towards H. pylori infection and its relationship with other microbiota. Randomized-controlled studies on patients with resistance H. pylori are needed. Moreover, In_vitro studies to evaluate the mechanisms by which CA may influence H. pylori are warranted.
CONCLUSION: The presented literature suggests potential avenues for the use of CA in the management of peptic ulcer disease and H.pylori infection.
METHODS: A PubMed and Google Scholar literature search was obtained on both pre-clinical and clinical studies related to CA and H.pylori infection.
RESULTS: Available clinical studies showed improvement in the eradication of H. pylori by about 10-20% when CA was added to the treatment regimens. This effect for CA could be related to several mechanisms including inhibition of H. pylori growth by binding to penicillin-binding proteins (PBPs), the transformation of H. pylori from the active filamentous form into coccoidal form, induction of the release of dopamine, modulation of immunological response towards H. pylori infection and its relationship with other microbiota. Randomized-controlled studies on patients with resistance H. pylori are needed. Moreover, In_vitro studies to evaluate the mechanisms by which CA may influence H. pylori are warranted.
CONCLUSION: The presented literature suggests potential avenues for the use of CA in the management of peptic ulcer disease and H.pylori infection.
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