2009
DOI: 10.1345/aph.1k288a
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Comment: Mesalamine-Associated Hypersensitivity Myocarditis in Ulcerative Colitis and the Kounis Syndrome

Abstract: exclude contemporarycoronary mast cell activationmanifestingas KS. However,this report shows that HSM and KS are very rarelydiagnosed diseasesratherthan very rare diseases.

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Cited by 8 publications
(5 citation statements)
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“…Yet, the exact mechanism by which mesalamine might prompt myocardial inflammation is not clearly identified. Rarely, mesalamine can induce hypersensitive reactions such as, hypersensitivity pneumonitis, angioedema, skin rashes, hypereosinophilia and thus, a mechanism of hypersensitivity to the drug rather than a direct cytotoxic effect is suspected [16]. The diagnosis of hypersensitivity myocarditis (HSM) is also suggested by the fact that, in all of the cases identified as being the result of mesalamine toxicity [13], there had been a clear improvement following the discontinuation of the drug.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Yet, the exact mechanism by which mesalamine might prompt myocardial inflammation is not clearly identified. Rarely, mesalamine can induce hypersensitive reactions such as, hypersensitivity pneumonitis, angioedema, skin rashes, hypereosinophilia and thus, a mechanism of hypersensitivity to the drug rather than a direct cytotoxic effect is suspected [16]. The diagnosis of hypersensitivity myocarditis (HSM) is also suggested by the fact that, in all of the cases identified as being the result of mesalamine toxicity [13], there had been a clear improvement following the discontinuation of the drug.…”
Section: Discussionmentioning
confidence: 99%
“…Different mechanisms could explain HSM but the exact one has not yet been identified. The most probable hypothesis seems to be an inhibition of cyclooxygenase-1 (COX1) by the drug, which may accelerate the metabolism of arachidonic acid toward lipoxygenase products such as, leukotrienes [6]. This overproduction of leukotriene metabolites may induce proinflammatory signaling, initiating the hypersensitive reaction by liberating eosinophil-stimulating cytokines, and will lead to the myocarditis.…”
Section: Discussionmentioning
confidence: 99%
“…Hypersensitivity reaction is probably a result of accelerated metabolism of arachidonic acid to leukotrienes due to cyclooxygenase-1 enzyme inhibition. Leukotrienes in turn result in overproduction of eosinophil stimulating cytokines which cause a hypersensitivity reaction resulting in myocarditis [16,17]. Hypersensitivity due to humoral-mediated response has also been suggested resulting in the formation of antibodies against mesalazine, with cross-reactivity to myocardium or pericardium [18].…”
Section: Mechanism Of Mesalazine Related Cardiotoxicitymentioning
confidence: 99%
“…Kounis et al explained the possible mechanism of the inhibition of cyclooxigenase-1 enzyme (COX-1) and, thus, overproduction of leucotriens which further promote an initiation of hypersensitivity reaction via eosinophil secreting factor induced by proinflammatory signals and, eventually, causing myocarditis. The relationship between mesalazine and myocarditis is thought to be due to hypersensitivity reaction rather than cytotoxic effects (2,3). Previous studies showed eosinophilic infiltration of the myocard in mesalazine associated myocarditis in biopsy (4).…”
Section: öZetmentioning
confidence: 99%
“…Mesalazine associated eosinophilic myocarditis or giant cell myocarditis was considered in our case. Because a provocative test with etiologic agent could lead fatal damage, it was not performed (2)(3)(4). Similarly, we did not perfom an endomyocardial biopsy because the patient refused to consent to the biopsy.…”
Section: öZetmentioning
confidence: 99%