Analysis of clinical characteristics of mesalazine-induced cardiotoxicity

Abstract

Background: Mesalazine is the first-line inflammatory bowel disease (IBD) treatment. However, it can cause fatal cardiotoxicity. We aimed to analyze the clinical characteristics of mesalazine-induced cardiotoxicity and provide evidence for clinical diagnosis, treatment, and prevention.Methods: We collected Chinese and English literature on mesalazine-induced cardiotoxicity from 1970 to 2021 for retrospective analysis.Results: A total of 52 patients (40 males and 12 females) were included, with a median age of 24.5 years (range 9–62) and a median onset time of 14 days (range 2–2880). Cardiotoxicity manifested as myocarditis, pericarditis, and cardiac pericarditis. The main clinical manifestations are chest pain (82.7%), fever (46.2%), and respiratory symptoms such as dyspnea and cough (40.4%). The levels of troponin T, creatine kinase, C-reactive protein, leukocyte count, erythrocyte sedimentation rate, and other biochemical markers were significantly increased. Cardiac imaging often suggests myocardial infarction, pericardial effusion, myocardial necrosis, and other symptoms of cardiac injury. It is essential to discontinue mesalamine immediately in patients with cardiotoxicity. Although corticosteroids are a standard treatment option, the benefits remain to be determined. Re-challenge of mesalamine should be carefully considered as cardiotoxic symptoms may reoccur.Conclusion: Mesalazine may cause cardiotoxicity in patients with inflammatory bowel disease, which should be comprehensively diagnosed based on clinical manifestations, biochemical indicators, and cardiac function imaging examinations. Mesalazine should be immediately discontinued, and corticosteroids may be an effective treatment for cardiotoxicity.

Berberine Alleviates Doxorubicin-Induced Myocardial Injury and Fibrosis by Eliminating Oxidative Stress and Mitochondrial Damage via Promoting Nrf-2 Pathway Activation

“…LVEDD and LVESD were increased in the Ber-pretreated group compared with the DOX group ( Figure 1 A,B). Usually, cardiac injury is accompanied by the release of enzymes such as creatine kinase (CK) into the blood [ 36 ]. In our study, as shown in Figure 1 C, DOX increased serum CK levels from 1378.8 ± 225.1 U to 2640 ± 443.8 U. Pretreatment with Ber markedly reduced the elevated CK content to 1586.5 ± 170.8 U.…”

Myocarditis Related to the Use of Mesalazine

“…Mesalazine has been shown to inhibit the activity of COX1 and enhance the metabolism of arachidonic acid into lipoxygenase products such as leukotrienes. The excessive production of lipoxygenase products can contribute to a pro-inflammatory signaling cascade, thereby promoting the development of allergic myocarditis [ 12 ]. This process involves the release of cytokines that stimulate eosinophils, leading to inflammation.…”

“…Furthermore, mesalazine has been found to induce the formation of reactive oxygen species, which disrupt mitochondrial membrane. This causes mitochondrial dysfunction and subsequent release of cytochrome c, eventually leading to cardiomyocyte apoptosis and eventually to cardiovascular dysfunction [ 12 ].…”

“…The study findings revealed no apparent link between the dosage of mesalazine and the occurrence of myocardial injury. Additionally, increasing the dose of mesalazine did not lead to a shorter onset time for cardiotoxicity [ 12 ]. These observations suggest that there is no apparent dose-dependent relationship between mesalazine and the development of myocardial injury or the timing of cardiotoxic manifestations.…”