Vedolizumab Safety During Pregnancy and Lactation in a Patient with Ulcerative Colitis: A Case Report.

Background: Inflammatory bowel disease (IBD) affects young adults of reproductive age, and questions related to pregnancy and breastfeeding are common in clinical practice. Most medications used to treat IBD are considered safe during pregnancy, except methotrexate and small molecules such as tofacitinib. Despite few studies regarding vedolizumab (VDZ) safety, it appears to be safe during pregnancy. Therefore, this study aimed to report the management of ulcerative colitis in pregnant patient refractory to anti-tumor necrosis factor (TNF) agents using VDZ. Case Report: A female, 38 years old, with ulcerative colitis was refractory to conventional treatment with mesalazine, sulfasalazine, and azathioprine. She was hospitalized at six weeks of gestation with severe acute colitis requiring the use of infliximab (IFX) to induce remission. She had a spontaneous abortion at nine weeks of gestation after the second dose of IFX. Since there was no endoscopic improvement after six months of IFX treatment, VDZ treatment was initiated. During the VDZ infusion period, the patient discovered that she was pregnant with twins, leading to the discussion of the risks and benefits of continuing the VDZ. The patient presented with disease clinical remission with the use of VDZ, and the babies were born at 34 weeks of gestation without complications. Breastfeeding was also performed without complications. Conclusion: Continued VDZ medication is safe during pregnancy and breastfeeding, with adverse events similar to anti-TNF therapy.

Acute heart failure as an adverse event of tumor necrosis factor inhibitor therapy in inflammatory bowel disease: A review of the literature.

Tumor necrosis factor inhibitors (anti-TNFs) are widely used therapies for the treatment of inflammatory bowel diseases (IBD); however, their administration is not risk-free. Heart failure (HF), although rare, is a potential adverse event related to administration of these medications. However, the exact mechanism of development of HF remains obscure. TNFα is found in both healthy and damaged hearts. Its effects are concentration- and receptor-dependent, promoting either cardio-protection or cardiomyocyte apoptosis. Experimental rat models with TNFα receptor knockout showed increased survival rates, less reactive oxygen species formation, and improved diastolic left ventricle pressure. However, clinical trials employing anti-TNF therapy to treat HF had disappointing results, suggesting abolishment of the cardioprotective properties of TNFα, making cardiomyocytes susceptible to apoptosis and oxidation. Thus, patients with IBD who have risk factors should be screened for HF before initiating anti-TNF therapy. This review aims to discuss adverse events associated with the administration of anti-TNF therapy, with a focus on HF, and propose some approaches to avoid cardiac adverse events in patients with IBD.