Atrial fibrillation (AF) is a common cardiac arrhythmia that is associated with severe consequences, including symptoms, hemodynamic instability, increased cardiovascular mortality, and stroke. While other arrhythmias such as torsades de pointes and sinus bradycardia are more typically thought of as drug-induced, AF may also be precipitated by drug therapy, although ascribing causality to drug-associated AF is more difficult than with other drug-induced arrhythmias. Drug-induced AF is more likely to occur in patients with risk factors and comorbidities that commonly coexist with AF, such as advanced age, alcohol consumption, family history of AF, hypertension, thyroid dysfunction, sleep apnea, and heart disease. New-onset AF has been associated with cardiovascular drugs such as adenosine, dobutamine, and milrinone. In addition, medications such as corticosteroids, ondansetron, and antineoplastic agents such as paclitaxel, mitoxantrone, and anthracyclines have been reported to induce AF. Whether bisphosphonate drugs are associated with new onset AF remains controversial and requires further study. The potential contribution of specific drug therapy should be considered when patients present with new onset AF.

Both calcium channel blockers (CCBs) and β blockers (BBs) are associated with fatal substance exposures within the United States. Cases of overdose with these agents have the potential to be both complex and difficult to manage. A variety of pharmacologic treatment options are available for clinicians to use to help mitigate harm from these poisonings. Hyperinsulinemic-euglycemic therapy (HIET) was once regarded as a last-ditch effort to treat patients in highly refractory cases. In recent years, this therapy has become a routine therapy in the treatment of CCB/BB overdose. This article provides a literature review regarding HIET in cases of overdose with CCB and BB agents. Relevant literature articles from 1997-2018 were identified and reviewed using the PubMed and Embase databases. The following search terms were used to identify potential articles: "hyperinsulinemic-euglycemic therapy," "overdose," "calcium channel blocker," "beta blocker," and "insulin." Articles published in the English language were included in this review. A manual search of reference lists was also conducted. Much of the literature is limited to case reports, series, retrospective chart reviews, and small prospective studies. The success rate observed in published case series ranged from 80.4-100%. Regular insulin is most commonly dosed at an initial bolus of 1 unit/kg followed by a regular insulin infusion of 0.5-1 unit/kg/hour. Euglycemia is often maintained using intravenous fluids containing dextrose. Hyperinsulinemic-euglycemic therapy exhibited a promising safety profile, provided close monitoring is conducted. More research is needed to determine optimal strategies for maintaining euglycemia, ideal monitoring parameters, and consistent efficacy goals.

Published case reports have documented the relationship between exenatide use and acute kidney injury. However, to our knowledge, no cases of this adverse effect with liraglutide, another glucagon-like peptide-1 receptor agonist approved for the treatment of type 2 diabetes mellitus, have been reported. We describe a 53-year-old Caucasian woman who came to a community hospital with severe and progressively worsening gastrointestinal symptoms for several weeks, leading to dehydration and development of acute kidney injury. Laboratory results showed an increase in her serum creatinine concentration to 22.8 mg/dl and blood urea nitrogen to 150 mg/dl; she also had lost 8.9 kg in the previous month. One month earlier, the patient had begun liraglutide 1.8 mg/day subcutaneously for uncontrolled type 2 diabetes. Use of the Naranjo adverse drug reaction probability scale indicated a possible relationship (score of 3) between the patient's development of acute kidney injury and liraglutide. Renal biopsy and laboratory testing were helpful in ruling out other potential causes of renal failure and adverse drug reactions due to other drugs such as ciprofloxacin and quinapril. After the reports of the renal biopsy were obtained, liraglutide was determined to be a likely cause of acute tubular necrosis. The patient was successfully treated with discontinuation of liraglutide, volume repletion, and hemodialysis. To our knowledge, this is the first documented case of liraglutide-induced acute tubular necrosis. Clinicians should be aware of this possible complication and closely follow liraglutide's dosage titration recommendations in the package insert. Patients should also be educated about the need to report unusual or prolonged gastrointestinal symptoms.