Iron may accumulate in excess due to a mutation in the HFE gene that upregulates absorption or when it is ingested or infused at levels that exceed the body's ability to clear it. Excess iron deposition in parenchymal tissue causes injury and ultimately organ dysfunction. Diabetes mellitus and hepatic cirrhosis due to pancreas and liver damage are just two examples of diseases that result from iron overload. Despite the rapid growth of information regarding iron metabolism and iron overload states, the most effective treatment is still serial phlebotomies. We present a patient who developed iron overload due to chronic ingestion of oral ferrous sulfate. This case illustrates the importance of querying geriatric patients regarding their use of nonprescription iron products without a medical indication.

Loperamide, an over-the-counter antidiarrheal, works on the µ opioid receptor with minimal opioid activity if taken as directed. Recently, it has gained popularity as the "poor man's methadone" at supratherapeutic dosing. Opioid antagonism with naloxone is beneficial in reversing respiratory depression but has no effect on cardiotoxicity due to the human ether-a-go-go-related gene (hERG). We present the case of a 34-year-old female who presented for syncope after taking 48 tablets of 2 mg loperamide.On arrival, she was obtunded with variable heart block and a QTc of 560 ms.Subsequently, due to further QT prolongation from loperamide to 656 ms, she developed Torsades de Pointes requiring defibrillation at 120 J twice. Ultimately, she was discharged home with psychiatric and substance abuse outpatient follow-up. Patients and healthcare providers face new challenges with the increase in loperamide misuse due to easy access and delayed identification. It is important for clinicians to recognize and be familiar with loperamide overdose given the potential for multiorgan failure and increased mortality.

IntroductionLactobacillus species causing infective endocarditis is rare. Most reported cases arise from the oral ingestion of Lactobacillus via dairy or nutritional supplements in patients with congenital valve disease or replacement. We present a case of native valve bacterial endocarditis caused by Lactobacillus arising from dental abscesses. Additionally, there was an error in identification of the Lactobacillus as Corynebacterium, which led to inadequate treatment.Presentation of caseA 51-year-old male presented to an outside clinic with several weeks of subjective fevers and malaise. The provider obtained two sets of blood cultures. Both grew Gram-positive bacilli identified as Corynebacterium. Once hospitalized he persistently had positive blood cultures despite treatment with vancomycin and gentamicin. The specimens were sent to a reference lab. The cultures were confirmed to be Lactobacillus zeae resistant to vancomycin and gentamicin. Once he was started on appropriate therapy his blood cultures showed no further growth of bacteria. The infected teeth were removed as it was felt they were the source of the bacteremia.DiscussionThis case presents two interesting topics in one encounter. First, Lactobacillus is not a common culprit in endocarditis. Secondly, the incorrect identification of the gram-positive bacilli bacteria led to prolonged bacteremia in our patient.ConclusionThe patient was evaluated by cardiothoracic surgery at our facility and it was determined that he would likely need a mitral valve replacement versus repair. The decision was made to treat the patient with six weeks Penicillin-VK prior to the operation. He is currently completing his antibiotic therapy.