Loperamide-induced cardiogenic syncope: a case report of a life-threatening presentation of an over-the-counter drug.

Background: Loperamide at supratherapeutic doses can cause cardiac toxicity, presenting as cardiogenic shock, prolonged QT, malignant arrhythmias, or in severe cases sudden cardiac death. Surreptitious loperamide use is difficult to diagnose. We present an interesting case of loperamide use presenting with polymorphic ventricular tachycardia, cardiogenic shock. Case summary: A 25-year-old female presented with multiple syncopal episodes for 12 months with an electrocardiogram showing a Brugada-like pattern for which she underwent implantable cardioverter-defibrillator placement. One day following the procedure, she developed cardiogenic shock and was transferred to our tertiary care centre. Extensive workup was unrevealing. She responded well to supportive management, recovering from shock and was transferred to the floor. Unfortunately, she again developed cardiogenic shock, ultimately leading to cardiac arrest. Given the unclear cause for her cardiovascular symptoms, futher medication history was obtained. It was revealed that she was taking 100-150 tablets of loperamide per day. The decision was made to treat with intralipid emulsion therapy empirically given the strong suspicion for loperamide toxicity. The patient recovered well with supportive care. Loperamide levels returned elevated at 190 ng/mL. Repeated studies showed improvement of the conduction block, resolution of arrhythmias, and recovery of right and left ventricular function. Discussion: Acute loperamide toxicity can present as biventricular failure, with difficult-to-control arrhythmias. It requires a high index of suspicion. Treatment for loperamide toxicity is mainly supportive, lipid emulsion therapy can be considered in severe or refractory cases.

Abnormality of Contingent Negative Variation Correlates with Parkinson's Disease Severity.

Objective: We sought to assess the influence of Parkinson's disease (PD) on contingent negative variation (CNV). Patients and Methods: This prospective study included 49 patients with PD (69.7±16.5; 35 male) and 35 age- and sex-matched controls. The PD cohort was subdivided, according to the Hoehn-Yahr Scale, Unified Parkinson's Disease Rating Scale (UPDRS), and UPDRS Part III, into 30 cases of uncomplicated PD and 19 cases of advanced PD. CNV was recorded over the frontal and central vertex with a linked bimastoid reference using a dual-stimulus paradigm with interstimulus intervals (ISIs) of 1.7 and 2.0 seconds. Results: In advanced PD, the amplitude of the late CNV over the central vertex was markedly reduced (p<0.005) at ISI of 1.7 seconds and correlated negatively with UPDRS (r=-0.32; p<0.003) and motor score (UPDRS Part III) (r=-0.45; p<0.002). Conclusion: Late CNV amplitude was significantly abnormal in PD and correlated with the severity of the motor manifestations.

Euglycemic Diabetic Ketoacidosis Due to SGLT2 Inhibitor in a Patient With Gitelman Syndrome: A Therapeutic Dilemma.

Euglycemic diabetic ketoacidosis (DKA) is a rarely reported side effect of sodium-glucose cotransporter-2 inhibitor (SGLT2i) empagliflozin. A 51-year-old female with Gitelman syndrome and type 2 diabetes mellitus (DM) presented with abdominal pain after a recent hospitalization for acute pancreatitis. Her diabetes medications included metformin, pioglitazone, and empagliflozin. Diabetic ketoacidosis was suspected; however, glucose levels were below the cutoff for DKA; therefore, she was diagnosed with euglycemic DKA. Her pancreatitis workup was insignificant. Severe symptomatic hypokalemia despite aggressive repletion limited the management of DKA with insulin infusion therapy. As her ketonemia resolved, she was initiated on subcutaneous insulin with a small but acceptable decrease in potassium. The therapeutic dilemma of managing euglycemic DKA due to SGLT2i in a patient with Gitelman syndrome has not been previously described.

Pregabalin-Induced Myopathy in a Double Lung Transplant Recipient.

Pregabalin is a gamma-aminobutyric acid (GABA) derivative that was commercially approved by the Food and Drug Administration (FDA) in 2004. It is commonly used in the treatment of diabetic neuropathy, peripheral neuropathy, and spinal cord injury. We present the case of a 36-year-old Caucasian male double lung transplant recipient who presented with an 18-month history of fatigue and muscle weakness. He had elevated creatinine kinase level and his muscle biopsy showed evidence of drug-induced myopathy that improved after the cessation of pregabalin. We present a case of drug-induced myopathy as a rare complication of pregabalin therapy in a double lung transplant recipient.

Abnormally high levels of anti-collagen type IV IgG antibodies in the serum of patients with a clinically isolated syndrome correlate with an increased risk of conversion to MS.

OBJECTIVE: To investigate anti-collagen-type-IV serum antibodies (ACIVAbs) levels in patients with clinically isolated syndrome (CIS), and to determine their predictive value for conversion into multiple sclerosis (MS). MATERIAL AND METHODS: Serum levels of IgM and IgG ACIVAbs in 40 untreated patients with CIS (13 male, mean age 34.85±11.4 years, range 16-58 years) were compared to those of 27 gender- and age-matched healthy controls. ACIVAbs were quantified using ELISA. Patients were followed for 5 years by clinical examination and MRI studies. RESULTS: Thirty two patients (80%) converted to MS (converted CIS, C-CIS group) while the rest 8 (20%) did not (non-converted CIS, NC-CIS). The C-CIS patients had significantly higher levels of IgG ACIVAb compared to NC-CIS while the IgM levels did not differ between C-CIS and NC-CIS. Conversion to MS occurred in 66% of patients with IgG ACIVAbs levels exceeding the 95th percentile found in controls. IgG ACIVAbs levels correlated positively with the serum levels of matrix metalloproteinases type 9 (r = 0.37; p = 0.003) and inversely with those of tissue inhibitor of metalloproteinases type 1 (r = -0.43; p = 0.0008). CONCLUSION: High serum levels of IgG ACIVAbs in patients with CIS correlate strongly with increased risk of conversion to MS.