The Use of Plasmapheresis in a Severe Case of Amiodarone-Induced Thyrotoxicosis.

Amiodarone-induced thyrotoxicosis (AIT) can be difficult to treat since amiodarone's long half-life leads to a persistent effect on thyroid function. We present a case of a 74-year-old male with severe AIT who presented with altered mentation and ultimately required intubation and intensive care for management of thyroid storm. Standard medical therapy for treatment of thyroid storm was initiated immediately, but the patient remained unresponsive with worsening biochemical parameters with increasing total T3 levels and sustained elevated levels of free T4 after 5 days of medical management. Due to the lack of a clinical and biochemical response to conventional medical therapy, the patient was started on plasmapheresis and underwent a total of 7 cycles of plasmapheresis over a period of 10 days. He significantly improved with plasmapheresis and was successfully bridged to a total thyroidectomy, which was completed without complications.

Isoproterenol Induced Insulin Resistance Leading to Diabetic Ketoacidosis in Type 1 Diabetes Mellitus.

Isoproterenol is known to cause insulin resistance and is often used to treat bradyarrhythmias from atrioventricular block. We report a case of isoproterenol induced diabetic ketoacidosis in a 77-year-old female patient treated with isoproterenol for atrioventricular block prior to insertion of permanent pacemaker. Diabetic ketoacidosis (DKA) developed within hours of starting an isoproterenol drip, and there were no other precipitating factors at that time. DKA resolved quickly after discontinuing isoproterenol and starting insulin drip. DKA is a common complication of diabetes mellitus, with about 140,000 hospital admissions for DKA in 2009. While the rate of DKA has increased by nearly 50% between 1988 and 2009, the rate of mortality has decreased. There are many causes of diabetic ketoacidosis, such as medication noncompliance, infection, pancreatitis, stroke, myocardial infarction, and many others. Isoproterenol may lead to diabetic ketoacidosis by increasing insulin resistance.

Insulin in the medical management of postprandial hypoglycemia in a patient with type 2 diabetes after gastric bypass surgery.

Objective. We evaluated a 47-year-old woman with a history of type 2 diabetes and severe obesity who developed postprandial hypoglycemia after undergoing Roux-en-Y gastric bypass surgery and losing 60% of her total body weight. We studied her insulin secretion and blood glucose dynamics and were able to tailor a therapeutic regimen involving insulin that eliminated episodes of hypoglycemia. Methods. We studied blood glucose levels during a prolonged fast, performed continuous glucose monitoring studies using a subcutaneous glucose sensor, and evaluated regional pancreatic insulin secretion using selective arterial calcium stimulation. Results. Continuous glucose monitoring revealed that the patient had early (1-2 hr) postprandial hyperglycemia followed by late (3-4 hr) postprandial hypoglycemia. Biochemical studies confirmed endogenous pancreatogenous insulin secretion as the cause of episodic hypoglycemia, but imaging studies and selective arterial calcium stimulation failed to localize an insulinoma. The patient was treated with preprandial doses of insulin aspart in order to attenuate the early postprandial hyperglycemia, and the late hypoglycemic episodes were avoided. Conclusion. We describe an interesting and novel nonsurgical approach to the prevention of postprandial hypoglycemia in a patient with noninsulinoma pancreatogenous hypoglycemia after gastric bypass.

Safe and simple emergency department discharge therapy for patients with type 2 diabetes mellitus and severe hyperglycemia.

OBJECTIVE: To investigate the safety and effectiveness of 2 simple discharge regimens for use in patients with type 2 diabetes mellitus (DM2) and severe hyperglycemia, who present to the emergency department (ED) and do not need to be admitted. METHODS: We conducted an 8-week, open-label, randomized controlled trial in 77 adult patients with DM2 and blood glucose levels of 300 to 700 mg/dL seen in a public hospital ED. Patients were randomly assigned to receive glipizide XL, 10 mg orally daily (G group), versus glipizide XL, 10 mg orally daily, plus insulin glargine, 10 U daily (G+G group). The primary outcome was to maintain safe fasting glucose and random glucose levels of <350 and <500 mg/dL up to 4 weeks and <300 and <400 mg/dL, respectively, thereafter and to have no return ED visits (responders). RESULTS: Baseline characteristics were similar between the 2 treatment groups. The primary outcome was achieved in 87% of patients in both treatment groups. The enrollment mean blood glucose values of 440 and 467 mg/dL in the G and G+G groups, respectively, declined by the end of week 1 to 298 and 289 mg/dL and by week 8 to 140 and 135 mg/dL, respectively. Homeostasis model assessment of beta-cell function and early insulin response improved 7-fold and 4-fold, respectively, in responders at the end of the 8-week study. CONCLUSION: Sulfonylurea with and without use of a small dose of insulin glargine rapidly improved blood glucose levels and beta-cell function in patients with DM2. Use of sulfonylurea alone once daily can be considered a safe discharge regimen for such patients and an effective bridge between ED intervention and subsequent follow-up.