Challenges with glucagon-like peptide-1 (GLP-1) agonist initiation: a case series of semaglutide overdose administration errors.

BACKGROUND: Prescriptions of semaglutide, a glucagon-like peptide-1 receptor agonist administered weekly for Type 2 diabetes mellitus and obesity, are increasing. Adverse effects from semaglutide overdose are poorly described. We report adverse effects from three unintentional semaglutide overdoses upon initiation. CASE REPORTS: Case 1: A 53-year-old man unintentionally injected semaglutide 2 mg instead of the recommended 0.1 mg. Case 2: A 45-year-old woman unintentionally injected semaglutide 2.4 mg instead of 0.25 mg. Case 3: A 33-year-old woman injected semaglutide 1.7 mg. All three of these patients developed nonspecific gastrointestinal symptoms. No patient experienced hypoglycemia. DISCUSSION: These unintentional semaglutide overdoses occurred due to deficits in patient and prescriber knowledge, and evasion of regulated access to pharmaceuticals. Nonspecific gastrointestinal symptoms predominated. The potential for hypoglycemia following glucagon-like peptide-1 agonist overdose is unclear, though it did not occur in our patients. It is thought that glucagon-like peptide-1 agonists are unlikely to cause hypoglycemia because their effects are glucose-dependent and diminish as serum glucose concentrations approach euglycemia. There is, however, an increase in hypoglycemia when glucagon-like peptide-1 agonists are combined with sulfonylureas. CONCLUSIONS: This case series highlights the critical role of patient education and training upon initiation of semaglutide therapy to minimize administration errors and adverse effects from injection of glucagon-like peptide-1 receptor agonists.

Insulin concentrations following termination of high-dose insulin euglycemic therapy.

INTRODUCTION: High-dose insulin therapy is used in patients with calcium channel blocker and beta-adrenergic antagonist overdoses. The pharmacokinetics of insulin are scantly reported following high-dose insulin therapy. We present two cases of persistently elevated insulin concentrations following high-dose insulin therapy. CASE REPORTS: A 50-year-old woman and a 45-year-old man experienced hypotension after overdosing on amlodipine and atenolol. They were treated with high-dose insulin therapy for 54 hours at 2 units/kilogram/hour and 48 hours at 10 units/kilogram/hour, respectively. Following termination, serum insulin elimination was studied. Insulin concentrations remained greater than 1,000 µU/mL (fasting reference 2.6-24.9 µU/mL) for longer than 4 hours (case 1) and 11 hours (case 2) and greater than 300 µU/mL for longer than 8 hours and 21 hours, respectively. Insulin concentrations decreased with apparent first-order elimination half-lives of 13.0 hours and 6.0 hours. DISCUSSION: Following high-dose insulin therapy, insulin concentrations remained elevated for longer than expected based on normal pharmacokinetics in therapeutic dosing. Three previous cases reported insulin half-lives of between 2.2 hours and 18.7 hours. The current cases add to the existing data that insulin has a variable but prolonged half-life following high-dose insulin therapy. CONCLUSIONS: These findings suggest that patients are at prolonged risk of hypoglycemia following cessation of high-dose insulin infusions.

Assessing the Role of Initial Serum Calcium Concentration in Patients with Ethylene Glycol Poisoning.

INTRODUCTION: Assays for ethylene glycol (EG) with a rapid turn-around time are not routinely available. Clinicians must rely on historical features and readily available clinical tests, combined with clinical acumen, to guide the initial management of suspected EG poisoning. Hypocalcemia has been suggested as a clue supporting the diagnosis of EG poisoning in patients presenting with an unexplained high anion gap metabolic acidosis (HAGMA). A previous small study challenged this assumption. METHODS: This was a retrospective case series of one state's poison control system of confirmed EG-poisoned patients between September 2017 and April 2021. The definition of EG poisoning was based on suspected EG ingestion and a serum EG concentration > 5 mg/dL. Patients who were suspected to have EG toxicity but did not have a confirmed EG concentration or the EG concentration was less than 5 mg/dL were excluded. Routine laboratory studies were recorded for all patients. Comparisons between serum calcium on presentation to presenting blood pH, bicarbonate, anion gap, and creatinine were assessed for correlation. RESULTS: There was no correlation between the presenting calcium and either pH or creatinine. There was a weak positive correlation between the initial serum calcium and anion gap, a weak negative correlation between the initial serum calcium and bicarbonate. CONCLUSION: On hospital presentation, hypocalcemia was not associated with EG poisoning, even in patients with a HAGMA. A normal serum calcium on presentation does not exclude the diagnosis of EG poisoning.

A "madd"-ening confounding: fruit seeds mimicking enteral drug concealment by computed tomography.

OBJECTIVE: To highlight the similarity between madd fruit seeds and enteral drug concealment ("body packing") on computed tomography when evaluated by Hounsfield Units. CASE REPORT: A 13-year-old girl from Senegal presented to the Emergency Department with severe abdominal pain. Examination showed right lower quadrant tenderness with rebound. Computed tomography scan of the abdomen and pelvis revealed smooth, well circumscribed, multiple intraluminal foreign bodies measuring up to 2 cm in size with Hounsfield Units measuring up to 200. The emergency department radiologist reported that these were suspicious for "body packer packets" of either opioids or cocaine, based on their appearance and Hounsfield Unit characteristics. Dietary history later revealed consuption of madd fruit (Saba senegalensis) seeds, which can cause bezoar formation and intestinal obstruction. CONCLUSION: Madd fruit seeds may appear similar to drug packets on computed tomography with similar Hounsfield Unit characteristics. History and clinical context are paramount to avoid misdiagnosis.

A 70-Year-Old Woman Presenting with Confusion and Muscle Spasms Due to Serotonin Syndrome Associated with Paroxetine and Quetiapine Treatment.

BACKGROUND Serotonin toxicity, often referred to as 'serotonin syndrome,' is a drug-induced condition due to excess serotonin released from brain synapses, resulting in symptoms that may be autonomic, neuromuscular, and/or cognitive in nature. Most cases involve more than 1 of the following drug regimens: monoamine oxidase inhibitors (MAOIs), serotonin releasers, selective serotonin reuptake inhibitors (SSRIs), or serotonin-norepinephrine reuptake inhibitors (SNRIs). This report is of a 70-year-old woman who presented with confusion and muscle spasms due to serotonin toxicity associated with paroxetine and quetiapine treatment. CASE REPORT An elderly woman with dementia presented to the Emergency Department with fever, altered mental status, labile blood pressures, and inducible clonus. No known medication dosage increases had been made, nor had any new serotonergic agents been added to the patient's drug regimen. She underwent a thorough workup in the Emergency Department and later during her hospitalization. A presumptive diagnosis of serotonin toxicity was made early on during her stay, with the etiology attributed to use of paroxetine and quetiapine. Clinical improvement was observed after benzodiazepine administration, discontinuation of offending agents, and a brief cyproheptadine course. The patient survived her hospital stay and was ultimately discharged to hospice care with a return to her baseline level of functioning. CONCLUSIONS Diagnosing serotonin toxicity requires a high degree of clinical suspicion and can occur in the absence of increased dosage of existing, or initiation of new, serotonergic agents.