Patient Case Report: Gabapentin-Induced Hypoglycemia.

PURPOSE: Gabapentin is an analog of gamma-aminobutyric acid (GABA), but its complete mechanism is not well understood. Common adverse effects from gabapentin include somnolence, sedation, and dizziness. Hyperglycemia is listed as a possible adverse drug reaction in the labeling. Case reports describe hypoglycemia in patients with diabetes, peritoneal dialysis, and/or incomplete medication records. The following case report details a hypoglycemia episode as a potential result of a gabapentin use in a patient without diabetes. SUMMARY: A 47-year old, 68 kg, white female presented to the emergency department with altered mental status. Her blood glucose level was 33 mg/dL. Gabapentin was started 1 week prior to the hypoglycemia episode. Her past medical history, concomitant medications, and other laboratory findings were not likely causes of her severe hypoglycemia. CONCLUSION: Gabapentin appears to have effects on several voltage-gated calcium channels. Hypoglycemia may be due to gabapentin binding to the alpha2delta subunit of the calcium channels in the pancreas. Future research should investigate gabapentin and the potential for hypoglycemia.

Evaluating the effects of dexmedetomidine compared to propofol as adjunctive therapy in patients with alcohol withdrawal.

BACKGROUND: In severe alcohol withdrawal (AW), benzodiazepines may be inadequate to control symptoms. In many situations, benzodiazepine dosing escalates despite no additional efficacy and introduces potential toxicities. Severe cases of AW may require additional agents to control symptoms. Case reports and studies have shown benefits with dexmedetomidine and propofol in severe AW, but these agents have not been compared with one another. This study compares the effects of dexmedetomidine and propofol on benzodiazepine and haloperidol utilization in patients with AW. METHODS: A retrospective chart review was completed on 41 patients with AW who received adjunctive dexmedetomidine or propofol. The primary objective was to compare benzodiazepine and haloperidol utilization before and after initiation of dexmedetomidine or propofol. Secondary measures included AW and sedation scoring, analgesic use, intensive care unit length of stay, rates of intubation, and adverse events. RESULTS: Among the dexmedetomidine and propofol groups, significant reductions in benzodiazepine (P≤0.0001 and P=0.043, respectively) and haloperidol (P≤0.0001 and P=0.026, respectively) requirements were observed. These reductions were comparable between groups (P=0.933 and P=0.465, respectively). A trend toward decreased intensive care unit length of stay in the dexmedetomidine group (123.6 hours vs 156.5 hours; P=0.125) was seen. Rates of intubation (14.7% vs 100%) and time of intubation (19.9 hours vs 97.6 hours; P=0.002) were less in the dexmedetomidine group. Incidence of hypotension was 17.6% in the dexmedetomidine group vs 28.5% in the propofol group. Incidence of bradycardia was 17.6% in the dexmedetomidine group vs 0% in the propofol group. No differences were observed in other secondary outcomes. CONCLUSION: In patients with severe AW who require sedation, both dexmedetomidine and propofol have unique and advantageous properties. Both agents appear to have equivalent efficacy in reducing AW-related symptoms and benzodiazepine and haloperidol requirements. These results should be validated in a larger, prospective trial.