DETERMINING INSULIN DOSE AT THE TIME OF DISCHARGE IN A HIGH-RISK POPULATION: IS THERE ROOM FOR IMPROVEMENT?

OBJECTIVE: To evaluate the adequacy of the insulin dose prescribed at hospital discharge in a high-risk population and assess patient characteristics that influence insulin dose requirement in the immediate postdischarge period. METHODS: This was a retrospective study conducted at Parkland Health System. We included all patients admitted to a medical floor who received an insulin prescription at discharge and had at least one follow-up visit within 6 months of discharge. All data were extracted by a detailed manual review of each electronic medical record. RESULTS: At the postdischarge follow-up (N = 797, median 33 days from discharge), 60% of patients required an insulin dose adjustment; 47% of the patients required a dose decrease. Significant predictors of a decrease insulin requirement postdischarge included (multiple regression beta coefficient [95% confidence interval]): newly diagnosed diabetes, -12.7 (-17.7, -7.7); ketosis-prone diabetes, -8.4 (-15, -1.8); glycated hemoglobin A1c (HbA1c), <10% (86 mmol/mol) -7.0 (-11.4, -2.6); discharge insulin total daily dose, -5.3 (-9.3, -1.3); and metformin prescription, -4.9 (-8.4, -1.3). CONCLUSION: An insulin dose adjustment (most commonly a decrease) was necessary shortly after discharge in more than half of our patients. A better model to estimate insulin dose at discharge is needed along with short-term follow-up after discharge for insulin titration. A pre-emptive insulin dose reduction at discharge should be considered for patients with newly diagnosed diabetes, ketosis-prone diabetes, metformin prescription, and those with HbA1c <10% at presentation. ABBREVIATIONS: DKA = diabetic ketoacidosis; HbA1c = glycated hemoglobin A1c; KPDM = ketosis-prone diabetes mellitus; TDD = total daily dose.

Marked lowering of high-density lipoprotein cholesterol levels due to high dose bexarotene therapy.

CONTEXT: Bexarotene is a retinoid X receptor agonist, which is currently used for the treatment of cutaneous T-cell lymphoma (CTCL). It is known to induce central hypothyroidism as well as dyslipidemia including elevation of triglycerides (TG) and low-density lipoprotein cholesterol along with slight lowering of high-density lipoprotein cholesterol (HDL-C). Marked lowering of HDL-C has never been previously reported in bexarotene-treated patients and whether it is related to hypothyroidism remains unclear. CASE REPORT: A 49-year-old African female with a history of CTCL on treatment with bexarotene of 300 mg/d, presented with serum total cholesterol level of 249 mg/dL (6.4 mmol/L), TG level of 92 mg/dL (1.03 mmol/L), HDL-C level of 78 mg/dL (2.02 mmol/L), thyroid stimulating hormone (TSH) of 0.68 µIU/mL, and free thyroxine level of 0.5 ng/dL. Six months later, on increasing the bexarotene dose to 600 mg daily, serum TG increased to 310 mg/dL (3.5 mmol/L) and HDL-C dropped to 3 to 5 mg/dL (0.077-0.13 mmol/L), whereas the TSH was undetectable (0.01 µIU/mL). Despite adequate levothyroxine replacement to 225 µg daily resulting in free thyroxine levels up to 1.5 ng/dL, HDL-C remained extremely low of 4 to 9 mg/dL (0.103-0.233 mmol/L). Bexarotene was discontinued due to poor response of CTCL, 3 months after which her HDL-C levels returned to baseline of 80 to 90 mg/dL (2.07-2.33 mmol/L). CONCLUSIONS: High dose bexarotene can markedly lower HDL-C levels, which normalize on discontinuation of the drug. Lowering of HDL-C with bexarotene may be due to an increase in cholesterol ester transfer protein activity and appears to be independent of central hypothyroidism.