Assessment of hyperglycemia after calcium channel blocker overdoses involving diltiazem or verapamil*

Abstract

Serum glucose concentrations correlate directly with the severity of the calcium channel blocker intoxication. The percentage increase of the peak glucose concentration is a better predictor of severity of illness than hemodynamic derangements. If validated prospectively, serum glucose concentration alone might be an indicator to begin hyperinsulinemia-euglycemia therapy.

Successful treatment of a patient with obesity, type 2 diabetes and hypertension with the paleolithic ketogenic diet

“…These included bisoprolol, acetylsalicylic acid and amlodipine. Bisoprolol and amlodipine, which belong to beta-blocker and calcium channel blocker type antihypertensives, respectively, are known for their effect to adversely affect glucose metabolism [15,16]. Glucose parameters further deteriorated in 2012.…”

The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential

“…There is no evidence for muscle weakness from block of Ca V 1.1 channels in skeletal muscle, increased hearing thresholds from inhibition of Ca V 1.3 in cochlear inner hair cells, visual impairment from block of Ca V 1.4 in retinal photoreceptors, or CNS disturbances from block of Ca V 1.2 and or Ca V 1.3 in the brain. Suppression of insulin secretion and hyperglycemia occur only at toxic plasma levels after CCB overdose (Levine et al, 2007). However, this side effect plays no role at therapeutic doses in clinical practice.…”

“…Glucagon-secreting a cells express both Ca V 1.2 and Ca V 1.3, in addition to Ca V 2 channels (Vignali et al, 2006). High doses of CCBs (achieved during intoxication) reduce insulin secretion and cause hyperglycemia, supporting the important role of LTCCs for insulin secretion in humans (Levine et al, 2007). However, the therapeutic (vasodilating) plasma concentrations of DHPs that lower blood pressure do not cause a clinically relevant inhibition of pancreatic LTCCs or hormone secretion in the endocrine pancreas.…”

Glucose, Blood Pressure, and Cardiovascular Risk

“…15 As a group, the calcium channel blockers show no major effect on glucose metabolism, although some reports have linked overdoses of certain calcium channel blockers (verapamil and diltiazem) with severe hyperglycemia. 16 Data concerning ␤-blockers are variable. Older agents, such as propranolol and metoprolol, have been associated with worsening glycemic control and increased diabetes risk, possibly because of inhibition of pancreatic insulin secretion through blockade of ␤2-adrenergic receptors, inhibition of peripheral glucose uptake, and resultant unopposed ␣2-adrenergic receptor-mediated stimulation of hepatic glycogenolysis.…”