Metoprolol Insulin

GR is a 68-year-old African-American male who presents to the emergency department with dizziness and loss of speech that began 1 hour ago. His past medical history is significant for hypertension, diabetes mellitus, hypercholesterolemia, and benign prostatic hypertrophy (BPH). Social history is significant for smoking 1 pack per day for the last 38 years. Current medications include metoprolol 50 mg twice daily, insulin NPH 20 units twice daily, and simvastatin 20 mg daily. 

Suicide by insulin has been reported in a 68-year-old, non-diabetic physician who had also taken metoprolol and alcohol. The blood metoprolol concentration was 0.4 microgram/ml (usual target range 0.035-0.5 micro-gram/ml) and alcohol 122 mg/dl (27 mmol/1). C-pep-tide could not be detected, serum insulin was 1849 iU/ml (normal fasting concentration below 16 pU/ml) (284). 

However, contrary to popular belief, beta-adrenoceptor antagonists do not by themselves increase the risk of hypoglycemic episodes in insulin-treated diabetics, in whom their use was concluded to be generally safe (192). Indeed, in 20 such patients treated with diet or diet plus oral hypoglycemic agents, both propranolol and metoprolol produced small but significant increases in blood... 

A pulsed depolarizing iontophoretic system has been developed by Advance Co. [26] that delivers a current of frequency 40 Hz and an on-off duty of 30% to deliver a significant amount of metoprolol into the blood without any observed skin irritation or erythema at the site of application. Okabe et al. [26] hypothesized that the high-frequency pulses provided low skin impedance in addition, the capacitance of the skin was restored to its initial state at the start of each pulse cycle. Chien et al. [89] reported that a sine waveform induced a faster hypoglycemic effect with insulin, with the peak at approximately 2 hours, than either a trapezoidal (7 hours) or a square waveform (12 hours) however, the duration of the hypoglycemia was also shorter (11 hours) compared with the other two waveforms [89]. 

Some beta-blockers demonstrate p, selectivity. At low doses, metoprolol and atenolol predominantly antagonize the receptors on cardiac tissues with less activity on P2-receptors. Therefore, they are less likely to cause bronchospasm in patients with COPD or asthma. The nonselective beta-blockers also have the disadvantage of masking hypoglycemic symptoms, especially in insulin-dependent diabetics. Blocking P2-receptors also leaves the alpha-mediated vasoconstriction unopposed and, as a result, may worsen Raynaud s disease or peripheral vascular disease. Some beta-blockers, such as labetolol and carvedilol, also possess alpha-blocking properties. 

Clinically important, potentially hazardous interactions with acebutolol, amitriptyline, amoxapine, atenolol, betaxolol, carteolol, clomipramine, desipramine, dexmethylphenidate, doxepin, esmolol, imipramine, insulin detemir, insulin glulisine, metoprolol, nadolol, nortriptyline, oxprenolol, penbutolol, pindolol, propranolol, protriptyline, sulpiride, timolol, tricyclic antidepressants, trimipramine, verapamil... 

Metoprolol did not affect the insulin-response to tolbutamide in one study 4 ... 

Newman RJ. Comparison of propranolol, metoprolol, and acebutolol on insulin-induced hypoglycaemia. BMJ (1976) 2,447-9-... 

Viberti GC, Keen H, Bloom SR. Beta blockade and diabetes mellitus effect of o qnenolol and metoprolol on the metabolic, cardiovascular, and hmiuxial re nse to insulin-induced h3fpoglycemia in insulin-dependent diabetics. Metabolism (1980) 29, 873-9. 

Ostman J, Amer P, Haglund K, Juhlin-Dannfelt A, Nowak J, Wennlund A. Effect of metoprolol and alprenolol cn the metabolic, hormonal, and haemortynamic re x>nse to insulin-induced l poglycaemia in hypertensive, insulin-dependent diabetics. Acta Med Scand ( 9 2) 211,381-5. 

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