INTERACTION BETWEEN BETA BLOCKERS AND INSULIN

Interaction between Beta Blockers and Insulin increases the risk and severity of hypoglycemia (low blood sugar) in patients

EFFECT

Additionally, beta-blockers can mask some of the hypoglycemic symptoms such as tremor, palpitation, and rapid heartbeat, making it harder to identify an oncoming episode. Other hypoglycemic symptoms such as headache, dizziness, drowsiness, nervousness, confusion, nausea, hunger, weakness and suddenness are not affected. If you have any questions or doubts through your doctor. You may need more frequent monitoring of your blood glucose levels, especially if you are prone to developing hypoglycemia. Any other drugs you use, including vitamins and herbs, should be told to the doctor.

SEVERITY

Moderate

ONSET

Rapid

SUBSTANTIABILITY

Possible

CLINICAL MANAGEMENT

In the treatment of diabetic patients, cardioselective beta-blockers are usually considered safer than non-cardioselective drugs. Nonetheless, caution is recommended if administered to patients treated with insulin or oral antidiabetic agents that may induce hypoglycemia (e.g., insulin secretagogues), as cardioselectivity is not absolute and larger doses of beta-1 selective agents that face some of the same risks as non-selective agents. Patients should be informed of the need for daily blood glucose monitoring and be mindful of the risk of masking other signs of hypoglycemia, such as tremor and tachycardia. Other symptoms, such as headache, dizziness, drowsiness, confusion, nausea, hunger, weakness, and suddenness may not be affected, however. On diabetic patients diagnosed with ophthalmic beta-blockers, the same precautions apply.

PROBABLE MECHANISM

Beta-blockers can inhibit some of the normal physiologic hypoglycemic response. Hypoglycemic signs such as tremor and tachycardia may be absent making it harder for patients to detect an oncoming episode. Moreover, numerous effects have been reported on glucose metabolism, generally with non-cardioselective beta-blockers (e.g., propranolol, pindolol, timolol) but sometimes with comparatively beta-1 selective agents (e.g., atenolol, metoprolol, nebivolol). Specifically, inhibition of catecholamine-mediated glycogenolysis and mobilization of glucose in conjunction with beta-blockade may potentiate insulin-induced hypoglycemia in diabetics and delay normal blood glucose recovery levels.

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