7 Interactions found for:

The following applies to the ingredients: Metoprolol and Empagliflozin (found in Jardiance)

MONITOR: Sodium-glucose co-transporter 2 (SGLT-2) inhibitors may potentiate the hypotensive effects of antihypertensive agents, including beta-blockers. Inhibition of glucose and sodium co-transport produces mild diuresis and transient natriuresis, resulting in intravascular volume contraction. Volume depletion-related adverse reactions including hypotension, postural dizziness, orthostatic hypotension, syncope, and dehydration can occur after initiating treatment with SGLT-2 inhibitors, and the risk may be increased with concomitant use of other agents that can lower blood pressure.

MONITOR: Beta-blockers may inhibit some of the normal physiologic responses to hypoglycemia, which, when combined with antidiabetic agents such as sodium-glucose co-transporter 2 (SGLT-2) inhibitors, may potentiate the risk for adverse events. Symptoms of hypoglycemia, such as tremors and tachycardia, may be absent, making it more difficult for patients to recognize an oncoming episode. In addition, multiple effects on glucose metabolism have been reported, usually with the noncardioselective beta-blockers (e.g., propranolol, pindolol, timolol) but occasionally also with relatively beta-1 selective agents (e.g., atenolol, metoprolol, nebivolol). Specifically, inhibition of catecholamine-mediated glycogenolysis and glucose mobilization in association with beta-blockade can potentiate insulin-induced hypoglycemia in diabetics and delay the recovery of normal blood glucose levels. Prolonged and severe hypoglycemia may occur, although these events have rarely been reported. Significant increases in blood pressure and bradycardia can also occur during hypoglycemia in diabetics treated with insulin and beta-blockers due to the antagonism of epinephrine's effect on beta-2 adrenergic receptors, which leads to unopposed alpha-adrenergic effects, including vasoconstriction. On the other hand, decreased glucose tolerance and decreased glucose-induced insulin secretion have also been reported with various beta-blockers. For example, cardioselective beta-blockers like atenolol have been noted to increase insulin resistance while others such as metoprolol and the noncardioselective propranolol are known to increase hepatic glycogenolysis and gluconeogenesis, which may contribute to hyperglycemia. However, beta-blockers with intrinsic sympathomimetic activity and alpha-adrenergic activity, such as pindolol, or those with alpha-blocking effects, such as carvedilol, are reported to have a lesser impact on insulin sensitivity and may even have neutral or mildly positive effects on glycemic control due to vasodilating and insulin-sensitizing effects. The extent to which these opposing effects manifest clinically and whether one effect will predominate are unclear.

MANAGEMENT: Caution is advised if SGLT-2 inhibitors are coadministered with beta-blockers, particularly in the elderly and patients with impaired renal function. Prior to initiating SGLT-2 inhibitors, volume status should be assessed and corrected, if necessary. If volume depletion occurs, treatment with SGLT-2 inhibitors should be interrupted until the condition is corrected. Clinical and laboratory monitoring are recommended during therapy, including electrolytes, fluid status, renal function, and blood pressure. In addition, cardioselective beta-blockers are generally considered safer than noncardioselective agents in the treatment of diabetic patients. Nevertheless, caution is advised if they are prescribed to patients on SGLT-2 inhibitor therapy, as cardioselectivity is not absolute and larger doses of beta-1 selective agents may pose some of the same risks as nonselective agents. Patients should be advised of the need for regular blood glucose monitoring, due to the potential for developing hypoglycemia or hyperglycemia. They should also be made aware that certain symptoms of hypoglycemia such as tremor and tachycardia may be masked. However, other symptoms such as headache, dizziness, drowsiness, confusion, nausea, hunger, weakness, and perspiration may be unaffected. The same precautions are applicable in diabetic patients treated with ophthalmic beta-blockers.

The following applies to the ingredients: Metoprolol

ADJUST DOSING INTERVAL: The bioavailability of metoprolol may be enhanced by food.

MANAGEMENT: Patients may be instructed to take metoprolol at the same time each day, preferably with or immediately following meals.

The following applies to the ingredients: Metoprolol

ADJUST DOSING INTERVAL: Concurrent administration with calcium salts may decrease the oral bioavailability of atenolol and possibly other beta-blockers. The exact mechanism of interaction is unknown. In six healthy subjects, calcium 500 mg (as lactate, carbonate, and gluconate) reduced the mean peak plasma concentration (Cmax) and area under the concentration-time curve (AUC) of atenolol (100 mg) by 51% and 32%, respectively. The elimination half-life increased by 44%. Twelve hours after the combination, beta-blocking activity (as indicated by inhibition of exercise tachycardia) was reduced compared to that with atenolol alone. However, during a 4-week treatment in six hypertensive patients, there was no difference in blood pressure values between treatments. The investigators suggest that prolongation of the elimination half-life induced by calcium coadministration may have led to atenolol cumulation during long-term dosing, which compensated for the reduced bioavailability.

MANAGEMENT: It may help to separate the administration times of beta-blockers and calcium products by at least 2 hours. Patients should be monitored for potentially diminished beta-blocking effects following the addition of calcium therapy.

The following applies to the ingredients: Empagliflozin (found in Jardiance)

GENERALLY AVOID: Alcohol may cause hypoglycemia or hyperglycemia in patients with diabetes. Hypoglycemia most frequently occurs during acute consumption of alcohol. Even modest amounts can lower blood sugar significantly, especially when the alcohol is ingested on an empty stomach or following exercise. The mechanism involves inhibition of both gluconeogenesis as well as the counter-regulatory response to hypoglycemia. Episodes of hypoglycemia may last for 8 to 12 hours after ethanol ingestion. By contrast, chronic alcohol abuse can cause impaired glucose tolerance and hyperglycemia. Moderate alcohol consumption generally does not affect blood glucose levels in patients with well controlled diabetes. A disulfiram-like reaction (e.g., flushing, headache, and nausea) to alcohol has been reported frequently with the use of chlorpropamide and very rarely with other sulfonylureas.

MANAGEMENT: Patients with diabetes should avoid consuming alcohol if their blood glucose is not well controlled, or if they have hypertriglyceridemia, neuropathy, or pancreatitis. Patients with well controlled diabetes should limit their alcohol intake to one drink daily for women and two drinks daily for men (1 drink = 5 oz wine, 12 oz beer, or 1.5 oz distilled spirits) in conjunction with their normal meal plan. Alcohol should not be consumed on an empty stomach or following exercise.