Drug Interactions between guanadrel and nateglinide
This report displays the potential drug interactions for the following 2 drugs:
- guanadrel
- nateglinide
Interactions between your drugs
guanadrel nateglinide
Applies to: guanadrel and nateglinide
MONITOR: Postganglionic adrenergic blocking agents may potentiate the hypoglycemic effects of insulin and insulin secretagogues (e.g., sulfonylureas, meglitinides). Limited data have demonstrated possible hypoglycemic activity with agents such as guanethidine and reserpine. The mechanism may involve depletion of catecholamine stores from adrenergic nerve endings, which can interfere with glycogenolysis and other mechanisms related to regulation of blood glucose levels. In one case report, a diabetic patient required an insulin dose increase following discontinuation of guanethidine therapy. Another study found improved glucose tolerance in three patients with type II diabetes given guanethidine 50 to 90 mg/day. Postganglionic adrenergic blocking agents can also diminish the physiological response to hypoglycemia induced by insulin and insulin secretagogues, as catecholamines are responsible for certain symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes.
MANAGEMENT: Close monitoring for the development of hypoglycemia is recommended when postganglionic adrenergic blocking agents are coadministered with insulin or insulin secretagogues, particularly in patients with advanced age and/or renal impairment. Insulin and oral antidiabetic dosages may require adjustment if an interaction is suspected. Patients should be instructed about the need for regular monitoring of blood glucose levels and be aware that certain symptoms of hypoglycemia such as tremor and tachycardia may be masked during antiadrenergic therapy. However, other symptoms such as headache, dizziness, drowsiness, nausea, hunger, and sweating may be unaffected. Patients should be observed for loss of glycemic control when antiadrenergic therapy is withdrawn.
References
- Gupta KK (1968) "Guanethidine and diabetes." Br Med J, 2, p. 697-8
- Gupta KK (1969) "The antidiabetic action of guanethidine." Postgrad Med J, 45, p. 455-6
- Gupta KK (1968) "Guanethidine and glucose tolerance in diabetics." Br Med J, 3, p. 679
Drug and food interactions
nateglinide food
Applies to: nateglinide
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.
References
- Jerntorp P, Almer LO (1981) "Chlorpropamide-alcohol flushing in relation to macroangiopathy and peripheral neuropathy in non-insulin dependent diabetes." Acta Med Scand, 656, p. 33-6
- Jerntorp P, Almer LO, Holin H, et al. (1983) "Plasma chlorpropamide: a critical factor in chlorpropamide-alcohol flush." Eur J Clin Pharmacol, 24, p. 237-42
- Barnett AH, Spiliopoulos AJ, Pyke DA, et al. (1983) "Metabolic studies in chlorpropamide-alcohol flush positive and negative type 2 (non-insulin dependent) diabetic patients with and without retinopathy." Diabetologia, 24, p. 213-5
- Hartling SG, Faber OK, Wegmann ML, Wahlin-Boll E, Melander A (1987) "Interaction of ethanol and glipizide in humans." Diabetes Care, 10, p. 683-6
- (2002) "Product Information. Diabinese (chlorpropamide)." Pfizer U.S. Pharmaceuticals
- (2002) "Product Information. Glucotrol (glipizide)." Pfizer U.S. Pharmaceuticals
- "Product Information. Diabeta (glyburide)." Hoechst Marion-Roussel Inc, Kansas City, MO.
- Skillman TG, Feldman JM (1981) "The pharmacology of sulfonylureas." Am J Med, 70, p. 361-72
- (2002) "Position Statement: evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes related complications. American Diabetes Association." Diabetes Care, 25(Suppl 1), S50-S60
- Cerner Multum, Inc. "UK Summary of Product Characteristics."
guanadrel food
Applies to: guanadrel
MONITOR: Many psychotherapeutic and CNS-active agents (e.g., anxiolytics, sedatives, hypnotics, antidepressants, antipsychotics, opioids, alcohol, muscle relaxants) exhibit hypotensive effects, especially during initiation of therapy and dose escalation. Coadministration with antihypertensives and other hypotensive agents, in particular vasodilators and alpha-blockers, may result in additive effects on blood pressure and orthostasis.
MANAGEMENT: Caution and close monitoring for development of hypotension is advised during coadministration of these agents. Some authorities recommend avoiding alcohol in patients receiving vasodilating antihypertensive drugs. Patients should be advised to avoid rising abruptly from a sitting or recumbent position and to notify their physician if they experience dizziness, lightheadedness, syncope, orthostasis, or tachycardia.
References
- Sternbach H (1991) "Fluoxetine-associated potentiation of calcium-channel blockers." J Clin Psychopharmacol, 11, p. 390-1
- Shook TL, Kirshenbaum JM, Hundley RF, Shorey JM, Lamas GA (1984) "Ethanol intoxication complicating intravenous nitroglycerin therapy." Ann Intern Med, 101, p. 498-9
- Feder R (1991) "Bradycardia and syncope induced by fluoxetine." J Clin Psychiatry, 52, p. 139
- Ellison JM, Milofsky JE, Ely E (1990) "Fluoxetine-induced bradycardia and syncope in two patients." J Clin Psychiatry, 51, p. 385-6
- Rodriguez de la Torre B, Dreher J, Malevany I, et al. (2001) "Serum levels and cardiovascular effects of tricyclic antidepressants and selective serotonin reuptake inhibitors in depressed patients." Ther Drug Monit, 23, p. 435-40
- Cerner Multum, Inc. "Australian Product Information."
- Pacher P, Kecskemeti V (2004) "Cardiovascular side effects of new antidepressants and antipsychotics: new drugs, old concerns?" Curr Pharm Des, 10, p. 2463-75
- Andrews C, Pinner G (1998) "Postural hypotension induced by paroxetine." BMJ, 316, p. 595
Therapeutic duplication warnings
No warnings were found for your selected drugs.
Therapeutic duplication warnings are only returned when drugs within the same group exceed the recommended therapeutic duplication maximum.
See also
Drug Interaction Classification
Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit. | |
Moderately clinically significant. Usually avoid combinations; use it only under special circumstances. | |
Minimally clinically significant. Minimize risk; assess risk and consider an alternative drug, take steps to circumvent the interaction risk and/or institute a monitoring plan. | |
No interaction information available. |
Further information
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