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About Eric Brandt
Expertise
I am a practicing pharmacist.On my drug information website, I have answered hundreds of questions to date. The articles posted on my site include Parkinson`s disease. depression, menopause, diabetes, sleep and aging, congestive heart failure, calcium channel blockers, thyroid hormone replacement therapy, ADHD, multiple sclerosis an more.

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I have experience in retail as well as hospital pharmacy pracice. Currently working in a hospital pharmacy. I am experienced in drug information. Over the last 6 years I have developed a successful web site for drug information.

The addressfor my drug information website is http://www.druginformation.bc.caThere you can read articles on varios areas of health interest. You can also leave me questions which I will personally answer. I also have a free health information newsletter called The Caplet. To subscribe send e-mail to thecaplet-subscribe@topica.com
 
   

You are here:  Experts > Health/Fitness > Pharmacology > Pharmacy > propranolol and increase of blood sugar

Topic: Pharmacy



Expert: Eric Brandt
Date: 4/1/2008
Subject: propranolol and increase of blood sugar

Question
sir, I have read in internet that propranolol -beta blocker can raise blood sugar even than calciam chanel blocker..is it true?

Answer
Hi,
Here is a reference I found on this subject.
1)  Beta-blocking agents appear to present minimal risk of altering glucose control in nondiabetic patients. Hypoglycemia occurs predominantly in Type-I diabetics (insulin dependent) receiving beta-blockers; the hypoglycemic response may be prolonged, exacerbated, or symptomatically altered. Propranolol may induce hypoglycemia by blocking catecholamine-induced glycogenolysis. In Type-II diabetics, the incidence of hypoglycemia with beta-blockers is much lower. However, hyperglycemia is more common in Type-II diabetics as a result of beta-blocker inhibition of insulin release. Beta-blockers should be avoided in Type-I diabetics if possible, primarily in patients prone to developing hypoglycemia. Since glucose regulation is mediated in part by beta-2-receptors, beta-1-selective agents may cause less of an alteration in glucose, insulin, and glucagon concentrations in diabetic patients (Mills & Horn, 1985a; Chin et al, 1984; Hansten, 1983; Abramson & Arky, 1968a; MacKintosh, 1967a); (Kotler, 1966).
2)  A prospective cohort study involving 12,550 adults (aged 45 to 64 years) without diabetes found that type II diabetes mellitus is nearly 2.5 times as likely to develop in patients with hypertension compared with normotensive patients. In addition, hypertensive patients receiving beta-blockers had a 28% higher risk of developing type II diabetes mellitus than hypertensive patients not receiving any antihypertensive therapy. Hypertensive patients receiving thiazide diuretics, ACE inhibitors, or calcium antagonists were not at a greater risk of developing diabetes than hypertensive patients not receiving any antihypertensive therapy (Gress et al, 2000; Sowers & Bakris, 2000). Previous clinical trials have yielded conflicting results regarding the potential risk of developing diabetes from use of beta- blockers in hypertensive patients. One study reported that obese elderly patients receiving diuretics and beta-blockers were at a greater risk of developing type II diabetes mellitus than normotensive patients (Mykkanen et al, 1994); whereas other studies found no increased risk of hyperglycemia or diabetes for patients taking beta- blockers (Savage et al, 1998; Neaton et al, 1993).
3)  Two pediatric cases of propranolol-induced hypoglycemia have been reported. The children were receiving 7.2 to 14 mg/kg/day of propranolol for behavior disorders. The authors suggest that children being treated with propranolol at doses greater than 4 mg/kg/day, are in a fasting state, and/or concurrently receiving methylphenidate may be at an increased risk for hypoglycemia (Chavez et al, 1999).
4)  There are numerous case reports of hypoglycemic episodes occurring in patients receiving propranolol (Zeligs & Lockhart, 1984; Grajower et al, 1980; Kallen et al, 1980; Belton et al, 1980); (Mackintosh, 1967)(Simpson, 1967); (Kotler et al, 1966).
5)  Chronic hemodialysis patients have a predisposition to developing hypoglycemia secondary to impaired glycogenolysis, inadequate hepatic and renal gluconeogenesis, and increased glucose utilization. This predisposition can be exacerbated by propranolol which inhibits glycogenolysis and gluconeogenesis (Pun et al, 1985). It appears that propranolol interferes with the compensatory responses to hypoglycemia. It is well known that propranolol can interfere with the sympathetic symptoms of hypoglycemia by virtue of its beta blocking action. In other words, reflex tachycardia, tremor, and nervousness do not occur when a patient becomes hypoglycemic while receiving propranolol. Diaphoresis, however, is unchanged or increased (Gilman et al, 1990; Popp et al, 1984; Zeligs & Lockhart, 1984; Young & Koda-Kimble, 1988).


Thank you for using Allexperts
sincerely,
Eric Brandt, B.Sc. Pharm

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