Patient Profile for Robert Doe
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General Information
ID: 5555
Prescriber: M.D.
Name: Robert Doe
Address: Street
City: Anycity
State: State
Zip: 55555
Country: USA
Phone: 123.234.5678
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Current Conditions
• arterial thromboembolism prophylaxis
• benign prostatic hyperplasia (BPH)
• cardiac arrhythmias
• cardiopulmonary bypass (multiple (4))
• defibrillation (cardioversion)
• diabetes mellitus Type II
• fatigue
• gastritis
• heart failure
• hypercholesterolemia
• hypertension
• insomnia severe
• muscle cramps
• nutritional supplementation
• renal impairment
• syncope
• vertigo
• weakness severe
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Current Allergies
No allergies noted
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Current Medications
• Medication
• Aspirin Dosage: 81mg Sig: tab 1 daily for heart
• B Complex H.P.™ Sig: tab 1 daily
• Cyanocobalamin, Vitamin B{12} Dosage: 500mcg Sig: spray in mouth every morning
• Flomax® Dosage: 0.4mg Sig: tab 1 daily for prostate
• Glyburide Dosage: 2.5mg Sig: tab 1 at breakfast
• Iron Salts Dosage: liquid Sig: 10cc daily
• Lisinopril Dosage: 10mg Sig: tab 1 daily
• Metoprolol Dosage: 50mg Sig: tab 1 twice a day
• Olay™ Vitamins Beauty Nutrients Ester-C® Alpha Lipoic Collagen Support Dosage: 50mg Sig: tab 1 daily
• Preventive Nutrition® Coenzyme Q-10 Sig: tab 1 twice a day
• Simvastatin Dosage: 40mg Sig: tab 1 in the evening daily
• Trazodone Dosage: 100mg Sig: tab 1 and a half (150mg) at bedtime
• Vitamin E Dosage: 400 U Sig: tab 1 twice a day
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Dosing Parameters
Gender: Male
Birthdate: 2/27/1920
Weight: 68.18 kgs
Height: 172.72 cm
Ideal Body Weight: 68.61 kgs
Body Surface Area: 1.81 m²
Serum Creatinine: 1.2 mg/dL
Creatinine Clearance: 44.19 mL/min
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Notes
Title: Initial Assessment & Interview
Date: 11/15/2004
This 84 year old white male presents with numerous physical problems that seem to be a result of current drug therapy. Although I didn’t get to meet him face to face, I had a very pleasant visit by phone. He was very open and mentally alert and discussed his problems in much detail. The assessment on his “Geriatric Depression Scale” quiz indicates a high degree of anxiety and depression scoring a value of 12. The patient presents with extreme muscle weakness, dizziness, depression, unsteady gait, very concerned about his lack of ability to play golf and serious fatigue with the least amount of exercise. After a lengthy discussion with the patient and with the information supplied to me, it is apparent that many of his problems are drug related and he can be helped into a higher state of quality of life.
Although it has been said, by his physician, that the drugs he is taking keep him alive, there are alternative measures and drug therapies that would better fit into his life style and afford him the pleasures he once enjoyed. Based on labs presented, maintaining an 84 year old patient at a 5.6% HGA1c will cause serious episodes of hypoglycemia during the day and in combination with the sulfonylurea (glyburide) exacerbates this condition mid-morning and after. His lipid panel is well within range for a much less drastic therapy than use of statin (Simvastatin) drug therapy and will surely exacerbate symptoms of weakness, fatigue, gait changes and loss of liver and renal function. A serious condition Rhabdomyolysis, ( a waisting away of muscle tissue) is present in all geriatric patients just by the fact of getting old. This condition is exacerbated by the statin drugs and should not be used in patients over 70 years of age unless seriously high cholesterol and LDL levels occur. With a cholesterol level of 126 and an LDL of 69, the use of Simvastatin is not advised. Many of the neutropharmaceuticals could be stopped, although, as we will discuss, some are important to continue. Use of ACE drug therapy in this patient is unnecessary since an alpha blocker (Flomax) and beta blocker (Metoprolol) are used. These two drugs are also implicated in the diabetes and depression the patient experiences. Based on the fact that the patient’s mind is clear and his will to do better is strong, changes to a more geriatric friendly drug therapy management program will surely improve his quality of life.
Title: Initial Assessment & Interview (follow-up)
Date: 12/13/2004
I did a follow-up call to Mr. Doe to see how the lowered dosing of Glyberide and Lisinopril affected his blood sugars and blood pressure. We had a pleasant talk and in his opinion he could see no difference in the values recorded with the new dosing. I had anticipated this result but I needed to wait for three or four weeks of therapy at this level to make sure that my recommendations would improve the overall health outlook picture.
Title: Drug Therapy Assessment & Recommendations
Date: 12/15/2004
Review of the drug therapy currently prescribed resulted in the following problem areas:
Aspirin - to continue
Vitamin B12 - 500mcg tablets should be stopped and changed to monthly injections of 1000mcg IM each month. Lack of intrinsic factor in the stomach makes absorption of B12 almost impossible.
Iron salts - based on laboratory results are not needed at this time.
Flomax - used to treat the BPH is a very good choice and should be continued.
Glyburide - Use of sulfonylurea in this age patient with type II diabetes is contraindicated. Diet alone could be all that is needed to control the condition. The use of steroid therapy a while back that precipitated the hyperglycemia then led to the use of the antidiabetic agent- this medication should not have been started until 30 to 60 days after the problems with the hyperglycemia and use of steroid therapy. Taking the sulfonylurea after breakfast starting the day with a blood sugar in the 90’s will lead to hypoglycemia and weakness, dizziness, fatigue and depression, all of which are present at this time.
Lisinopril - an ACE inhibitor, is not indicated in this patient. Need for nephroprotection at 84 is unreasonable. Problems with orthostatic hypotension, dizziness, syncope all are experienced by the patient.
Metoprolol - Use of a beta blocker in a diabetic exacerbates lose of glucose control. Common problems with depression are seen in the geriatric patient. Use of cardioprotection at 84 is of little value. Use of calcium channel blocker from the benzothiazepine group, diltiazem, will provide the needed antihypertensive and cardiac support to allow for fewer adverse events and better quality of life.
Simvastatin - A perfect contraindication of this drug with this patient is clear. Rhabdomyolysis symptoms are present and will prevail in deteriorating his physical condition and quality of life. The Coenzyme Q10 on board has surely slowed this process but need for control of lipids can be accomplished in other ways. All studies indicate that risks are too great to use statin therapy unless critical conditions are present. Using the assumption that elevated homocystine and methylmalonic acid levels are high, use of Vitamin B12, B6 and folic acid will bring down cholesterol and LDL levels and improve HDL in most geriatrics. I feel strongly that removal of the simvastatin will allow the patient to regain much strength and allow for him to get back to playing golf.
Trazadone - This drug is not very successful in treating the geriatric patient. It is a very weak SSRI and has many side effects consistent with the age and condition of this patient. Need for an antidepressant-antianxiety drug therapy is apparent based on a score of 3 on the depression scale assessment and indications of general boredom. Use of Effexor XR a SSRI and SNRI given at bedtime improves sleep and provides the necessary support for anxiety and depression. As he regains his strength and is able to participate in his hobbies again, this drug can probably be removed. The patient will know when this change should occur.
Drug Therapy Management
Stop B Complex HP
Stop Vitamin B12 tablets
Stop Glyburide
Stop Iron Salts
Stop Lisinopril
Stop Olay Vitamins
Stop Simvastatin
Stop Trazadone
New Drug Therapy
Aspirin EC 325mg - 1 tablet daily
Vitamin B6 200mg - tablet 1 daily
Folic Acid 1mg - tab 1 daily
Vitamin B12 1000mcg Inj. - 1000mcg IM weekly x 4 weeks then 1000mcg IM monthly
Flomax 0.4mg - cap 1 daily
Diltiazem CD 180mg - cap 1 daily…. Then taper to discontinue Metoprolol 50mg daily for four days, then 50mg every other day for 4 days and discontinue completely…..
Centrum Silver - tab 1 daily
Coenzyme Q 10 - tab 1 two times a day for 4 more months and discontinue
Effexor XR 37.5mg at bedtime for 5 days, then 75mg at bedtime for 5 days, then 112.5mg at bedtime.
Vitamin E 400 units - cap 1 daily
Fish Oil 1000mg – cap 1 daily
ANYTHING NOT LISTED ABOVE DISCONTINUE COMPLETELY
Continue to keep your blood pressure log and record your beginning AM blood pressure and your ending PM blood pressure with pulses. After about 10 days on the diltiazem cd 180mg evaluation of mean blood pressures will indicate a need to titrate the drug up to 240mg daily or down to 120mg daily…
Continue your blood sugar log and don’t worry about a 200 blood sugar. The latest studies show that in the geriatric patient, allowing for higher HGA1c in the range of 7 to 8 % makes for better quality of life. This may show at times blood sugars that are from 175 to 225 and that is alright. Your next HGA1c in 90 days will show just how good the mean glucose control has been. The mean glucose control is the most important, not the snapshot of a finger stick.
Get new labs in 90 days with new lipid panel to evaluate your progress and need for adjustments in your drug therapy management.
Remember that it will take time to see all the changes that the new drug therapy will produce. After completing the titration processes that are required, you should see big improvements relating to the complaints recorded. The additional vitamin supplements should also make you feel better after 30 days or so. Further titration of the diltiazem dosing may be needed until we reach your dose. Continue to keep your blood pressure and pulse log. This is very important. Talk to you friends and see if they want to assist you by allowing you to start back playing a few holes at a time until your stamina returns, which may take 4 or 5 months. Continuing the Coenzyme Q10 will help you regain muscle tone. Walk a little farther each day and push yourself to make this muscle tone reappear. Continue your diet and stay away from white foods. White foods being bread, potatoes, rice, candy or just complicated carbohydrates. The Atkin’s Diet candies with 0 to 2 net carbs can be consumed without affecting your blood sugar. You may want to sample these.
Let me remind you that this drug therapy regimen is thoroughly thought out and should be followed in its entirety. Choosing only bits and pieces of it may keep us from reaching our mutual goal of improvement in your quality of life and health. I am as close as your phone, so if problems occur please call me. I look forward to hearing from you after your visit with your doctor. I am always available to talk to your doctor if necessary. After the changes are made I want you to call me if any drug problem or symptom occurs during your entire rehab process, but would like review this overall progress in 90 to 120 days by phone.
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Drug Interactions
Aspirin, ASA (Aspirin) and Glyburide
Severity: Moderate
Displacement of glyburide from protein binding sites by other drugs may lead to enhanced hypoglycemic action. In vitro, the protein binding exhibited by glyburide is predominantly non-ionic. Drugs such as clofibrate (and possibly fenofibrate), phenylbutazone, salicylates, and sulfonamides displace the ionic-binding sulfonylureas (e.g., chlorpropamide, tolbutamide, tolazamide) from serum proteins to a far greater extent than the non-ionic binding glyburide.[29] However, this difference in protein binding has not been shown to result in fewer drug-drug interactions with glyburide versus other sulfonylureas in clinical use. Aspirin, ASA has been shown to decrease both glyburide protein binding and glyburide AUC.[1309] Additionally, salicylates, by inhibiting prostaglandin synthesis, can indirectly increase insulin secretion. Thus, salicylates can decrease blood sugar. If any of these drugs are administered or discontinued in patients receiving oral antidiabetic agents, patients should be monitored for hypoglycemia.
Salicylates, by inhibiting prostaglandin E2 synthesis, can indirectly increase insulin secretion. Thus, salicylates can decrease blood sugar and may potentiate the effects of other antidiabetic agents. This mechanism may explain how salicylates can potentiate the clinical effects of sulfonylureas, however, displacement of sulfonylureas from protein binding sites has also been reported.[1310] In large doses, salicylates uncouple oxidative phosphorylation, deplete hepatic and muscle glycogen, and cause hyperglycemia and glycosuria. After acute overdose or use of greater than maximum recommended daily dosages, salicylates can cause either hypoglycemia or hyperglycemia. Large doses of aspirin should be used cautiously in patients receiving antidiabetic agents.[5232]
Aspirin, ASA (Aspirin) and Lisinopril
Severity: Low
Aspirin, ASA may reduce the vasodilatory efficacy of ACE inhibitors by inhibiting the synthesis of vasodilatory prostaglandins. This interaction has been documented primarily in heart failure patients.[5718] [6060] However, the established benefits of using aspirin in combination with an ACE inhibitor in patients with ischemic heart disease and left ventricular dysfunction generally outweigh this concern.[5718] [6060] Patients receiving concurrent salicylates and ACE inhibitor therapy should be monitored for antihypertensive or vasodilatory efficacy; the dose of the ACE inhibitor can be adjusted if indicated based on clinical evaluation.
The efficacy of antihypertensive agents needs to be carefully assessed during aspirin usage. During antihypertensive therapy with beta-blockers, high concentrations of vasodilatory prostaglandins are produced in response to reflex-mediated pressor mechanisms (e.g., sympathetic tone). Concurrent use of beta-blockers with aspirin may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.[5717] Aspirin can increase the risk of renal insufficiency in patients receiving diuretics, secondary to the effects of aspirin on renal blood flow. Aspirin inhibits renal prostaglandin production, which causes salt and water retention and decreased renal blood flow. Thus, the effectiveness of diuretics in patients with underlying renal or cardiovascular disease may be diminished by the concomitant administration of aspirin.[5717] Aspirin may decrease the hyperuricemic effect of hydrochlorothiazide, HCTZ and furosemide. Concomitant use of aspirin and potassium-sparing diuretics, such as triamterene or spironolactone, may cause hyperkalemia.[5717] The hyponatremic and hypotensive effects of angiotensin converting enzyme (ACE) inhibitors may be diminished by concurrent use of aspirin; the inhibition of cyclooxygenase by aspirin prevents the formation of vasodilatory prostaglandins.[5717] Furthermore, reduced renal blood flow is expected from the decreased pressure gradient created in the glomeruli when aspirin is used with an ACE inhibitor.[5718] Low-dose aspirin (e.g., 81 mg/day) may be less likely to attenuate the antihypertensive or cardioprotective effects of ACE inhibitors; however, the dose-related effect is controversial.[6439] The established benefits of using low-dose aspirin in combination with an ACE inhibitor in patients with ischemic heart disease and left ventricular dysfunction generally outweigh concerns, especially with appropriate renal function and serum potassium monitoring.[5718] [6060] [6439] Monitor the patient's blood pressure, renal function, and clinical status for the desired responses and adjust therapy accordingly.
Aspirin, ASA (Aspirin) and Metoprolol
Severity: Low
The efficacy of antihypertensive agents needs to be carefully assessed during aspirin usage. During antihypertensive therapy with beta-blockers, high concentrations of vasodilatory prostaglandins are produced in response to reflex-mediated pressor mechanisms (e.g., sympathetic tone). Concurrent use of beta-blockers with aspirin may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.[5717] Aspirin can increase the risk of renal insufficiency in patients receiving diuretics, secondary to the effects of aspirin on renal blood flow. Aspirin inhibits renal prostaglandin production, which causes salt and water retention and decreased renal blood flow. Thus, the effectiveness of diuretics in patients with underlying renal or cardiovascular disease may be diminished by the concomitant administration of aspirin.[5717] Aspirin may decrease the hyperuricemic effect of hydrochlorothiazide, HCTZ and furosemide. Concomitant use of aspirin and potassium-sparing diuretics, such as triamterene or spironolactone, may cause hyperkalemia.[5717] The hyponatremic and hypotensive effects of angiotensin converting enzyme (ACE) inhibitors may be diminished by concurrent use of aspirin; the inhibition of cyclooxygenase by aspirin prevents the formation of vasodilatory prostaglandins.[5717] Furthermore, reduced renal blood flow is expected from the decreased pressure gradient created in the glomeruli when aspirin is used with an ACE inhibitor.[5718] Low-dose aspirin (e.g., 81 mg/day) may be less likely to attenuate the antihypertensive or cardioprotective effects of ACE inhibitors; however, the dose-related effect is controversial.[6439] The established benefits of using low-dose aspirin in combination with an ACE inhibitor in patients with ischemic heart disease and left ventricular dysfunction generally outweigh concerns, especially with appropriate renal function and serum potassium monitoring.[5718] [6060] [6439] Monitor the patient's blood pressure, renal function, and clinical status for the desired responses and adjust therapy accordingly.
During antihypertensive therapy with beta-blockers, high concentrations of vasodilatory prostaglandins are produced in response to reflex-mediated pressor mechanisms (e.g., sympathetic tone). Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.[5717]
Aspirin, ASA (Aspirin) and Ascorbic Acid, Vitamin C (Olay™ Vitamins Beauty Nutrients Ester-C® Alpha Lipoic Collagen Support)
Severity: Low
Agents that acidify the urine should be avoided in patients receiving high-dose salicylates. Urine acidifying agents (e.g., ammonium chloride, ascorbic acid, vitamin C, potassium chloride, or phosphate salts) may increase renal tubular reabsorption of salicylic acid and possibly increase salicylic acid levels. However, if the urine is acidic prior to administration of an acidifying agent, the increase in salicylic acid concentrations should be minimal. Increases in salicylic acid levels are more likely in patients receiving acidifying agents with a baseline urinary pH > 6.5.
Acidification of the urine by ascorbic acid will alter the excretion of certain other drugs administered concurrently.[5449] Agents that acidify the urine should be avoided in patients receiving high-dose salicylates. Urine acidifying agents may increase renal tubular reabsorption of salicylic acid and possibly increase salicylic acid levels. However, if the urine is acidic prior to administration of an acidifying agent, the increase in salicylic acid concentrations should be minimal. Increases in salicylic acid levels are more likely in patients with a urinary pH > 6.5.
Niacin, Niacinamide (found in B Complex H.P.™) and Glyburide
Severity: Moderate
Niacin, Niacinamide interferes with glucose metabolism and can result in hyperglycemia; monitor patients on antidiabetic agents for loss of blood glucose control if niacin therapy is added.[6158]
Niacin (nicotinic acid) interferes with glucose metabolism and can result in hyperglycemia; monitor patients on antidiabetic agents for loss of blood glucose control if niacin therapy is added.
Niacin, Niacinamide (found in B Complex H.P.™) and Lisinopril
Severity: Moderate
Clonidine has been shown to inhibit niacin-induced flushing. This interaction is harmless unless niacin augments the hypotensive actions of clonidine. Finally, clinicians should keep in mind that cutaneous vasodilation induced by niacin may become problematic if high-dose niacin is used concomitantly with other antihypertensive agents, especially peripheral vasodilators such as epoprostenol, nitrates, calcium-channel blockers, or others, particularly in the setting of acute myocardial infarction, unstable angina, or other acute hemodynamic compromise.
Niacin, Niacinamide (found in B Complex H.P.™) and Metoprolol
Severity: Moderate
Clonidine has been shown to inhibit niacin-induced flushing. This interaction is harmless unless niacin augments the hypotensive actions of clonidine. Finally, clinicians should keep in mind that cutaneous vasodilation induced by niacin may become problematic if high-dose niacin is used concomitantly with other antihypertensive agents, especially peripheral vasodilators such as epoprostenol, nitrates, calcium-channel blockers, or others, particularly in the setting of acute myocardial infarction, unstable angina, or other acute hemodynamic compromise.
Niacin, Niacinamide (found in B Complex H.P.™) and Simvastatin
Severity: Moderate
Cyclosporine, fibric acid derivatives (e.g., gemfibrozil, fenofibrate, clofibrate), and antilipemic doses of niacin (i.e., vitamin B3 as nicotinic acid) may increase the risk of myopathy, rhabdomyolysis and acute renal failure (see Adverse Reactions);[5336] however, in some cases simvastatin has been used safely in combination with these agents.
This risk may be increased at higher doses of simvastatin. In patients taking gemfibrozil or cyclosporine, the simvastatin dose should not exceed 10 mg/day PO to reduce the risk of myopathy (see Dosage section).[5336] The risk of myopathy is increased by gemfibrozil, and to a lesser extent by other fibrates or niacin >= 1 g/day.[5336] Fibrates or doses of niacin >= 1 g/day are independently associated with myopathy.[5336 The serious risk of myopathy or rhabdomyolysis should be weighed carefully versus the benefits of combined 'statin' and fibrate therapy; there is no assurance that periodic monitoring of CK will prevent the occurrence of severe myopathy and renal damage.[5336]
Rare cases of rhabdomyolysis have been reported in patients taking niacin (nicotinic acid) in lipid-altering doses (i.e., >=1 g/day) and HMG-CoA reductase inhibitors (i.e., 'statins') concurrently.[5506] Patients undergoing combined therapy should be carefully monitored for myopathy or rhabdomyolysis, particularly in the early months of treatment or during periods of upward dose titration of either drug. Since compounds in went yeast, Monascus purpureus are pharmacologically similar to the HMG-CoA reductase inhibitors,[5911] clinicians and patients should use this dietary supplement cautiously in combination with niacin, particularly in non-prescription use.
Niacin, Niacinamide (found in B Complex H.P.™) and Aspirin, ASA (Aspirin)
Severity: Low
Niacin is known to induce the release of prostacyclin, which may be the mechanism of niacin-induced flushing, especially after immediate-release dosage forms. Aspirin, ASA has been shown to offset this adverse reaction if administered 30 minutes before the niacin dose. Concomitant administration of aspirin is reported to decrease the metabolic clearance of nicotinic acid according to manufacturer's data, but the clinical relevance of this finding is not known. In general, the interaction between ASA or and niacin is beneficial, although clinicians should note that both drugs, when administered in high doses, are potentially hepatotoxic. A recently published study demonstrated that niacin dosage forms that are more likely to produce flushing are less likely to be hepatotoxic.[221] Ibuprofen has also been reported to minimize niacin-induced flushing.
Tamsulosin (Flomax®) and Lisinopril
Severity: Low
No pharmacokinetic interaction occurred when tamsulosin was co-administered with either digoxin, furosemide, or theophylline. In addition, tamsulosin did not potentiate the hypotensive effects of atenolol, enalapril, furosemide, or nifedipine.[6419] However, since the symptoms of orthostasis (e.g., postural hypotension, dizziness and vertigo) are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.[6419] Tamsulosin should not be used with other alpha-blockers.[6419]
Tamsulosin (Flomax®) and Metoprolol
Severity: Low
No pharmacokinetic interaction occurred when tamsulosin was co-administered with either digoxin, furosemide, or theophylline. In addition, tamsulosin did not potentiate the hypotensive effects of atenolol, enalapril, furosemide, or nifedipine.[6419] However, since the symptoms of orthostasis (e.g., postural hypotension, dizziness and vertigo) are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.[6419] Tamsulosin should not be used with other alpha-blockers.[6419]
Glyburide and Metoprolol
Severity: Moderate
Beta-blockers exert complex actions on the body's ability to regulate blood glucose. Beta-blockers can prolong hypoglycemia by interfering with glycogenolysis (secondary to blocking the compensatory actions of epinephrine) or can promote hyperglycemia (by inhibiting insulin secretion and decreasing tissue sensitivity to insulin). Since insulin secretion is mediated via beta2-receptors, beta-blockers, particularly nonselective agents, can directly antagonize the major beneficial effect of sulfonylureas. Also, beta-blockers can blunt the tachycardic response and exaggerate the hypertensive response to hypoglycemia.
Thus, beta-blockers may interact pharmacodynamically with antidiabetic agents. No pharmacokinetic interaction has been observed between beta-blockers and antidiabetic agents. Selective beta-blockers, such as acebutolol, atenolol, metoprolol, or penbutolol, antagonize beta2-receptors less than nonselective agents and, as a result, may cause fewer problems with blood glucose regulation, although all beta-blockers can still mask the tachycardic response to hypoglycemia.[6141]
Beta-blockers exert complex actions on the body's ability to regulate blood glucose.[6141] |