Hydrochlorothiazide / propranolol Disease Interactions

There are 25 disease interactions with hydrochlorothiazide / propranolol:

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Asthma/Copd

Severe Potential Hazard, High plausibility

Applies to: Chronic Obstructive Pulmonary Disease, Asthma

In general, beta-adrenergic receptor blocking agents (i.e., beta-blockers) should not be used in patients with bronchospastic diseases. Beta blockade may adversely affect pulmonary function by counteracting the bronchodilation produced by catecholamine stimulation of beta-2 receptors. If beta-blocker therapy is necessary in these patients, an agent with beta-1 selectivity (e.g., atenolol, metoprolol, betaxolol) is considered safer, but should be used with caution nonetheless. Cardioselectivity is not absolute and can be lost with larger doses.

References

  1. Horvath JS, Woolcock AJ, Tiller DJ, Donnelly P, Armstrong J, Caterson R "A comparison of metoprolol and propranolol on blood pressure and respiratory function in patients with hypertension." Aust N Z J Med 8 (1978): 1-6
  2. Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, Hauser SL, Longo DL, eds. "Harrison's Principles of Internal Medicine. 14th ed." New York, NY: McGraw-Hill Health Professionals Division (1998):
  3. Falliers CJ, Vincent ME, Medakovic M "Effect of single doses of labetalol, metoprolol, and placebo on ventilatory function in patients with bronchial asthma: interaction with isoproterenol." J Asthma 23 (1986): 251-60
View all 29 references

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Bradyarrhythmia/Av Block

Severe Potential Hazard, High plausibility

Applies to: Heart Block, Sinus Node Dysfunction

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with sinus bradyarrhythmia or heart block greater than the first degree (unless a functioning pacemaker is present). Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to exacerbate these conditions.

References

  1. "Product Information. Corgard (nadolol)." Bristol-Myers Squibb, Princeton, NJ.
  2. "Product Information. Sectral (acebutolol)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
  3. "Product Information. Trandate (labetalol)." Glaxo Wellcome, Research Triangle Park, NC.
View all 21 references

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Cardiogenic Shock/Hypotension

Severe Potential Hazard, High plausibility

Applies to: Cardiogenic Shock, Hypotension

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with hypotension or cardiogenic shock. Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to further depress cardiac output and blood pressure, which can be detrimental in these patients.

References

  1. "Product Information. Levatol (penbutolol)." Reed and Carnrick, Jersey City, NJ.
  2. "Product Information. Blocadren (timolol)." Merck & Co, Inc, West Point, PA.
  3. "Product Information. Visken (pindolol)." Sandoz Pharmaceuticals Corporation, East Hanover, NJ.
View all 23 references

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Diabetes

Severe Potential Hazard, High plausibility

Applies to: Diabetes Mellitus

Beta-adrenergic receptor blocking agents (aka beta-blockers) may mask symptoms of hypoglycemia such as tremors, tachycardia and blood pressure changes. In addition, the nonselective beta-blockers (e.g., propranolol, pindolol, timolol) may inhibit catecholamine-mediated glycogenolysis, thereby potentiating insulin-induced hypoglycemia and delaying the recovery of normal blood glucose levels. Since cardioselectivity is not absolute, larger doses of beta-1 selective agents may demonstrate these effects as well. Therapy with beta-blockers should be administered cautiously in patients with diabetes or predisposed to spontaneous hypoglycemia.

References

  1. "Product Information. Lopressor (metoprolol)." Novartis Pharmaceuticals, East Hanover, NJ.
  2. "Product Information. Kerlone (betaxolol)." Searle, Skokie, IL.
  3. "Product Information. Coreg (carvedilol)." SmithKline Beecham, Philadelphia, PA.
View all 21 references

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Hemodialysis

Severe Potential Hazard, High plausibility

Applies to: hemodialysis

Therapy with beta-adrenergic receptor blocking agents (aka beta-blockers) should be administered cautiously in patients requiring hemodialysis. When given after dialysis, hemodynamic stability should be established prior to drug administration to avoid marked falls in blood pressure. The hemodynamic status should be closely monitored before and after the dose.

References

  1. "Product Information. Levatol (penbutolol)." Reed and Carnrick, Jersey City, NJ.
  2. "Product Information. Blocadren (timolol)." Merck & Co, Inc, West Point, PA.
  3. "Product Information. Visken (pindolol)." Sandoz Pharmaceuticals Corporation, East Hanover, NJ.
View all 14 references

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Hypersensitivity

Severe Potential Hazard, High plausibility

Applies to: Allergies

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) in patients with a history of allergic reactions or anaphylaxis may be associated with heightened reactivity to culprit allergens. The frequency and/or severity of attacks may be increased during beta-blocker therapy. In addition, these patients may be refractory to the usual doses of epinephrine used to treat acute hypersensitivity reactions and may require a beta-agonist such as isoproterenol.

References

  1. "Product Information. Sectral (acebutolol)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
  2. "Product Information. Zebeta (bisoprolol)." Lederle Laboratories, Wayne, NJ.
  3. "Product Information. Coreg (carvedilol)." SmithKline Beecham, Philadelphia, PA.
View all 16 references

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Pvd

Severe Potential Hazard, High plausibility

Applies to: Peripheral Arterial Disease, Cerebrovascular Insufficiency

Due to their negative inotropic and chronotropic effects on the heart, beta-adrenergic receptor blocking agents (aka beta-blockers) reduce cardiac output and may precipitate or aggravate symptoms of arterial insufficiency in patients with peripheral vascular disease. In addition, the nonselective beta-blockers (e.g., propranolol, pindolol, timolol) may attenuate catecholamine-mediated vasodilation during exercise by blocking beta-2 receptors in peripheral vessels. Therapy with beta-blockers should be administered cautiously in patients with peripheral vascular disease. Close monitoring for progression of arterial obstruction is advised.

References

  1. "Product Information. Cartrol (carteolol)." Abbott Pharmaceutical, Abbott Park, IL.
  2. Coppeto JR "Transient ischemic attacks and amaurosis fugax from timolol." Ann Ophthalmol 17 (1985): 64-5
  3. "Product Information. Trandate (labetalol)." Glaxo Wellcome, Research Triangle Park, NC.
View all 25 references

Propranolol (Includes Hydrochlorothiazide/propranolol) ↔ Liver Disease

Severe Potential Hazard, High plausibility

Applies to: Liver Disease

Propranolol is primarily metabolized by the liver. Patients with liver disease may be at greater risk for adverse effects from propranolol due to decreased drug clearance. Therapy with propranolol should be administered cautiously in patients with liver disease. Dosage adjustments may be necessary.

References

  1. George CF, Orme ML, Buranapong P, et al "Contribution of the liver to overall elimination of propranolol." J Pharmacokinet Biopharm 4 (1976): 17-27
  2. Arthur MJ, Tanner AR, Patel C, et al "Pharmacology of propranolol in patients with cirrhosis and portal hypertension." Gut 26 (1985): 14-9
  3. Silber BM, Holford NH, Riegelman S "Dose-dependent elimination of propranolol and its major metabolites in humans." J Pharm Sci 72 (1983): 725-32
View all 11 references

Thiazides (Includes Hydrochlorothiazide/propranolol) ↔ Anuria

Severe Potential Hazard, High plausibility

Applies to: Anuria

The use of thiazide diuretics is contraindicated in patients with anuria.

References

  1. "Product Information. Diuril (chlorothiazide)." Merck & Co, Inc, West Point, PA.
  2. "Product Information. Renese-R (reserpine-polythiazide)." Pfizer US Pharmaceuticals, New York, NY.
  3. "Product Information. Enduron (methyclothiazide)." Abbott Pharmaceutical, Abbott Park, IL.
View all 9 references

Thiazides (Includes Hydrochlorothiazide/propranolol) ↔ Electrolyte Losses

Severe Potential Hazard, High plausibility

Applies to: Hypokalemia, Diarrhea, Electrolyte Abnormalities, Hyperaldosteronism, Hyponatremia, Magnesium Imbalance, Malnourished, Vomiting, Ventricular Arrhythmia, Dehydration

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

References

  1. Peters RW, Hamilton J, Hamilton BP "Incidence of cardiac arrhythmias associated with mild hypokalemia induced by low-dose diuretic therapy for hypertension." South Med J 82 (1989): 966-9,
  2. Jorgensen FS, Brunner S "The long-term effect of bendroflumethiazide on renal calcium and magnesium excretion and stone formation in patients with recurring renal stones." Scand J Urol Nephrol 8 (1974): 128-31
  3. Medical Research Council Working Party on Mild to Moderate Hypertension. "Ventricular extrasystoles during thiazide treatment: substudy of MRC mild hypertension trial." Br Med J (Clin Res Ed) 287 (1983): 1249-53
View all 77 references

Thiazides (Includes Hydrochlorothiazide/propranolol) ↔ Liver Disease

Severe Potential Hazard, High plausibility

Applies to: Liver Disease

Patients with severe liver disease or cirrhosis are very susceptible to thiazide-induced hypokalemic hypochloremic alkalosis. Blood ammonia concentrations may be further increased in patients with previously elevated concentrations. Hepatic encephalopathy and death have occurred secondary to the electrolyte alterations accompanying diuretic use. Therapy with thiazide diuretics should be administered cautiously in patients with impaired hepatic function or progressive liver disease, and discontinued promptly if signs of impending hepatic coma appear (e.g., tremors, confusion, and increased jaundice).

References

  1. Sherlock S, Senewiratne B, Scott A, Walker JG "Complications of diuretic therapy in hepatic cirrhosis." Lancet 1 (1966): 1049-52
  2. "Product Information. Zaroxolyn (metolazone)." Rhone-Poulenc Rorer, Collegeville, PA.
  3. "Product Information. Metahydrin (trichlormethiazide)." Hoechst Marion-Roussel Inc, Kansas City, MO.
View all 12 references

Thiazides (Includes Hydrochlorothiazide/propranolol) ↔ Lupus Erythematosus

Severe Potential Hazard, Moderate plausibility

Applies to: Lupus Erythematosus

The use of thiazide diuretics has been reported to possibly exacerbate or activate systemic lupus erythematosus. Reported cases have generally been associated with chlorothiazide and hydrochlorothiazide. Therapy with thiazide diuretics should be administered cautiously in patients with a history or risk of SLE.

References

  1. "Product Information. Zaroxolyn (metolazone)." Rhone-Poulenc Rorer, Collegeville, PA.
  2. "Product Information. Renese-R (reserpine-polythiazide)." Pfizer US Pharmaceuticals, New York, NY.
  3. "Product Information. Metahydrin (trichlormethiazide)." Hoechst Marion-Roussel Inc, Kansas City, MO.
View all 14 references

Thiazides (Includes Hydrochlorothiazide/propranolol) ↔ Renal Function Disorders

Severe Potential Hazard, High plausibility

Applies to: Renal Dysfunction

Thiazide diuretics may be ineffective when the glomerular filtration rate is low (GFR < 25 mL/min) because they are not expected to be filtered into the renal tubule, their site of action. In addition, thiazide diuretics decrease the GFR and may precipitate azotemia in renal disease. Cumulative effects may also develop because most of these drugs are excreted unchanged in the urine by glomerular filtration and active tubular secretion. Therapy with thiazide diuretics should be administered cautiously at reduced dosages in patients with renal impairment. If renal function becomes progressively worse, as indicated by rising BUN or serum creatinine levels, an interruption or discontinuation of thiazide therapy should be considered.

References

  1. Klunk LJ, Ringel S, Neiss ES "The disposition of 14C-indapamide in man." J Clin Pharmacol 23 (1983): 377-84
  2. Riess W, Dubach UC, Burckhardt D, Theobald W, Vuillard P, Zimmerli M "Pharmacokinetic studies with chlorthalidone (Hygroton) in man." Eur J Clin Pharmacol 12 (1977): 375-82
  3. el-Meheiry MM, Nabih AE, Soliman MD "A clinical study of a new diuretic, Trichlormethiazide." J Trop Med Hyg 69 (1966): 209-14
View all 41 references

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Chf

Moderate Potential Hazard, High plausibility

Applies to: Congestive Heart Failure

Beta-adrenergic receptor blocking agents (aka beta-blockers) in general should not be used in patients with overt congestive heart failure (CHF). Sympathetic stimulation may be important in maintaining the hemodynamic function in these patients, thus beta-blockade can worsen the heart failure. However, therapy with beta-blockers may be beneficial and can be administered cautiously in some CHF patients provided they are well compensated and receiving digitalis, diuretics, an ACE inhibitor, and/or nitrates. Carvedilol, specifically, is indicated for use with these agents in the treatment of mild to severe heart failure of ischemic or cardiomyopathic origin. There is also increasing evidence that the addition of a beta-blocker to standard therapy can improve morbidity and mortality in patients with advanced heart failure, although it is uncertain whether effectiveness varies significantly with the different agents. Data from one meta-analysis study suggest a greater reduction of mortality risk for nonselective beta-blockers than for beta-1 selective agents.

References

  1. "Product Information. Corgard (nadolol)." Bristol-Myers Squibb, Princeton, NJ.
  2. "Product Information. Kerlone (betaxolol)." Searle, Skokie, IL.
  3. Tcherdakoff P "Side-effects with long-term labetalol: an open study of 251 patients in a single centre." Pharmatherapeutica 3 (1983): 342-8
View all 47 references

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Hyperlipidemia

Moderate Potential Hazard, Moderate plausibility

Applies to: Hyperlipidemia

Beta-adrenergic receptor blocking agents (aka beta-blockers) may alter serum lipid profiles. Increases in serum VLDL and LDL cholesterol and triglycerides, as well as decreases in HDL cholesterol, have been reported with some beta-blockers. Patients with preexisting hyperlipidemia may require closer monitoring during beta-blocker therapy, and adjustments made accordingly in their lipid-lowering regimen.

References

  1. Gordon NF, Scott CB, Duncan JJ "Effects of atenolol versus enalapril on cardiovascular fitness and serum lipids in physically active hypertensive men." Am J Cardiol 79 (1997): 1065-9
  2. Samuel P, Chin B, Schoenfeld BH, et al "Comparison of the effect of pindolol versus propranolol on the lipid profile in patients treated for hypertension." Br J Clin Pharmacol 24 (1987): s63-4
  3. Lithell H, Andersson PE "Metabolic effects of carvedilol in hypertensive patients." Eur J Clin Pharmacol 52 (1997): 13-7
View all 39 references

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Hyperthyroidism

Moderate Potential Hazard, High plausibility

Applies to: Hyperthyroidism

When beta-adrenergic receptor blocking agents (aka beta-blockers) are used to alleviate symptoms of hyperthyroidism such as tachycardia, anxiety, tremor and heat intolerance, abrupt withdrawal can exacerbate thyrotoxicosis or precipitate a thyroid storm. To minimize this risk, cessation of beta-blocker therapy, when necessary, should occur gradually with incrementally reduced dosages over a period of 1 to 2 weeks. Patients should be advised not to discontinue treatment without first consulting with the physician. Close monitoring is recommended during and after therapy withdrawal.

References

  1. "Product Information. Kerlone (betaxolol)." Searle, Skokie, IL.
  2. "Product Information. Lopressor (metoprolol)." Novartis Pharmaceuticals, East Hanover, NJ.
  3. "Product Information. Coreg (carvedilol)." SmithKline Beecham, Philadelphia, PA.
View all 15 references

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Hyperthyroidism Pks

Moderate Potential Hazard, High plausibility

Applies to: Hyperthyroidism

During chronic administration, the clearance of beta-blockers that are primarily metabolized by the liver (e.g., labetalol, metoprolol, penbutolol, propranolol) may be increased in patients with hyperthyroidism due to increased liver blood flow and enhanced activity of drug-metabolizing enzymes. Pharmacokinetic studies have demonstrated an approximately 50% increase in systemic clearance of propranolol during long-term therapy. In general, the dosage required to achieve therapeutic blood concentrations in such patients may be higher than that required in euthyroid patients and should be individualized.

References

  1. Feely J "Clinical pharmacokinetics of beta-adrenoceptor blocking drugs in thyroid disease." Clin Pharmacokinet 8 (1983): 1-16
  2. O'Connor P, Feely J "Clinical pharmacokinetics and endocrine disorders. Therapeutic implications." Clin Pharmacokinet 13 (1987): 345-64

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Iop

Moderate Potential Hazard, Moderate plausibility

Applies to: Glaucoma/Intraocular Hypertension

Systemic beta-adrenergic receptor blocking agents (aka beta-blockers) may lower intraocular pressure. Therefore, patients with glaucoma or intraocular hypertension may require adjustments in their ophthalmic regimen following a dosing change or discontinuation of beta-blocker therapy.

References

  1. "Product Information. Blocadren (timolol)." Merck & Co, Inc, West Point, PA.
  2. "Product Information. Sectral (acebutolol)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
  3. "Product Information. Trandate (labetalol)." Glaxo Wellcome, Research Triangle Park, NC.
View all 15 references

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Ischemic Heart Disease

Moderate Potential Hazard, High plausibility

Applies to: Ischemic Heart Disease

Heightened sensitivity to catecholamines may occur after prolonged use of beta-adrenergic receptor blocking agents (aka beta-blockers). Exacerbation of angina, myocardial infarction and ventricular arrhythmias have been reported in patients with coronary artery disease following abrupt withdrawal of therapy. Cessation of beta-blocker therapy, whenever necessary, should occur gradually with incrementally reduced dosages over a period of 1 to 2 weeks in patients with coronary insufficiency. Patients should be advised not to discontinue treatment without first consulting with the physician. In patients who experience an exacerbation of angina following discontinuation of beta-blocker therapy, the medication should generally be reinstituted, at least temporarily, along with other clinically appropriate measures.

References

  1. "Product Information. Betapace (sotalol)." Berlex, Richmond, CA.
  2. "Product Information. Levatol (penbutolol)." Reed and Carnrick, Jersey City, NJ.
  3. "Product Information. Visken (pindolol)." Sandoz Pharmaceuticals Corporation, East Hanover, NJ.
View all 19 references

Beta-Blockers (Includes Hydrochlorothiazide/propranolol) ↔ Myasthenia Gravis

Moderate Potential Hazard, Low plausibility

Applies to: Myoneural Disorder

Beta-adrenergic receptor blocking agents (aka beta-blockers) may potentiate muscle weakness consistent with certain myasthenic symptoms such as diplopia, ptosis, and generalized weakness. Several beta-blockers have been associated rarely with aggravation of muscle weakness in patients with preexisting myasthenia gravis or myasthenic symptoms.

References

  1. Coppeto JR "Timolol-associated myasthenia gravis." Am J Ophthalmol 98 (1984): 244-5
  2. Herishanu Y, Rosenberg P "Beta-blockers and myasthenia gravis." Ann Intern Med 83 (1975): 834-5
  3. "Product Information. Blocadren (timolol)." Merck & Co, Inc, West Point, PA.
View all 7 references

Thiazides (Includes Hydrochlorothiazide/propranolol) ↔ Diabetes

Moderate Potential Hazard, Moderate plausibility

Applies to: Diabetes Mellitus, Abnormal Glucose Tolerance

Thiazide diuretics may cause hyperglycemia and glycosuria in patients with diabetes. They may also precipitate diabetes in prediabetic patients. These effects are usually reversible following discontinuation of the drugs. Therapy with thiazide diuretics should be administered cautiously in patients with diabetes mellitus, glucose intolerance, or a predisposition to hyperglycemia. Patients with diabetes mellitus should be monitored more closely during thiazide therapy, and their antidiabetic regimen adjusted accordingly.

References

  1. "Product Information. Diuril (chlorothiazide)." Merck & Co, Inc, West Point, PA.
  2. Nielsen S, Schmitz A, Knudsen RE, Dollerup J, Mogensen CE "Enalapril versus bendroflumethiazide in type 2 diabetes complicated by hypertension." Q J Med 87 (1994): 747-54
  3. Diamond MT "Hyperglycemic hyperosmolar coma associated with hydrochlorothiazide and pancreatitis." N Y State J Med 72 (1972): 1741-2
View all 36 references

Thiazides (Includes Hydrochlorothiazide/propranolol) ↔ Hyperlipidemia

Moderate Potential Hazard, Moderate plausibility

Applies to: Hyperlipidemia

Thiazide diuretics may increase serum triglyceride and cholesterol levels, primarily LDL and VLDL. Whether these effects are dose-related and sustained during chronic therapy are unknown. Patients with preexisting hyperlipidemia may require closer monitoring during thiazide therapy, and adjustments made accordingly in their lipid-lowering regimen

References

  1. Ames RP "A comparison of blood lipid and blood pressure responses during the treatment of systemic hypertension with indapamide and with thiazides." Am J Cardiol 77 (1996): b12-6
  2. Freis ED "The efficacy and safety of diuretics in treating hypertension." Ann Intern Med 122 (1995): 223-6
  3. Slotkoff L "Clinical efficacy and safety of indapamide in the treatment of edema." Am Heart J 106 (1983): 233-7
View all 23 references

Thiazides (Includes Hydrochlorothiazide/propranolol) ↔ Hyperparathyroidism

Moderate Potential Hazard, Moderate plausibility

Applies to: Hyperparathyroidism

Urinary calcium excretion is decreased by thiazide diuretics during chronic administration. Pathologic changes in the parathyroid gland with hypercalcemia and hypophosphatemia have been reported during prolonged therapy. However, the common complications of hyperparathyroidism such as renal lithiasis, bone resorption, and peptic ulceration have not been seen. Clinicians should be cognizant of these effects when prescribing or administering thiazide therapy to patients with hyperparathyroidism. These drugs should be discontinued before carrying out tests for parathyroid function.

References

  1. Lindy S, Tarssanen L "Serum calcium and phosphorus in patients treated with thiazides and furosemide." Acta Med Scand 194 (1973): 319-22
  2. "Product Information. Lozol (indapamide)." Rhone-Poulenc Rorer, Collegeville, PA.
  3. Paloyan E, Farland M, Pickleman JR "Hyperparathyroidism coexisting with hypertension and prolonged thiazide administration." JAMA 210 (1969): 1243-5
View all 27 references

Thiazides (Includes Hydrochlorothiazide/propranolol) ↔ Hyperuricemia

Moderate Potential Hazard, High plausibility

Applies to: Gout

Thiazide diuretics decrease the rate of uric acid excretion. Hyperuricemia occurs frequently but is usually asymptomatic and rarely leads to clinical gout except in patients with a history of gout or chronic renal failure. Therapy with thiazide diuretics should be administered cautiously in such patients.

References

  1. "Product Information. Thalitone (chlorthalidone)." Monarch Pharmaceuticals Inc, Bristol, TN.
  2. "Product Information. Diuril (chlorothiazide)." Merck & Co, Inc, West Point, PA.
  3. Beling S, Vukovich RA, Neiss ES, Zisblatt M, Webb E, Losi M "Long-term experience with indapamide." Am Heart J 106 (1983): 258-62
View all 20 references

Thiazides (Includes Hydrochlorothiazide/propranolol) ↔ Thyroid Function Tests

Moderate Potential Hazard, Moderate plausibility

Applies to: Thyroid Disease

Thiazide diuretics may decrease serum PBI (protein-bound iodine) levels without associated thyroid disturbance. Clinicians should be cognizant of this effect when prescribing or administering thiazide therapy to patients with thyroid disorders.

References

  1. Bech K, Skovsted L, Siersbaek-Nielsen K, Hansen JM "Influence of thiazides on thyroid parameters in man." Acta Endocrinol (Copenh) 89 (1978): 673-8
  2. "Product Information. Thalitone (chlorthalidone)." Monarch Pharmaceuticals Inc, Bristol, TN.
  3. "Product Information. Renese-R (reserpine-polythiazide)." Pfizer US Pharmaceuticals, New York, NY.
View all 10 references

You should also know about...

hydrochlorothiazide / propranolol drug Interactions

There are 1073 drug interactions with hydrochlorothiazide / propranolol

hydrochlorothiazide / propranolol alcohol/food Interactions

There are 5 alcohol/food interactions with hydrochlorothiazide / propranolol

Drug Interaction Classification

The classifications below are a general guideline only. It is difficult to determine the relevance of a particular drug interaction to any individual given the large number of variables.

Major Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit.
Moderate Moderately clinically significant. Usually avoid combinations; use it only under special circumstances.
Minor 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.

Do not stop taking any medications without consulting your healthcare provider.

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