Class: Thiazide Diuretics
VA Class: CV701
CAS Number: 58-93-5
Brands: Accuretic, Aldactazide, Aldoril, Atacand HCT, Avalide, Benicar HCT, Capozide, Diovan HCT, Dyazide, Hydra-Zide, HydroDIURIL, Hyzaar, Inderide, Lopressor HCT, Lotensin HCT, Maxzide, Micardis HCT, Microzide, Moduretic, Monopril HCT, Prinzide, Teveten HCT, Timolide, Uniretic HCT, Vaseretic, Zestoretic, Ziac
Introduction
Thiazide diuretic and antihypertensive agent.a
Uses for Hydrochlorothiazide
Hypertension
Used alone or in combination with other antihypertensive agents for all stages of hypertension.b f 110
Thiazides have well-established benefits, can be useful in achieving goal BP alone or combined with other antihypertensive drugs, enhance the antihypertensive efficacy of multidrug regimens, and are more affordable than other agents.b f
JNC 7 recommends that thiazides be used as initial therapy for the treatment of uncomplicated hypertension in most patients, either alone or combined with other classes of antihypertensive drugs with demonstrated benefit (e.g., ACE inhibitors, angiotensin II receptor antagonists, β-blockers, calcium-channel blockers).f
Most hypertension outcome studies have involved thiazides, which generally have been unsurpassed in preventing cardiovascular complications of hypertension and are relatively inexpensive and well tolerated.f
The principal goal of preventing and treating hypertension is to reduce the risk of cardiovascular and renal morbidity and mortality, including target organ damage.f The higher the baseline BP, the more likely the development of MI, heart failure, stroke, and renal disease.f
Effective antihypertensive therapy reduces the risk of stroke by about 34–40%, MI by about 20–25%, and heart failure by more than 50%.f
Antihypertensive drug therapy is recommended for all patients with SBP/DBP ≥140/90 mm Hg who fail to respond to lifestyle/behavioral modifications.f
Initial antihypertensive therapy with drugs generally is recommended for anyone with diabetes mellitus, chronic renal impairment, or heart failure having SBP ≥130 mm Hg or DBP≥80 mm Hg.f
Black hypertensive patients generally tend to respond better to monotherapy with diuretics or calcium-channel blockers than to monotherapy with ACE inhibitors, angiotensin II receptor antagonists, or β-blockers.f 100
Thiazides are preferred in hypertensive patients with osteoporosis. Secondary beneficial effect in hypertensive geriatric patients of reducing the risk of osteoporosis secondary to effect on calcium homeostasis and bone mineralization.
Thiazide diuretics (unlike potassium-sparing diuretics) may be used in patients who are at an increased risk for developing hyperkalemia (e.g., those receiving an ACE inhibitor).112
Although hypertension during pregnancy responds well to thiazides, and the drugs had been used widely in the past for preeclampsia and eclampsia,b g such use no longer is recommended and other antihypertensives (e.g., methyldopa, hydralazine, labetalol) currently are preferred.f
Although rarely induces acute gout, generally avoid or use with caution in hypertensive patients with a history of gout or elevated uric acid concentrations.f
Edema (General)
Management of edema resulting from various causes; diagnose etiology before use.b
Edema caused by renal disease or by corticosteroids or estrogens may be relatively resistant to treatment.b
Ineffective in patients with Scr or BUN concentrations greater than twice normal.b
May be ineffective in patients with a GFR of <15–25 mL/minute; even when GFR is 25–50 mL/minute, more potent (e.g., loop) diuretics may be indicated.b
No substantial difference in clinical effects or toxicity of comparable thiazide or thiazide-like diuretics, except metolazone may be more effective in edema with renal impairment.b
Edema in CHF
Management of edema associated with CHF.b c
Used in conjunction with moderate sodium restriction (≤3 g of sodium daily), an ACE inhibitor, and usually a β-adrenergic blocking agent, with or without a cardiac glycoside.c d
Beneficial effects are additive with those of cardiac glycosides and/or ACE inhibitors.c
Unless contraindicated or not tolerated, all patients with mild to severe CHF secondary to left ventricular systolic dysfunction (ejection fraction less than 35–40%) generally should receive therapy with a diuretic in conjunction with an ACE inhibitor with or without a cardiac glycoside or a β-adrenergic blocking agent.d
Diuretic therapy and sodium restriction are not routinely necessary in patients with left ventricular systolic dysfunction and no or minimal overt signs or symptoms of heart failure (NYHA functional class I heart failure);d d diuretics should be added to ACE inhibitor therapy if volume overload develops or if symptoms of heart failure continue.
Concomitant diuretic therapy usually is indicated in patients with symptomatic heart failure (NYHA class II or greater) because of the likelihood of sodium and fluid retention.d
Do not use diuretics as monotherapy in CHF even if symptoms (e.g., peripheral edema, pulmonary congestion) are well controlled; diuretics alone do not prevent progression of heart failure.
Diuretics produce rapid symptomatic benefits, relieving pulmonary and peripheral edema more rapidly (within hours or days) than cardiac glycosides, ACE inhibitors, or β-blockers (in weeks or months).
Once fluid retention has resolved in CHF, diuretic therapy should be maintained to prevent recurrence of fluid retention. Ideally, diuretic therapy should be adjusted according to changes in body weight (as an indicator of fluid retention) rather than maintained at a fixed dosage.
Diuretics should be continued in CHF and comorbid conditions (e.g., hypertension) where ongoing therapy with the drugs is indicated.
Edema Secondary to Nephrotic Syndrome
May be useful if the patient fails to respond to corticosteroid therapy.b
More likely to become refractory to thiazides than edema associated with CHF, and more potent diuretics may be required.b
Edema in Pregnancy
Generally responds well to thiazides except when caused by renal disease.b
Thiazides should not be used for routine therapy in pregnant women with mild edema who are otherwise healthy.b
Diabetes Insipidus
Has been used widely in the treatment of diabetes insipidus†.b
Effective in both the neurohypophyseal and nephrogenic forms of the disease, decreasing urine volume by up to 50%.b
Particularly useful in nephrogenic diabetes insipidus, since this form of the disease is unresponsive to vasopressin or lypressin and chlorpropamide.b
Useful in patients who are allergic or refractory to vasopressin or lypressin and has been used in combination with one of these hormones and a low-salt diet in patients who excrete an exceptionally large volume of urine.b
Renal Tubular Acidosis
Has been used with success in the treatment of electrolyte disturbances associated with renal tubular acidosis†.b
Renal Calculus Formation
Has been used with success in the prophylaxis of renal calculus formation associated with hypercalciuria†.b
Hydrochlorothiazide Dosage and Administration
Administration
Administer orally.a
Dosage
Individualize according to requirements and response.a Use lowest dosage necessary to produce desired clinical effect.109
If added to potent hypotensive agent regimen, initially reduce hypotensive dosage to avoid the possibility of severe hypotension.a
Pediatric Patients
Usual Dosage
Oral
Infants <6 months of age: Up to 3 mg/kg daily, in 2 divided doses; up to 37.5 mg daily.109
Infants 6 months to 2 years of age: Usually, 1–2 mg/kg daily, in a single or 2 divided doses, up to 37.5 mg daily.109
Children 2–12 years of age: 1–2 mg/kg daily, in a single or 2 divided doses, up to 100 mg daily.a
Hypertension
Oral
Initially, 1 mg/kg once daily.111 Increase dosage as necessary up to a maximum of 3 mg/kg (up to 50 mg) once daily.111
Adults
Hypertension
BP Monitoring and Treatment Goals
Carefully monitor BP during initial titration or subsequent upward adjustment in dosage.d
Avoid large or abrupt reductions in BP.d
Adjust dosage at approximately monthly intervals (more aggressively in high-risk patients [stage 2 hypertension, comorbid conditions]) if BP control is inadequate at a given dosage; it may take months to control hypertension adequately while avoiding adverse effects of therapy.d
SBP is the principal clinical end point, especially in middle-aged and geriatric patients.d Once the goal SBP is attained, the goal DBP usually is achieved.
The goal is to achieve and maintain a lifelong SBP <140 mm Hg and a DBP <90 mm Hg if tolerated.d
The goal in hypertensive patients with diabetes mellitus or renal impairment is to achieve and maintain a SBP <130 mm Hg and a DBP <80 mm Hg.d
Monotherapy
Oral
Initially, 12.5–25 mg daily.101 102 110 112
Gradually increase until the desired therapeutic response is achieved or adverse effects become intolerable, up to 50 mg daily.101 102 109
If adequate response is not achieved at maximum dosage, add or substitute another hypotensive agent.101 102 109 110
Maintenance
Usually, 12.5–50 mg once daily.102 109 110
Combination Therapy
Oral
Initially, administer each drug separately to adjust dosage.a
May use fixed combination if optimum maintenance dosage corresponds to drug ratio in combination preparation.a
Administer each drug separately whenever dosage adjustment is necessary.a
Alternatively, may initially use certain (low-dose hydrochlorothiazide/other antihypertensive) fixed combinations for potentiation of antihypertensive effect and minimization of potential dose-related adverse effects of each drug.102
Edema
Oral
Usually, 25–100 mg daily in 1–3 divided doses.109
Many patients also may respond to intermittent therapy (e.g., alternate days, 3–5 days weekly); decreased risk of excessive diuretic response and resulting electrolyte imbalance.109
Prescribing Limits
Pediatric Patients
Usual Dosage
Oral
Infants <2 years of age: Maximum 37.5 mg daily.109
Children 2–12 years of age: Maximum 100 daily.109
Hypertension
Oral
Maximum 3 mg/kg (up to 50 mg) once daily.111
Adults
Hypertension
Oral
Maximum before switching/adding alternative drug is 50 mg daily.101 102 109
Higher dosages had been used in the past (up to 200 mg daily)e but no longer are recommended because of the risk of adverse effects (e.g., markedly decreased serum potassium).101 Instead, switch to or add alternative drug.
Special Populations
Hepatic Impairment
No specific dosage recommendations for hepatic impairment; caution because of risk of precipitating hepatic coma.a 109
Renal Impairment
No specific dosage recommendations for renal impairment; caution because of risk of precipitating azotemia.a 109
Geriatric Patients
Initiate therapy at the lowest dosage (12.5 mg daily); may adjust dosage in increments of 12.5 mg if needed.112
Cautions for Hydrochlorothiazide
Contraindications
Anuria.b 109
Known hypersensitivity to hydrochlorothiazide, other thiazides, or any ingredient in the formulation.b
Although manufacturers state allergy to other sulfonamide derivatives is a contraindication,109 evidence to support cross-sensitivity is limited, and history of sensitivity to sulfonamide anti-infectives (“sulfa sensitivity”) should not be considered an absolute contraindication.
Warnings/Precautions
Warnings
Severe Renal Impairment
Use with caution; thiazides decrease GFR and may precipitate azotemia.b 109
Effects may be cumulative in impaired renal function.b 109
Hepatic Impairment
Use with caution in hepatic impairment or progressive liver disease (particularly with associated potassium deficiency); electrolyte imbalance may precipitate hepatic coma.b 109
Discontinue immediately if signs of impending hepatic coma appear.b
Hypotensive Agents
May potentiate effects of other hypotensive agents.109 Although additive or potentiated antihypertensive effects usually are used to therapeutic advantage,f hypotension could occur.109 b (See Interactions.)
Lupus Erythematosus
Possible exacerbation or activation of systemic lupus erythematosus.109
Lithium
Generally, do not use with lithium salts.109 (See Interactions.)
Sensitivity Reactions
Hypersensitivity
May occur with or without history of allergy or bronchial asthma.109
Sulfonamide cross-sensitivity unlikely. (See Contraindications under Cautions.)
General Precautions
Electrolyte Imbalance
Monitor for fluid or electrolyte imbalance (hyponatremia, hypochloremic alkalosis, hypokalemia).b 109
Observe for signs of electrolyte imbalance (e.g., dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, confusion, seizures, oliguria, muscle pains, cramps, muscular fatigue, hypotension, tachycardia, nausea, vomiting).109
Perform periodic serum electrolyte determinations (particularly of potassium, sodium, chloride, and bicarbonate); institute measures to maintain normal serum concentrations if necessary.b
Serum and urinary electrolyte measurements are especially important with diabetes mellitus, vomiting, diarrhea, parenteral fluid therapy, or expectations of excessive diuresis.b
Weekly (or more frequent) electrolyte measurement recommended early in treatment; possible to extend interval between measurements to ≥3 months when electrolyte response has stabilized.b
Hypokalemia
May occur after brisk diuresis, when cirrhosis is present, or with prolonged therapy; inadequate oral electrolyte intake may contribute.109
May cause cardiac arrhythmias, exaggerate cardiac response to cardiac glycoside toxicity (increase ventricular irritability).109
Use potassium-sparing diuretics and/or potassium supplementation to avoid or treat hypokalemia.109
Hypochloremia
Generally mild, usually does not require specific treatment except in renal or hepatic impairment.109
Chloride replacement may be required for metabolic acidosis.109
Hyponatremia
Dilutional hyponatremia may occur in edematous patients in hot weather; appropriate treatment usually is water restriction rather than salt administration except when hyponatremia is life-threatening.109
In actual salt depletion, appropriate replacement is treatment of choice.109
Gout
Hyperuricemia or precipitation of gout may occur.109
Hyperglycemia
In diabetic patients, dosage adjustment of insulin or oral hypoglycemics may be required; hyperglycemia may occur and latent diabetes mellitus may become evident.109
Sympathectomy
Antihypertensive effect may be enhanced after sympathectomy.109
Hypomagnesemia
May increase magnesium urinary excretion, resulting in hypomagnesemia.109
Hypercalcemia
May decrease calcium urinary excretion, cause slight intermittent serum calcium increase in absence of known calcium metabolism disorder; marked hypercalcemia may indicate hyperparathyroidism.109
Discontinue prior to performing parathyroid tests.109
Hyperlipidemia
May increase cholesterol and triglyceride concentrations.109
Clinical importance of these changes is unknown.b Diet low in saturated fat and cholesterol usually compensates.b
Hypotensive Effects
Orthostatic hypotension rarely occurs.b
Specific Populations
Pregnancy
Category B.109
Although hypertension during pregnancy responds well to thiazides, and the drugs had been used widely in the past for preeclampsia and eclampsia,b g such use no longer is recommended and other antihypertensives (e.g., methyldopa, hydralazine, labetalol) currently are preferred.f Diuretics are not recommended for pregnancy-induced hypertension because of the maternal hypovolemia associated with this form of hypertension; decreased placental perfusion is possible.g Diuretics are considered second-line agents for control of chronic hypertension in pregnant women.f
Thiazides should not be used as routine therapy in pregnant women with mild edema who are otherwise healthy.b
Edema associated with pregnancy generally responds well to thiazides except when caused by renal disease.b
Lactation
Distributed into milk.g h 109 Discontinue nursing or the drug.109
Although hydrochlorothiazide use generally is considered compatible with breast-feeding,g h thiazides can reduce milk volume and thus suppress lactation.f g
Pediatric Use
No controlled studies in children; use is supported by experience and published literature about hypertension treatment in children.109 111
Geriatric Use
Elderly may be at increased risk of dilutional hyponatremia, especially underweight females with poor oral fluid and electrolyte intake or excessive low-sodium nutritional supplement intake.b (See Hyponatremia under Warnings/Precautions.)
Increased incidence of adverse effects and excessive reduction in BP in those >65 years of age.112 (See Geriatric Patients under Dosage and Administration.)
Hepatic Impairment
Use caution.b (See Hepatic Impairment under Warnings.)
Renal Impairment
Use caution.b (See Severe Renal Impairment under Warnings.)
Consider interruption or discontinuance if progressive renal impairment (rising nonprotein nitrogen, BUN, or serum creatinine) occurs.109
Common Adverse Effects
Potassium depletion, hyperuricemia (usually asymptomatic rarely leading to gout).b Hypochloremic alkalosis in patients at risk (e.g., hypokalemic patients).b Hyperglycemia and glycosuria in diabetics.b
Interactions for Hydrochlorothiazide
Specific Drugs and Laboratory Tests
Drug or Test
|
Interaction
|
Comments
|
|---|
Alcohol
|
Increased risk of postural hypotension with thiazidesb
|
|
Amphetamine
|
Thiazides may cause slightly more alkaline urinary pH; may decrease urinary excretion of some amines (e.g., amphetamine) with concurrent useb
|
Urine pH change is not great during thiazide use and, toxic blood concentrations of amines usually do not occurb
Monitor for signs of toxicity after initiation of thiazides in patients receiving amphetamineb
|
Amphotericin B
|
Additive/potentiated potassium loss b
|
Severe potassium depletion may occur when used concomitantlyb
|
Anticoagulants, oral
|
Postulated that may antagonize oral anticoagulant effectsb
|
Confirmatory evidence is lackingb
|
Antidiabetic agents (sulfonylureas)
|
Thiazide hyperglycemic effect may exacerbate diabetes mellitus, increase antidiabetic agent requirements, and/or cause temporary loss of diabetic control or secondary failure to antidiabetic agentb
|
|
Barbiturates
|
Increased risk of postural hypotension with thiazidesb
|
|
Cholestyramine or colestipol resin
|
May bind thiazides, reduce their GI absorption, with cholestyramine reportedly producing greater binding in vitrob
|
Administer thiazides at least 2 hours before cholestyramine or colestipol when used concomitantlyb
|
Corticosteroids
|
Additive/potentiated potassium loss b
|
Severe potassium depletion may occur when used concomitantlyb
|
Corticotropin
|
Additive/potentiated potassium loss b
|
Severe potassium depletion may occur when used concomitantlyb
|
Diazoxide
|
May potentiate diazoxide hyperglycemic, hypotensive, and hyperuricemic effectsb
|
Use concomitantly with cautionb
|
Digitalis glycosides
|
Thiazide-induced electrolyte disturbances (principally hypokalemia, but also hypomagnesemia and hypercalcemia) may increase digitalis toxicity riskb
|
Perform periodic electrolyte determinations with concomitant use; correct hypokalemia if warrantedb
|
Hypotensive agents
|
Increased hypotensive effects of most other hypotensive agents b
Addition of thiazide to stabilized regimen with potent hypotensive agent (e.g., guanethidine sulfate, methyldopa, ganglionic blocking agent) may cause severe postural hypotensionb
|
Usually used to therapeutic advantageb
|
Insulin
|
May exacerbate diabetes mellitus, increase insulin requirements, cause temporary loss of diabetic control, or secondary failure to insulinb
|
|
Lithium
|
Thiazides (sometimes used with lithium to reduce lithium-induced polyuria) reduced renal lithium clearance within several daysb
Can increase serum lithium concentrations and the risk of lithium intoxicationb
|
Occasionally used to therapeutic advantage to reduce lithium-induced polyuria, but reduce lithium dosage by about 50% and monitor serum lithium carefully.b Generally, avoid concomitant use because of increased lithium toxicity risk.b
|
Methenamine
|
Urinary alkalinization may decrease the effectiveness of methenamine compounds which require a urinary pH of ≤5.5 for optimal activityb
|
Monitor urine pH during concurrent therapyb
|
Neuromuscular blocking agents (e.g., tubocurarine chloride or gallamine triethiodide [both no longer commercially available in the US])
|
May cause prolonged neuromuscular blockadeb
|
Confirmatory evidence lackingb
|
NSAIAs
|
Increased risk of NSAIA-induced renal failure secondary to prostaglandin inhibition and decreased renal blood flowb
NSAIAs may interfere with the natriuretic, diuretic, and antihypertensive response to diuretics b
|
Monitor closely for possible adverse effects and/or attenuation of diuretic-induced therapeutic effects during concomitant useb
|
Opiates
|
Increased risk of postural hypotension with thiazidesb
|
|
Probenecid
|
Blocks thiazide-induced uric acid retentionb
Also blocks renal tubular secretion of thiazide, but effect on thiazide duration of action apparently not studiedb
Apparently enhances excretion of calcium, magnesium, and citrate during thiazide therapy, but urinary calcium concentrations remain below normalb
Sodium, potassium, ammonia, chloride, bicarbonate, phosphate, and titratable acid excretion apparently not affected by concomitant probenecid and thiazide therapyb
|
Used to therapeutic advantageb
|
Quinidine
|
Thiazides may cause slightly more alkaline urinary pH; may decrease urinary excretion of some amines (e.g., quinidine) with concurrent useb
|
Urine pH change is not great during thiazide use, and toxic blood concentrations of amines usually do not occurb
Monitor for signs of toxicity after initiation of thiazideb
|
Test, Amylase (serum)
|
Values may be increased substantially in both asymptomatic patients and in patients developing acute pancreatitis who are receiving thiazidesb
|
|
Test, Corticosteroids (urinary) (Glenn-Nelson technique)
|
Decreased values by interfering in vitro with the absorbance in the modified Glenn-Nelson technique for urinary 17-hydroxycorticosteroids; may also decrease urinary cortisol excretionb
|
Importance of effect on urinary corticosteroids is unclearb
|
Test, Estrogens (spectrophotometric assay of total urinary estrogen; assay of estradiol)
|
Hydrochlorothiazide causes falsely decreased values by interfering with formation of the Kober chromogen, and with the assay of estriol by degrading estriol at the acid hydrolytic stage of the assay; does not occur with chlorothiazideb
|
|
Test, Histamine for pheochromocytoma
|
False-negative resultsb
|
|
Test, Parathyroid function tests
|
May elevate serum calcium in the absence of known disorders of calcium metabolismb
|
Discontinue thiazides prior to performing parathyroid function testsb
|
Test, Phenolsulfonphthalein (PSP)
|
Thiazides compete with phenolsulfonphthalein (PSP) for secretion by the proximal renal tubulesb
|
Importance unknownb
|
Test, Phentolamine
|
False-negative resultsb
|
|
Test, Protein-bound iodine (PBI)
|
Values may be decreased, although usually not to subnormalb
|
|
Test, Triiodothyronine resin uptake
|
Decreased slightly, but 24-hour I 131 uptake is not affectedb
|
|
Test, Tyramine
|
False-negative resultsb
|
|
Vasopressors (e.g., norepinephrine)
|
Possible decreased arterial responsiveness to vasopressor amines b
|
Clinical importance not established;b decrease in pressor response not sufficient to preclude vasopressor use109
|
Hydrochlorothiazide Pharmacokinetics
Absorption
Bioavailability
Variable absorption from GI tract.b
Onset
Diuretic effect: Within 2 hours; peak effect in 3–6 hours.b 109
Hypotensive effect: Generally 3–4 days.b
Duration
Diuretic effect: 6–12 hours.b 109
Food
Food decreases rate and extent of absorption of Microzide capsules.112
Distribution
Extent
Distributed in the extracellular space.a b
Does not cross blood-brain barrier.a
Readily crosses the placenta.a b g
Distributed into breast milk.a g h
Elimination
Metabolism
Not metabolized.a
Elimination Route
Excreted unchanged in urine;a ≥61% eliminated in 24 hours.a
Half-life
5.6–15 hours.a
Special Populations
In patients with uncompensated CHF or impaired renal function, excretion may be delayed.b Effect of hemodialysis on elimination of the drug has not been determined.112
Stability
Storage
Oral
Capsules
Tight containers at <40°C, preferably at 15–30°C; protect from light, moisture, and freezing.112
Oral Solution
Tight containers at <40°C, preferably at 15–30°C.a Avoid freezing.a
Tablets
Tight containers at <40°C, preferably at 15–30°C; protect from light, moisture, and freezing.109 a
ActionsActions
Exact mechanism of diuretic action is unclear; may act by altering metabolism of the tubular cells.b
Enhances excretion of sodium, chloride, and water by interfering with the transport of sodium ions across the renal tubular epithelium.b
Primary site of diuretic action appears to be the cortical diluting segment of the nephron.b
GFR decreases, but unclear whether secondary to a direct effect on renal vasculature or to the decrease in intravascular fluid volume or an increase in tubular pressure caused by the inhibition of sodium and water reabsorption.b The fall in GFR is not important in the mechanism of action.b
Enhances urinary excretion of potassium secondary to increased amount of sodium at distal tubular site of sodium-potassium exchange.b
Increases urinary bicarbonate excretion (although to a lesser extent than chloride excretion) but change in urinary pH is usually minimal; diuretic efficacy is not affected by the acid-base balance of the patient.b
Hypocalciuric effect is thought to result from a decrease in extracellular fluid (ECF) volume, although calcium reabsorption in the nephron may be increased; also, slight or intermittent elevations in serum calcium concentration.b
Rate of uric acid excretion is decreased, probably because of competitive inhibition of uric acid secretion or a decrease in ECF volume and a secondary increase in uric acid reabsorption.b
Hypotensive activity in hypertensive patients; also augments the action of other hypotensive agents.b Precise mechanism of hypotensive action has not been determined, but postulated that part of this effect is caused by direct arteriolar dilation.b
Advice to Patients
Advise patient of signs of electrolyte imbalance (e.g., dryness of the mouth, thirst, weakness, lethargy, drowsiness, restlessness, confusion, seizures, oliguria, muscle pains or cramps, muscular fatigue, hypotension, tachycardia, GI disturbances such as nausea and vomiting).b
Advise patients of importance of compliance with scheduled determinations of serum electrolyte concentrations (particularly potassium, sodium, chloride, and bicarbonate).b
Advise hypertensive patients of importance of continuing lifestyle/behavioral modifications that include weight reduction (for those who are overweight or obese), dietary changes to include foods that are rich in potassium and calcium and moderately restricted in sodium (adoption of the Dietary Approaches to Stop Hypertension [DASH] eating plan), increased physical activity, smoking cessation, and moderation of alcohol intake.
Advise that lifestyle/behavioral modifications reduce BP, enhance antihypertensive drug efficacy, and decrease cardiovascular risk and remain an indispensable part of the management of hypertension.
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs as well as any concomitant illnesses.
Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.
Importance of informing patients of other important precautionary information. (See Cautions.)
Preparations
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Hydrochlorothiazide
Routes
|
Dosage Forms
|
Strengths
|
Brand Names
|
Manufacturer
|
|---|
Oral
|
Capsules
|
12.5 mg*
|
Hydrochlorothiazide Capsules
|
|
|
|
|
Microzide
|
Watson
|
|
Solution
|
50 mg/5 mL*
|
Hydrochlorothiazide Solution
|
|
|
Tablets
|
25 mg*
|
Hydrochlorothiazide Tablets
|
|
|
|
|
HydroDIURIL (scored)
|
Merck
|
|
|
50 mg*
|
Hydrochlorothiazide Tablets
|
|
|
|
|
HydroDIURIL (scored)
|
Merck
|
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Amiloride Hydrochloride and Hydrochlorothiazide
Routes
|
Dosage Forms
|
Strengths
|
Brand Names
|
Manufacturer
|
|---|
Oral
|
Tablets
|
5 mg of Anhydrous Amiloride Hydrochloride and Hydrochlorothiazide 50 mg*
|
Amiloride Hydrochloride and Hydrochlorothiazide Tablets
|
|
|
|
|
Moduretic (scored)
|
Merck
|
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Captopril and Hydrochlorothiazide
Routes
|
Dosage Forms
|
Strengths
|
Brand Names
|
Manufacturer
|
|---|
Oral
|
Tablets
|
25 mg Captopril and Hydrochlorothiazide 15 mg*
|
Capozide (scored)
|
Par
|
|
|
|
Captopril and Hydrochlorothiazide Tablets
|
|
|
|
25 mg Captopril and Hydrochlorothiazide 25 mg*
|
Capozide (scored)
|
Par
|
|
|
|
Captopril and Hydrochlorothiazide Tablets
|
|
|
|
50 mg Captopril and Hydrochlorothiazide 15 mg*
|
Capozide (scored)
|
Par
|
|
|
|
Captopril and Hydrochlorothiazide Tablets
|
|
|
|
50 mg Captopril and Hydrochlorothiazide 25 mg*
|
Capozide (scored)
|
Par
|
|
|
|
Captopril and Hydrochlorothiazide Tablets
|
|
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Enalapril Maleate and Hydrochlorothiazide
Routes
|
Dosage Forms
|
Strengths
|
Brand Names
|
Manufacturer
|
|---|
Oral
|
Tablets
|
5 mg Enalapril Maleate and Hydrochlorothiazide 12.5 mg*
|
Enalapril Maleate and Hydrochlorothiazide Tablets
|
|
|
|
|
Vaseretic
|
Biovail
|
|
|
10 mg Enalapril Maleate and Hydrochlorothiazide 25 mg*
|
Enalapril Maleate and Hydrochlorothiazide Tablets
|
|
|
|
|
Vaseretic
|
Biovail
|
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Methyldopa and Hydrochlorothiazide
Routes
|
Dosage Forms
|
Strengths
|
Brand Names
|
Manufacturer
|
|---|
Oral
|
Tablets, film-coated
|
250 mg Methyldopa and Hydrochlorothiazide 15 mg*
|
Methyldopa and Hydrochlorothiazide Tablets
|
|
|
|
250 mg Methyldopa and Hydrochlorothiazide 25 mg*
|
Aldoril
|
Merck
|
|
|
|
Methyldopa and Hydrochlorothiazide Tablets
|
|
Metoprolol Tartrate and Hydrochlorothiazide
Routes
|
Dosage Forms
|
Strengths
|
Brand Names
|
Manufacturer
|
|---|
Oral
|
Tablets
|
50 mg Metoprolol Tartrate and Hydrochlorothiazide 25 mg
|
Lopressor HCT (scored)
|
Novartis
|
|
|
100 mg Metoprolol Tartrate and Hydrochlorothiazide 25 mg
|
Lopressor HCT (scored)
|
Novartis
|
|
|
100 mg Metoprolol Tartrate and Hydrochlorothiazide 50 mg
|
Lopressor HCT (scored)
|
Novartis
|
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Propranolol Hydrochloride and Hydrochlorothiazide
Routes
|
Dosage Forms
|
Strengths
|
Brand Names
|
Manufacturer
|
|---|
Oral
|
Tablets
|
40 mg Propranolol Hydrochloride and Hydrochlorothiazide 25 mg*
|
Inderide (scored)
|
Wyeth
|
|
|
|
Propranolol Hydrochloride and Hydrochlorothiazide Tablets
|
|
|
|
80 mg Propranolol Hydrochloride and Hydrochlorothiazide 25 mg*
|
Inderide (scored)
|
Wyeth
|
|
|
|
Propranolol Hydrochloride and Hydrochlorothiazide Tablets
|
|
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Spironolactone and Hydrochlorothiazide
Routes
|
Dosage Forms
|
Strengths
|
Brand Names
|
Manufacturer
|
|---|
Oral
|
Tablets, film-coated
|
25 mg Spironolactone and Hydrochlorothiazide 25 mg*
|
Aldactazide
|
Pfizer
|
|
|
|
Spironolactone and Hydrochlorothiazide Tablets
|
|
|
|
50 mg Spironolactone and Hydrochlorothiazide 50 mg*
|
Aldactazide (scored)
|
Pfizer
|
Timolol Maleate and Hydrochlorothiazide
Routes
|
Dosage Forms
|
Strengths
|
Brand Names
|
Manufacturer
|
|---|
Oral
|
Tablets
|
10 mg Timolol Maleate and Hydrochlorothiazide 25 mg
|
Timolide
|
Merck
|
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary)
