INFORMATION FOR HEALTH PROFESSIONALS
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Capozide is available as:
scored, white tablets providing captopril/hydrochlorothiazide, 50mg/25mg (biconvex round; 9.5mm diameter; scored on one side and imprinted SQUIBB 390 on the other)
or
scored, distinct orange-mottled white tablets providing captopril/hydrochlorothiazide, 25mg/15mg (biconvex rounded squares; 7.6 x 7.6mm dimensions; with quadrisect bars engraved on one side and imprinted SQUIBB CAPOZIDE 338 on the other.
The beneficial effects of captopril in hypertension and heart failure result primarily from the suppression of the renin-angiotensin-aldosterone system. There is no consistent correlation, however, between renin levels and response to the medicine. Renin, an enzyme synthesized by the kidneys, is released into the circulation where it acts on a plasma globulin substrate to produce angiotensin I. Angiotensin I is then converted enzymatically by angiotensin-converting enzyme to the octapeptide angiotensin II, a potent endogenous vasoconstrictor substance. Angiotensin II also stimulates aldosterone secretion from the adrenal cortex, thereby contributing to sodium and fluid retention and potassium loss. Captopril prevents the conversion of angiotensin I to angiotensin II by inhibition of angiotensin-converting enzyme. Serum concentrations of aldosterone are decreased and as a result, small increases in serum potassium may occur along with sodium and fluid loss. Increased concentrations of bradykinin or prostaglandin E2 may also have a role in the therapeutic effect of captopril. Captopril produces a reduction in peripheral resistance in hypertensive patients with either no change or an increase in cardiac output. Treatment with captopril may induce regression of left ventricular hypertrophy in hypertensive patients. Reduction of blood pressure occurs within 30 minutes and is often maximal 60 to 90 minutes after administration of an individual dose of captopril. The duration of effect appears to be dose related.
Hydrochlorothiazide is a thiazide diuretic. The precise mechanism of the antihypertensive effect of the thiazides is unknown. Thiazides affect the renal tubular mechanism of electrolyte reabsorption and increase excretion of sodium and chloride in approximately equivalent amounts. Natriuresis causes a secondary loss of potassium and bicarbonate. Hydrochlorothiazide increases plasma renin activity, increases aldosterone secretion, and decreases serum potassium. Concurrent captopril administration attenuates the potassium loss associated with hydrochlorothiazide. Peripheral vascular resistance is reduced. Onset of diuretic action following oral administration occurs in 2 hours and the peak action in about 4 hours, and persists for 6 to 12 hours.
Following oral administration of Capozide rapid absorption of captopril occurs with peak blood levels at about one hour. Although the presence of food in the gastrointestinal tract reduces the absorption of captopril this does not appear to substantially reduce its antihypertensive efficacy. After administration of a radio labelled oral dose, the apparent elimination half life for total radioactivity in blood is about 12 hours for the 12 to 48 hour time interval. The half life of unchanged drug is approximately 2 hours. About 75% of a dose of captopril is excreted in the urine; 50% as unchanged drug, and the remainder as the disulphide dimer of captopril and captopril -cysteine disulphide. Approximately 25 to 30% of the circulating drug is protein bound. Excretion of captopril is reduced in patients with renal impairment.
Absorption of hydrochlorothiazide following oral administration of Capozide is relatively rapid with 68% to 80% absorption of an oral dose. Hydrochlorothiazide has a plasma half-life of 3 to 4 hours. It is rapidly eliminated by the kidney, mainly as unchanged drug. There is preferential binding to red blood cells. Hydrochlorothiazide should be used with caution in patients with impaired hepatic function or progressive liver disease, since minor alterations of fluid and electrolyte balance may precipitate hepatic coma.
There are no significant differences in the pharmacokinetic profile between that of the combination and those of the single components.
Capozide is indicated for the treatment of patients with hypertension, who are not adequately controlled on monotherapy. Capozide is therefore not indicated as first line therapy.
Capozide is also indicated for the treatment of patients with heart failure who have not responded adequately to or cannot be controlled by conventional therapy.
This fixed combination medicine is not indicated for initial therapy of hypertension and the dose should be adjusted to the individual patient's needs.
Capozide may be administered either once or twice daily.
Dosage may be varied by use of either Capozide 25mg/15mg or Capozide 50mg/25mg. The usual dose is Capozide 50mg/25mg once a day.
If additional control beyond that provided by the 50mg/25mg b.d. Capozide dose is indicated, it is recommended that other antihypertensive agents be added to the regimen.
Captopril has been used in conjunction with a diuretic and digitalis with the dosage of each individually titrated. The combination tablet should not be used to initiate therapy; however, once the optimal dose of captopril and diuretic has been established, Capozide may be substituted for continued therapy.
Because captopril and hydrochlorothiazide are excreted primarily by the kidneys, excretion rates are reduced in patients with impaired renal function. These patients will take longer to reach steady-state captopril levels and will reach higher steady-state levels for a given daily dose than patients with normal renal function. Therefore, these patients may respond to smaller or less frequent doses of Capozide. After the desired therapeutic effect has been achieved, the dose intervals should be increased or the total daily dose reduced until the minimal effective dose is achieved. When concomitant diuretic therapy is required in patients with severe renal impairment, a loop diuretic (eg, frusemide), rather than a thiazide diuretic is preferred for use with captopril; therefore, for patients with severe renal dysfunction the captopril-hydrochlorothiazide combination tablet is not usually recommended.
A history of previous hypersensitivity to captopril, thiazides, any sulfonamide derived medicine or the inactive ingredients of Capozide Tablets.
Pregnancy (see Use In Pregnancy)
Patients with a history of hereditary and/or idiopathic angioedema or angioedema associated with previous treatment with an angiotensin converting enzyme inhibitor.
Anuria
Possibly because angiotensin-converting enzyme is essential for degradation of endogenous bradykinin, patients receiving ACE inhibitors are subject to a variety of adverse reactions producing effects ranging from relatively mild, such as cough (see Cough this section), to serious such as the following:
Severe life-threatening angioedema has been reported rarely with most of the angiotensin converting enzyme (ACE) inhibitors. The overall incidence is approximately 0.1% to 0.2%. There seems to be no sex difference in the incidence of angioedema or in the predisposition to angioedema in patients with heart failure or hypertension. In the majority of reported cases, the symptoms occurred during the first week of therapy. The aetiology is thought to be non-immunogenic and may be related to accentuated bradykinin activity. Usually the angioedema involves non-pitting oedema of the skin and oedema of the subcutaneous tissues and mucous membranes.
Angioedema of the face, extremities, lips, tongue, glottis and/or larynx has been reported in patients treated with ACE inhibitors. In such a case, the product should be discontinued promptly and appropriate monitoring instituted to ensure complete resolution of the symptoms. In instances when swelling has been confined to the face and lips, angioedema has generally resolved either without treatment or with antihistamines. Angioedema associated with laryngeal oedema is potentially life threatening. Where involvement of the tongue, glottis, or larynx is likely to cause airway obstruction appropriate therapy, including adrenalin and oxygen administration, should be carried out promptly or the patient hospitalised. Patients who respond to medical treatment should be observed carefully for a possible re-emergence of symptoms of angioedema.
There are reports where changing the patient over to another ACE inhibitor was followed by recurrence of oedema and others where it was not. Because of the potential severity of this rare event another ACE inhibitor should not be used in patients with a history of angioedema to a drug of this class.
Two patients undergoing desensitising treatment with hymenoptera venom while receiving another ACE inhibitor, enalapril, sustained life-threatening anaphylactoid reactions. In the same patients, these reactions were avoided when the ACE inhibitor was temporarily withheld, but they reappeared upon inadvertent rechallenge. Therefore, caution should be used in patients treated with ACE inhibitors undergoing such desensitization procedures.
Patients haemodialyzed with high-flux polyacrylonitrile ("AN69") membranes are highly likely to experience anaphylactoid reactions if they are treated with ACE inhibitors. Anaphylactiod reactions have also been reported in patients undergoing low-density lipoprotein apheresis with dextran sulfate absorption. These combinations should therefore be avoided, either by use of a different class of medication or alternative membranes (eg, cuprophane or polysulphone PSF for haemodialysis).
Proteinuria has been seen in less than 1% of patients receiving captopril, but this has been predominantly in those who had prior renal disease, or in those given relatively high doses (in excess of 150mg per day), or both. Alterations in renal function (as assessed by blood urea nitrogen and serum creatinine) were infrequent in these patients and did not occur in those who had no prior renal disease. In patients without prior evidence of renal disease the incidence of proteinuria was 0.5%. In those patients without prior evidence of renal disease and receiving 150mg of captopril or less per day the incidence was 0.2%. Nephrotic syndrome (hypoalbuminaemia, oedema, and protein excretion greater than 3 grams per day) occurred in about one-fifth of the proteinuric patients. In most cases, proteinuria subsided or cleared within 6 months whether or not captopril was continued. Although membranous glomerulopathy was found in biopsies taken from some proteinuric patients, a causal relationship to captopril has not been established since pretreatment biopsies were not taken and membranous glomerulopathy has been shown to occur in hypertensive patients not receiving captopril.
Patients with prior renal disease or those taking captropril at doses greater than 150mg per day, should have urinary protein estimations (dipstick) done prior to treatment and periodically thereafter. If these show increasing amounts of urinary protein, a 24-hour quantitative determination of urinary protein should be done. If this exceeds one gram per day, the benefits and risks of continuing Capozide should be evaluated.
Neutropenia has occurred in some patients receiving captopril but the risk of neutropenia is dependent on the clinical status of the patient especially the presence of pre-existing impaired renal function, collagen vascular disease, immunosuppressant therapy, or a combination of these complicating factors.
In clinical studies with captopril involving 4,132 uncomplicated hypertensive patients, neutropenia occurred in one patient (0.02% of patients). However, all patients receiving Capozide should be told to report any signs of infection (eg, sore throat, fever). Serious infections resulting from the neutropenia and which proved fatal in a few cases occurred only in patients with impaired renal function. A complete white blood count should be done immediately when infection is present. If the infection occurs during the first three months of therapy, Capozide should be discontinued until the results of the blood count are known. In patients with renal impairment not associated with collagen vascular disease and complicated by coadministration of immunosuppressant drugs, neutropenia occurred in 0.3% of cases. Daily doses of captopril were relatively high in these patients.
In patients with collagen vascular disease (eg, systemic lupus erythematosus, scleroderma), particularly those with coexisting renal impairment, Capozide should be prescribed only after an assessment of benefit and risk and then with caution since neutropenia has occurred in 8 of 124 such patients in clinical trials. Similar caution should be exercised in patients receiving immunosuppressant drugs.
Neutropenia was noted 2½ to 13 weeks after captopril had been started. Thus, for patients with impaired renal function, collagen vascular disease, or who are receiving immunosuppressant drugs, white blood cell and differential counts should be performed prior to therapy, every 2 weeks during the first 3 months of Capozide therapy and periodically thereafter. If the neutrophil count falls below 1000/mm3, Capozide should be discontinued and the patient's course should be followed. In clinical trials, neutrophil counts returned to normal in about 2 weeks in most cases upon discontinuing captopril.
Thiazide diuretics also have been reported rarely to cause agranulocytosis and bone marrow depression.
Two year studies with captopril doses of 50 to 1350mg/kg/day in mice and rats failed to show any evidence of carcinogenic potential. Captopril studies in rats have revealed no impairment of fertility.
No long-term hydrochlorothiazide studies in animals have been performed to evaluate carcinogenic potential, mutagenesis, or whether this drug affects fertility in males or females.
Although most patients will tolerate the antihypertensive effects of Capozide well, they may occasionally experience dizziness or lightheadedness, usually mild, indicative of hypotension, that may occur within one hour of the first dose. In most instances, symptoms are relieved simply by instructing the patient to lie down.
Hypotension is most likely to occur in patients who are volume- and/or salt-depleted as a result of prolonged diuretic therapy, salt restriction, dialysis, diarrhoea, or vomiting. Volume and/or salt depletion should be corrected before initiating therapy with Capozide.
The likelihood of an exaggerated hypotensive reaction can be predicted early if the patient is under medical supervision during the first hour after initial dosing; and if necessary, it can be rapidly reversed by intravenous infusion of normal saline.
A hypotensive episode following the initial dose of Capozide should not preclude further titration of the medicine.
Thiazides may potentiate the action of other hypertensive drugs (see Interactions ). In addition, the antihypertensive effects of thiazide diuretics may be increased in the postsympathectomy patient.
In patients with congestive heart failure, with or without associated renal insufficiency, ACE inhibitor therapy may cause excessive hypotension, which may be associated with oliguria, azotemia, and rarely with acute renal failure and death. In such patients, Capozide therapy should be initiated under close medical supervision. Patients should be followed closely for the first two weeks for treatment and whenever the dose is increased.
Capozide should be used with caution in patients with renal disease. Patients with bilateral renal artery stenosis have developed increases in blood urea nitrogen and serum creatinine after reduction of blood pressure with captopril usually administered along with a diuretic. Capozide, therefore, would not be appropriate for patients with severe renal impairment since loop diuretics (eg, frusemide) rather than a thiazide are preferred for such patients. Azotemia may be induced by thiazides in patients with impaired renal function. Some patients with heart failure have experienced a reduction in renal function during long-term treatment with captopril that usually stabilized at the reduced level.
Capozide should also be used with caution in patients with impaired hepatic function or progressive liver disease, since minor alterations of fluid and electrolyte balance may precipitate hepatic coma.
Capozide, as with any medicine that reduces vascular resistance, should be used only with extreme caution in patients with haemodynamically significant aortic stenosis because of the potentially harmful consequences of reduced coronary perfusion secondary to the reduced blood pressure.
Rarely, ACE inhibitors have been associated with a syndrome that starts with cholestatic jaundice and progresses to fulminant hepatic necrosis and sometimes death. The mechanism of this syndrome is not understood. Patients receiving ACE inhibitors who develop jaundice or marked elevations of hepatic enzymes should discontinue the ACE inhibitor and receive appropriate medical follow-up.
Determination of serum electrolytes to detect possible electrolyte imbalance should be performed at appropriate intervals.
Thiazides, including hydrochlorothiazide, can cause fluid or electrolyte imbalance (hypokalemia, hyponatremia, and hypochloraemic alkalosis). Patients should be periodically observed for clinical signs or symptoms of fluid and electrolyte imbalance, such as dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, nausea or vomiting. Although hypokalemia may develop when thiazide diuretics are used, especially with brisk diuresis or in the presence of severe cirrhosis, concurrent therapy with captopril reduces diuretic-induced hypokalemia. The net effect of Capozide may be to elevate, reduce or leave serum potassium unchanged. Hypokalemia, should it occur, can sensitize or exaggerate the response of the heart to the toxic effects of digitalis (eg, increased ventricular irritability). Chloride deficit is generally mild and usually does not require treatment. Calcium excretion is decreased by thiazides. Pathological changes in the parathyroid gland with hypercalcemia and hypophosphatemia have been observed in a few patients on prolonged thiazide therapy. The common complications of hyperparathyroidism such as renal lithiasis, bone resorption, and peptic ulceration have not been seen. Thiazides should be discontinued before carrying out tests for parathyroid function. Thiazides have been shown to increase the urinary excretion of magnesium, which may result in hypomagnesaemia.
Hyperuricemia may occur, and an acute attack of gout may be precipitated in certain patients receiving thiazide therapy. Insulin requirements in diabetic patients may be altered and latent diabetes mellitus may become manifested during thiazide administration. Increases in cholesterol and triglyceride levels have been associated with thiazide diuretic therapy.
Cough has been reported with the use of ACE inhibitors, including captopril.
Characteristically the cough is nonproductive, persistent and resolves after discontinuation of therapy. ACE inhibitor-induced cough should be considered as part of the differential diagnosis of cough.
Thiazide diuretics have been reported to cause exacerbation or activation of systemic lupus erythematosus.
Captopril may cause a false-positive urine test for acetone.
When used in pregnancy during the second and third trimester, ACE inhibitors can cause injury and even death to the developing foetus. When pregnancy is detected Capozide should be discontinued as soon as possible. In humans, exposure of the mother to ACE inhibitors in the second and third trimesters of pregnancy has been associated with foetal and neonatal injury, including hypotension, neonatal skull hypoplasia, anuria, reversible and irreversible renal failure and death. Oligohydramnios has been reported, presumably as a consequence of decreased renal function, in the foetus; in this setting oligohydramnios has been associated with foetal limb contractures, craniofacial deformation and hypoplastic lung development. Prematurity, intrauterine growth retardation and patent ductus arteriosus have been reported, although it is not clear whether these occurrences were due to the ACE inhibitor exposure. Consequently women who become pregnant whilst taking Capozide should be switched to alternative, appropriate anti-hypertensive therapy.
Like captopril, thiazides cross the placenta and can cause foetal or neonatal jaundice, thrombocytopenia, and other adverse reactions which have occurred in the adult.
Female patients of childbearing age should be told about the consequences of second- and third-trimester exposure to ACE inhibitors as well as the possible effects of thiazides. Women should be instructed to notify their doctor immediately if pregnancy is suspected.
Both captopril and hydrochlorothiazide appear in breast milk. If Capozide is deemed essential, the patient should stop nursing.
In patients undergoing major surgery or during anaesthesia the use of Capozide may lead to hypotension which can be corrected by volume expansion. It may also increase the response to tubocurarine. (See Interactions )
Safety and effectiveness of Capozide in children have not been established.
Adverse effects that have been reported when the captopril component of Capozide is administered alone are:
The rash associated with captopril is usually pruritic and maculopapular, rarely urticarial. It generally occurs during the first month of treatment, and is usually self-limited and reversible; it may respond to antihistamine therapy. In the majority of patients the rash resolves with continuation of therapy at the same or reduced dosage.
Pruritus, flushing, erythema multiform (including Stevens-Johnson syndrome) exfoliative dermatitis, bullous pemphigus, a reversible pemphigoid-like lesion, photosensitivity and angioedema have also been reported with captopril therapy.
2% of patients receiving 150mg or less per day of captopril developed a diminution or loss of taste perception. At doses in excess of 150mg per day 7% of patients experienced this effect. Taste impairment is reversible and usually self-limited (2 to 3 months). In most patients the condition resolved with the continuation of therapy. Stomatitis, resembling aphthous ulcers, anorexia, gastric irritation, nausea, vomiting, cramping, diarrhoea, constipation, glossitis, dyspepsia, abdominal pain, peptic ulcer, dizziness, headache, malaise, dry mouth, cholestatic jaundice, and pancreatitis, have been reported. Elevations of liver enzymes have been noted in a few patients receiving captopril although no causal relationship has been found. Rare cases of hepatocellular injury with secondary cholestasis have also been reported in association with captopril administration (See Warnings and Precautions, Hepatic Failure ).
Proteinuria (see Warnings and Precautions ) and transient elevations of BUN and creatinine have occurred with the use of captopril (see Warnings and Precautions ). Electrolyte disturbances, renal failure, nephrotic syndrome, polyuria, oliguria and urinary frequency have been reported
Neutropenia, agranulocytosis, anaemia (including aplastic and haemolytic) thrombocytopenia and pancytopenia
Hypotension (dizziness, syncope, orthostatic hypotension) may occur after initiation of Capozide therapy. Patients with heart failure, renin-dependent hypertension or who are significantly volume-depleted (see Warnings and Precautions ) are particularly at risk. Tachycardia, chest pain and palpitations have each been observed in approximately 1% of captopril treated patients. Angina pectoris, myocardial infarction, Raynaud's syndrome and congestive heart failure have occurred in 0.3% of captopril patients. Cardiac arrest, cerebrovascular accident/insufficiency, rhythm disturbances have also been reported.
Angioedema has been reported in approximately 0.1% of captopril treated patients. Angioedema involving the upper airways has caused fatal airways obstruction.
Cough has been reported in 0.5-2% of patients treated with captopril in clinical trials. Bronchospasm, eosinophilic pneumonitis, dyspnoea and rhinitis have also been reported.
Symptomatic hyponatremia.
Myalgia, myasthenia.
Ataxia, confusion, depression, nervousness, somnolence, fatigue, insomnia, paraesthesia, headache.
Blurred vision.
Impotence.
Asthenia, gynaecomastia, alopecia.
(See Warnings and Precautions, Use in Pregnancy ).
Hydrochlorothiazide therapy has been associated with the following adverse effects:
Anorexia, gastric irritation, nausea, vomiting, cramping, diarrhea, constipation, jaundice (intrahepatic cholestatic jaundice), pancreatitis, and sialadenitis.
Dizziness, vertigo, parasthesias, headache, and xanthopsia.
Leukopenia, agranulocytosis, thrombocytopenia, aplastic anaemia, and haemolytic anaemia.
Orthostatic hypotension.
Purpura, photosensitivity, rash, urticaria, necrotizing angiitis (vasculitis; cutaneous vasculitis), fever, respiratory distress including pneumonitis, and anaphylactic reactions.
Hyperglycaemia, glycosuria, hyperuricemia, muscle spasm, weakness, restlessness, and transient blurred vision. Impotence has been observed with some thiazide diuretics used in high dosage.
Patients on diuretics and especially those in whom diuretic therapy was recently instituted, as well as those on severe dietary salt restriction or dialysis, may occasionally experience a precipitous reduction of blood pressure usually within the first hour after receiving the initial dose of captopril.
The possibility of hypotensive effects with captopril can be minimized by either discontinuing the diuretic or increasing the salt intake approximately one week prior to initiation of treatment with captopril or initiating therapy with small doses (6.5 or 12.5mg). Alternatively, provide medical supervision for at least one hour after the initial dose.
Nitroglycerin or other nitrates or other drugs having vasodilator activity should, be administered cautiously, and a lower dosage considered.
Captopril's effect will be augmented by antihypertensive agents that cause renin release. For example, diuretics (eg, thiazides) may activate the renin-angiotensin-aldosterone system.
The sympathetic nervous system may be especially important in supporting blood pressure in patients receiving captopril alone or with diuretics. Therefore, agents affecting sympathetic activity (eg, ganglionic blocking agents or adrenergic neuron blocking agents) should be used with caution. Beta-adrenergic blocking drugs add some further antihypertensive effect to captopril, but the overall response is less than additive.
Since captopril decreases aldosterone production, elevation of serum potassium may occur. Potassium-sparing diuretics such as spironolactone, triamterene, or amiloride, or potassium supplements, should be given only for documented hypokalemia, and then with caution and the patient's serum potassium monitored frequently, since they may lead to a significant increase in serum potassium. Salt substitutes containing potassium should also be used with caution.
In some patients, these agents can reduce the effects of diuretics. It has been reported that indomethacin may reduce the antihypertensive effect of captopril, especially in cases of low renin hypertension. Other nonsteroidal anti-inflammatory agents (eg, aspirin) may also have this effect.
Increased serum lithium levels and risk of lithium toxicity have been reported in patients receiving concomitant lithium and ACE inhibitor therapy. The risk of lithium toxicity is further increased by the use of hydrochlorothiazide. Thus Capozide and lithium should be coadministered with caution, and frequent monitoring of serum lithium levels is recommended.
When administered concurrently the following medicines may interact with thiazide diuretics:
Potentiation of orthostatic hypotension may occur.
Hyperglycaemia induced by thiazides may require dosage adjustment of the antidiabetic drug.
Dosage adjustments of antigout medication may be necessary, since hydrochlorothiazide may raise the level of blood uric acid. Increase in dosage of probenecid or sulfinpyrazone may be necessary.
Thiazide diuretics may increase serum calcium levels due to decreased excretion. If calcium must be prescribed, serum calcium levels should be monitored and calcium dosage adjusted accordingly.
May delay or decrease absorption of hydrochlorothiazide. Thiazide diuretics should be taken at least one hour before or four to six hours after these medications.
Additive effect or potentiation. Potentiation occurs with ganglionic or peripheral adrenergic blocking drugs. Hydrochlorothiazide may interact with diazoxide; blood glucose, serum uric acid levels, and blood pressure should be monitored.
Intensified electrolyte depletion, particularly hypokalemia.
Effects of preanaesthetic and anaesthetic agents may be potentiated; adjust dosage of these agents accordingly and if possible, hydrochlorothiazide therapy should be discontinued one week prior to surgery.
Possible decreased response to pressor amines but not sufficient to preclude their use. Caution should be exercised.
Possible increased responsiveness to the muscle relaxant; dosage adjustments may be required. Fluid and electrolyte imbalances should be monitored and corrected prior to surgery if feasible.
In the event of overdosage with Capozide, hypotension would be the most important problem. Volume expansion with an intravenous infusion of normal saline is the treatment of choice to normalize the blood pressure.
Captopril is removed by haemodialysis. The degree to which hydrochlorothiazide is removed by haemodialysis has not been clearly established.
Store below 30°C. Protect from moisture.
Prescription medicine.
Tablets:
50mg/25mg in calendar blister packs of 30 tablets.
25mg/15mg in calendar blister packs of 30 tablets.
Both strengths contain the following inactive ingredients: lactose, microcrystalline cellulose, pregelatinized starch, magnesium stearate and stearic acid. Capozide 25mg/15mg tablets also contain FD&C yellow No.6.
Bristol-Myers Squibb (NZ) Limited
Stanway Business Park
Tower 2, Level 1
646 Great South Road
Ellerslie, Auckland
NEW ZEALAND
Telephone Number: (09) 571 5250; Toll Free Number: 0800 80 40 80
7 March 1997.