xanthopsia
Hydrochlorothiazide, HCTZ (Microzide) Adverse Reactions
Adverse GI effects associated with thiazide therapy include abdominal pain, anorexia, gastric irritation, nausea/vomiting, cramps, diarrhea, constipation, sialadenitis, and pancreatitis.
Patients receiving hydrochlorothiazide should be monitored closely for signs of electrolyte imbalance including hyponatremia, hypokalemia, hypomagnesemia, and hypochloremia. Patients should be aware of the symptoms of these disturbances (e.g., lassitude, mental confusion, fatigue, faintness, dizziness, muscle cramps, tachycardia, headache, paresthesia, thirst, anorexia, nausea, or vomiting), and report these signs immediately. Thiazides also can decrease urinary calcium excretion, resulting in hypercalcemia.
Hypokalemia is one of the most common adverse effects associated with thiazide diuretic therapy and can lead to cardiac arrhythmias. This effect is especially important to consider in patients receiving cardiac glycoside therapy because potassium depletion increases the risk of cardiac toxicity. Hyperaldosteronism, secondary to cirrhosis or nephrosis, can predispose patients to hypokalemia when hydrochlorothiazide is administered. Low dietary-potassium intake, potassium-wasting states, or administration of potassium-wasting drugs also can predispose patients to hydrochlorothiazide-induced hypokalemia. Patients receiving hydrochlorothiazide therapy may require supplemental potassium to prevent hypokalemia or metabolic alkalosis.
Hypochloremic alkalosis can occur with hypokalemia during hydrochlorothiazide therapy, and it is particularly likely to occur in patients with other losses of potassium and/or chloride such as through severe vomiting, diarrhea, excessive sweating, GI drainage, paracentesis, or potassium-losing renal diseases.
Patients receiving hydrochlorothiazide can develop a dilutional hyponatremia, but it usually is asymptomatic and moderate. Withdrawal of the drug, fluid restriction, and potassium or magnesium supplementation typically will return the serum sodium concentration to normal, but severe hyponatremia can occur. Geriatric patients are especially susceptible to developing hyponatremia, so care should be taken when diuretics are administered to these patients.
Hydrochlorothiazide reportedly has caused azotemia and interstitial nephritis, resulting in reversible renal failure. These effects have occurred mainly in patients with preexisting renal disease.
Hydrochlorothiazide can produce glycosuria and hyperglycemia in diabetic patients. Blood and/or urine glucose levels should be assessed more carefully in diabetic patients receiving hydrochlorothiazide.
Thiazide diuretics are well known to cause hyperuricemia. The Framingham Study showed that acute gout occurred in only 20% of patients with hyperuricemia. Thiazide diuretics appear to interfere with proximal tubule secretion of uric acid since thiazides are also organic acids and they compete with uric acid for binding at this site. Since thiazides reduce the clearance of uric acid, patients with gout or hyperuricemia may have exacerbations of their disease.
Hypercholesterolemia and/or hypertriglyceridemia have been associated with thiazide diuretic therapy. Although elevations in total cholesterol concentrations of 8% can negate the protection against coronary heart disease provided by a 5 mmHg reduction in blood pressure, data from long-term studies suggest diuretic-induced cholesterol changes are not clinically significant and do not contribute to coronary heart disease risk. After approximately one year of treatment, total serum cholesterol concentrations will subside to baseline or lower, suggesting diuretic-induced cholesterol changes are not a significant coronary heart disease risk factor.
Orthostatic hypotension and hypotension can occur during hydrochlorothiazide therapy and can be exacerbated by alcohol, narcotics, or antihypertensive drugs.
Thiazide diuretics have been associated with intrahepatic cholestatic jaundice (rare), and hyperbilirubinemia. Caution should be used when thiazides are administered to jaundiced infants due to the risk of hyperbilirubinemia.
Adverse CNS effects associated with thiazide therapy include dizziness, headache, paresthesias, vertigo, and xanthopsia.
While their incidence is rare, agranulocytosis, aplastic anemia, pancytopenia, hemolytic anemia, leukopenia, and thrombocytopenia have been reported with thiazide diuretic therapy.
Other adverse effects reported with hydrochlorothiazide include blurred vision, muscle spasm, impotence, and weakness.
Due to the diuretic action of hydrochlorothiazide, polyuria can be troublesome for some patients during therapy.
Adverse dermatologic reactions to hydrochlorothiazide and other thiazide diuretics are uncommon but may occur. These reactions include purpura, photosensitivity, rash, alopecia, urticaria, erythema multiforme including Stevens-Johnson syndrome, exfoliative dermatitis including toxic epidermal necrolysis (TEN), and polyarteritis nodosa.
[ Last revised: 8/5/2004 11:57:00 AM ]
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