Thiazide hyperglycemia caused

In long-term treatment, the thiazides may produce hypokalemia, hyperglycemia hyperuricemia, and a 5% increase in plasma cholesterol indapamide has been shown not to increase plasma cholesterol or lipids at therapeuLic doses. Thiazides can cause hyponatremia in patients with large Water intake while on the drug hyponatremia may be associated with nausea, vomiting, and headaches. 

Like all diuretics, the thiazides can cause electrolyte abnormalities, such as hypokalemia and hyponatremia, and dehydration. These complications are uncommon in patients with uncomplicated hypertension, but are more common in patients with heart failure or decompensated hepatic cirrhosis with secondary hyperaldosteronism. Until a patient is accustomed to the effect of a diuretic, dizziness may be experienced. Serum lipid concentrations are slightly raised acutely and hyperglycemia can occur during long-term therapy. Rare effects are thrombocytopenia, rashes, drug fever, cholestatic jaundice, pancreatitis, and precipitation of hepatic... 

Diuretic drugs often cause a mild reduction of the plasma potassium concentration hyponatremia may be observed. Hypercalcemia may occur with hemoconcentration, but occasionally the free-ionized and the protein-bound fraction is increased. Thiazides cause hyperglycemia and reduce glucose tolerance, especially in diabetics. Thiazides may cause prerenal azotemia with hyperuricemia as a result of decreased renal blood flow and GFR as a result of reduced blood volume. Thiazides, like other diuretics, by causing hemoconcentration increase the plasma concentration of lipids. Many thiazides induce microsomal enzymes and thus affect lipoprotein concentrations. 

Interaction of thiazides with beta-blockers can cause a greater risk of hyperglycemia than if either component is given separately (166,167). 

The medications that cause hyperglycemia are glucocorticoids, thiazide diuretics, and epinephrine. 

The thiazide diuretics, also called sulfonamide or ben-zothiadiazide diuretics, vary in their actions. For instance, the potency of hydrochlorothiazide (Hydro-Diuril and Esidrix) is ten times greater than that of chlorothiazide (Diuril), but the drugs have equal efficacy. The duration of action of hydrochlorothiazide, which is 6 to 12 hours, equals that of chlorothiazide. On the other hand, chlorthalidone (Hygroton) has a duration of action lasting 48 hours. Some thiazide derivatives inhibit carbonic anhydrase, which is unrelated to their diuretic activity. Those that are active in this respect may, at sufficient doses, have the same effect on bicarbonate excretion as does acetazola-mide. They cause a moderate loss of sodium (5 to 10% of the filtered load), chloride, and water, and the clearance of free water is impaired. They may cause metabolic alkalosis (resorption of bicarbonate and loss of hydrogen ions), hyperuricemia (enhanced resorption of uric acid), or hyperglycemia (due to directly inhibited insulin release and to hypokalemia). 

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