remains constant so that calcium is retained within the body. Higher levels of retained calcium are associated with increased bone mineral density and fewer fractures in individuals with osteoporosis. By a poorly understood mechanism, thiazides directly stimulate osteoblast differentiation and bone mineral formation, further slowing the course of osteoporosis. Other uses Bromine intoxication can be treated by giving intravenous saline with either thiazides or Loop diuretics. Contraindications Contraindications include: Hypotension Allergy to sulphur-containing medications Gout Kidney failure Lithium therapy Hypokalemia May worsen diabetes Thiazides reduce the clearance of uric acid since they compete for the same transporter, and therefore raise the levels of uric acid in the blood. Hence, they are prescribed with caution in patients with gout or hyperuricemia. Chronic administration of thiazides is associated with the increase of insulin resistance which can lead to hyperglycemia. Thiazides cause loss of blood potassium, while conserving blood calcium. Thiazides can decrease placental perfusion and adversely affect the fetus, so should be avoided in pregnancy. Adverse effects Hypokalemia – Thiazide diuretics reduce potassium concentration in blood through two indirect mechanisms: inhibition of sodium-chloride symporter at distal convoluted tubule of a nephron and stimulation of aldosterone that activates Na+/K+-ATPase at collecting duct. Inhibition of sodium-chloride symporter increases availability of sodium and chloride in urine. When the urine reaches the collecting duct, the increase in sodium and chloride availability activates Na+/K+-ATPase, which increases the absorption of sodium and excretion of potassium into the urine. Long term administration of thiazide diuretics reduces total body blood volume. This activates the renin–angiotensin system, stimulates the secretion of aldosterone, thus activating Na+/K+-ATPase, increasing excretion of potassium in urine. Therefore, ACE inhibitor and thiazide combination is used to prevent hypokalemia. Hyperglycemia Hyperlipidemia Hyperuricemia Hypercalcemia Hyponatremia Hypomagnesemia Hypocalciuria Mechanism of action Thiazide diuretics control hypertension in part by inhibiting reabsorption of sodium (Na+) and chloride (Cl−) ions from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive Na+-Cl− symporter. The term "thiazide" is also often used for drugs with a similar action that do not have the thiazide chemical structure, such as chlorthalidone and metolazone. These agents are more properly termed thiazide-like diuretics. Thiazide diuretics also increase calcium reabsorption at the distal tubule. By lowering the sodium concentration in the tubule epithelial cells, thiazides indirectly increase the activity of the basolateral Na+/Ca2+ antiporter to maintain intracellular Na+ level, facilitating Ca2+ to leave the epithelial cells into the renal