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Eprosartan / hydrochlorothiazide Side Effects

Medically reviewed by Last updated on May 14, 2023.

Applies to eprosartan / hydrochlorothiazide: oral tablet.


Do not use hydrochlorothiazide and eprosartan if you are pregnant. Stop using this medication and tell your doctor right away if you become pregnant.

If you have diabetes, do not use hydrochlorothiazide and eprosartan together with any medication that contains aliskiren (Amturnide, Tekturna, Tekamlo, Valturna).

Get emergency medical help if you have signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat.

In rare cases, this medicine can cause a condition that results in the breakdown of skeletal muscle tissue, leading to kidney failure. Call your doctor right away if you have unexplained muscle pain, tenderness, or weakness especially if you also have fever, unusual tiredness, and dark colored urine.

Call your doctor at once if you have:

  • eye pain, vision problems;

  • a light-headed feeling, like you might pass out;

  • shortness of breath (even with mild exertion), swelling, rapid weight gain;

  • fever;

  • little or no urinating;

  • jaundice (yellowing of the skin or eyes); or

  • dry mouth, increased thirst, drowsiness, restless feeling, confusion, increased urination, fast heart rate, feeling light-headed, fainting, or seizure (convulsions).

Common side effects may include:

  • stomach pain;

  • back pain;

  • dizziness, drowsiness;

  • headache;

  • runny or stuffy nose, sore throat; or

  • dry cough.

This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects.

For Healthcare Professionals

Applies to eprosartan / hydrochlorothiazide: oral tablet.


Angiotensin II receptor blockade, unlike ACE inhibition, has no impact on the processing of peptides such as bradykinin and substance P, two peptides able to induce cough.

The incidence of cough was not significantly different and averaged 3.5% and 2.6%, respectively, in patients who were given eprosartan and placebo. In comparative studies, the average incidence of cough among patients enalapril ranged from 6.1% to 12.8%, nearly two to three times the incidence of cough among patients given eprosartan (1.5% to 6.5%).[Ref]

Respiratory side effects of eprosartan have included upper respiratory tract infection (8%), rhinitis (4%), pharyngitis (4%), cough (4%), asthma (<1%), and epistaxis (<1%). Respiratory side effects associated with HCTZ are rare, and include approximately 30 case reports of acute noncardiogenic pulmonary edema. These cases are thought to be due to idiosyncrasy or a hypersensitivity mechanism.[Ref]


Cardiovascular side effects of eprosartan reported in less than 1% of patients have included angina pectoris, bradycardia, abnormal ECG, extrasystoles, atrial fibrillation, hypotension (including orthostatic hypotension), tachycardia, palpitations, and peripheral ischemia. The risk of orthostatic hypotension is greater in patients with intravascular salt or volume depletion. Cardiac arrhythmias, including ventricular ectopy and complete AV heart block, are associated with hypokalemia and hyponatremia due to HCTZ. Hypotension has been reported in association with HCTZ-induced pulmonary edema. Orthostatic hypotension may occur and may rarely be associated with syncope, particularly in the elderly.[Ref]


A prospective study of 34 patients who received oral thiazide-type diuretics for 14 years without interruption revealed an increased average fasting blood glucose level after treatment. Withdrawal of thiazide therapy for 7 months in 10 of the patients resulted in average reductions of 10% in the fasting blood glucose and 25% in the 2-hour glucose tolerance test values. A control group was not reported.[Ref]

Endocrine side effects of eprosartan have included increased sweating in less than 1% of patients. Endocrinologic problems associated with thiazide diuretics include glucose intolerance and a potentially deleterious effect on the lipid profile. This may be important in some patients with or who are at risk for diabetes or coronary artery disease. A single case of recurrent parathyroid adenoma is reported, although the association is probably coincidental.[Ref]


Thiazide diuretics may increase serum cholesterol and triglycerides, resulting in increased risk of cholesterol gallstone formation. Reports of bowel strictures associated with thiazide ingestion have been reported in the 1960's although these patients were on a combination HCTZ-potassium product.[Ref]

Gastrointestinal side effects of eprosartan have included abdominal pain (2%). Anorexia, constipation, dry mouth, esophagitis, flatulence, gastritis, gastroenteritis, gingivitis, nausea, periodontitis, toothache, and vomiting have been reported in less than 1% of patients. A case of dysgeusia and burning mouth syndrome has been reported. Gastrointestinal side effects associated with HCTZ are unusual, and include case reports of pancreatitis and acute cholecystitis.[Ref]


In general, eprosartan has been well tolerated. Prior to FDA approval, data have shown that the incidence of adverse drug events (ADEs) associated the use of eprosartan was similar to the incidence of ADEs associated with the use of placebo. The most frequently occurring ADEs associated with the use of eprosartan (but as prevalent among placebo patients) included headache, dizziness, myalgia, sinusitis, diarrhea, bronchitis, dyspepsia, edema, and chest pain. The majority of ADEs were mild to moderate in severity. In placebo-controlled trials, 4% of treated patients discontinued therapy due to an ADE, compared with 6.5% of patients given placebo.[Ref]


Genitourinary side effects associated with eprosartan have included urinary tract infection (1%). Albuminuria, cystitis, hematuria, micturition frequency, polyuria, renal calculus, and urinary incontinence have been reported in less than 1% of patients.[Ref]


Hematologic side effects of eprosartan have included anemia and purpura in less than 1% of patients, decrease in hemoglobin of more than 20% (0.1%), leukopenia (0.3%), neutropenia (1.3%), and thrombocytopenia (0.3%). Hematologic side effects associated with HCTZ are rare. Cases of immune-complex hemolytic anemia, aplastic anemia, and thrombocytopenia have been reported.[Ref]


Hepatic side effects of eprosartan have included minor increases in AST (SGOT), ALT (SGPT), and alkaline phosphatase in less than 1% of patients. One case of elevated ALT >3.5 times ULN has been reported.[Ref]


Metabolic side effects associated with eprosartan have included hypertriglyceridemia (1%); and increased creatine phosphokinase, diabetes mellitus, glycosuria, gout, hypercholesterolemia, hyperglycemia, hyperkalemia, hypokalemia, and hyponatremia in less than 1% of patients. Metabolic side effects associated with HCTZ are common, especially when doses greater than 50 mg per day are used. Mild hypokalemia (decrease of 0.5 mEq/L) occurs in up to 50% of patients, and may predispose patients to cardiac arrhythmias. Metabolic alkalosis, hyponatremia, hypomagnesemia, hypercalcemia, hyperglycemia, and elevated serum uric acid levels are also relatively common. Hydrochlorothiazide (HCTZ) may increase serum cholesterol.[Ref]

Since HCTZ may increase total serum cholesterol by 11%, LDL lipoprotein cholesterol by 12%, and VLDL lipoprotein cholesterol levels by 50%, and may reduce insulin secretion, it should be used with caution in diabetic patients and in those with hypercholesterolemia. True glucose intolerance may develop in approximately 3% of patients. It is typically reversible within six months after discontinuation of therapy.

Hyperuricemia may be an important consideration in patients with a history of gout. Hypophosphatemia and low serum magnesium concentrations may occur, but are usually clinically insignificant except in malnourished patients.[Ref]


Musculoskeletal side effects of eprosartan have included arthralgia (2%), arthritis, arthrosis, skeletal pain, tendonitis, leg cramps, and back pain in less than 1% of patients. In addition, rare reports of rhabdomyolysis have been reported during postmarketing experience in patients receiving angiotensin II receptor blockers. Musculoskeletal side effects associated with HCTZ are unusual, and include case reports of myalgias and chills. Preservation of mineral bone density has also been observed in older patients.[Ref]

Nervous system

Nervous system side effects of eprosartan have included anxiety, ataxia, insomnia, migraine, neuritis, nervousness, paresthesia, somnolence, tremor, vertigo, and tinnitus in less than 1% of patients. A nervous system side effect, cerebrovascular insufficiency, has been associated with HCTZ-induced plasma volume contraction.[Ref]


Ocular side effects associated with eprosartan have included conjunctivitis, abnormal vision, and xerophthalmia in less than 1% of patients.

Ocular side effects have included idiosyncratic reactions to the hydrochlorothiazide component resulting in acute transient myopia and acute angle-closure glaucoma.[Ref]


Other side effects associated with eprosartan affecting the body as a whole have included viral infection (2%), injury (2%), and fatigue (2%). Alcohol intolerance, asthenia, substernal chest pain, peripheral edema, fever, hot flushes, influenza-like symptoms, malaise, rigors, pain, herpes simplex, otitis externa, and otitis media have been reported in less than 1% of patients.[Ref]


Psychiatric side effects of eprosartan have included depression (1%).[Ref]


Although hydrochlorothiazide has been used to treat nephrogenic diabetes insipidus, a case report in which the drug was believed to have caused this condition has been reported.[Ref]

Renal side effects of eprosartan have included minor increases in creatinine (0.6%) and BUN (1.3%). The use of angiotensin II receptor antagonists in patients whose renal function depends on the renin-angiotensin-aldosterone system (i.e., congestive heart failure) has been associated with oliguria and/or progressive azotemia and rarely acute renal failure and/or death. Increases in serum creatinine and BUN have been reported with other angiotensin II receptor antagonists in patients with unilateral or bilateral renal artery stenosis. Renal insufficiency, manifest as an increase in serum creatinine and BUN may occur due to HCTZ-induced intravascular volume depletion. Rare cases of interstitial nephritis have been reported.[Ref]


Dermatologic side effects reported in less than 1% of patients taking eprosartan have included eczema, furunculosis, pruritus, rash, and maculopapular rash. Dermatologic reactions of HCTZ include case reports of erythema annular centrifugum, acute eczematous dermatitis, and morbilliform and leukocytoclastic vasculitis. Thiazides may induce phototoxic dermatitis. In addition, a rare, distinct entity with clinical and laboratory features indistinguishable from those of subacute cutaneous lupus erythematosus is associated with HCTZ.[Ref]

A 67-year-old woman with hypothyroidism, hypercalcemia, depression, and hypertension developed facial erythema, headaches, tremors, confusion and personality changes associated with a new positive ANA and anti-nRNP, and a skin biopsy consistent with lupus erythematosus while taking hydrochlorothiazide (HCTZ), levothyroxine, and amitriptyline. The eruption resolved upon discontinuation of HCTZ, but she later developed a higher ANA titer associated with symptomatic diffuse interstitial pulmonary infiltrates. She was successfully treated with corticosteroids.[Ref]


Hypersensitivity (usually nausea, vomiting, diarrhea, and rash) has been reported in less than 1% of patients taking HCTZ. Rare cases of acute pulmonary edema, interstitial cystitis, and interstitial nephritis, and anaphylaxis have been reported.[Ref]

There have been approximately 34 known cases of thiazide-induced pulmonary edema, encompassing 52 episodes of pulmonary edema, as of 1991 (per a 1996 review). In some cases, doses as small as 12.5 mg were associated with the development of pulmonary edema. The average time to onset of this adverse reaction is 44 minutes, women carry a relative risk of 9:1, and the average age is 56 years. The mortality rate is 6%. Some experts consider this side effect grossly underreported.[Ref]


There are rare case reports of hydrochlorothiazide-induced immune hemolytic anemia. The following illustrates a fatal case:

A 53-year-old man with hypertension developed nausea, vomiting, diarrhea, and progressive anorexia and weakness associated with scleral icterus, anemia with spherocytosis, dark red urine with proteinuria, bilirubinuria, hemoglobinuria, and elevated lactic dehydrogenase levels 18 months after beginning hydrochlorothiazide and methyldopa. Haptoglobin was less than 50 mg per dl. Direct and indirect Coombs tests were positive. The patient died suddenly; autopsy revealed no obvious cause of death, left ventricular hypertrophy, and mild coronary atherosclerosis.[Ref]

Immunologic side effects associated with HCTZ are rare, and include case reports of allergic vasculitis and hemolytic anemia. There are numerous case reports of patients developing a rash histologically identical to subacute cutaneous lupus following HCTZ administration.[Ref]


1. Klein MD. Noncardiogenic pulmonary edema following hydrochlorothiazide ingestion. Ann Emerg Med. 1987;16:901-3.

2. Beaudry C, Laplante L. Severe allergic pneumonitis from hydrochlorothiazide. Ann Intern Med. 1973;78:251-3.

3. Hoegholm A, Rasmussen SW, Kristensen KS. Pulmonary oedema with shock induced by hydrochlorothiazide: a rare side effect mimicking myocardial infarction. Br Heart J. 1990;63:186.

4. Biron P, Dessureault J, Napke E. Acute allergic interstitial pneumonitis induced by hydrochlorothiazide [published erratum appears in Can Med Assoc J 1991 Sep 1;145(5):391]. Can Med Assoc J. 1991;145:28-34.

5. Gould L, Reddy CV, Zen B, Singh BK. Life-threatening reaction to thiazides. N Y State J Med. 1980;80:1975-6.

6. Prupas HM, Brown D. Acute idiosyncratic reaction to hydrochlorothiazide ingestion. West J Med. 1983;138:101-2.

7. Grace AA, Morgan AD, Strickland NH. Hydrochlorothiazide causing unexplained pulmonary oedema. Br J Clin Pract. 1989;43:79-81.

8. Levay ID. Hydrochlorothiazide-induced pulmonary edema. Drug Intell Clin Pharm. 1984;18:238-9.

9. Fine SR, Lodha A, Zoneraich S, Mollura JL. Hydrochlorothiazide-induced acute pulmonary edema. Ann Pharmacother. 1995;29:701-3.

10. Biron P. Thiazide-induced pulmonary edema. Ann Pharmacother. 1996;30:415-6.

11. Fine SR, Lodha A, Zoneraich S, Mollura JL. Thiazide-induced pulmonary edema. Ann Pharmacother. 1996;30:416.

12. Waeber B, Burnier M, Nussberger J, Brunner HR. Experience with angiotensin II antagonists in hypertensive patients. Clin Exp Pharmacol Physiol. 1996;23 ( Suppl:s142-6.

13. Product Information. Teveten (eprosartan). SmithKline Beecham. 2001.

14. Oparil S. Eprosartan versus enalapril in hypertensive patients with angiotensin-converting enzyme inhibitor-induced cough. Curr Ther Res Clin Exp. 1999;60:1-14.

15. Bernal C, Patarca R. Hydrochlorothiazide-induced pulmonary edema and associated immunologic changes. Ann Pharmacother. 1999;33:172-4.

16. Gavras I, Gavras H. Safety and tolerability of eprosartan. Pharmacotherapy. 1999;19:s102-7.

17. Chittivelu S. Hydrochlorothiazide-induced pulmonary edema and associated immunologic changes. Ann Pharmacother. 1999;33:1010-1.

18. Product Information. Teveten HCT (eprosartan-hydrochlorothiazide). Biovail Pharmaceuticals Canada. 2003.

19. Bohm M, Sachse A. Safety and tolerability of eprosartan in combination with hydrochlorothiazide. Drug Saf. 2002;25:599-611.

20. Pollare T, Lithell H, Berne C. A comparison of the effects of hydrochlorothiazide and captopril on glucose and lipid metabolism in patients with hypertension. N Engl J Med. 1989;321:868-73.

21. Papademetriou V, Fletcher R, Khatri IM, Freis ED. Diuretic-induced hypokalemia in uncomplicated systemic hypertension: effect of plasma potassium correction on cardiac arrhythmias. Am J Cardiol. 1983;52:1017-22.

22. Ragnarsson J, Hardarson T, Snorrason SP. Ventricular dysrhythmias in middle-aged hypertensive men treated either with a diuretic agent or a beta-blocker. Acta Med Scand. 1987;221:143-8.

23. Hollifield JW, Slaton PE. Thiazide diuretics, hypokalemia and cardiac arrhythmias. Acta Med Scand Suppl. 1981;647:67-73.

24. Krishna GG, Narins RG. Hemodynamic consequences of diuretic-induced hypokalemia. Am J Kidney Dis. 1988;12:329-31.

25. Mahabir RN, Laufer ST. Clinical evaluation of diuretics in congestive heart failure. A detailed study in four patients. Arch Intern Med. 1969;124:1-7.

26. Holland OB, Kuhnert L, Pollard J, Padia M, Anderson RJ, Blomqvist G. Ventricular ectopic activity with diuretic therapy. Am J Hypertens. 1988;1:380-5.

27. Mouallem M, Friedman E, Shemesh Y, Mayan H, Pauzner R, Farfel Z. Cardiac conduction defects associated with hyponatremia. Clin Cardiol. 1991;14:165-8.

28. Grunwald MH, Halevy S, Livni E. Allergic vasculitis induced by hydrochlorothiazide: confirmation by mast cell degranulation test. Isr J Med Sci. 1989;25:572-4.

29. Weir MR, Wright JT, Jr Ferdinand KC, Cook CA, Champion D, Wong S, Jenkins PA, Kong BW. Comparison of the efficacy and metabolic effects of nicardipine and hydrochlorothiazide in hypertensive black men and women. J Hum Hypertens. 1993;7:141-7.

30. Freis ED. The efficacy and safety of diuretics in treating hypertension. Ann Intern Med. 1995;122:223-6.

31. Klimiuk PS, Davies M, Adams PH. Primary hyperparathyroidism and thiazide diuretics. Postgrad Med J. 1981;57:80-3.

32. Fager G, Berglund G, Bondjers G, Elmfeldt D, Lager I, Olofsson SO, Smith U, Wiklund O. Effects of anti-hypertensive therapy on serum lipoproteins. Treatment with metoprolol, propranolol and hydrochlorothiazide. Artery. 1983;11:283-96.

33. Belleau LJ, Lebel M, Brossard JJ. Merits of adding a beta blocker (acebutolol) to a diuretic (hydrochlorothiazide) in the treatment of hypertension. J Clin Pharmacol. 1982;22:20-7.

34. Murphy MB, Kohner E, Lewis PJ, Schumer B, Dollery CT. Glucose intolerance in hypertensive patients treated with diuretics: a fourteen-year follow-up. Lancet. 1982;2:1293-5.

35. Bell DS. Insulin resistance. An often unrecognized problem accompanying chronic medical disorders. Postgrad Med. 1993;93:99-103,.

36. Kasiske BL, Ma JZ, Kalil RS, Louis TA. Effects of antihypertensive therapy on serum lipids. Ann Intern Med. 1995;122:133-41.

37. Harper R, Ennis CN, Heaney AP, Sheridan B, Gormley M, Atkinson AB, Johnston GD, Bell PM. A comparison of the effects of low- and conventional-dose thiazide diuretic on insulin action in hypertensive patients with NIDDM. Diabetologia. 1995;38:853-9.

38. Burnier M, Hagman M, Nussberger J, Biollaz J, Armagnac C, Brouard R, Weber B, Brunner HR. Short-term and sustained renal effects of angiotensin II receptor blockade in healthy subjects. Hypertension. 1995;25:602-9.

39. van den Meiracker AH, Admiraal PJ, Janssen JA, Kroodsma JM, de Ronde WA, Boomsma F, Sissmann J, Blankestijn PJ, Mulder PG, Man In 't Veld AJ. Hemodynamic and biochemical effects of the AT1 receptor antagonist irbesartan in hypertension. Hypertension. 1995;25:22-9.

40. Rosenberg L, Shapiro S, Slone D, Kaufman DW, Miettinen OS, Stolley PD. Thiazides and acute cholecystitis. N Engl J Med. 1980;303:546-8.

41. Dietz MW. Iatrogenic jejunal ulcer. Am J Roentgenol Radium Ther Nucl Med. 1967;99:136-8.

42. Reinus FZ, Weinberger HA, Fischer WW. Medication-induced ulceration of the small bowel. Am J Surg. 1966;112:97-101.

43. Wagner W, Longerbeam JK, Smith LL, Feikes HL. Drug-induced ulcers of the small bowel causing intestinal obstruction or perforation. Am Surg. 1967;33:7-11.

44. Campbell JR, Knapp RW. Small bowel ulceration associated with thiazide and potassium therapy: review of 13 cases. Ann Surg. 1966;163:291-6.

45. Smith BL, Tedeschi A, Lane CD. Pancreatitis with a twist. Hosp Pract (Off Ed). 1988;23:150,.

46. Diamond MT. Hyperglycemic hyperosmolar coma associated with hydrochlorothiazide and pancreatitis. N Y State J Med. 1972;72:1741-2.

47. Holland GW. Stenosing ulcers of the small bowel associated with thiazide and potassium therapy. N Z Med J. 1965;64:383-5.

48. Castells X, Rodoreda I, Pedros C, Cereza G, Laporte JR. Drug points: Dysgeusia and burning mouth syndrome by eprosartan. BMJ. 2002;325:1277.

49. Hoss DM, Nierenberg DW. Severe shaking chills and fever following hydrochlorothiazide administration. Am J Med. 1988;85:747.

50. Garratty G, Houston M, Petz LD, Webb M. Acute immune intravascular hemolysis due to hydrochlorothiazide. Am J Clin Pathol. 1981;76:73-8.

51. Eisner EV, Crowell EB. Hydrochlorothiazide-dependent thrombocytopenia due to IgM antibody. JAMA. 1971;215:480-2.

52. Kuller L, Farrier N, Caggiula A, Borhani N, Dunkle S. Relationship of diuretic therapy and serum magnesium levels among participants in the Multiple Risk Factor Intervention Trial. Am J Epidemiol. 1985;122:1045-59.

53. Fichman MP, Vorherr H, Kleeman CR, Telfer N. Diuretic-induced hyponatremia. Ann Intern Med. 1971;75:853-63.

54. Papademetriou V, Price M, Notargiacomo A, Gottdiener J, Fletcher RD, Freis ED. Effect of diuretic therapy on ventricular arrhythmias in hypertensive patients with or without left ventricular hypertrophy. Am Heart J. 1985;110:595-9.

55. Polanska AI, Baron DN. Hyponatraemia associated with hydrochlorothiazide treatment . Br Med J. 1978;1:175-6.

56. Pinnock CA. Hyponatraemia associated with hydrochlorothiazide treatment . Br Med J. 1978;1:48.

57. Hakim R, Tolis G, Goltzman D, Meltzer S, Friedman R. Severe hypercalcemia associated with hydrochlorothiazide and calcium carbonate therapy. Can Med Assoc J. 1979;121:591-4.

58. Itescu S, Haskell LP, Tannenberg AM. Thiazide-induced clinically significant hypophosphatemia . Clin Nephrol. 1987;27:161-2.

59. Byatt CM, Millard PH, Levin GE. Diuretics and electrolyte disturbances in 1000 consecutive geriatric admissions. J R Soc Med. 1990;83:704-8.

60. Bain PG, Egner W, Walker PR. Thiazide-induced dilutional hyponatraemia masquerading as subarachnoid haemorrhage . Lancet. 1986;2:634.

61. Benfield GF, Haffner C, Harris P, Stableforth DE. Dilutional hyponatraemia masquerading as subarachnoid haemorrhage in patient on hydrochlorothiazide/amiloride/timolol combined drug . Lancet. 1986;2:341.

62. Duarte CG, Winnacker JL, Becker KL, Pace A. Thiazide-induced hypercalcemia. N Engl J Med. 1971;284:828-30.

63. Seelig CB. Magnesium deficiency in two hypertensive patient groups. South Med J. 1990;83:739-42.

64. Peters RW, Hamilton J, Hamilton BP. Incidence of cardiac arrhythmias associated with mild hypokalemia induced by low-dose diuretic therapy for hypertension. South Med J. 1989;82:966-9,.

65. Kone B, Gimenez L, Watson AJ. Thiazide-induced hyponatremia. South Med J. 1986;79:1456-7.

66. Jones IG, Pickens PT. Diabetes mellitus following oral diuretics. Practitioner. 1967;199:209-10.

67. Berlin I. Prazosin, diuretics, and glucose intolerance. Ann Intern Med. 1993;119:860.

68. Frierson JH, Marvel SL, Thomas GM. Hydrochlorothiazide-induced pulmonary edema with severe acute myocardial dysfunction. Clin Cardiol. 1995;18:112-4.

69. Pickkers P, Schachter M, Hughes AD, Feher MD, Sever PS. Thiazide-induced hyperglycaemia: a role for calcium-activated potassium channels? Diabetologia. 1996;39:861-4.

70. Ilson BE, Martin DE, Boike SC, Jorkasky DK. The effects of eprosartan, an angiotensin II AT(1) receptor antagonist, on uric acid excretion in patients with mild to moderate essential hypertension. J Clin Pharmacol. 1998;38:437-41.

71. Frassetto LA, Nash E, Morris RC, Sebastian A. Comparative effects of potassium chloride and bicarbonate on thiazide-induced reduction in urinary calcium excretion. Kidney Int. 2000;58:748-52.

72. Sebastian A. Thiazides and bone. Am J Med. 2000;109:429-30.

73. Magil AB, Ballon HS, Cameron EC, Rae A. Acute interstitial nephritis associated with thiazide diuretics. Clinical and pathologic observations in three cases. Am J Med. 1980;69:939-43.

74. Dorn MR, Walker BK. Noncardiogenic pulmonary edema associated with hydrochlorothiazide therapy. Chest. 1981;79:482-3.

75. Magil AB. Drug-induced acute interstitial nephritis with granulomas. Hum Pathol. 1983;14:36-41.

76. Delevett AF, Recalde M. Diuretic-induced renal colic. JAMA. 1973;225:992.

77. Goette DK, Beatrice E. Erythema annulare centrifugum caused by hydrochlorothiazide-induced interstitial nephritis. Int J Dermatol. 1988;27:129-30.

78. Alted E, Navarro M, Cantalapiedra JA, Alvarez JA, Blasco MA, Nunez A. Non-cardiogenic pulmonary edema after oral ingestion of hydrochlorothiazide . Intensive Care Med. 1987;13:364-5.

79. Burnier M, Roch-Ramel F, Brunner HR. Renal effects of angiotensin II receptor blockade in normotensive subjects. Kidney Int. 1996;49:1787-90.

80. Ziai F, Ots M, Provoost AP, Troy JL, Rennke HG, Brenner BM, Mackenzie HS. The angiotensin receptor antagonist, irbesartan, reduces renal injury in experimental chronic renal failure. Kidney Int Suppl. 1996;57:s132-6.

81. Bjornberg A, Gisslen H. Thiazides: A cause of necrotising vasculitis? Lancet. 1965;2:982-3.

82. Reed BR, Huff JC, Jones SK, Orton PW, Lee LA, Norris DA. Subacute cutaneous lupus erythematosus associated with hydrochlorothiazide therapy. Ann Intern Med. 1985;103:49-51.

83. Diffey BL, Langtry J. Phototoxic potential of thiazide diuretics in normal subjects. Arch Dermatol. 1989;125:1355-8.

84. Robinson HN, Morison WL, Hood AF. Thiazide diuretic therapy and chronic photosensitivity. Arch Dermatol. 1985;121:522-4.

85. Parodi A, Romagnoli M, Rebora A. Subacute cutaneous lupus erythematosus-like eruption caused by hydrochlorothiazide. Photodermatol. 1989;6:100-2.

86. Goodrich AL, Kohn SR. Hydrochlorothiazide-induced lupus erythematosus: a new variant? J Am Acad Dermatol. 1993;28:1001-2.

87. Rich MW, Eckman JM. Can hydrochlorothiazide cause lupus? J Rheumatol. 1995;22:1001.

88. Brown CW, Deng JS. Thiazide diuretics induce cutaneous lupus-like adverse reaction. J Toxicol Clin Toxicol. 1995;33:729-33.

89. Geanon JD, Perkins TW. Bilateral acute angle-closure glaucoma associated with drug sensitivity to hydrochlorothiazide. Arch Ophthalmol. 1995;113:1231-2.

90. Beck ML, Cline JF, Hardman JT, Racela LS, Davis JW. Fatal intravascular immune hemolysis induced by hydrochlorothiazide. Am J Clin Pathol. 1984;81:791-4.

91. Shirey RS, Bartholomew J, Bell W, Pollack B, Kickler TS, Ness PM. Characterization of antibody and selection of alternative drug therapy in hydrochlorothiazide-induced immune hemolytic anemia. Transfusion. 1988;28:70-2.

Further information

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Some side effects may not be reported. You may report them to the FDA.