[Inappropriate antidiuretic hormone secretion syndrome associated with ramipril treatment].

Farmacia Hospitalaria 01/2010; 34(3):154-5. DOI: 10.1016/j.farma.2009.10.004
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    ABSTRACT: A 63-year-old white female who was being treated for hypertension with lisinopril presented with seizures, altered mental status, and a serum sodium of 101 mEq/L. Serum sodium prior to initiation of lisinopril therapy was 137 mEq/L. The hyponatremia was corrected and did not recur after lisinopril was stopped. The hyponatremia may have been a result of polydipsia and inappropriate antidiuresis secondary to ACE-inhibitor therapy.
    The American Journal of the Medical Sciences 04/1992; 303(3):177-9. DOI:10.1097/00000441-199203000-00009 · 1.52 Impact Factor
  • Journal of the American Geriatrics Society 01/1996; 43(12):1448-9. DOI:10.1111/j.1532-5415.1995.tb06638.x · 4.22 Impact Factor
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    ABSTRACT: To describe a case of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) associated with lisinopril therapy. A 76-year-old white woman who was being treated with lisinopril and metoprolol for hypertension presented with headaches accompanied by nausea and a tingling sensation in her arms. Her serum sodium was 109 mEq/L, with a serum osmolality of 225 mOsm/kg, urine osmolality of 414 mOsm/kg, and spot urine sodium of 122 mEq/L. Diclofenac 75 mg qd for osteoarthritic pain and lisinopril 10 mg qd for hypertension was begun in 1990. Lisinopril was increased to 20 mg qd in August 1994 and to 20 mg bid pm in August 1996 for increasing blood pressure; metoprolol 50 mg qd was added in July 1996. A diagnosis of SIADH was postulated and further evaluation was undertaken to exclude thyroid and adrenal causes. After lisinopril was discontinued and the patient restricted to 1000 mL/d of fluid, serum sodium gradually corrected to 143 mEq/L. The patient was discharged taking metoprolol alone for her hypertension; serum sodium has remained > or =138 mEq/L through April 1999, 32 months after discharge, despite daily use of diclofenac. Angiotensin-converting enzyme (ACE) inhibitors in antihypertensive doses may block conversion of angiotensin I to angiotensin II in the peripheral circulation, but not in the brain. Increased circulating angiotensin I enters the brain and is converted to angiotensin II, which may stimulate thirst and release of antidiuretic hormone from the hypothalamus, eventually leading to hyponatremia. SIADH should be considered a rare, but possible, complication of therapy with lisinopril and other ACE inhibitors.
    Annals of Pharmacotherapy 03/2000; 34(2):176-9. DOI:10.1345/aph.19116 · 2.92 Impact Factor

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