Syndrome of Inappropriate Antidiuretic Hormone Secretion Associated with Lisinopril

Shaikh, Zakir Hussain; Taylor, Harris C.; Maroo, Praful; Llerena, Luis

doi:10.1345/aph.19116

Cited by 28 publications

(16 citation statements)

References 17 publications

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“…Increasing circulating angiotensin I enters the brain and is converted to angiotensin II, which may stimulate thirst and the release of antidiuretic hormone from the hypothalamus, eventually leading to hyponatremia. 10 Mahon et al 18 demonstrated a 5-fold increase in plasma antidiuretic hormone concentrations after intracerebroventricular injection of angiotensin II in the forebrain of Lister hooded rats. Indeed, in rats, a dose-dependent effect of captopril on water intake has been described.…”

Section: Discussionmentioning

confidence: 99%

“…For the following reasons, we considered hyponatremia in our patient as an adverse drug reaction associated with ACE inhibitors. ACE inhibitors-including captopril, lisinopril, and enalapril-have been reported previously as a cause of severe hyponatremia [4][5][6][7][8][9][10][11] (Table Serum sodium I). Seventeen cases of severe hyponatremia induced by ACE inhibitor therapy have been reported in the literature-5 with captopril, 3 with lisinopril, and 9 with enalapril, including our patient.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Angiotensin‐converting enzyme inhibitor‐induced syndrome of inappropriate secretion of antidiuretic hormone: Case report and review of the literature

Izzedine

Fardet

Launay-Vacher

et al. 2002

Clin Pharma and Therapeutics

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Seventeen cases of severe hyponatremia induced by angiotensin-converting enzyme (ACE) inhibitor therapy have been reported in the literature. The mechanism of severe hyponatremia induced by ACE inhibitor is not clear. A 60-year-old white man with a history of idiopathic dilated cardiomyopathy was treated with enalapril, 20 mg daily, that had been started 2 weeks before heart transplantation. The serum sodium level was 138 mmol/L before initiation of enalapril therapy and 127 mmol/L just before cardiac surgery. In the post-heart transplantation period, enalapril therapy was withdrawn for the perianesthesia period, and the serum sodium level increased from 127 to 140 mmol/L. One month later, viral myocarditis developed in the patient and enalapril was reintroduced at 20 mg daily. Two weeks later, natremia decreased. Enalapril was discontinued. Three days later the serum sodium level rose to 140 mmol/L. Severe symptomatic hyponatremia induced by the syndrome of inappropriate secretion of antidiuretic hormone should be considered a rare but possible complication associated with ACE inhibitor therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Angiotensin‐converting enzyme inhibitor‐induced syndrome of inappropriate secretion of antidiuretic hormone: Case report and review of the literature

Izzedine

Fardet

Launay-Vacher

et al. 2002

Clin Pharma and Therapeutics

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“…Of course, it is the preservation of bradykinin's (endothelium-dependent, nitric oxideand prostacyclin-mediated) vasodilator effect that is thought to lend added salutary value to ACE inhibition. Still other adverse reactions, such as syndrome of inappropriate ADH secretion, although appearing to still be ACE inhibitor classdependent, are more esoteric, although enhanced brain angiotensin levels arising from hyper-reninaemia have been suggested to play a role [25,26]. The incidence of taste disturbance seems to be restricted to the use of sulfhydryl-containing agents such as captopril and is easily avoided by selecting an alternative chemical class of ACE inhibitor.…”

Section: Acementioning

confidence: 99%

Therapeutic inhibition of the renin angiotensin aldosterone system

Laight¹

2009

Expert Opinion on Therapeutic Patents

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Each intervention has merits and demerits with implications for RAAS 'escape' phenomena, 'dual inhibition' therapy, long-term clinical efficacy and adverse drug reactions. Renin inhibitors offer the most complete RAAS inhibition, but more downstream interventions are likely to recruit supplementary anti-RAAS mediators and receptor signalling pathways. Furthermore, managing hyperkalaemia-stimulated aldosterone escape during combined ACE inhibitor and angiotensin receptor blocker treatment may realise the full clinical potential of dual inhibition therapy.

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“…Diese in der Klinik häufig eingesetzten Medikamente hemmen die periphere -nicht die zentrale -Konversion von Angiotensin I in Angiotensin II. Das peripher ansteigende Angiotensin I kann zentral in Angiotensin II umgewandelt werden, welches das Durstzentrum und die ADH-Freisetzung stimuliert [30].…”

Section: Syndrom Der Inappropriaten Adh-sekretionunclassified

Akute symptomatische Hyponatriämie bei einem 70-jährigen Patienten

Samie¹,

Theilmann

2002

Medizinische Klinik

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This etiologic correlation was reported in literature by many authors. However, these SIADHs were associated with a big subdural hematoma which needed neurosurgical intervention in most of the cases. Our patient is unique in that his symptoms were caused by a small subdural hematoma, which did not need surgical intervention. The patient was treated with cautious saline infusion, administration of a loop diuretic and fluid restriction with improvement of both his clinical and metabolic state. As large water loads may result in severe hyponatremia in these patients, moderate fluid restriction appears to be effective in long-term management even after stabilization/normalization of serum sodium. There are no sufficient data about the incidence of asymptomatic hyponatremia due to SIADH resulting from minor head injury, because most of these patients are asymptomatic and therefore they do not receive clinical attention.

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Syndrome of Inappropriate Antidiuretic Hormone Secretion Associated with Lisinopril

Abstract: SIADH should be considered a rare, but possible, complication of therapy with lisinopril and other ACE inhibitors.

Cited by 28 publications

References 17 publications

Angiotensin‐converting enzyme inhibitor‐induced syndrome of inappropriate secretion of antidiuretic hormone: Case report and review of the literature

Angiotensin‐converting enzyme inhibitor‐induced syndrome of inappropriate secretion of antidiuretic hormone: Case report and review of the literature

Therapeutic inhibition of the renin angiotensin aldosterone system

Akute symptomatische Hyponatriämie bei einem 70-jährigen Patienten

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