Acute severe hyponatremia induced by aceclofen in a male patient with central diabetes insipidus

Bergoglio, Marina Teresita; Izquierdo, Eva; Martín, Silvia Veses; Mijares, Antonio Hernández

doi:10.1016/j.endonu.2012.06.012

Cited by 3 publications

(3 citation statements)

References 6 publications

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“…Bergoglio et al described a 46-year-old man, taking desmopressin for CDI, who was admitted for symptomatic hyponatremia with a sodium of 113 mEq/L (113 mmol/L). The only change in his usual medication regime had been the addition of 200 mg/day of aceclofen for back pain [ 4 ]. The patient was reported to be euvolemic and had documented normal sodium levels prior to aceclofen.…”

Section: Discussionmentioning

confidence: 99%

“…Opioids and non-steroidal anti-inflammatory drugs (NSAIDS) have both been reported individually, to cause hyponatremia, typically secondary to SIADH [ 1 – 3 ]. Rarely, have they been reported to cause hyponatremia in an individual with CDI [ 4 , 5 ]. The mechanism for the hyponatremia would have to be different in this situation given that patients with DI do not produce ADH.…”

Section: Introductionmentioning

confidence: 99%

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Central diabetes insipidus and pain medications – a risky combination

Pinto

Mokashi

Cummings

2021

Clin Diabetes Endocrinol

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Background Central Diabetes Insipidus (CDI) results from decreased production of antidiuretic hormone (ADH) leading to an inability to concentrate urine. CDI is treated with desmopressin (DDAVP). Rarely reported in the literature, opioids and non-steroidal anti-inflammatories (NSAIDs) can induce hyponatremia in individuals treated for CDI. Case presentation A 10-year-old boy with septo-optic dysplasia and CDI was treated with DDAVP 1.6 mg orally TID maintaining normal sodium levels. Post admission for a femur fracture, he was discharged on ibuprofen and hydromorphone. Sodium was 136 mmol/l two days before discharge. He returned to the ED after having a seizure at home. He was euvolemic and mildly lethargic. Sodium was low at 108 mmol/l. DDAVP and hydromorphone were held and he was fluid restricted, but the sodium remained low. Sodium began to rise when Ibuprofen was stopped. Intermittent small doses of DDAVP were given to facilitate gradual correction of hyponatremia. At discharge, sodium had normalized. Conclusion Hyponatremia has occasionally been described as a side effect of opioids and rarely of NSAIDs in patients with CDI. Stimulation of the thirst centre may play a role with opioids while a decrease in urine output may be the mechanism with NSAIDs.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Central diabetes insipidus and pain medications – a risky combination

Pinto

Mokashi

Cummings

2021

Clin Diabetes Endocrinol

View full text Add to dashboard Cite

show abstract

“…However, literature shows that in some people with preexisting renal disease or disorders of fluid imbalance such as central diabetes insipidus, NSAIDs can cause syndrome of inappropriate antidiuretic hormone (SIADH) secretion, further leading to symptomatic hyponatremia. [ 1 ] Examples include ketorolac, diclofenac, and indomethacin. [ 2 ] Here, we present a case of aceclofenac-induced SIADH in an elderly female with no preexisting renal disease.…”

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confidence: 99%