|LETTER TO THE EDITOR
|Year : 2023 | Volume
| Issue : 3 | Page : 196-197
A case of acute symptomatic hyponatremia secondary to aceclofenac-induced syndrome of inappropriate antidiuretic hormone
Vishal Mangal1, Mohit Kumar1, Anil Vasudeva2
1 Department of Internal Medicine, Military Hospital, Ambala, Haryana, India
2 Department of Hospital Administration, Military Hospital, Ambala, Haryana, India
|Date of Submission||11-May-2023|
|Date of Decision||06-Jul-2023|
|Date of Acceptance||13-Jul-2023|
|Date of Web Publication||01-Aug-2023|
Department of Internal Medicine, Military Hospital, Ambala - 133 001, Haryana
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Mangal V, Kumar M, Vasudeva A. A case of acute symptomatic hyponatremia secondary to aceclofenac-induced syndrome of inappropriate antidiuretic hormone. Indian J Pharmacol 2023;55:196-7
|How to cite this URL:|
Mangal V, Kumar M, Vasudeva A. A case of acute symptomatic hyponatremia secondary to aceclofenac-induced syndrome of inappropriate antidiuretic hormone. Indian J Pharmacol [serial online] 2023 [cited 2023 Dec 4];55:196-7. Available from: https://www.ijp-online.com/text.asp?2023/55/3/196/382570
Nonsteroidal anti-inflammatory drugs (NSAIDs) are most commonly used as analgesics. Although there are various side effects associated with NSAID use, they are generally innocuous in patients with no history of liver or kidney disease. 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. Examples include ketorolac, diclofenac, and indomethacin. Here, we present a case of aceclofenac-induced SIADH in an elderly female with no preexisting renal disease.
A 75-year-old female, a known case of hypertension and on regular treatment with angiotensin receptor blockers and calcium channel blockers, was brought by her daughter-in-law to the accident and emergency department with complaints of altered sensorium of 1-day duration. There was no history of fever, nausea, vomiting, or focal neurological deficit. On general physical examination, her vital parameters were essentially normal; however, she was disoriented to time, place, and person. A careful history revealed intake of tablet aceclofenac for about a week for right-sided shoulder pain. Laboratory investigations showed normal hematological and biochemical parameters; however, her serum sodium level was 123.3meq/L. A clinical diagnosis of acute symptomatic euvolemic hypotonic hyponatremia was established. She was managed with 100 mL of 3% sodium chloride infusion.
Further, etiological workup showed urine osmolality of 554 mOsmol/L, spot urine sodium was 143.3 meq/L, and serum uric acid was 3.6 mg/dL. Thyroid function test and serum cortisol level were within the normal limits. She underwent brain magnetic resonance imaging to rule out other causes of altered sensorium, which showed multiple lacunar infarcts and cerebral atrophy. As per Bartter and Schwartz's criteria, a diagnosis of SIADH was established, likely secondary to aceclofenac. The patient was managed with oral salt and fluid restriction and aceclofenac was stopped. Over the next 3 days, her serum sodium level improved to 132 mEq/L along with a marked improvement in her clinical condition. The patient was discharged with the advice to avoid NSAIDs without prior consultation.
Prostaglandins are produced in the kidneys and have a role in maintaining the fluid and electrolyte balance. Although the effect is generally not clinically significant, in patients with multiple comorbidities and preexisting renal disease, the inhibition of prostaglandins by NSAIDs can lead to fluid and electrolyte imbalance. Prostaglandins have an inhibitory effect on ADH, and therefore, NSAIDs, by inhibiting the prostaglandins, exaggerate the water-resorptive effects of ADH. This can lead to hyponatremia in patients taking NSAIDs. However, this side effect of NSAIDs is rare, considering that prostaglandins in the brain stimulate the secretion of ADH and the water excess developed due to the initial rise in ADH also gives negative feedback resulting in the subsequent decrease in ADH and normalization of serum sodium levels. In our case, the patient had no identifiable risk factors for developing hyponatremia with NSAID use. Although rare, ACE inhibitors and amlodipine are also known to cause SIADH. However, since the patient had been taking them for about a year, aceclofenac was the cause of acute symptomatic hyponatremia. Cessation of aceclofenac and water restriction leads to the improvement of symptoms despite continuing oral anti-hypertensives. This is the first case of acute symptomatic hyponatremia caused by aceclofenac-induced SIADH in an elderly female without any preexisting risk factors.
Although rampantly prescribed by many medical practitioners and also self-prescribed as an over-the-counter drug, NSAID use should be checked for the possibility of SIADH, especially in patients with preexisting renal diseases or other risk factors potentiating a fluid and electrolyte imbalance such as hypovolemia or concurrent medications known to cause ADH release.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
| » References|| |
Bergoglio MT, Solá Izquierdo E, Veses Martin S, Hernández Mijares A. Acute severe hyponatremia induced by aceclofen in a male patient with central diabetes insipidus. Endocrinol Nutr 2013;60:338-40.
Lim SY, Panikkath R, Prabhakar S. Syndrome of inappropriate antidiuretic hormone secretion associated with prolonged keterolac use. Clin Nephrol Case Stud 2014;2:5-8.
Liamis G, Milionis H, Elisaf M. A review of drug-induced hyponatremia. Am J Kidney Dis 2008;52:144-53.