© 2019 Journal of Basic and Clinical Pharmacy 12 Case Report INTRODUCTION Hyponatremia, defined as a serum sodium concentration below 135 mmol/L, is the most common electrolyte imbalance encountered in clinical practice, occurring in 15%-30% of acutely or chronically hospitalized patients. [1] It causes a diverse spectrum of clinical symptoms ranging from mild to life threatening, with higher overall mortality. [2,3]. Several populations are at increased risk of developing hyponatremia, including intensive care unit, postoperative, psychiatric, elderly, and nursing home patients. [4-8] Euvolemic hyponatremia occurs when the water intake exceeds the excretion by kidney. SIADH is the most common cause of euvolemic hyponatremia. e criteria necessary for its diagnosis were originally defined by Bartter and Schwartz in 1967. [9] [Table 1]. Many causes have been implicated with SIADH like tumors, CNS disorders, pulmonary infections and medications. Drugs known to mimic the action of Arginine Vasopressin [AVP], stimulate its release, or enhance its action can cause SIADH. [10-13] Selective Serotonin-Reuptake Inhibitors for example can also enhance the Arginine Vasopressin [AVP] effect, especially in the elderly, females, those taking diuretics, or those with low baseline plasma sodium concentrations. [10,12] Wide range of medications contribute to cause SIADH such as Phenothiazines, Tricyclic anti-depressant [TCA], Serotonin Reuptake Inhibitors, Opiate derivatives, Carbamazepine and Others. ere are only a few reported cases about SIADH induced by Pregabalin. is is a case report of patient who developed hyponatremia secondary to SAIDH aſter being started on Pregabalin. CASE REPORT A 28-year-old male patient presented to emergency department on December 20 th 2018 with an acute onset of abnormal movements characterized by up-rolling of both eyes, non-purposeful rapid unequal movements of both upper and lower limbs and clenching of teeth. His other symptoms were generalized fatigue and weakness associated with decreased oral intake over the last two days. He had been on Gabapentin for peripheral neuropathy which was stopped and he was switched to Pregabalin 75 mg twice daily a week before this presentation. He has a past medical history of autosomal recessive combined cerebellar and peripheral ataxia with hearing loss, diabetes mellitus, hypothyroidism, von Willebrand disease and intellectual disability. His laboratory investigation showed serum sodium 115 mmol/L. He appeared mildly dehydrated and therefore the initial working diagnosis was hypovolemic hyponatremia. He received 1 liter of intravenous 0.9% Normal Saline, which improved his sodium level to 119 mmol/L. Following this he was kept on 0.9% Normal Saline at 30 ml/hour and his sodium reached to 121 mmol/L. As there was no significant improvement in his serum sodium levels and the patient remained lethargic, he was given 2% hypertonic saline, despite which his serum sodium level did not improve and was at 120 m mmol/L. Further laboratory investigations showed normal thyroid function and normal serum cortisol. His urinary sodium excretion and urine osmolality osmolality were high. [Table 2]. On the basis of the above findings, diagnosis of SIADH was made. His treatment was altered and his fluid intake was restricted to less than 1 liter per day. Following this, serum sodium levels gradually improved to reach 135 mmol/L. [Table 3] DISCUSSION e first case report of the SIADH was done by Bartter and Schwartz in October 1957, of two bronchogenic carcinoma patients, who developed significant euvolemic hyponatremia. [1,9] Syndrome of Inappropriate Antidiuresis is diagnosed when euvolemic hyponatremia is present accompanied with low serum osmolality and inappropriately elevated urine osmolality with normal renal, thyroid and adrenal function. [14,15] [Table 1], Syndrome of inappropriate anti-diuresis [SIAD] can be due to either increased release of antidiuretic hormone [independently from effective serum osmolality or circulating volume] from pituitary This is an open access article distributed under the terms of the Creative Commons Attribution Noncommercial Share Alike 3.0 License, which allows others to remix, tweak, and build upon the work non commercially, as long as the author is credited and the new creations are licensed under the identical terms. For reprints contact: invoice@jbclinpharm.org Cite this article as: Metwali H, Hasan H, Yousuf M. Pregabalin Induced Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH) Secretion: A Case Report. J Basic Clin Pharma 2019;10: 45-48. Pregabalin Induced Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH) Secretion: A Case Report Metwali H, Hasan H, Yousuf M King Abdul Aziz Medical City, Western Region, Jeddah, Saudi Arabia ABSTRACT Pregabalin is now being frequently used to treat many medical conditions such as fibromyalgia, diabetic peripheral neuropathy, post herpetic neuralgia and as adjunctive therapy for seizure. Hyponatremia is the most frequent electrolyte abnormality seen in hospitalized patients. And, Syndrome of Inappropriate Anti-diuretic Hormone Secretion (SIADH) is a common cause of euvolemic hyponatremia. Despite Hyponatremia, SIADH and use of Pregabalin being common in clinical practice, there are only a few case reports of Pregabalin induced SIADH causing hyponatremia which are reported in our literature. The aim of this case report is to add to the existing reports about the incidence of hyponatremia due to pregabalin which will alert the prescriber to monitor serum sodium levels and identify the cause of hyponatremia in patients newly started on pregabalin. Key words: Pregabalin; Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH) Correspondence: Hend Metwali, Pharm, Clinical Pharmacist, Pharmaceutical Care Department at King Abdullah International Medical Research Center / King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City –Jeddah Saudi Arabia E-mail: metwalihe@nhga.med.sa metwalihe@nhga.med.sa Access this article online Website: www.jbclinpharm.org Quick Response Code: