Sahebi Keivan, Foroozand Hassan, Bahmei Mohammad, Taghizadeh Raziee, Zare Samane, Inaloo Soroor
Student Research Committee, School of Medicine, Shiraz University of Medicine, Shiraz, Iran.
Pediatric Neurology Department, Nemazee Hospital, Shiraz, Iran.
Heliyon. 2025 Jan 9;11(2):e41675. doi: 10.1016/j.heliyon.2025.e41675. eCollection 2025 Jan 30.
The widespread use of glucocorticoids in clinical practice may occasionally be complicated by hypokalemic paralysis. Previously, only a few cases of glucocorticoid-induced hypokalemic paralysis in healthy adults had been reported. Intriguingly, cases of B12-induced hypokalemia have previously been reported in patients with pernicious anemia. Recently, we experienced a case of hypokalemic paralysis in an adolescent following intramuscular injections of dexamethasone and vitamin B12. Upon exclusion of other causes, a presumptive diagnosis of glucocorticoid-induced hypokalemic paralysis, with a possible but uncertain contribution from B12 supplementation, was made for the patient. After potassium replacement therapy, the patient fully recovered and was discharged after five days. Although glucocorticoids are known to cause hypokalemia through mechanisms such as enhanced transcellular shift or renal excretion, the potential role of vitamin B12 in worsening this effect remains unclear. It is hypothesized that B12 supplementation under certain conditions could influence electrolyte balance and potentially amplify the hypokalemic effects of glucocorticoids. However, this hypothesis is based on a few cases, and further pathophysiological and clinical studies are needed to clarify whether B12 supplementation exacerbates hypokalemia induced by glucocorticoids or if the observation is coincidental or context-specific. Meanwhile, clinicians should be cautious when prescribing glucocorticoids, particularly in combination with B12 supplements. This includes ensuring that both are administered only when clinically indicated, monitoring vital signs and serum potassium levels in at-risk patients, and considering alternatives when appropriate.
糖皮质激素在临床实践中的广泛应用偶尔可能并发低钾性麻痹。此前,仅有少数健康成年人发生糖皮质激素诱导的低钾性麻痹的病例报道。有趣的是,此前曾有恶性贫血患者发生维生素B12诱导的低钾血症的病例报道。最近,我们遇到一例青少年在肌内注射地塞米松和维生素B12后发生低钾性麻痹的病例。在排除其他病因后,对该患者作出了糖皮质激素诱导的低钾性麻痹的推测性诊断,维生素B12补充剂可能但不确定地起了作用。经补钾治疗后,患者完全康复,5天后出院。虽然已知糖皮质激素可通过增强跨细胞转移或肾脏排泄等机制导致低钾血症,但维生素B12在加重这种效应方面的潜在作用仍不清楚。据推测,在某些情况下补充维生素B12可能影响电解质平衡,并可能放大糖皮质激素的低钾效应。然而,这一假设基于少数病例,需要进一步的病理生理学和临床研究来阐明补充维生素B12是否会加重糖皮质激素诱导的低钾血症,或者这种观察结果是巧合还是与特定情况有关。同时,临床医生在开具糖皮质激素处方时应谨慎,尤其是与维生素B12补充剂联用时。这包括仅在临床有指征时才给予两者,监测高危患者的生命体征和血清钾水平,并在适当的时候考虑替代方案。