ArticleHeliyon2025
Hypokalemic paralysis in an adolescent following dexamethasone and B12 injection: A case report and literature review.
Article in Heliyon, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Thyrotoxic Hypokalemic Periodic Paralysis: Pathophysiological Mechanisms.Endocrinology and metabolism (Seoul, Korea) · 2025Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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