Bonnar Clare E, Brazil John F, Okiro Julie O, Giblin Louise, Smyth Yvonne, O'Shea Paula M, Finucane Francis M
Centre for Diabetes, Endocrinology & Metabolism.
Department of Nephrology, Endocrinology & Metabolism.
Endocrinol Diabetes Metab Case Rep. 2021 Oct 1;2021. doi: 10.1530/EDM-21-0060.
A 32-year-old Caucasian male presented to the emergency department with a one-day history of acute severe bilateral lower limb weakness, three days after competing in a bodybuilding competition. He consumed large quantities of carbohydrate-rich foods following the competition. His past medical history was significant for anxiety, and family history was non-contributory. Examination was normal except for reduced power and hyporeflexia in both legs, despite his muscular physique. He was noted to have severe hypokalaemia (K+= 1.9 mmol/L). His thyroid function tests were consistent with thyrotoxicosis. He reported taking thyroxine and several other agents to facilitate muscle mass generation before the bodybuilding competition. His presentation was reminiscent of thyrotoxic periodic paralysis, albeit uncommon with Caucasian ethnicity. He also had transient hyperglycaemia at presentation with concomitant hyperinsulinaemia, which could be attributed to the carbohydrate load and may have exacerbated his hypokalaemia through a transcellular shift. Urine toxicology screen subsequently ruled out the use of diuretics but confirmed the presence of a long-acting beta agonist (clenbuterol) which, along with other substances, may have aggravated the hypokalaemia further. After 12 h of i.v. replacement, the potassium level normalised and leg weakness resolved. The patient agreed to stop taking thyroxine and beta agonists and was well during the clinic visit at one month follow-up. This case highlights the potential for thyrotoxicosis factitia to exacerbate hypokalaemia and muscle weakness from other causes in bodybuilders presenting with acute severe weakness, irrespective of ethnicity.
In patients presenting with muscle weakness and hypokalaemia, early consideration of thyrotoxicosis is essential, even in the absence of a past history of thyroid disease or specific symptoms of thyrotoxicosis, in order to allow prompt initiation of appropriate treatment and to prevent recurrence. Bodybuilders may constitute a uniquely 'at-risk' group for thyrotoxic periodic paralysis secondary to thyrotoxicosis factitia, especially where there is concomitant use of beta-adrenergic agonists, even in the absence of diuretic use. Although rare and usually described in patients of Asian or Polynesian ethnicity, this case highlights that thyrotoxic periodic paralysis secondary to thyrotoxicosis factitia can also occur in patients with Caucasian ethnicity. We speculate that consuming large quantities of carbohydrates may induce hyperinsulinaemia, which could theoretically contribute to worse hypokalaemia, though mechanistic studies would be needed to explore this further.
一名32岁的白人男性在参加健美比赛三天后，因急性严重双侧下肢无力一天而就诊于急诊科。比赛后他食用了大量富含碳水化合物的食物。他既往有焦虑病史，家族史无特殊。尽管他体型强壮，但体格检查除双下肢肌力减弱和反射减退外均正常。他被发现有严重低钾血症（血钾=1.9 mmol/L）。他的甲状腺功能检查结果与甲状腺毒症相符。他报告在健美比赛前服用甲状腺素及其他几种药物以促进肌肉生长。他的表现让人联想到甲状腺毒症性周期性瘫痪，尽管在白人中并不常见。他就诊时还伴有短暂性高血糖及同时出现的高胰岛素血症，这可能归因于碳水化合物负荷，并且可能通过细胞内转移加重了他的低钾血症。尿液毒理学筛查随后排除了利尿剂的使用，但证实存在长效β激动剂（克仑特罗），其与其他物质一起可能进一步加重了低钾血症。静脉补钾12小时后，血钾水平恢复正常，下肢无力症状缓解。患者同意停用甲状腺素和β激动剂，在一个月后的门诊随访时情况良好。该病例强调，对于出现急性严重无力的健美运动员，无论种族如何，人为甲状腺毒症都有可能加重由其他原因引起的低钾血症和肌无力。
对于出现肌无力和低钾血症的患者，即使没有甲状腺疾病既往史或甲状腺毒症的特定症状，早期考虑甲状腺毒症也至关重要，以便及时开始适当治疗并预防复发。健美运动员可能是人为甲状腺毒症继发甲状腺毒症性周期性瘫痪的独特“高危”群体，特别是在同时使用β肾上腺素能激动剂的情况下，即使没有使用利尿剂。虽然罕见且通常在亚洲或波利尼西亚种族患者中描述，但该病例表明人为甲状腺毒症继发的甲状腺毒症性周期性瘫痪也可发生在白人患者中。我们推测大量摄入碳水化合物可能会诱发高胰岛素血症，理论上这可能导致更严重的低钾血症，不过还需要进行机制研究以进一步探讨这一点。
