The Journal of clinical endocrinology and metabolism · 2022
Hyperthyroidism in Graves Disease Causes Sleep Disorders Related to Sympathetic Hypertonia.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Matsumoto Kazuhisa, Izawa Shoichiro, Fukaya Kenji, Matsuda Eriko, Fujiyama Misato, Matsuzawa Kazuhiko, Okura Tsuyoshi, Kato Masahiko, Taniguchi Shin-Ichi, Yamamoto Kazuhiro
Аннотация
CONTEXT: It is well known that Graves disease (GD) causes sleep disorders (SDs). However, the characteristics and associated factors of SD and its clinical course post hyperthyroidism normalization remain unclear.
OBJECTIVE: To clarify the characteristics and associated factors of subjective SD and its clinical course after GD treatment.
METHODS: From November 2017 to October 2020, we enrolled 72 participants (22 newly diagnosed with GD with untreated hyperthyroidism, 20 previously diagnosed with GD with normal thyroid function, and 30 normal controls) with no other underlying SD-related diseases. We compared the groups at enrollment and conducted prospective observations after 12 months of treatment on participants with newly diagnosed GD. Main outcome measures were differences and changes in the Pittsburgh Sleep Quality Index (PSQI) global and component sleep quality scores.
RESULTS: PSQI global sleep quality scores (P = .036) and sleep disturbance scores (P = .011) were significantly different among the 3 groups, and were highest in the untreated hyperthyroidism group. Multiple regression analysis demonstrated that free thyroxine level, which was positively correlated with sympathetic tone (ST) as evaluated by pulse rate, and urinary total metanephrines was associated with poorer PSQI global sleep quality scores independently of other factors (P = .006). Prospective observation showed that PSQI global sleep quality scores (P = .018) and sleep disturbance scores (P = .011) significantly improved with thyroid function normalization and ST attenuation.
CONCLUSION: Hyperthyroidism caused by GD augmented ST and exacerbated subjective SD. Normalization of hyperthyroidism caused by GD improved subjective SD.
OBJECTIVE: To clarify the characteristics and associated factors of subjective SD and its clinical course after GD treatment.
METHODS: From November 2017 to October 2020, we enrolled 72 participants (22 newly diagnosed with GD with untreated hyperthyroidism, 20 previously diagnosed with GD with normal thyroid function, and 30 normal controls) with no other underlying SD-related diseases. We compared the groups at enrollment and conducted prospective observations after 12 months of treatment on participants with newly diagnosed GD. Main outcome measures were differences and changes in the Pittsburgh Sleep Quality Index (PSQI) global and component sleep quality scores.
RESULTS: PSQI global sleep quality scores (P = .036) and sleep disturbance scores (P = .011) were significantly different among the 3 groups, and were highest in the untreated hyperthyroidism group. Multiple regression analysis demonstrated that free thyroxine level, which was positively correlated with sympathetic tone (ST) as evaluated by pulse rate, and urinary total metanephrines was associated with poorer PSQI global sleep quality scores independently of other factors (P = .006). Prospective observation showed that PSQI global sleep quality scores (P = .018) and sleep disturbance scores (P = .011) significantly improved with thyroid function normalization and ST attenuation.
CONCLUSION: Hyperthyroidism caused by GD augmented ST and exacerbated subjective SD. Normalization of hyperthyroidism caused by GD improved subjective SD.