Kaminsky P, Klein M, Duc M
Service de Médecine J, C.H.R.U. de nancy, Hôpitaux de Brabois, Vandoeuvre.
Ann Endocrinol (Paris). 1992;53(4):125-32.
Patients with thyroid deficiency often complain of muscular weakness, exercise intolerance, cramps and excessive fatiguability. Hypothyroidism induces a metabolic myopathy, with a fall of the energetic production, and especially of the mitochondrial metabolism. This is due to a global inhibition of the main oxidative pathways (substrate incorporation, substrate oxidation) and of the respiratory chain. A diminished energetic consumption is partially related to a transition in the myosin isoforms, which express a slower ATPase, and to an impairment of the trans-sarcolemic transports. Exercise intolerance could be due to an abnormal recruitment of several metabolic pathways, such as glycolysis, related to the mitochondrial metabolism impairment, and including an abnormal accumulation of protons and monovalent phosphate ions, which are involved in the alteration of the actin-myosin interaction, and also by an abnormal Ca++ metabolism. The decreased number of NA+/K+ ATPase dependent pumps could imply an abnormal intracellular Na+ level and explain the frequent disorders of the membrane excitability.
甲状腺功能减退的患者常主诉肌肉无力、运动不耐受、痉挛和过度易疲劳。甲状腺功能减退会引发一种代谢性肌病，伴有能量产生下降，尤其是线粒体代谢下降。这是由于主要氧化途径（底物掺入、底物氧化）和呼吸链受到全面抑制。能量消耗减少部分与肌球蛋白同工型转变有关，肌球蛋白同工型表达较慢的ATP酶，还与跨肌膜转运受损有关。运动不耐受可能是由于多种代谢途径的异常募集，如与线粒体代谢受损相关的糖酵解，包括质子和单价磷酸离子的异常积累，这些离子参与肌动蛋白-肌球蛋白相互作用的改变，也与异常的Ca++代谢有关。依赖Na+/K+ ATP酶的泵数量减少可能意味着细胞内Na+水平异常，并解释了频繁出现的膜兴奋性紊乱。
