[1]曹雯,夏萍,范尧夫,等.内分泌疾病的神经肌肉表现[J].国际内分泌代谢杂志,2015,(02):133-137.[doi:10.3760/cma.j.issn.1673-4157.2015.02.017]
 Cao Wen,Xia Ping,Fan Yaofu,et al.Neuromuscular manifestations of endocrine disorders[J].International Journal of Endocrinology and Metabolism,2015,(02):133-137.[doi:10.3760/cma.j.issn.1673-4157.2015.02.017]
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内分泌疾病的神经肌肉表现()
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
期数:
2015年02
页码:
133-137
栏目:
综述
出版日期:
2015-03-20

文章信息/Info

Title:
Neuromuscular manifestations of endocrine disorders
作者:
曹雯夏萍范尧夫徐书杭刘超
210028 南京,中国中医科学院江苏分院,南京中医药大学附属中西医结合医院内分泌代谢病院区
Author(s):
Cao WenXia PingFan YaofuXu ShuhangLiu Chao.
Endocrine and Diabetes Center,Jiangsu Province Hospital on Integration of Chinese and Western Medicine,Nanjing University of Traditional Chinese Medicine,Jiangsu Branch of China Academy of Chinese Medical Science,Nanjing 210028,China Corresponding author:Liu Chao,Email:liuchao@jsatcm.com
关键词:
内分泌疾病神经肌肉肌病维生素D甲状腺疾病
Keywords:
Endocrine disordersNeuromuscleMyopathyVitamin DThyroid disease
DOI:
10.3760/cma.j.issn.1673-4157.2015.02.017
摘要:
内分泌疾病的临床表现错综复杂,一些非特异性的病变如神经肌肉改变易于漏诊、误诊或误治。糖皮质激素分泌异常、甲状腺疾病、垂体功能紊乱、钙和维生素D代谢异常等多种内分泌代谢性疾病,均可以导致神经肌肉病变而呈现相应的临床特征,如肌肉软弱、肌肉萎缩、乏力等。通过对症处理以及对原发疾病的及时诊断和治疗,神经肌肉病变可以恢复或者缓解。
Abstract:
Endocrine diseases have complicated clinical manifestations. Some non-specific manifes-tations such as neuromuscular changes are easy to be misdiagnosed and mistreated.A variety of endocrine diseases,including glucocorticoids abnormalities,thyroid diseases,pituitary dysfunction,abnormal calcium and vitamin D metabolism,can cause neuromuscular alterations manifested by muscle weakness,muscle atrophy, muscle fatigue,etc. Through the diagnosis and treatment of underlying diseases,as well as symptomatic treatment,muscle lesions may be cured or alleviated.

参考文献/References:

[1] Schakmn O,Gilson HS.Mechanisms of muscle atrophy induced by glucocorticoids[J].Horm Res,2009,72(Suppl 1):36-41.  
[2] Braith R,Welsch M,Mills RJ,et al.Resistance exercise prevents glucocorticoid-induced myopathy in heart transplant recipients[J].Med Sci Sports Exerc,1998,30(4):483-489.  
[3] Mechanism KH.Diagnosis,and treatment of steroid myopathy[J].Brain Nerve,2013,65(11):1375-1380.  
[4] Khan MA,Larson E.Acute myopathy secondary to oral steroid therapy in a 49-year-old man:a case report[J].J Med Case Reports, 2011,5(1):82.  
[5] Awab A,Alilou W,Ei MR,et al.Rhabdomyolysis in severe acute asthma[J].Ann Fr Anesth Reanim,2009,28(2):171-172.  
[6] Barel M,Perez OA,Giozzet VA,et al.Exercise training prevents hyperinsulinemia,muscular glycogen loss and muscle atrophy induced by dexamethasone treatment[J].Eur J Appl Physiol,2010,108(5):999-1007.  
[7] Ruff RL,Simoncini L,Stuhmer W.Slow sodium channel inacti-vation in mammalian muscle:apossible role inregulating excitability[J].Muscle Nerve,1988,11(5):502-510.  
[8] Charmandari E,Nicolaides NC,Chrousos GP.Adrenal insuffi ciency[J].Lancet,2014,383(9935):2152-2167.  
[9] Segal J.A rapid,extranuclear effect of 3,5,3'-triiodothyronine on sugar uptake by several tissues in the rat in vivo.Evidence for a physiological role for the thyroid hormone action at the level of the plasma memebrane[J].Endocrinology,1989,124(6):2755-2764.
[10] Kim JY,Park KD,Richman DP.Treatment of myasthenia gravis based on its immunopathogenesis[J].J Clin Neurol,2011,7(4):173-183.
[11] Duyff RF,Van den Bosch J,Laman DM,et al.Neuromuscular findings in thyroid dysfunction:aprospective clinical and electro-diagnosticstudy[J].J Neurol Neurosurg Psychiatry,2000,68(6):750-755.
[12] Kumar KV,Manoj S.Visual vignette.Hypothyroidism-associated myopathy[J].Endocr Pract,2012,18(2):295.
[13] Miyauchi S,Matsuura B,Ueda T,et al.Interleukin-18 induces insulin resistance in the hyperthyroid state[J].Endocr J,2013, 60(4):449-455.
[14] Mamarabadi M,Razjouyan H,Moghaddasi M.Hypothyroidism the main thyroid dysfunction in Iranian patients with myasthenia gravis:a case serie[J].Iran J Neurol,2011,10(1-2):22-25.
[15] Stelmachowska-Banas M,Zielinski G,Zdunowski P,et al.The impact of transsphenoidal surgery on glucose homeostasis and insulin resistance in acromegaly[J].Neurol Neurochir Pol,2011, 45(4):328-334.
[16] Carrosco de la Fuente M,Gonz?仳lez-Albarr?仳n O,Pérez L?仵pez G,et al.Diabetic ketoacidosis as the first manifestation of a mixed growth hormone and prolactin-secreting tumor[J].Endocrinol Nutr,2010,57(10):507-509.
[17] Gopalan R,Schlesinger D,Vance ML,et al.Long-term outcomes after gamma knife radiosurgery for patients with a nonfunctioning pituitary adenoma[J].Neurosurgery,2011,69(2):284-293.
[18] Lewiecki EM,Miller PD.Skeletal effects of primary hyperparathy-roidism:bone mineral density and fracture risk[J].J Clin Densitom,2013,16(1):28-32.
[19] Okazaki R.Updates on rickets and osteomalacia:vitamin D deficiency:its pathophysiology and treatment[J].Clin Calcium,2013,23(10):1483-1489.
[20] Reisin RC,Martínez O,Mor?觃n M,et al.Thyrotoxic periodic paralysis in caucasians.Report of 8 cases[J].Neurologia,2000, 15(6):222-225.
[21] Glerup H,Mikkelsen K,Poulsen L,et al.Hypovitaminosis D myopathy without biochemical signs of osteomalacic bone involvement[J].Calcif Tissue Int,2000,66(6):419-424.
[22] Wieliczko M,Dycewska M.Hypocalcemia[J].Wiad Lek,2013,66(4):303-306.
[23] Yamashita H,Murakami T,Noguchi S,et al.Postoperative tetany in Graves' disease:important role of vitamin D metabolites[J].Ann Surg,1999,229(2):237-245.
[24] Ishikawa T,Inagaki H,Kanayama M,et al.Hypocalcemic hyper-CK-emia in hypoparathyroidism[J].Brain Dev,1990,12(2):249-252.

备注/Memo

备注/Memo:
通信作者:刘超,Email: liuchao@jsatcm.com
更新日期/Last Update: 2015-03-20