Dtsch Med Wochenschr 2018; 143(16): 1174-1180
DOI: 10.1055/s-0043-121381
Dossier
© Georg Thieme Verlag KG Stuttgart · New York

Osteoarthropathien und Myopathien bei Schilddrüsenerkrankungen

Osteoarthropathies and Myopathies associated with Disorders of the Thyroid Endocrine System
Volker Nehls
Weitere Informationen

Publikationsverlauf

Publikationsdatum:
07. August 2018 (online)

Abstract

Triiodothyronine (T3) is a key regulator of bone, muscle and articular cartilage. Musculoskeletal symptoms of hyperthyroidism include loss of bone mass finally leading to osteoporosis and weakness of the skeletal musculature. Hypothyroidism on the other side frequently leads to muscle stiffness and cramping and, occasionally, results in rhabdomyolysis. To prevent terminal differentiation of chondrocytes with consecutive cartilage degeneration, cartilage probably depends on exact regulation of local T3 availability by the intracellular deiodinase system. Recent findings underline the importance of local T3 generation by deiodinase type 2 and support the existence of local hypo- or hyperthyroidism.

In the review, the implications of the recent literature for current understanding of osteoarthritis, myopathies and diabetic osteoarthropathy will be discussed. Further emphasis will be placed on the association of autoimmune thyroiditis with musculoskeletal diseases and fibromyalgia.

Triiodthyronin (T3) ist unverzichtbar für die Entwicklung des muskuloskelettalen Systems [1]. Sowohl bei der Hyperthyreose als auch Hypothyreose kommt es zu krankhaften Veränderungen an Knochen, Gelenken und Muskeln, am häufigsten Hashimoto-Thyreoiditis und Morbus Basedow. Neue Konzepte und Vorstellungen in der molekularen Thyreologie fließen zunehmend in die Therapie ein und müssen in der internistischen Praxis Berücksichtigung finden.

 
  • Literatur

  • 1 Bassett JH, Williams GR. Role of Thyroid Hormones in Skeletal Development and Bone Maintenance. Endocr Rev 2016; 37 (02) 135-187 . doi:10.1210/er.2015-1106
  • 2 Arrojo EDrigo R, Fonseca TL, Werneck-de-Castro JP. et al. Role of the type 2 iodothyronine deiodinase (D2) in the control of thyroid hormone signaling. Biochim Biophys Acta 2013; 1830 (07) 3956-3964 . doi:10.1016/j.bbagen.2012.08.019
  • 3 Delling G, Kummerfeldt K, von Recklinghausen FD. A reminiscence on the occasion of the centenary of his publication Osteitis fibrosa or deformans, osteomalacia and osteoplastic carcinosis in their interrelationships. Dtsch Med Wochenschr 1991; 116: 1976-1979
  • 4 Aubert CE, Floriani C, Bauer DC. et al. Thyroid Function Tests in the Reference Range and Fracture: Individual Participant Analysis of Prospective Cohorts. J Clin Endocrinol Metab 2017; 102 (08) 2719-2728 . doi:10.1210/jc.2017-00294
  • 5 Doury P, Dirheimer Y, Pattin S. Algodystrophy: Diagnosis and Therapy of a Frequent Disease of the Locomotor Apparatus. Heidelberg: Springer; 1981
  • 6 Sanches CP, Vianna AGD, Barreto FC. The impact of type 2 diabetes on bone metabolism. Diabetol Metab Syndr 2017; 9: 85 . doi:10.1186/s13098-017-0278-1
  • 7 Williams MF, London DA, Husni EM. et al. Type 2 diabetes and osteoarthritis: a systematic review and meta-analysis. J Diabetes Complications 2016; 30 (05) 944-950 . doi:10.1016/j.jdiacomp.2016.02.016
  • 8 Drigo RA, Fonseca TL, Castillo M. et al. Endoplasmic Reticulum Stress Decreases Intracellular Thyroid Hormone Activation via an eIF2a-Mediated Decrease in Type 2 Deiodinase Synthesis. Mol Endocrinol 2011; 25 (12) 2065-2075 . doi:10.1210/me.2011-1061
  • 9 Wajner SM, Goemann IM, Bueno AL. et al. IL-6 promotes nonthyroidal illness syndrome by blocking thyroxine activation while promoting thyroid hormone inactivation in human cells. J Clin Invest 2011; 121 (05) 1834-1845 . doi:10.1172/JCI44678
  • 10 Nagase H, Nagasawa Y, Tachida Y. et al. Deiodinase 2 upregulation demonstrated in osteoarthritis patients cartilage causes cartilage destruction in tissue-specific transgenic rats. Osteoarthritis Cartilage 2013; 21 (03) 514-523 . doi:10.1016/j.joca.2012.12.013
  • 11 Bomer N, Cornelis FM, Ramos YF. et al. The effect of forced exercise on knee joints in Dio2(-/-) mice: type II iodothyronine deiodinase-deficient mice are less prone to develop OA-like cartilage damage upon excessive mechanical stress. Ann Rheum Dis 2016; 75 (03) 571-577 . doi:10.1136/annrheumdis-2014-206608
  • 12 Bomer N, den Hollander W, Ramos YF. et al. Underlying molecular mechanisms of DIO2 susceptibility in symptomatic osteoarthritis. Ann Rheum Dis 2015; 74 (08) 1571-1579 . doi:10.1136/annrheumdis-2013-204739
  • 13 Muhammad H, Rais Y, Miosge N. et al. The primary cilium as a dual sensor of mechanochemical signals in chondrocytes. Cell Mol Life Sci 2012; 69 (13) 2101-2107 . doi:10.1007/s00018-011-0911-3
  • 14 van der Spek AH, Fliers E, Boelen A. Thyroid hormone metabolism in innate immune cells. J Endocrinol 2017; 232 (02) R67-R81
  • 15 Mancini A, Di Segni C, Raimondo S. et al. Thyroid Hormones, Oxidative Stress, and Inflammation. Mediators Inflamm 2016; 6757154. DOI: 10.1155/2016/6757154.
  • 16 Linquette M, Lefebvre J, Racadot A. et al. Production rate and mean plasma concentration of cortisol in hyperthyroidism. Ann Endocrinol (Paris) 1976; 37 (05) 331-345
  • 17 Price SA, Thondam S, Bondugulapati LN. et al. Significant attenuation of stimulated cortisol in early Graves disease without adrenal autoimmunity. Endocr Pract 2012; 18 (06) 924-930 . doi:10.4158/EP12002.OR
  • 18 Bloise FF, Cordeiro A, Ortiga-Carvalho TM. Role of thyroid hormone in skeletal muscle physiology. J Endocrinol 2018; 236 (01) R57-R68 . doi:10.1530/JOE-16-0611
  • 19 Chang CC, Cheng CJ, Sung CC. et al. A 10-year analysis of thyrotoxic periodic paralysis in 135 patients: focus on symptomatology and precipitants. Eur J Endocrinol 2013; 169 (05) 529-536 . doi:10.1530/EJE-13-0381
  • 20 Elnady BM, Kamal NM, Shaker RH. et al. Prevalence and clinical significance of nonorgan specific antibodies in patients with autoimmune thyroiditis as predictor markers for rheumatic diseases. Medicine (Baltimore) 2016; 95 (38) e4336 . doi:10.1097/MD.0000000000004336