All Title Author
Keywords Abstract


Hypothyroidism Induced Severe Rhabdomyolysis in a Hemodialysis Patient

DOI: 10.1155/2014/501890

Full-Text   Cite this paper   Add to My Lib

Abstract:

Hypothyroidism occurs relatively common and is a significant cause of morbidity and mortality during the course of chronic kidney disease. Rhabdomyolysis is a potentially life-threatening condition characterised by necrosis of muscular tissue and rarely associates with hypothyroidism. Here we describe a case of rhabdomyolysis due to severe hypothyroidism in a 56-year-old female hemodialysis patient. 1. Introduction Thyroid dysfunction is relatively common in patients with chronic kidney disease (CKD) when compared to general population [1, 2]. Both hormonal changes including alterations in TRH, TSH, and iodine clearance as well as presence of associating autoimmune disorders (type 1 diabetes mellitus or systemic lupus erythematosus) and comorbidities such as HCV infection or treatment with drugs having adverse thyroid effects (e.g., amiodarone) are thought to be responsible for thyroid dysfunction [2–4]. Thyroid dysfunction particularly hypothyroidism is a significant cause of cardiovascular mortality and morbidity in CKD patients [5–10]. In hemodialysis patients, however, the frequency of acute complications and neuromuscular effects of hypothyroidism are not known. Rhabdomyolysis is a rapid breakdown of skeletal muscle tissue leading to release of its contents into systemic circulation [11]. Rhabdomyolysis, a life-threatening condition, may occur due to physical factors including trauma, convulsions, or overexertion as well as to chemical and hormonal causes [11]. Hypothyroidism associated rhabdomyolysis is rare in nonuremic patients. Hypothyroidism induced rhabdomyolysis in dialysis patients has not been reported as far as we know. Here we present a case of rhabdomyolysis in a hemodialysis patient on amiodarone treatment receiving antithyroid therapy for subclinical hyperthyroidism. 2. Case Presentation A 56-year-old female with a past medical history of end stage diabetic nephropathy, interstitial pulmonary disease, congestive heart failure, and atrial fibrillation presented to nephrology outpatient clinics with complaints of nausea and fatigue. She was back on routine hemodialysis 4 times a week for 18 months (she underwent a renal transplantation 10 years ago). She provided a history of subclinical hyperthyroidism detected six months ago for which antithyroid treatment was started because of the diagnosis of a thyroid nodule. She stated that she missed her follow-up appointments. Her medications included warfarin 5?mg, diltiazem 30?mg, amiodarone 400?mg (started for atrial fibrillation with rapid ventricular response), propylthiouracil 300?mg,

References

[1]  J. C. Lo, G. M. Chertow, A. S. Go, and C.-Y. Hsu, “Increased prevalence of subclinical and clinical hypothyroidism in persons with chronic kidney disease,” Kidney International, vol. 67, no. 3, pp. 1047–1052, 2005.
[2]  M. Chonchol, G. Lippi, G. Salvagno, G. Zoppini, M. Muggeo, and G. Targher, “Prevalence of subclinical hypothyroidism in patients with chronic kidney disease,” Clinical Journal of the American Society of Nephrology, vol. 3, no. 5, pp. 1296–1300, 2008.
[3]  E. M. Kaptein, “Thyroid hormone metabolism and thyroid diseases in chronic renal failure,” Endocrine Reviews, vol. 17, no. 1, pp. 45–63, 1996.
[4]  S. Disthabanchong and A. Treeruttanawanich, “Oral sodium bicarbonate improves thyroid function in predialysis chronic kidney disease,” American Journal of Nephrology, vol. 32, no. 6, pp. 549–556, 2010.
[5]  C. M. Rhee, E. K. Alexander, I. Bhan, and S. M. Brunelli, “Hypothyroidism and mortality among dialysis patients,” Clinical Journal of the American Society of Nephrology, vol. 8, no. 4, pp. 593–601, 2013.
[6]  C. Zoccali, F. Benedetto, F. Mallamaci et al., “Low triiodothyronine and cardiomyopathy in patients with end-stage renal disease,” Journal of Hypertension, vol. 24, no. 10, pp. 2039–2046, 2006.
[7]  E. Tatar, F. Kircelli, G. Asci et al., “Associations of triiodothyronine levels with carotid atherosclerosis and arterial stiffness in hemodialysis patients,” Clinical Journal of the American Society of Nephrology, vol. 6, no. 9, pp. 2240–2246, 2011.
[8]  E. Tatar, M. S. Demirci, F. Kircelli et al., “The association between thyroid hormones and arterial stiffness in peritoneal dialysis patients,” International Urology and Nephrology, vol. 44, pp. 601–606, 2012.
[9]  J. J. Carrero, A. R. Qureshi, J. Axelsson et al., “Clinical and biochemical implications of low thyroid hormone levels (total and free forms) in euthyroid patients with chronic kidney disease,” Journal of Internal Medicine, vol. 262, no. 6, pp. 690–701, 2007.
[10]  E. Tatar, F. Kircelli, and E. Ok, “The contribution of thyroid dysfunction on cardiovascular disease in patients with chronic kidney disease,” Atherosclerosis, vol. 227, no. 1, pp. 26–31, 2013.
[11]  F. Y. Khan, “Rhabdomyolysis: a review of the literature,” Netherlands Journal of Medicine, vol. 67, no. 9, pp. 272–283, 2009.
[12]  R. F. Duyff, J. van den Bosch, D. M. Laman, B.-J. Potter van Loon, and W. H. J. P. Linssen, “Neuromuscular findings in thyroid dysfunction: a prospective clinical and electrodiagnostic study,” Journal of Neurology Neurosurgery and Psychiatry, vol. 68, no. 6, pp. 750–755, 2000.
[13]  F. Monzani, N. Caraccio, G. Siciliano, L. Manca, L. Murri, and E. Ferrannini, “Clinical and biochemical features of muscle dysfunction in subclinical hypothyroidism,” Journal of Clinical Endocrinology and Metabolism, vol. 82, no. 10, pp. 3315–3318, 1997.
[14]  M. Altay, M. Duranay, and M. Ceri, “Rhabdomyolysis due to hypothyroidism,” Nephrology Dialysis Transplantation, vol. 20, no. 4, pp. 847–848, 2005.
[15]  T. J. Kiernan, M. Rochford, and J. H. McDermott, “Simvastatin induced rhabdomyolysis and an important clinical link with hypothyroidism,” International Journal of Cardiology, vol. 119, no. 3, pp. 374–376, 2007.
[16]  R. L. Satarasinghe, R. Ramesh, A. A. A. Riyaaz, P. A. K. G. Gunarathne, and A. P. de Silva, “Hypothyroidism is a predisposing factor for fenofibrate-induced rhabdomyolysis—patient report and literature review,” Drug Metabolism and Drug Interactions, vol. 22, no. 4, pp. 279–283, 2007.
[17]  E. M. Kaptein, R. B. Wilcox, and J. C. Nelson, “Assessing thyroid hormone status in a patient with thyroid disease and renal failure: from theory to practice,” Thyroid, vol. 14, no. 5, pp. 397–400, 2004.
[18]  S. Basaria and D. S. Cooper, “Amiodarone and the thyroid,” American Journal of Medicine, vol. 118, no. 7, pp. 706–714, 2005.
[19]  E. L. Batcher, X. C. Tang, B. N. Singh, S. N. Singh, D. J. Reda, and J. M. Hershman, “Thyroid function abnormalities during amiodarone therapy for persistent atrial fibrillation,” American Journal of Medicine, vol. 120, no. 10, pp. 880–885, 2007.
[20]  J. A. Franklyn, J. R. Davis, M. D. Gammage, W. A. Littler, D. B. Ramsden, and M. C. Sheppard, “Amiodarone and thyroid hormone action,” Clinical Endocrinology, vol. 22, no. 3, pp. 252–264, 1985.
[21]  A. Marot, J. Morelle, V. A. Chouinard, M. Jadoul, M. Lambert, and N. Demoulin, “Concomitant use of simvastatin and amiodarone resulting in severe rhabdomyolysis: a case report and review of the literature,” Acta Clinica Belgica, vol. 66, no. 2, pp. 134–136, 2011.

Full-Text

comments powered by Disqus