|Year : 2021 | Volume
| Issue : 2 | Page : 31-37
Hypothyroidism-associated rhabdomyolysis: A new case report and review of the reported cases
Fahmi Yousef Khan1, Theeb Osama Sulaiman2, Raza Ali Akbar1
1 Department of Medicine, Hamad General Hospital, Doha; Clinical Medicine, Weill Cornell Medical College, Ar-Rayyan, Qatar
2 Department of Medicine, Hamad General Hospital, Doha, Qatar
|Date of Submission||16-Nov-2021|
|Date of Acceptance||07-Jan-2022|
|Date of Web Publication||07-Oct-2022|
Dr. Fahmi Yousef Khan
Department of Medicine, Hamad General Hospital, Doha; Weill Cornell Medical College, P.O.Box: 3050, Ar-Rayyan
Source of Support: None, Conflict of Interest: None
Background: Hypothyroidism alone or in combination with other factors has the risk of triggering rhabdomyolysis. In this article, we aim to describe hypothyroidism-associated rhabdomyolysis and its outcomes.
Methods: We reported a new case of hypothyroidism-associated rhabdomyolysis and reviewed similar reported cases from the literature for in-depth knowledge.
Results: Eighty-one cases, including the one reported in this article, met the inclusion criteria for this review. The mean age of the patients was 45.6 ± 15.8 years. Out of these, 57 (70.4%) patients were males and 24 (29.6%) were females. The precipitating factor was absent in 45 (55.6%) cases. A total of 8 (9.9%) cases had chronic renal failure at time of presentation, while 25 (30.9%) had hypertension, 11 (13.6%) had diabetes mellitus, and 32 (39.5%) had dyslipidemia. The median creatine kinase (CK) level was 5885 U/L (Interquartile range: 3280.5–11550.5 U/L). Electromyography was performed in 12 patients with 10 (12.3%) cases showing myopathic changes including polyphasic potential and fiber necrosis. Muscle biopsy was performed in 7 (8.4%) cases, with Type II fiber atrophy observed in 4 (4.9%) biopsies. Sixty-two cases developed acute kidney injury, of which 14 (17.3%) required hemodialysis. All patients were treated with levothyroxine and most patients (67, 82.7%) were treated by hydration. All the reported patients made good recovery. A statistically nonsignificant correlation was found between CK and thyroid-stimulating hormone (r = 0.218; P = 0.052).
Conclusions: Rhabdomyolysis is a recognized complication of hypothyroidism even in the absence of additional risk factors. Clinicians should be aware of the impact of rhabdomyolysis and hypothyroidism on renal function and promptly initiate hormone replacement therapy and vigorous hydration to preserve the renal function.
Keywords: Acute kidney injury, hypothyroidism, myopathy, rhabdomyolysis
|How to cite this article:|
Khan FY, Sulaiman TO, Akbar RA. Hypothyroidism-associated rhabdomyolysis: A new case report and review of the reported cases. Imam J Appl Sci 2021;6:31-7
|How to cite this URL:|
Khan FY, Sulaiman TO, Akbar RA. Hypothyroidism-associated rhabdomyolysis: A new case report and review of the reported cases. Imam J Appl Sci [serial online] 2021 [cited 2022 Nov 26];6:31-7. Available from: https://www.e-ijas.org/text.asp?2021/6/2/31/358062
| Introduction|| |
Rhabdomyolysis is a potentially life-threatening syndrome characterized by the breakdown of skeletal muscle resulting in the subsequent release of intracellular contents into the circulatory system. The etiologic spectrum of rhabdomyolysis is extensive, including major causes such as toxins and medications, trauma, excessive muscular activity, heat-related, muscle ischemia, and infections. Other rarer causes include electrolyte disturbance, hereditary metabolic abnormalities or structural abnormalities of the skeletal muscle cell, connective tissue disorders, and endocrine abnormalities. Hypothyroidism-associated rhabdomyolysis is a clinical condition which is usually triggered by some precipitating factors, such as the simultaneous use of statins along with heavy exercise. However, rhabdomyolysis due to hypothyroidism with no apparent precipitating factors has also been reported in the literature.,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,
In this case report, we describe a similar patient with no apparent precipitating factors for hypothyroidism-associated rhabdomyolysis. To better understand the topic, we reviewed 73 published case reports,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, of rhabdomyolysis associated with hypothyroidism retrieved from different sources including MEDLINE, PubMed, search engine Google, and EMBASE.
| Methods|| |
We reviewed the English-language literature and checked the relevant references from 1970 to 2019 to identify all known cases of rhabdomyolysis associated with hypothyroidism using multiple sources; MEDLINE, PubMed, search engine Google, and EMBASE using the terms “rhabdomyolysis and hypothyroidism,” “Hypothyroid myopathy,” “hypothyroidism-associated rhabdomyolysis,” and “hypothyroid rhabdomyolysis.” Manuscripts published in English were reviewed and relevant references were checked, and authors were contacted where possible. In addition, we also present a new case report.
Inclusion and exclusion criteria
All cases with biochemical diagnosis of primary hypothyroidism (with or without clinical signs) and serum creatine kinase (CK) level of more than ten times the upper limit of normal were included in this report.
We excluded cases if they fulfilled at least one of the following criteria: abstracts, insufficient clinical or laboratory data, serum CK level <10 times the upper limit of normal, endocrinopathies other than primary hypothyroidism (panhypopituitarism, Cushing syndrome), or presence of primary muscle disease.
For all reports of rhabdomyolysis caused by hypothyroidism, the information extracted included if available: patient's age and sex, clinical and laboratory features, concomitant drugs, associated medical conditions as well as therapeutic interventions and outcome.
The gathered information was transferred to the computer utilizing the with SPSS software (v 25; IBM Corp, Armonk, NY, USA). Descriptive statistics of qualitative and quantitative data were expressed as frequency along with percentage and mean (±SD). Pearson's Chi-square and exact tests were used to test the differences in the proportion of categorical variables, and independent t-tests were used for evaluating the difference between the means of two continuous variables. Pearson correlation analysis was performed to examine the linear relationship between serum CK and TSH level. P < 0.05 was considered statistically significant.
| Case Report|| |
A 35-year-old man was admitted to our hospital with a 2-day history of lower limb muscular pain. The patient also noted that his urine had turned dark brown for the preceding 24 h. On further questioning, he reported cold intolerance and somnolence for 6 months. Other medical history was unremarkable. He was not taking any medications and denied any abuse of alcohol or drugs including anabolic steroids. There was no personal or family history of muscle or thyroid disease. On physical examination, the patient was alert and oriented. There was no pedal edema or palpable goiter and the skin examination was normal. His temperature was 36.7°C, blood pressure was 120/70 mmHg, and pulse rate was 72 beats/min. The range of motion in the lower extremities was limited by the pain and tenderness and there was no delayed relaxation of ankle jerk. The rest of his clinical examination was unremarkable.
The laboratory investigations revealed a hemoglobin level of 12 g/dL (NR: 13–17 g/dl) and a total leukocyte count of 5.1 × 103/μL (4–10 × 103/uL) with a normal differential and a platelet count of 153,000/μL (NR: 150–400 × 103/uL). Blood chemistry revealed aspartate aminotransferase of 81 U/L (NR: 5–34 U/L); alanine aminotransferase, 75 U/L (NR: 0–55 U/L); blood urea nitrogen 8.8 mmol/L (NR: 1.17–3.64 mmol/L); and serum creatinine 210 μmol/L (NR: 64–100 μmol/L). An arterial blood gas analysis at room air was performed which showed H 7.2 (NR: 7.35–7.45), PaO2 88 mmHg (NR: 83–108 mmHg), and PaCO2 31 mmHg (NR: 35–45 mmHg). His fasting lipid profile showed a total cholesterol of 6.1 mmol/L (NR: <5.1 mmol/L), LDL cholesterol 4.2 mmol/L (NR: 3.36–4.12 mmol/L), and triglyceride 1.2 mmol/L (NR: <1.7 mmol/L). His myoglobin was elevated 1230 ng/ml (NR: 28–72 ng/ml) and the CK level was elevated (12331 U/L; NR: 22–100 U/L) with normal CK MB fraction and cardiac troponin levels. The urine myoglobin test result was positive. Urinalysis did not reveal any hematuria, pyuria, or ketonuria.
The patient was admitted to the intensive care unit with a provisional diagnosis of acute kidney injury (AKI) secondary to rhabdomyolysis. Early and aggressive hydration was initiated and urinary output was measured hourly with cautious monitoring of serum potassium and other electrolytes levels. During hospitalization, the patient's thyroid function tests were obtained which showed thyroid-stimulating hormone (TSH) of 100 mIU/L (NR: 0.45–4.5) and serum-free thyroxin (FT4) of 4.2pmol/L (NR: 9–20). Both serum antithyroglobulin antibody and antimicrosomal antibody were positive at high titers, consistent with primary autoimmune hypothyroidism. The antinuclear antibody was negative.
The patient was diagnosed with primary autoimmune hypothyroidism associated with rhabdomyolysis and AKI. Vigorous hydration was continued with cautious monitoring of serum potassium and other electrolyte levels to treat rhabdomyolysis and AKI, whereas hypothyroidism was treated with L-thyroxin at a dosage of 100 μg/day.
In the following days, the patient significantly improved with levels of CK and serum creatinine declining considerably towards normalization. The patient was subsequently discharged 16 days after hospitalization. He was then seen in the medical outpatient's clinic 12 weeks after discharge. He remained clinically asymptomatic and his labs revealed normal CK and serum creatinine levels.
| Results Of The Case Reviews|| |
In addition to our case, 74 reports with 80 cases meeting the criteria were included in this review. [Table 1] describes all of the 81 cases of hypothyroidism-associated rhabdomyolysis including our current reported case. The mean age of the patients was 45.6 ± 15.8 (9–75 years), out of which 57 (70.4%) were males and 24 (29.6%) were females. Precipitating factor was absent in 55 cases (67.9%). A total of 8 patients (9.9%) had chronic kidney disease chronic renal failure at time of presentation, while 25 (30.9%) had hypertension, 11 (13.6%) had diabetes mellitus, and 32 (39.5%) had dyslipidemia [Table 2].
|Table 1: Summary of reported cases of rhabdomyolysis associated with hypothyroidism|
Click here to view
|Table 2: Summary of reported cases of rhabdomyolysis associated with hypothyroidism|
Click here to view
The clinical manifestations of rhabdomyolysis associated with hypothyroidism include muscle pain, muscle swelling, muscle tenderness, backache, darkened urine, and generalized muscle weakness [Table 1].
The median CK level was 5885 U/L (Interquartile range: 3280.5–11550.5 U/L). Detection of blood/urine myoglobin was reported in 48 patients, with 41 positives. Electromyography was performed in 12 patients with 10 (12.3%) cases showing myopathic changes including polyphasic potential and fiber necrosis. Two cases (2.5%) exhibited normal electromyography. Muscle biopsy was performed in 7 (8.4%) cases, with Type II fiber atrophy observed in 4 (4.9%) biopsies, while 3 (3.7%) biopsies were reported normal.
Sixty-two cases of rhabdomyolysis were complicated with AKI, of which 14 (17.3%) required dialysis. All patients were treated with levothyroxine, and most patients, 67 (82.7%), were treated by hydration. All the reported patients made good recovery.
There were no significant differences between patients with and without AKI regarding the age, serum CK, and TSH levels [Table 3]. Moreover, a statistically nonsignificant correlation was found between CK and TSH (r = 0.218; P = 0.052), CK and FT4 (r = −0.109; P = 0.363), and CK and FT3 (r = −0.035; P = 0.827).
|Table 3: Demographic and clinical characteristics of the patients with and without acute renal failure|
Click here to view
| Discussion|| |
Myopathy is a common clinical feature of patients with hypothyroidism, affecting approximately 79% of the cases. It presents with nonspecific symptoms of myalgias, muscle cramps, fatigue, and muscle weakness, particularly exacerbated with exertion and exercise. If hypothyroidism is left untreated, the patient may develop significant muscle disease such as rhabdomyolysis resulting in severe functional limitations. The most common laboratory finding in patients with hypothyroid myopathy is elevated serum CK, which occurs in 57%–90% of cases.,,, In asymptomatic patients, CK elevation is usually mild, <10 times the upper normal limits. Although the diagnostic CK level for rhabdomyolysis should be >10 times the upper normal limit, it is not clear whether or not the severity of rhabdomyolysis is related to the degree of CK elevation.
Our case, as well as the cases reviewed, highlights several important points.
First, rhabdomyolysis can occur in patients with primary hypothyroidism of various etiologies, with autoimmune thyroiditis being the most common etiology. Moreover, we found rhabdomyolysis can precede or follow the diagnosis of hypothyroidism. In our review, 60 cases, including ours, had rhabdomyolysis at presentation and retrospectively diagnosed with hypothyroidism. Accordingly, thyroid status should be evaluated when treating a patient suffering from unexplained rhabdomyolysis and AKI.
Second, contrary to what is known among researchers, regarding the significant role of some factors such as lipid-lowering drugs, alcohol, or exercise in triggering rhabdomyolysis in patients with hypothyroidism, rhabdomyolysis occurred in 55 (67.9%) of the cases reviewed, including ours, in the absence of additional precipitating factors. This indicates that rhabdomyolysis due to hypothyroidism alone is not as rare as some authors have previously suggested. The precise pathophysiology of rhabdomyolysis in hypothyroidism is currently not clear. Skeletal muscle has been recognized as a key thyroid hormone target for contractile function, regeneration, and transport as well as for metabolism and glucose disposal. Thyroid hormone deficiency leads to a reduced mitochondrial oxidative capacity, abnormal glycogenolysis, and an insulin-resistant state of the cell. This leads to selective atrophy of Type 2 muscle fibers (fast-twitching type) as they are dependent on glycolysis for energy, causing a switch to slow-twitching Type 1 fibers, low myosin ATPase activity, and low adenosine triphosphate that was seen clinically as slowing of muscle contraction.,, Moreover, decreased muscle carnitine, which was found in patients with hypothyroid myopathy, could also be a possible mechanism underlying hypothyroid myopathy. All these changes might sensitize muscle cells to other factors related to muscle injury and increase the risk of rhabdomyolysis.
Third, we only found that 14 (17.3%) cases presented with dark urine; otherwise, the clinical presentation of hypothyroidism-associated rhabdomyolysis was nonspecific and generally indistinguishable from hypothyroid myopathy. Therefore, a high index of suspicious is needed to detect this complication as early as possible. Unexplained muscle pain or weakness in hypothyroid patients must raise the suspicion of rhabdomyolysis, and therefore, CK level, being the most sensitive indicators of myocyte injury in rhabdomyolysis, should be evaluated.
Fourth, in general, AKI develops in almost a third to half (33%–45%) of all patients with rhabdomyolysis., However, our review showed that over three-quarter (76.5%) of patients with hypothyroidism-associated rhabdomyolysis developed AKI, which is higher than the range reported for AKI in rhabdomyolysis patients in general. Based on some reports that showed an association between hypothyroidism and impaired renal function,,, the increased number of AKI among the reviewed cases can be attributed to the dual effect of hypothyroidism and rhabdomyolysis on the kidney, which may aggravate the occurrence of AKI. Hence, clinicians should be aware of the impact of rhabdomyolysis and hypothyroidism on renal function and initiate hormone replacement and vigorous hydration as early as possible to preserve renal function.
Fifth, we did not find a significant correlation between CK level and thyroid function tests such as TSH, FT4, and FT3 levels, which dispute any significant relation between the degree of muscle involvement and the severity of hypothyroidism. This is consistent with the findings of Hartl et al. but contrary to the findings of Hekimsoy and Oktem.
Finally, our review showed that the overall outcome of hypothyroid-associated rhabdomyolysis is generally good as all the reviewed patients recovered. In general, rapid remission of symptoms is achieved after the initiation of thyroxin. In addition, early and vigorous hydration to preserve renal function, and treating the underlying causes, played a crucial role in the safe outcome of the reviewed cases. Around one in 6 cases (17.3%) with AKI required dialysis. All patients suffering from AKI secondary to hypothyroid-associated rhabdomyolysis achieved a premorbid health status which they had prior to their presentation.
| Conclusions|| |
Rhabdomyolysis is a recognized complication of hypothyroidism even in the absence of additional risk factors. The clinical presentation of hypothyroidism-associated rhabdomyolysis is nonspecific and a high index of suspicious is needed to detect it as early as possible. Measurement of CK, therefore, has an important role in the evaluation of all hypothyroid patients presenting with muscular weakness. AKI is a serious potential consequence of hypothyroidism-associated rhabdomyolysis which needs early identification, prevention, and aggressive management. Hence, clinicians should be aware of the impact of rhabdomyolysis and hypothyroidism on renal function and promptly initiate hormone replacement and vigorous hydration to preserve the renal function.
This study was approved by MRC (Project Ref. No: MRC-04-21-436).
Declaration of patient consent:
The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The Guardian understands that names and initials will not be published, and due efforts will be made to conceal the identity, but anonymity cannot be guaranteed
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Khan FY. Rhabdomyolysis: A review of the literature. Neth J Med 2009;67:272-83.
Swaminath D, Limsuwat C, Islam E. Acute kidney injury and rhabdomyolysis as an initial presentation of Hashimoto's thyroiditis. Southwest Respir Crit Care Chron 2013;1:35-8.
Cai Y, Tang L. Rare acute kidney injury secondary to hypothyroidism-induced rhabdomyolysis. Yonsei Med J 2013;54:172-6.
Mooraki A, Broumand B, Neekdoost F, Amirmokri P, Bastani B. Reversible acute renal failure associated with hypothyroidism: Report of four cases with a brief review of literature. Nephrology (Carlton) 2003;8:57-60.
Abbas MH, Nagib AM, Khaled MM, Donia AF. Adolescent with hypothyroidism induced rhabdomyolysis and acute kidney injury. J Clin Case Rep 2015;5:498.
Nikolaidou C, Gouridou E, Ilonidis G, Boudouris G. Acute renal dysfunction in a patient presenting with rhabdomyolysis due to Hypothyroidism attributed to Hashimoto's Disease. Hippokratia 2010;14:281-3.
Ulu R, Gözel N, Yiğit İP, Gürel A, Doğukan A. Acute kidney injury secondary to hypothyroidism-induced rhabdomyolysis. Turk Neph Dial Transpl 2016;25 Suppl 1:62-4.
Chang ZY, Boo AY, Tulsidas H. Rhabdomyolysis: A rare complication of hypothyroidism. Proc Singapore Healthc 2015;24:188-90.
Windpessl M, Wang Y, Lassnig E, Wallner M. Rhabdomyolysis due to severe hypothyroidism culminating in uremic encephalopathy. Ren Fail 2014;36:829-30.
Ulyanovskiy P, Dergan D, Abbas S, Manes P, Erlikh I. Refractory acute kidney injury secondary to hypothyroid-induced myopathy: A contemporary case report. J Med Cases 2017;8:8-10.
Comak E, Koyun M, Kiliçarslan-Akkaya B, Bircan I, Akman S. Severe rhabdomyolysis and acute renal failure in an adolescent with hypothyroidism. Turk J Pediatr 2011;53:586-9.
Ardalan MR, Ghabili K, Mirnour R, Shoja MM. Hypothyroidism-induced rhabdomyolysis and renal failure. Ren Fail 2011;33:553-4.
Zare-Khormizi MR, Rahmanian M, Pourrajab F, Akbarnia S. Massive pericardial effusion and rhabdomyolysis secondary to untreated severe hypothyroidism: The first report. Acta Clin Belg 2014;69:375-8.
Naz A, Issa M. Rhabdomyolysis and acute renal impairment in a patient with hypothyroidism: A case report. Case Rep Med 2014;2014:139170.
Altay M, Ceri M, Unverdi S, Duranay M. An unusual cause of acute renal failure: Hypothyroidism. NDT Plus 2010;3:386-7.
Halverson PB, Kozin F, Ryan LM, Sulaiman AR. Rhabdomyolysis and renal failure in hypothyroidism. Ann Intern Med 1979;91:57-8.
Katipoglu B, Ates I, Acehan F, Meteris A, Yılmaz N. Rhabdomyolysis case based on hypothyroidism. Endocrinol Diabetes Metab Case Rep 2016;2016:16-0083.
Madhu SV, Jain R, Kant S, Prakash V, Kumar V. Myopathy presenting as a sole manifestation of hypothyroidism. J Assoc Physicians India 2010;58:569-70.
Sathyan S, George S, Vijayan P. Hypothyroidism: A reversible cause of 'acute kidney injury' – A series of 5 cases. Int J Adv Med 2015;2:423-5.
Seo CG, Kim KJ, Park E, Kim NH, Kim JH, Kim HY, et al.
Untreated primary hypothyroidism with simultaneous rhabdomyolysis, pericardial effusion, and sudden sensorineural hearing loss: A case report. BMC Endocr Disord 2019;19:52.
Freeston J, Gough A. Reversible myopathy and renal impairment. J R Soc Med 2004;97:124-5.
Farias Moeller R, Zecavati N, Sherafat-Kazemzadeh R, Aleinikoff S, Rennert W. Adolescent with rhabdomyolysis due to undiagnosed hypothyroidism. Case Rep Pediatr 2011;2011:670673.
Rabhi M, Chaari J, Toloune F. Rhabdomyolysis disclosing hypothyroidism. Eur J Intern Med 2006;17:220.
Galli-Tsinopoulou A, Stylianou C, Kokka P, Panagopoulou P, Nousia-Arvanitakis S. Rhabdomyolysis, renal failure, pericardial effusion, and acquired von Willebrand disease resulting from hypothyroidism in a 10-year-old girl. Thyroid 2008;18:373-5.
Neves PD, Bridi RA, Balbi AL, Ponce D. Hypothyroidism and acute kidney injury: An unusual association. BMJ Case Rep 2013;2013:bcr2013200585.
Bhansali A, Chandran V, Ramesh J, Kashyap A, Dash RJ. Acute myoedema: An unusual presenting manifestation of hypothyroid myopathy. Postgrad Med J 2000;76:99-100.
Riggs JE. Acute exertional rhabdomyolysis in hypothyroidism: The result of a reversible defect in glycogenolysis? Mil Med 1990;155:171-2.
Altay M, Duranay M, Ceri M. Rhabdomyolysis due to hypothyroidism. Nephrol Dial Transplant 2005;20:847-8.
Jain S, Bhargava K, Sawlani KK, Daga MK, Gaiha M. Myoglobinuria and transient acute renal failure in a patient revealing hypothyroidism. J Assoc Physicians India 1999;47:444-6.
Barahona MJ, Mauri A, Sucunza N, Paredes R, Wägner AM. Hypothyroidism as a cause of rhabdomyolysis. Endocr J 2002;49:621-3.
Kisakol G, Tunc R, Kaya A. Rhabdomyolysis in a patient with hypothyroidism. Endocr J 2003;50:221-3.
Kuo HT, Jeng CY. Overt hypothyroidism with rhabdomyolysis and myopathy: A case report. Chin Med J (Engl) 2010;123:633-7.
Mangaraj S, Sethy G, Sen RK, Rout RN. Hypothyroidism presenting as acute kidney injury. J Health Spec 2014;2:28-30. [Full text]
Espiritu RP, Stan MN. Rhabdomyolysis after withdrawal of thyroid hormone in a patient with papillary thyroid cancer. Endocr Pract 2008;14:1023-6.
Birewar S, Oppenheimer M, Zawada ET Jr. Hypothyroid acute renal failure. S D J Med 2004;57:109-10.
Sekine N, Yamamoto M, Michikawa M, Enomoto T, Hayashi M, Ozawa E, et al.
Rhabdomyolysis and acute renal failure in a patient with hypothyroidism. Intern Med 1993;32:269-71.
Mazokopakis EE. Unusual causes of rhabdomyolysis. Intern Med J 2008;38:364-7.
Salehi N, Agoston E, Munir I, Thompson GJ. Rhabdomyolysis in a patient with severe hypothyroidism. Am J Case Rep 2017;18:912-8.
Akin D, Ozmen S. Acute renal failure in two cases with hypothyroidism related rhabdomyolysis. Int J Case Rep Images 2014;5:195-7.
Ahmed GS, Zaid HM, Moloney M. Hashimoto's thyroiditis presenting as Hoffman's syndrome, rhabdomyolysis and acute kidney injury. BMJ Case Rep 2014;2014:bcr2013203269.
Zorkin NG, Golts M, Fernandes VC. Severe hypothyroidism presenting with acute mania and psychosis: A case report and literature review. Bipolar Disord 2017;3:116.
Choi YA, Lee SJ, Kim SY, Chang YK. Rhabdomyolysis induced by hypothyroidism in a kidney transplant recipient. Kidney Res Clin Pract 2011;30:120-4.
Somaratne S, Arachchi WK, Munidasa D. A rare presentation of a common condition: Polymyositis like syndrome in hypothyroidism. Galle Med J 2007;12:57.
Joshi B, Jones D, Rochford A, Giblin L. Hypothyroidism and associated acute renal failure. J R Soc Med 2009;102:199-200.
Boryushkina V, Ahmed S, Quadri K, Ramdass A. Recurrent rhabdomyolysis induced by severe hypothyroidism. Cureus 2019;11:e4818.
Gurala D, Rajdev K, Acharya R, Idiculla PS, Habib S, Krzyzak M. Rhabdomyolysis in a young patient due to hypothyroidism without any precipitating factor. Case Rep Endocrinol 2019;2019:4210431.
Lin HW. Rhambdomyolysis induced by hypothyroidism in a patient with hypopharyngeal cancer: A case report and review of the literature. J Intern Med Taiwan 2013;24:418-23.
Leonardi A, Penta L, Cofini M, Lanciotti L, Principi N, Esposito S. Rhabdomyolysis in a young girl with Van Wyk-Grumbach syndrome due to severe Hashimoto thyroiditis. Int J Environ Res Public Health 2018;15:704.
Cengizhan MS, Çelik M. A postpartum rhabdomyolysis patient due to hypothyroidism. Int J Fam Commun Med 2018;2:158-9.
Neal JM, Yuhico RJ. “Myxedema madness” associated with newly diagnosed hypothyroidism and obstructive sleep apnea. J Clin Sleep Med 2012;8:717-8.
Mohamed MF, Mahgoub AB, Sardar S, Elzouki AN. Acute psychosis and concurrent rhabdomyolysis unveiling diagnosis of hypothyroidism. BMJ Case Rep 2019;12:e231579.
Scott KR, Simmons Z, Boyer PJ. Hypothyroid myopathy with a strikingly elevated serum creatine kinase level. Muscle Nerve 2002;26:141-4.
Chaudhary N, Duggal AK, Makhija P, Puri V, Khwaja GA. Statin-induced bilateral foot drop in a case of hypothyroidism. Ann Indian Acad Neurol 2015;18:331-4.
] [Full text]
Jbara Y, Bricker D. Rhabdomyolysis in the setting of induced hypothyroidism and statin therapy: A case report. Eur Thyroid J 2015;4:62-4.
Ehelepola ND, Sathkumara SM, Bandara HM, Kalupahana KL. Atorvastatin-diltiazem combination induced rhabdomyolysis leading to diagnosis of hypothyroidism. Case Rep Med 2017;2017:8383251.
Rando LP, Cording SA, Newnham HH. Successful reintroduction of statin therapy after myositis: Was there another cause? Med J Aust 2004;180:472-3.
Little C, Hamilton S, Shik J. Rhabdomyolysis causing acute kidney injury in a patient with multiple risk factors and an underlying inflammatory muscle disease: A case report. UBCMJ 2012;4:20-2.
Ambapkar SN, Shetty N, Dwivedy A, Malve HO. Statin-induced rhabdomyolysis in patient with renal failure and underlying undiagnosed hypothyroidism. Indian J Crit Care Med 2016;20:305-7.
] [Full text]
Tatar E, Isikyakar T, Yeniay KP, Uzuner HH, Sevinc Ok E. Hypothyroidism induced severe rhabdomyolysis in a hemodialysis patient. Case Rep Med 2014;2014:501890.
Kedzia A, Krysiak R, Madej A, Okopień B. Is every case of muscle damage during hypolipemic therapy the side effect of this therapy? A case report. Pol Arch Med Wewn 2007;117:473-6.
Clouâtre Y, Leblanc M, Ouimet D, Pichette V. Fenofibrate-induced rhabdomyolysis in two dialysis patients with hypothyroidism. Nephrol Dial Transplant 1999;14:1047-8.
Vold PL, Weiss PJ. Rhabdomyolysis from tourniquet trauma in a patient with hypothyroidism. West J Med 1995;162:270-1.
Lochmüller H, Reimers CD, Fischer P, Heuss D, Müller-Höcker J, Pongratz DE. Exercise-induced myalgia in hypothyroidism. Clin Investig 1993;71:999-1001.
Satarasinghe RL, Ramesh R, Riyaaz AA, Gunarathne PA, de Silva AP. Hypothyroidism is a predisposing factor for fenofibrate-induced rhabdomyolysis-patient report and literature review. Drug Metabol Drug Interact 2007;22:279-83.
Yeter E, Keles T, Durmaz T, Bozkurt E. Rhabdomyolysis due to the additive effect of statin therapy and hypothyroidism: A case report. J Med Case Rep 2007;1:130.
Evans RM, Watanabe I, Singer PA. Central changes in hypothyroid myopathy: A case report. Muscle Nerve 1990;13:952-6.
Nelson SR, Phillips AO, Hendry BM. Hypothyroidism and rhabdomyolysis in a marathon runner. Nephrol Dial Transplant 1993;8:375-6.
Sousa AA, Kronit HS, Neves Fde A, Amato AA. Fenofibrate-induced rhabdomyolysis in a patient with chronic kidney disease: An unusual presenting feature of hypothyroidism. Arq Bras Endocrinol Metabol 2009;53:383-6.
Bar SL, Holmes DT, Frohlich J. Asymptomatic hypothyroidism and statin-induced myopathy. Can Fam Physician 2007;53:428-31.
Ahn P, Min HJ, Park SH, Lee BM, Choi MJ, Yoon JW, et al.
Rhabdomyolysis and acute kidney injury associated with hypothyroidism and statin therapy. Endocrinol Metab (Seoul) 2013;28:331-4.
Zhang R, Ran HH, Lu CY, Gao W, Huang Y, Gao YL, et al.
Rhabdomyolysis induced by simvastatin-diltiazem interaction in unrecognized hypothyriodism. J Geriatr Cardiol 2010;7:126-8.
Hung YT, Yeung VT. Hypothyroidism presenting as hypercholesterolaemia and simvastatin-induced myositis. Hong Kong Med J 2000;6:423-4.
Peringat J, Manappallil RG, Karadan U. Rhabdomyolysis: A rare complication of Hashimoto's thyroiditis precipitated by statin therapy. BMJ Case Rep 2018;2018:bcr2017223229.
Ram R, Swarnalatha G, Ramesh V, Rao KN, Dakshinamurty KV. Rhabdomyolysis induced acute renal failure secondary to statins. Indian J Nephrol 2013;23:211-3.
] [Full text]
Qari FA. Severe rhabdomyolysis and acute renal failure secondary to use of simvastatin in undiagnosed hypothyroidism. Saudi J Kidney Dis Transpl 2009;20:127-9.
] [Full text]
Sindoni A, Rodolico C, Pappalardo MA, Portaro S, Benvenga S. Hypothyroid myopathy: A peculiar clinical presentation of thyroid failure. Review of the literature. Rev Endocr Metab Disord 2016;17:499-519.
Madariaga MG. Polymyositis-like syndrome in hypothyroidism: Review of cases reported over the past twenty-five years. Thyroid 2002;12:331-6.
McKeran RO, Slavin G, Ward P, Paul E, Mair WG. Hypothyroid myopathy. A clinical and pathologaical study. J Pathol 1980;132:35-54.
Giampietro O, Clerico A, Buzzigoli G, Del Chicca MG, Boni C, Carpi A. Detection of hypothyroid myopathy by measurement of various serum muscle markers-myoglobin, creatine kinase, lactate dehydrogenase and their isoenzymes. Correlations with thyroid hormone levels (free and total) and clinical usefulness. Horm Res 1984;19:232-42.
Hekimsoy Z, Oktem IK. Serum creatine kinase levels in overt and subclinical hypothyroidism. Endocr Res 2005;31:171-5.
Doran GR. Serum enzyme disturbances in thyrotoxicosis and myxoedema. J R Soc Med 1978;71:189-94.
Mullur R, Liu YY, Brent GA. Thyroid hormone regulation of metabolism. Physiol Rev 2014;94:355-82.
Wile CM, Young A, Jones DA, Edward RH. Muscle relaxation rate, fiber type composition and energy turnover in hyper and hypothyroid patients. Clin Sci 1979;57:375-84.
Rhee CM. The interaction between thyroid and kidney disease: An overview of the evidence. Curr Opin Endocrinol Diabetes Obes 2016;23:407-15.
Iglesias P, Bajo MA, Selgas R, Díez JJ. Thyroid dysfunction and kidney disease: An update. Rev Endocr Metab Disord 2017;18:131-44.
Rao NS, Chandra A, Malhotra KP. Severe hypothyroidism-associated acute renal failure – A case series from North India and review of literature. Thyroid Res Pract 2019;16:121-7. [Full text]
Hartl E, Finsterer J, Grossegger C, Kroiss A, Stöllberger C. Relationship between thyroid function and skeletal muscle involvement in subclinical and overt hypothyroidism. Endocrinologist 2001;11:217-21.
[Table 1], [Table 2], [Table 3]