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Case Reports in Endocrinology

Volume 2019, Article ID 4210431, 3 pages
https://doi.org/10.1155/2019/4210431

Case Report
Rhabdomyolysis in a Young Patient due to Hypothyroidism
without Any Precipitating Factor

Dhineshreddy Gurala ,1 Kartikeya Rajdev ,1 Roshan Acharya,1 Pretty Sara Idiculla,2

Saad Habib,1 and Michael Krzyzak3
1
Resident, Internal Medicine, Staten Island University Hospital, Northwell Health, Staten Island, NY, USA
2
Foreign Medical Graduate, Sree Gokulam Medical College and Research Foundation, Alamthara, India
3
Hospitalist, Internal Medicine, Staten Island University Hospital, Northwell Health, Staten Island, NY, USA

Correspondence should be addressed to Dhineshreddy Gurala; dineshgurala@gmail.com

Received 6 August 2019; Revised 27 September 2019; Accepted 21 October 2019; Published 3 December 2019

Academic Editor: Osamu Isozaki

Copyright © 2019 Dhineshreddy Gurala et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.

Hypothyroidism is characterized by decreased hormone production, which results in various clinical manifestations in different
organ systems. Muscular symptoms are common in patents with clinical hypothyroidism which includes muscle cramps, myalgia,
and mild to moderate elevation of creatinine kinase less than five times the upper limit of normal. However, rhabdomyolysis due
to hypothyroidism is rare and in most of the reported cases a precipitating factor has been found. We report a unique case of a
35-year-old male with no past medical history who presented with rhabdomyolysis due to newly diagnosed hypothyroidism without
any precipitating factors and was treated successfully with intravenous fluids and levothyroxine.

1. Introduction for one week prior to presentation. It initially started in his

neck which progressed to his shoulder, trunk, and bilateral
Hypothyroidism is found in 4.6% of the U.S. population, with lower extremities and was associated with excessive fatigue
0.3% presenting clinically and 4.3% being subclinical [1]. and recent weight gain of 4.54 kg over two weeks. Review of
Muscle involvement in hypothyroidism is common, involving systems was negative for dry skin, thinning of hair, fever, chills,
79% of patients [2]. Muscular manifestations range from mus- upper respiratory tract infection, weakness in upper or lower
cle weakness, myalgia, muscle cramps with mild to moderate extremities, double vision, changes in memory, or puffy skin.
elevation of creatinine kinase to more severe such as Hoffman’s He denied the use of illicit drugs, alcohol abuse, herbal med-
syndrome or rhabdomyolysis [3, 4]. Rhabdomyolysis due to ications, trauma or prolonged immobilization, and did not
skeletal muscle necrosis in hypothyroidism is rare [5, 6] and report any family history of thyroid disease. His vitals were
usually associated with precipitating factor such as statin med- stable with a heart rate of 70 beats per minute, and blood
ication or severe exercise, illicit drugs. However, without any pressure was 130/80 mm Hg. Physical examination was posi-
obvious precipitating factors, the incidence of rhabdomyolysis tive for diffuse mild muscle tenderness with normal 5/5 motor
is infrequent [3]. Here in we report a unique case of rhabdo- strength in upper and lower extremities. Electrocardiography
myolysis in young male due to hypothyroidism without any showed normal sinus rhythm. Laboratory examination
associated precipitating factors. revealed normal hemogram and serum electrolytes including
phosphate and calcium levels as shown in the Table 1. His
serum creatinine was 1.2 mg/dl (baseline creatinine is 1.0−1.2).
2. Case Presentation He had elevated serum creatinine kinase (CK) of 11760 U/L
and elevated lactate dehydrogenase (LDH) of 544 U/L. His
A 35-year-old male with no significant medical history pre- lipid profile was deranged with total cholesterol of 240 mg/dl,
sented to the emergency department with diffuse muscle pain triglyceride of 284 mg/dl, and LDL-cholesterol of 138 mg/dl.
2 Case Reports in Endocrinology

Table 1: Laboratory results. 3. Discussion

Variable Reference range Day 1 Day 2 Day 3 Hypothyroidism causes a broad spectrum of clinical manifes-
Hemoglobin tations such as generalized fatigue, dry skin, constipation,
14–18 15.6
(mg/dl) bradycardia, hypothermia, diastolic hypertension, and peri-
WBC count cardial effusion. Muscular symptoms range from muscle weak-
4.8–10.8 7.84
(K/µl) ness, stiffness, myalgia, muscle cramps to severe
Platelets (K/µl) 130–400 206 rhabdomyolysis, and pseudohypertrophy of the muscles
Glucose random (Hoffman’s syndrome) [3, 4].
70–99 94
(mg/dl) Rhabdomyolysis is defined by skeletal muscle necrosis and
Serum ­sodium release of intracellular muscle contents into the circulation.
135–146 137 138 141
(mmol/litre)
Common causes of rhabdomyolysis include seizure, trauma,
Serum potassium
3.5–5.0 4.3 3.8 3.8 medications such as a statin, illicit drugs (methadone), alcohol,
(mmol/litre)
Serum chloride
strenuous exercise, inflammatory myopathies (polymyositis),
98–110 96 97 101 electrolyte abnormalities (hyponatremia, hypokalemia, hypoc-
(mmol/litre)
Anion gap 7–14 15 13 14 alcemia), and some of the glycogen storage disorders [7].
BUN (mg/dl) 10–20 14 11 9 Rarely, it may also develop in patients with hypothyroidism
Serum creatinine
[8, 9]. The pathophysiology of rhabdomyolysis in hypothy-
0.7–1.5 1.2 1.3 1.2 roidism is still unclear. Myolysis is attributable to changes in
(mg/dl)
Calcium (mg/dl) 8.5–10.1 9.3 8.7 8.6 muscle fibers from fast twitching to slow twitching muscle
Magnesium fibers, deposition of glycosaminoglycans, poor contractility
1.8–2.4 1.9 of actin-myosin units, low myosin ATPase activity, or low ATP
(mg/dl)
TSH (µIU/ml) 0.27–4.2 111 100 turn over in the skeletal muscles [10]. Some of the possible
T4 (µg/dl) 4.6–12 0.5 explanations for these are inhibition of mitochondrial oxida-
LDH (U/l) 50–242 544 tive phosphorylation results in reduced ATP production and
0–225 9553 11760 7600
dysregulation of metabolic pathways such as the Kreb’s cycle,
CK (U/l)
fatty acid catabolism, and glycolytic energy production [11].
CRP (mg/dl) 0–0.4 0.27
Diagnosis of rhabdomyolysis is based on the elevation of
RF (IU/ml) 0–13 <10
creatinine kinase up to five times the standard limit. Our
CCP (units) 0–19 <8
patient had 50 times the usual limit of CK, had clinical symp-
Ds DNA (IU/ml) ≤29 <12 toms of hypothyroidism such as weight gain, extreme fatigue,
ESR (mm/hr) 0–10 3 and laboratory examination showed high TSH, low T4 and
TG (mg/dl) 40–150 284 dyslipidemia. Our patient did not have any other risk factors
HDL-cholesterol for the development of rhabdomyolysis and his work-up was
40–60 29
(mg/dl) negative for infectious, inflammatory, or autoimmune etiology.
LDL-cholesterol These findings led to the diagnosis of hypothyroidism induced
50–100 138
(mg/dl)
rhabdomyolysis.
Total-cholesterol
100–200 240 Initial management of rhabdomyolysis consists of intra-
(mg/dl)
venous fluids administration and to correct electrolyte abnor-
malities such as hyperkalemia, hyperphosphatemia,
hypocalcemia, hyperuricemia, and metabolic acidosis. Acute
His urine was bloody in appearance, and urine analysis was kidney injury (AKI) is one of the most common complications
negative for erythrocytes but was positive for urine with the reported frequency of AKI ranges from 15 to over
myoglobin. 50% [12, 13]. Early and aggressive fluid resuscitation is nec-
The patient was admitted to the hospital for rhabdomyol- essary to prevent acute kidney injury [12]. The type of fluid
ysis and was started on intravenous fluids. He was found to and rate of repletion are unclear, however, initial fluid resus-
have an TSH (Thyroid Stimulating Hormone) of 100 micro citation with isotonic saline at the rate of 100 to 200 ml/hour
IU/ml with a low free T4 level of 0.5 micro g/dl (Table 1). He is suggested to maintain or enhance renal perfusion, thereby
was diagnosed with hypothyroidism and treatment with lev- minimizing ischemic injury. Sequential monitoring of CK
othyroxine was initiated. Further work-up including levels, volume status of the patient, and urine output are
Rheumatoid Factor (RF), Cyclic Citrullinated Peptide (CCP) needed to monitor response to the treatment and to adjust the
Antibody, Antinuclear Antibody (ANA), Erythrocyte rate of intravenous fluids. Fluid repletion should be continued
Sedimentation Rate (ESR), C-Reactive Protein (CRP), ds until CK levels decreases to <5000 U/l and continue to fall.
DNA, Coombs test, HIV, and urine drug screen was normal. Measurement of TSH and free T4 every 4−6 weeks is necessary
Our patient showed significant improvement in his symptoms to assess the response. If TSH remains above the reference
and the CK levels went down to 7600 µ/l with hydration by range, the dose can be increased by 25 to 50 µg/day until ther-
the third day of hospitalization. He was eventually discharged apeutic goal has been achieved.
home on the fourth day of hospitalization and followed up as We suggest to keep hypothyroidism in one of the differen-
an out-patient. tial diagnosis in patients with rhabdomyolysis. According to
Case Reports in Endocrinology 3

the American Thyroid Association clinical guidelines, an [10] C. M. Wiles, A. Young, D. A. Jones, and R. H. Edwards, “Muscle
increase in serum concentration of either CK or LDH for at relaxation rate, fibretype composition and energy turnover in
least two weeks is enough to screen patients for hypothyroidism hyper- and hypo-thyroid patients,” Clinical Science, vol. 57, no. 4,
[13]. Our case illustrates the importance of screening for hypo- pp. 375–384, 1979.
thyroidism in patients with rhabdomyolysis, and symptoms of [11] P. D. Thompson, P. Clarkson, and R. H. Karas, “Statin-associated
hypothyroidism in the absence of other etiologies [14, 15]. myopathy,” JAMA, vol. 289, no. 13, pp. 1681–1690, 2003.
[12] P. A. Gabow, W. D. Kaehny, and S. P. Kelleher, “The spectrum
of rhabdomyolysis,” Medicine, vol. 61, no. 3, pp. 141–152, 1982.
4. Conclusion [13] G. Melli, V. Chaudhry, and D. R. Cornblath, “Rhabdomyolysis:
an evaluation of 475 hospitalized patients,” Medicine, vol. 84,
Rhabdomyolysis is a rare but potentially severe complication no. 6, pp. 377–385, 2005.
of hypothyroidism. Clinicians should be aware of this unique [14] J. L. Zimmerman and M. C. Shen, “Rhabdomyolysis,” Chest,
possibility and be cautious in patients presenting with symp- vol. 144, no. 3, pp. 1058–1065, 2013.
toms of hypothyroidism and muscular manifestations. It is [15] P. W. Ladenson, P. A. Singer, K. B. Ain et al., “American Thyroid
necessary to screen patients with elevated muscle enzymes for Association guidelines for detection of thyroid dysfunction,”
hypothyroidism, as recommended by the American Thyroid Archives of Internal Medicine, vol. 160, no. 11, pp. 1573–1575,
Association. Early diagnosis and prompt treatment of hypo- 2000.
thyroidism induced rhabdomyolysis are essential in prevent-
ing grave consequences.

Conflicts of Interest
The authors declare that they have no conflicts of interest.

References
  [1] J. G. Hollowell, N. W. Staehling, W. D. Flanders et al., “Serum
TSH, T4, and thyroid antibodies in the United States population
(1988 to 1994): National Health and Nutrition Examination
Survey (NHANES III),” The Journal of Clinical Endocrinology
& Metabolism, vol. 87, no. 2, pp. 489–499, 2002.
  [2] R. F. Duyff, J. Van den Bosch, D. M. Laman, B. J. van Loon, and
W. H. Linssen, “Neuromuscular findings in thyroid dysfunction:
a prospective clinical and electrodiagnostic study,” Journal of
Neurology, Neurosurgery & Psychiatry, vol. 68, no. 6, pp. 750–755,
2000.
  [3] A. A. Khaleeli, D. G. Griffith, and R. H. T. Edwards, “The clinical
presentation of hypothyroid myopathy and its relationship to
abnormalities in structure and function of skeletal muscle,”
Clinical Endocrinology, vol. 19, no. 3, pp. 365–376, 1983.
  [4] F. H. Norris Jr and B. J. Panner, “Hypothyroid myopathy. Clinical,
electromyographical, and ultrastructural observations,” Archives
of Neurology, vol. 14, no. 6, pp. 574–589, 1966.
  [5] A. Sindoni, C. Rodolico, M. A. Pappalardo, S. Portaro, and
S. Benvenga, “Hypothyroid myopathy: a peculiar clinical
presentation of thyroid failure. Review of the literature,” Reviews
in Endocrine and Metabolic Disorders, vol. 17, no. 4, pp. 499–519,
2016.
  [6] M. N. Chowta and N. K. Chowta, “Hypothyroidism-associated
rhabdomyolysis,” Indian Journal of Medical Sciences, vol. 62,
no. 12, p. 496, 2008.
 [7]  M. J. Barahona, A. Mauri, N. Sucunza, R. Paredes, and
A. M. Wägner, “Hypothyroidism as a cause of rhabdomyolysis,”
Endocrine Journal, vol. 49, no. 6, pp. 621–623, 2002.
  [8] B. Katipoglu, I. Ates, F. Acehan, A. Meteris, and N. Yılmaz,
“Rhabdomyolysis case based on hypothyroidism,” Endocrinology,
Diabetes & Metabolism Case Reports, vol. 2016, no. 1, 2016.
 [9]  N. Salehi, E. Agoston, I. Munir, and G. J. Thompson,
“Rhabdomyolysis in a patient with severe hypothyroidism,” The
American Journal of Case Reports, vol. 18, pp. 912–918, 2017.
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