Endocrine Myopathies

Back

Practice Essentials

A myopathy is considered any abnormal state of striated muscle. Clinically, the patient experiences muscle weakness, pain, cramps, muscle tenderness, and spasms in various degrees.

Diseases of the endocrine system, including the thyroid, parathyroid, adrenal gland, pituitary gland, and the islands of Langerhans of the pancreas, usually result in multisystem signs and symptoms. A myopathy can very often be present, but it rarely is the presenting symptom.

Major categories of endocrine myopathy include those associated with (1) adrenal dysfunction (as in adrenal insufficiency, glucocorticoid excess, and hyperaldosteronism); (2) thyroid dysfunction (as in hypothyroidism or thyrotoxicosis); (3) parathyroid dysfunction (as in hyperparathyroidism or hypoparathyroidism); (4) pituitary dysfunction (as in acromegaly or panhypopituitarism); and (5) pancreatic islands of Langerhans dysfunction (as in diabetic muscle infarction). Steroid myopathy is the most common endocrine myopathy.[1]

Pathophysiology

A myopathy is defined as an abnormality of the structure or function of skeletal muscle.[2]  Skeletal muscle has a complex structure, composed of intricately organized proteins arranged in a specific manner to allow for muscle contraction.[2]  Contraction of a muscle fiber is initiated by the action of the axon that innervates it, which is then transmitted to the inside of the muscle fiber by a structure called the transverse tubular system that results in the release of calcium from the endoplasmic reticulum.[2]  This calcium then leads to muscle contraction through a series of downstream events in an ATP-dependent process.[2]  Given this complex structure and function, the muscle fiber is susceptible to disturbances by a variety of systemic disorders, including inflammatory disorders, endocrinopathies, electrolyte imbalances, infections, drugs, toxins, and metabolic disorders.  Although endocrinopathies lead to alterations in cellular function and metabolic disturbances that can result in skeletal muscle dysfunction, the exact pathogenesis remains incompletely understood. The etiopathogenesis of specific endocrine myopathies are detailed below.

Adrenal dysfunction

Adrenal disorders associated with skeletal muscle dysfunction include primary adrenal insufficiency, glucocorticoid excess, and hyperaldosteronism. Adrenal hormone excess or deficiency secondary to pituitary disorders may also be associated with skeletal muscle dysfunction.

Primary adrenal insufficiency may be the result of autoimmune, infectious, or metastatic etiologies, with other causes including bilateral adrenal hemorrhage and specific drugs also included in the differential diagnoses. While acute adrenal crisis is associated with severe generalized weakness,[3]  muscle weakness is also a common manifestation of chronic Addison disease.[4]  Patients may also present with myalgias, lower extremity flexion contractures, and hyperkalemic periodic paralysis that improve with hormone replacement.[5, 6, 7]  The exact pathogenesis of this weakness is unclear and whether this represents a true myopathy remains to be elucidated. The postulated mechanisms include circulatory insufficiency, disturbances in carbohydrate metabolism, as well as electrolyte disturbances, namely, hyponatremia and hyperkalemia.[7]  

Glucocorticoid excess caused by Cushing’s syndrome, Cushing’s disease, ectopic adrenocorticotropic hormone (ACTH) production, and exogenous glucocorticoid administration are all associated with muscle weakness and atrophy, with predominant proximal muscle involvement.[7]  Interestingly, other disease states associated with increased glucocorticoid production such as sepsis, acidosis, and cancer, are also associated with muscle damage.[8] ​ Glucocorticoid excess may lead to muscle weakness via inhibition of protein synthesis, increased protein catabolism and altered carbohydrate metabolism.[7, 9, 10]

Hyperaldosteronism caused by pituitary or ectopic overproduction of ACTH, adrenal tumors, or exogenous corticosteroid administration has been associated with muscle weakness that is attributed to the associated hypokalemia.[11, 12] ​ Objective myopathy is rare in hyperaldosteronism, but case reports describe objective muscle weakness, elevated creatine kinase levels, and electromyographic findings of myopathy.[11, 13]

Thyroid dysfunction

Both hyperthyroidism and hypothyroidism are associated with myopathy.

Thyroid hormone deficiency may be congenital or acquired; acquired causes include autoimmune etiologies, iodine-deficient states and post-ablative or post-surgical hypothyroidism.[2]  Central hypothyroidism from hypopituitarism may also occur.[14]  Thyroid hormone deficiency has been commonly associated with neuromuscular symptoms,[15]  probably due to impaired muscle energy metabolism and slow protein turnover that occur with thyroid hormone deficiency.[15, 16, 17]

Thyroid hormone excess, or thyrotoxicosis, may result from Graves disease, toxic multinodular goiter, toxic adenoma, thyroiditis, exogenous thyroid hormone intake and, rarely, excessive thyroid-stimulating hormone (TSH) secretion from the pituitary gland.[14] ​ Thyrotoxic myopathy may  be secondary to a disturbance in the function of the muscle fibers from increased mitochondrial respiration, accelerated protein degradation and lipid oxidation, as well as enhanced beta-adrenergic sensitivity due to excessive amounts of thyroid hormone.[18]

Parathyroid dysfunction and vitamin D deficiency (osteomalacia)

Hypoparathyroidism is most commonly postsurgical, but may also occur due to genetic or autoimmune etiologies.[19]  Resistance to parathyroid hormone (PTH) can occur in hypomagnesemia.[19]  Hypoparathyroidism results in hypocalcemia, which in turn leads to neuromuscular irritability[20]  that manifests as tetany, with or without carpopedal spasm.  

Primary hyperparathyroidism, or hypersecretion of PTH from the parathyroid glands — from parathyroid adenomas, and less commonly from diffuse gland hyperplasia[19]  — has specific effects on skeletal muscle. Increased intracellular calcium, and protein degradation along with reduced calcium sensitivity of troponin, lead to hyperparathyroid myopathy, including muscle weakness and pain.[7]  

Secondary hyperparathyroidism occurs as a result of hypocalcemia from vitamin D deficiency and chronic renal failure.[19]  Elevated PTH levels may lead to hyperparathyroid myopathy by similar mechanisms as in primary hyperparathyroidism. Furthermore, the associated vitamin D deficiency and uremia can result in various downstream effects, resulting in myopathic features as well.  

Osteomalacia, the abnormal mineralization of bone seen in vitamin D deficiency and hypophosphatemia, is associated with myopathy via various mechanisms, including decreased protein synthesis, impaired excitation-contraction coupling, decreased myofibrillar ATPase activity, and impaired calcium uptake ability.[7]  

Pituitary dysfunction

Pituitary disorders, both hyposecretion and hypersecretion of hormones, are associated with myopathy.

Hypopituitarism is usually due to compression of the adenohypophysis from pituitary adenomas and rarely from trauma or infection. The muscle weakness in panhypopituitarism is largely due to the consequent reduction in thyroid and adrenal hormones, although reduced growth hormone levels also play a role.[7]  

Hyperpituitarism results from excessive secretion from tumors arising from specific pituitary cells, such as ACTH and growth hormone from corticotroph and somatotroph adenomas, respectively.

ACTH-secreting pituitary adenoma or Cushing’s disease may result in a proximal myopathy due to excess glucocorticoid secretion.[7, 21]

The muscle weakness in acromegaly has been postulated to occur via reduced membrane excitability and reduced muscle ATPase activity, while a concomitant increased muscle bulk may occur due to the effects of growth hormone on muscle protein metabolism.[7]  Interestingly, there are some reports that dysfunction of the hypothalamic-pituitary-adrenal axis plays a role in the pathogenesis of polymyalgia rheumatica.[22, 23]  

Pancreatic islets of Langerhans dysfunction

Diabetic muscle infarction (spontaneous diabetic myonecrosis) is a rare condition that can occur in patients with type 1 and type 2 diabetes and is thought to represent one of the vascular complications of diabetes.[24, 25]  It can present as painful muscle swelling, typically of the front of the thigh, and the exact pathogenesis is unclear.[25]

Epidemiology

Patients with endocrine dysfunctions frequently complain of vague fatigue and weakness that may be ignored, leading to delayed diagnosis if this was the sole manifestation.[26] A diagnosis of myopathy is sometimes made without histologic or electrophysiologic confirmation.  Therefore, the true prevalence of endocrine myopathy is difficult to ascertain.[27]

Corticosteroid myopathy remains the most common endocrine-related myopathy. Severe muscle weakness occurs in up to 21% of patients with exogenous glucocorticosteroid excess.[28]

The prevalence of specific endocrine myopathies is as follows:

Sex- and age-related demographics

Sex-related demographics are as follows:

Age-related demographics are as follows:

Prognosis

The prognosis depends on the underlying endocrine process. Hyperthyroidism, hypothyroidism, and other endocrine states may be fatal.

Myopathy may be painful, and the pain must be addressed either in the form of symptomatic therapies or curative treatments of the endocrine diseases. Myopathy often abates with correction of underlying disease. Prolonged weakness and partial recovery are common, especially in severe cases and in patients with delayed or suboptimal treatment.

The prognoses for various endocrine myopathies are as follows:

Morbidity/mortality

Myopathy may result in weakness and/or pain that may significantly influence the quality of life and impair daily function. Myopathy may also result in muscle atrophy.

Mortality is related to the underlying cause of myopathy. For example, myxedema coma may have a mortality rate between 50% (if treated aggressively) and 100%.[41]

Complications

Clinicians should be aware of the following potential complications that may arise:

History

When approaching a patient with a suspected myopathy, the age of onset, rapidity of progression, distribution of muscle involvement, and whether the symptoms are intermittent, stable, or progressive can help guide the diagnosis.[2]  In endocrine myopathies, multiple organ systems are usually involved and myopathy is only one part of the history, although exceptions do occur where myopathy may be the presenting feature. For systemic manifestations of endocrine diseases, please refer to respective Medscape Reference articles for more details. This article will focus on muscular manifestations of endocrine diseases. Endocrine myopathies may have an acute or chronic presentation, depending on the etiology, and they are typically characterized by proximal more than distal muscle weakness, with or without associated muscle pain, cramps, and/or spasms. The weakness is typically symmetric or rapidly becomes symmetric. Muscle atrophy may or may not be present.

Adrenal dysfunction

Hypoadrenalism

Acute adrenal crisis is associated with severe generalized weakness.[3]  Addison disease may be associated with chronic weakness, myalgias, and lower extremity flexion contractures.[5, 6, 7]  Some cases are also associated with hyperkalemic periodic paralysis that presents with intermittent muscle weakness.[7]

Hyperadrenalism

Cushing’s syndrome may present with the usual cushingoid features plus myalgias and proximal muscle weakness.[46] Corticosteroid-induced myopathy is the most common endocrine-related muscle disease and may be acute, as in the intensive care unit setting, or may be a more chronic process.[47]  While hyperaldosteronism may be associated with subjective muscle weakness, objective weakness is rare.[11, 12, 13]  

Thyroid dysfunction

The muscular manifestations of hypothyroidism are myriad and are summarized below:

General symptoms of thyrotoxicosis include weight loss, sweating, tremor, muscle wasting, and painless weakness. Occasionally, patients have myalgia, cramps, and bulbar and ocular muscle weakness. Ocular symptoms (diplopia, reduced blinking, lid lag) and skin disease may be present, especially in the case of Graves disease.

Onset of symptoms may be gradual in mild hyperthyroidism and more rapid in severe hyperthyroidism.[7]  

Thyrotoxic periodic paralysis is a condition characterized by transient attacks of proximal muscle weakness lasting minutes to days, with sparing of bulbar and respiratory muscles.[7]

Parathyroid dysfunction

Hypoparathyroidism results in hypocalcemia manifesting as perioral and distal parasthesias and numbness, tetany, carpopedal spasm, and muscle cramps. Muscle weakness, if present, is usually mild.

In primary hyperparathyroidism, muscle wasting, proximal muscle weakness, and painful muscle stiffness are common.[7]  Patients may also have muscle cramps and paresthesias.[53]  Although there is usually sparing of bulbar and sphincter muscles, there have been reports of respiratory muscle weakness.[54, 55]

Patients with secondary hyperparathyroidism have similar muscle symptoms to those with primary hyperparathyroidism but usually have a concomitant neuropathy.[7]

Patients with osteomalacia typically have proximal muscle weakness, pain, and wasting.[7]  

Pituitary dysfunction

In patients with hypopituitarism, the myopathy often results from secondary adrenal and thyroid dysfunction. Patients have severe muscle weakness with relatively preserved muscle mass.[7]

As with hypopituitarism, secondary adrenal effects may be responsible for the myopathy in hyperpituitarism. In acromegaly, patients typically have gradually progressive muscle weakness, often with increased muscle mass.

Pancreatic islets of Langerhans dysfunction

Diabetic muscle infarction is a rare condition that tends to occur in patients with poorly controlled diabetes and typically presents acutely with muscle swelling and pain, most commonly affecting the lower extremities.[25]  

Physical Examination

Physical examination should focus on the entire body, as the endocrine diseases usually present with multiple system findings. An endocrine tumor is in the differential diagnosis, and signs of a hormone-secreting tumor may be seen on examination.

A detailed neurologic examination is required, including a complete assessment of power, tone, muscle bulk, and deep tendon reflexes. Early recognition of bulbar muscle weakness and respiratory muscle weakness is essential, as these can lead to life-threatening complications.

In general, there is predominant proximal rather than distal muscle involvement. Muscle atrophy may or may not be present. Muscle stretch reflexes are usually present (may be depressed) even in weak muscles.

The following patterns may be observed in specific endocrine myopathies.

Adrenal dysfunction

Hypoadrenalism

Hypoadrenalism may be associated with subjective muscle weakness, myalgias, and lower extremity flexion contractures.[5, 6, 7]

Hyperadrenalism

Glucocorticoid excess is typically associated with proximal muscle weakness and atrophy, with the lower extremities more affected than the upper extremities.[7]  Striated muscles of sphincters and those innervated by cranial nerves are spared.[7]  Although hyperaldosteronism may be associated with subjective muscle weakness, objective weakness is rare.[11, 12, 13]  

Thyroid dysfunction

Thyroid disorders may result in orbital myositis, a disorder that may impair ocular movement and therefore may clinically appear as eye muscle weakness.[56]

Hypothyroidism

Patients typically have symmetric proximal muscle weakness with reduced velocity of motor movements and delayed relaxation of deep tendon reflexes. Median neuropathy at the wrist commonly accompanies this diagnosis. Myxedema is a classic, yet often forgotten sign of hypothyroid myopathy characterized by a typical localized mounding of muscle tissue induced by a light pressure or tactile stimulus, elicited by flicking the bulk of the biceps muscle with the thumb and index finger.[57]

Hyperthyroidism

In addition to the findings of Graves disease, muscle weakness with atrophy of proximal muscles may be present. Distal muscle involvement has also been described.[27]  In rare cases, bulbar and respiratory muscles may be involved and it is important to exclude this involvement on examination. Deep tendon reflexes are typically normal, or in some cases, are brisk.[7, 27]  

Parathyroid dysfunction

Hypoparathyroidism

Tetany is a common finding. If the tetany is latent, it may be elicited on examination by hyperventilation or by specific maneuvers, including the Chvostek sign, where twitching of the facial muscles is caused by tapping the facial nerve, and the Trousseau sign, where carpopedal spasm is provoked by inflating a blood pressure cuff to block venous return.[7]  

Hyperparathyroidism

Hyperparathyroid myopathy typically manifests with symmetric proximal muscle weakness and wasting with brisk deep tendon reflexes.[7] Respiratory muscle weakness may be present.[54, 55]

Osteomalacia

Patients may have proximal muscle weakness and wasting.[7]  

Pituitary dysfunction

Hypopituitarism

Multiple endocrinopathies may result from pituitary dysfunction. The myopathy from pituitary disease may be a result of secondary adrenal or thyroid dysfunction or other endocrine disturbance. Patients have severe muscle weakness with relatively preserved muscle mass. A pituitary tumor may have focal mass effects.

Hyperpituitarism

Multiple endocrinopathies may result from pituitary dysfunction. Patients with acromegaly may have muscle weakness with increased muscle mass. Concomitant neuropathy, particularly of the median nerve is often present.[7]  Mass lesions may have local effects.

Pancreatic islets of Langerhans dysfunction

Diabetic muscle infarction

Typically presents acutely with muscle swelling and pain, most commonly affecting the lower extremities. Tenderness of the affected muscle group may be appreciated on examination.[25]  A few patients may have a mild fever.[24, 58]  Rarely, there may be associated erythema, warmth and induration.[58]  

Caveats

Physicians must be especially alert in the following scenarios:

Laboratory Studies

Because the diagnosis is made by elucidating the underlying endocrine abnormality, laboratory studies are considered in relation to the most likely etiologies.

Laboratory studies measuring hormone levels may help distinguish one endocrine myopathy from another. These tests are best ordered in consultation with an endocrinologist.

Creatine kinase (CK) levels may be normal or increased in various endocrine disorders, as follows:

Imaging Studies and Other Tests

Imaging studies

Imaging studies neither confirm nor exclude the presence of muscle disease. They may be of benefit in the diagnosis of endocrine disorders.

Other tests

Electromyography (EMG) may reveal the presence of a myopathy, but a normal examination does not rule out the diagnosis. Although commonly performed with nerve conduction study testing, needle EMG is direct invasive testing of muscle and therefore differs from nerve conduction study testing. Myopathy is a disorder of muscle, and the nerve conduction study portion of the electrophysiological examination should be normal; however, the endocrinopathies often also cause neuropathies or may be associated with other conditions (such as diabetes) in which neuropathies are common. This heterogeneity explains the great variability and lack of consensus regarding the electrophysiological findings in endocrine diseases.

Needle EMG examination preferentially studies the type I units, as these units fire selectively during weak muscle contraction. Thus, a disease process selectively involving type II units, such as steroid myopathy, may reveal no abnormalities on EMG.

EMG findings consistent with a myopathic process include the following:

Histologic Findings

Muscle biopsy is considered mainly to exclude other treatable or congenital muscle diseases, including myotonic dystrophy or congenital myopathies.[62, 63] Histologic changes associated with endocrine myopathies are variable and rarely specific. There is a striated muscle protein that may prove to be a disease progression marker.[64]

Histologic findings are as follows:

Medical and Surgical Care

Medical care

Treatment of endocrine myopathies involves correction of the underlying endocrine dysfunction, either surgically or medically. Care should be taken to avoid neurapraxic lesions. Beta-adrenergic–blocking agents may improve the strength of the muscles, especially respiratory muscles.

Surgical care

When the underlying cause of endocrine myopathies is found to be related to a hormone-secreting tumor or a tumor of the endocrine glands, it usually needs to be surgically removed.

Consultations

Endocrinology consultation is recommended.

Neurology consultation may be appropriate if neurological findings such as specific muscle weakness require elucidation; neurologists may also perform EMG examination to determine the presence of myopathic findings.

Physical medicine consultation may be helpful if the patient has suffered weakness and has not recovered fully.

Medication Summary

No specific medications are recommended for endocrine myopathies. Refer to the relevant Medscape Reference articles for the appropriate medical management of each endocrinopathy.

Author

Shireen R Chacko, MBBS, Resident Physician, Department of Internal Medicine, Albert Einstein Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Catherine Anastasopoulou, MD, PhD, FACE, Associate Professor of Medicine, The Steven, Daniel and Douglas Altman Chair of Endocrinology, Sidney Kimmel Medical College of Thomas Jefferson University; Einstein Endocrine Associates, Einstein Medical Center

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Neil A Busis, MD, Chief of Neurology and Director of Neurodiagnostic Laboratory, UPMC Shadyside; Clinical Professor of Neurology and Director of Community Neurology, Department of Neurology, University of Pittsburgh Physicians

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Academy of Neurology<br/>Serve(d) as a speaker or a member of a speakers bureau for: American Academy of Neurology<br/>Received income in an amount equal to or greater than $250 from: American Academy of Neurology.

Chief Editor

Nicholas Lorenzo, MD, CPE, MHCM, FAAPL, Co-Founder and Former Chief Publishing Officer, eMedicine and eMedicine Health, Founding Editor-in-Chief, eMedicine Neurology; Founder and Former Chairman and CEO, Pearlsreview; Founder and CEO/CMO, PHLT Consultants; Former Chief Medical Officer, MeMD Inc

Disclosure: Nothing to disclose.

Additional Contributors

Dianna Quan, MD, Professor of Neurology, Director of Electromyography Laboratory, University of Colorado School of Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Association of Neuromuscular and Electrodiagnostic Medicine; American Neuromuscular Foundation<br/>Serve(d) as a speaker or a member of a speakers bureau for: Alnylam<br/>Received research grant from: Alnylam; Momenta/Janssen; Avidity bioscience.

Wayne E Anderson, DO, FAHS, FAAN, Assistant Professor of Internal Medicine/Neurology, College of Osteopathic Medicine of the Pacific Western University of Health Sciences; Clinical Faculty in Family Medicine, Touro University College of Osteopathic Medicine; Clinical Instructor, Departments of Neurology and Pain Management, California Pacific Medical Center

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Ling Xu, MD to the development and writing of this article.

References

  1. Minetto MA, Lanfranco F, Motta G, Allasia S, Arvat E, D'Antona G. Steroid myopathy: some unresolved issues. J Endocrinol Invest. 2011 May. 34(5):370-5. [View Abstract]
  2. Selcen D. Muscle diseases. Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. 26. Philadelphia, PA: Elsevier; 2020. 2: 2501-08.
  3. Rushworth RL, Torpy DJ, Falhammar H. Adrenal Crisis. N Engl J Med. 2019 Aug 29. 381 (9):852-861. [View Abstract]
  4. Nerup J. Addison's disease--clinical studies. A report of 108 cases. Acta Endocrinol (Copenh). 1974 May. 76 (1):127-41. [View Abstract]
  5. Shapiro MS, Trebich C, Shilo L, Shenkman L. Myalgias and muscle contractures as the presenting signs of Addison's disease. Postgrad Med J. 1988 Mar. 64 (749):222-3. [View Abstract]
  6. Harbuz V, Bihan H, Salama J, Reach G, Cohen R. Flexion contractures possibly reflect the existence of hypocortisolism: two case reports. J Neurol. 2010 Jul. 257 (7):1129-33. [View Abstract]
  7. Ruff RL, Weissmann J. Endocrine Myopathies. Neurology Clinics. New York: McGraw Hill; August 1988. 6: 575-92.
  8. Vegiopoulos A, Herzig S. Glucocorticoids, metabolism and metabolic diseases. Mol Cell Endocrinol. 2007 Sep 15. 275 (1-2):43-61. [View Abstract]
  9. Kelly FJ, McGrath JA, Goldspink DF, Cullen MJ. A morphological/biochemical study on the actions of corticosteroids on rat skeletal muscle. Muscle Nerve. 1986 Jan. 9 (1):1-10. [View Abstract]
  10. Smith OL, Wong CY, Gelfand RA. Influence of glucocorticoids on skeletal muscle proteolysis in normal and diabetic-adrenalectomized eviscerated rats. Metabolism. 1990 Jun. 39 (6):641-6. [View Abstract]
  11. Relman AS. Diagnosis of primary aldosteronism. Am J Surg. 1964 Jan. 107:173-7. [View Abstract]
  12. Conn JW, Knopf RF, Nesbit RM. Clinical characteristics of primary aldosteronism from an analysis of 145 cases. Am J Surg. 1964 Jan. 107:159-72. [View Abstract]
  13. Atsumi T, Ishikawa S, Miyatake T, Yoshida M. Myopathy and primary aldosteronism: electronmicroscopic study. Neurology. 1979 Oct. 29 (10):1348-53. [View Abstract]
  14. Jonklaas J, Cooper DS. Thyroid. Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. 26. Philadelphia, PA: Elsevier; 2020. 2: 1462-76.
  15. Horak HA, Pourmand R. Endocrine myopathies. Neurol Clin. 2000 Feb. 18(1):203-13. [View Abstract]
  16. Monzani F, Caraccio N, Siciliano G, Manca L, Murri L, Ferrannini E. Clinical and biochemical features of muscle dysfunction in subclinical hypothyroidism. J Clin Endocrinol Metab. 1997 Oct. 82 (10):3315-8. [View Abstract]
  17. Argov Z, Arnold DL. MR spectroscopy and imaging in metabolic myopathies. Neurol Clin. 2000 Feb. 18 (1):35-52. [View Abstract]
  18. Lin SH, Huang CL. Mechanism of thyrotoxic periodic paralysis. J Am Soc Nephrol. 2012 Jun. 23(6):985-8. [View Abstract]
  19. Thakker RV. The parathyroid glands, hypercalcemia, and hypocalcemia. Goldman L, Schafer AI. Goldman-Cecil Medicine. 26. Philadelphia, PA: Elsevier; 2020. 2: 1611-22.
  20. Engel AG, Fransini-Armstrong C, eds. Endocrine myopathies. In: Myology. 2nd ed. McGraw-Hill. 1994.
  21. Tran M, Elias AN. Severe myopathy and psychosis in a patient with Cushing's disease macroadenoma. Clin Neurol Neurosurg. 2003 Dec. 106 (1):1-4. [View Abstract]
  22. Imrich R, Bosak V, Rovensky J. Polymyalgia rheumatica and temporal arteritis: the endocrine relations and the pathogenesis. Review. Endocr Regul. 2006 Sep. 40(3):83-9. [View Abstract]
  23. Cutolo M, Foppiani L, Minuto F. Hypothalamic-pituitary-adrenal axis impairment in the pathogenesis of rheumatoid arthritis and polymyalgia rheumatica. J Endocrinol Invest. 2002. 25 (10 Suppl):19-23. [View Abstract]
  24. Rocca PV, Alloway JA, Nashel DJ. Diabetic muscular infarction. Semin Arthritis Rheum. 1993 Feb. 22 (4):280-7. [View Abstract]
  25. Horton WB, Taylor JS, Ragland TJ, Subauste AR. Diabetic muscle infarction: a systematic review. BMJ Open Diabetes Res Care. 2015. 3 (1):e000082. [View Abstract]
  26. Shah DN, Chorya HP, Ramesh NN, et al. Myopathies of endocrine origin: A review for physicians. Dis Mon. 2024 Jan. 70 (1):101628. [View Abstract]
  27. Rodolico C, Bonanno C, Pugliese A, Nicocia G, Benvenga S, Toscano A. Endocrine myopathies: clinical and histopathological features of the major forms. Acta Myol. 2020 Sep. 39 (3):130-135. [View Abstract]
  28. Leszczyńska D, Szatko A, Papierska L, Zgliczyński W, Glinicki P. Musculoskeletal complications of Cushing syndrome. Reumatologia. 2023. 61 (4):271-82. [View Abstract]
  29. Alshekhlee A, Kaminski HJ, Ruff RL. Neuromuscular manifestations of endocrine disorders. Neurol Clin. 2002 Feb. 20 (1):35-58, v-vi. [View Abstract]
  30. Stewart PM. The Adrenal Cortex. Williams Textbook of Endocrinology. 12. Philadelphia: Elsevier Saunders; 12th May 2011.
  31. Urbanic RC, George JM. Cushing's disease--18 years' experience. Medicine (Baltimore). 1981 Jan. 60 (1):14-24. [View Abstract]
  32. Thorn GW, Dorrance S, Day E. Addison's disease: evaluation of synthetic desoxycorticosterone acetate therapy in 158 patients. Ann Intern Med. 1942. 16:1053-96.
  33. Olson BR, Klein I, Benner R, Burdett R, Trzepacz P, Levey GS. Hyperthyroid myopathy and the response to treatment. Thyroid. 1991. 1 (2):137-41. [View Abstract]
  34. Shane E, McClane KA, Olarte MR, Bilezikian JP. Hypoparathyroidism and elevated muscle enzymes. Neurology. 1980 Feb. 30 (2):192-5. [View Abstract]
  35. Patten BM, Bilezikian JP, Mallette LE, Prince A, Engel WK, Aurbach GD. Neuromuscular disease in primary hyperparathyroidism. Ann Intern Med. 1974 Feb. 80 (2):182-93. [View Abstract]
  36. Askari A, Vignos PJ Jr, Moskowitz RW. Steroid myopathy in connective tissue disease. Am J Med. 1976 Oct. 61 (4):485-92. [View Abstract]
  37. Mishra AK, Agarwal A, Gupta S, Agarwal G, Verma AK, Mishra SK. Outcome of adrenalectomy for Cushing's syndrome: experience from a tertiary care center. World J Surg. 2007 Jul. 31 (7):1425-32. [View Abstract]
  38. Duyff RF, Van den Bosch J, Laman DM, van Loon BJ, Linssen WH. Neuromuscular findings in thyroid dysfunction: a prospective clinical and electrodiagnostic study. J Neurol Neurosurg Psychiatry. 2000 Jun. 68 (6):750-5. [View Abstract]
  39. Patten BM, Pages M. Severe neurological disease associated with hyperparathyroidism. Ann Neurol. 1984 May. 15 (5):453-6. [View Abstract]
  40. Frame B, Heinze EG Jr, Block MA, Manson GA. Myopathy in primary hyperparathyroidism. Observations in three patients. Ann Intern Med. 1968 May. 68 (5):1022-7. [View Abstract]
  41. Mathew V, Misgar RA, Ghosh S, Mukhopadhyay P, Roychowdhury P, Pandit K, et al. Myxedema coma: a new look into an old crisis. J Thyroid Res. 2011. 2011:493462. [View Abstract]
  42. Salehi N, Agoston E, Munir I, Thompson GJ. Rhabdomyolysis in a Patient with Severe Hypothyroidism. Am J Case Rep. 2017 Aug 22. 18:912-918. [View Abstract]
  43. Katipoglu B, Ates I, Acehan F, Meteris A, Yılmaz N. Rhabdomyolysis case based on hypothyroidism. Endocrinol Diabetes Metab Case Rep. 2016. 2016:[View Abstract]
  44. Siafakas NM, Alexopoulou C, Bouros D. Respiratory muscle function in endocrine diseases. Monaldi Arch Chest Dis. 1999 Apr. 54(2):154-9. [View Abstract]
  45. Abisi S, Yong YP, Beech A, Oluwole A, Tennant W. Spontaneous sequential compartment syndrome of the lower limbs. Vasc Endovascular Surg. 2013 Oct. 47 (7):566-8. [View Abstract]
  46. Pivonello R, Isidori AM, De Martino MC, Newell-Price J, Biller BM, Colao A. Complications of Cushing's syndrome: state of the art. Lancet Diabetes Endocrinol. 2016 Jul. 4 (7):611-29. [View Abstract]
  47. Gupta A, Gupta Y. Glucocorticoid-induced myopathy: Pathophysiology, diagnosis, and treatment. Indian J Endocrinol Metab. 2013 Sep. 17 (5):913-6. [View Abstract]
  48. Panat SR, Jha PC, Chinnannavar SN, Chakarvarty A, Aggarwal A. Kocher debre semelaigne syndrome: a rare case report with orofacial manifestations. Oman Med J. 2013 Mar. 28 (2):128-30. [View Abstract]
  49. 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 Dec. 17 (4):499-519. [View Abstract]
  50. Rodolico C, Toscano A, Benvenga S, et al. Myopathy as the persistently isolated symptomatology of primary autoimmune hypothyroidism. Thyroid. 1998 Nov. 8(11):1033-8. [View Abstract]
  51. Achappa B, Madi D. Hoffmann's Syndrome- A Rare Form of Hypothyroid Myopathy. J Clin Diagn Res. 2017 May. 11 (5):OL01-OL02. [View Abstract]
  52. Winter S, Heiling B, Eckardt N, Kloos C, Axer H. Hoffmann's syndrome in the differential work-up of myopathic complaints: a case report. J Med Case Rep. 2023 Oct 31. 17 (1):473. [View Abstract]
  53. Turken SA, Cafferty M, Silverberg SJ, De La Cruz L, Cimino C, Lange DJ, et al. Neuromuscular involvement in mild, asymptomatic primary hyperparathyroidism. Am J Med. 1989 Nov. 87 (5):553-7. [View Abstract]
  54. Sorva A. Respiratory muscle weakness in primary hyperparathyroidism. J Am Geriatr Soc. 1996 Jan. 44 (1):104. [View Abstract]
  55. Gentric A, Pennec YL. Fatal primary hyperparathyroidism with myopathy involving respiratory muscles in an old woman. J Am Geriatr Soc. 1994 Dec. 42 (12):1306. [View Abstract]
  56. Costa RM, Dumitrascu OM, Gordon LK. Orbital myositis: diagnosis and management. Curr Allergy Asthma Rep. 2009 Jul. 9(4):316-23. [View Abstract]
  57. Vignesh G, Balachandran K, Kamalanathan S, Hamide A. Myoedema: A clinical pointer to hypothyroid myopathy. Indian J Endocrinol Metab. 2013 Mar. 17 (2):352. [View Abstract]
  58. Umpierrez GE, Stiles RG, Kleinbart J, Krendel DA, Watts NB. Diabetic muscle infarction. Am J Med. 1996 Sep. 101 (3):245-50. [View Abstract]
  59. 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 (4):232-42. [View Abstract]
  60. Doran GR. Serum enzyme disturbances in thyrotoxicosis and myxoedema. J R Soc Med. 1978 Mar. 71 (3):189-94. [View Abstract]
  61. Minetto MA, Lanfranco F, Botter A, Motta G, Mengozzi G, Giordano R, et al. Do muscle fiber conduction slowing and decreased levels of circulating muscle proteins represent sensitive markers of steroid myopathy? A pilot study in Cushing's disease. Eur J Endocrinol. 2011 Jun. 164 (6):985-93. [View Abstract]
  62. Romeo V. Myotonic Dystrophy Type 1 or Steinert's disease. Adv Exp Med Biol. 2012. 724:239-57. [View Abstract]
  63. Li Cavoli G, Mulè G, Rotolo U. Renal involvement in psychological eating disorders. Nephron Clin Pract. 2011. 119(4):c338-41; discussion c341. [View Abstract]
  64. Nilsson MI, Nissar AA, Al-Sajee D, Tarnopolsky MA, Parise G, Lach B, et al. Xin is a marker of skeletal muscle damage severity in myopathies. Am J Pathol. 2013 Dec. 183(6):1703-9. [View Abstract]
  65. Ferguson GT, Irvin CG, Cherniack RM. Effect of corticosteroids on respiratory muscle histopathology. Am Rev Respir Dis. 1990 Nov. 142 (5):1047-52. [View Abstract]