steroid myopathy ck

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Steroid myopathy ck

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Case 4: An year-old man with a 6 year history of mostly ocular myasthenia treated with pyridostigmine developed gradual worsening of his symptoms. After the second dexamethasone dose, he developed severe generalized weakness and new-onset breathing and swallowing difficulties.

He was discharged wheelchair-bound and dependent on intermittent respiratory support and assistance in ADL. Diagnosed as refractory myasthenia, treatment with steroids was continued. In retrospect, he described worsening of his symptoms after each dose of the steroids.

Steroid-induced myopathy was considered only after he had been treated with relatively high doses of steroids for over a year, too late to benefit when treatment was tapered. Glucocorticoid-induced myopathy is well-known in chronically treated patients. Some reports involve mechanically ventilated patients whose myopathy developed with concurrent use of neuromuscular blocking agents, prolonged muscle disuse, critical-care nutritional deficiencies and very high doses of corticosteroids.

The true extent of the problem is hard to estimate. Nevertheless, ASM can be considered a rare occurrence. Our cases and literature review demonstrate the great clinical diversity of ASM Table 1 2—12 , already noted by Askari et al. In contrast with early reports which involved very high doses of steroids, often given to ventilated patients with severe status asthmaticus, 2—5 and suggestions that patients treated with fluorinated corticosteroids are more susceptible, 7 our experience and the scant existing literature reveal that ASM is unpredictable and should be considered when patients treated with steroids regardless of dose, route of administration or length of treatment develop muscle weakness at any site Table 1.

The fact that no single test is diagnostic for this condition 9 , 10 adds to the difficulty in its timely recognition. Yet, even the relatively indolent course can be later followed by a more severe, chronic and possibly irreversible form if steroids are continued cases 3 and 4. Thus, when ASM is suspected, corticosteroid-dose should probably be reduced or omitted altogether if an alternative treatment is feasible.

The clinical characteristics of ASM, based on our four patients and the comprehensive review of additional patients reported in the literature is summarised in Table 2. Table 1. Acute, early onset myopathy associated with glucocorticoid treatment: cases from our clinic and the literature. Old age, malnutrition, immobilization, sedentary lifestyle and a prior muscle disease may all increase the risk of steroid myopathy.

Chronic steroid myopathy is mediated mainly through muscle fibre atrophy, affecting glycolytic more than oxidative fibres 15 and takes months to develop. The exact mechanism of ASM is unclear, but a direct effect on muscle contraction and energy production is likely. Steroids have numerous non-genomic effects. Thus, a high index of suspicion for steroid myopathy is warranted in any patient who develops new-onset fatigable or constant muscle weakness of any muscle group, independent of the dose or time frame following corticosteroid treatment.

This is even more important in patients with underlying neuromuscular diseases, in which the symptoms of steroid myopathy can be easily attributed to their pre-existing disease. In such cases, timely dose reduction, or preferably, drug discontinuation if possible, are likely to be followed by a significant improvement in muscle strength.

Currently, the great diversity in the presentation of early steroid myopathy; the frequent ascribing of symptoms to the primary disease; and poor awareness of this entity, all contribute to delayed recognition and belated treatment. Steroid myopathy. Clinical, histologic and cytologic observation. Johns Hopkins Med J ; : — Google Scholar. Acute hydrocortisone myopathy. Acute hydrocortisone myopathy in acute severe asthma.

Thorax ; 41 : — 2. Acute myopathy in severe acute asthma treated with intravenously administered corticosteroids. Am Rev Respir Dis ; : — 3. Acute myopathy and neuropathy in status asthmaticus: case report and literature review. Muscle Nerve ; 16 : 84 — Steroid myopathy in connective tissue disease. Kumar S. Steroid-induced myopathy following a single oral dose of prednisone.

Neurol India ; 51 : — 6. Khan MA , Larson E. Acute myopathy secondary to oral steroid therapy in a year-old man: a case report. J Med Case Rep ; 5 : Acute myopathy following short-term low-dose oral steroid therapy. J Ind Acad Clin Med ; 10 : 65 — 8. Acute myopathy following intra-muscular injection of compound betamethasone.

Medicine Baltimore ; 96 : e Steroid myopathy induced by epidural triamcinolone injection. Brit J Rheumatol ; 34 : — 6. Herzog AG. Proximal myopathy associated with inhaled steroids. JAMA ; : Dekhuizen PN , Decramer M. Steroid-induced myopathy and its significance to respiratory disease: a known disease rediscovered. Eur Respir J ; 5 : — Respiratory muscle fibres: specialisation and plasticity.

Thorax ; 59 : — Gupta A , Gupta Y. Glucocorticoid-induced myopathy: pathophysiology, diagnosis, and treatment. Indian J Endocrinol Metab ; 17 : — 6. The effects of non-genomic glucocorticoid mechanisms on bodily functions and the central neural system. A critical evaluation of findings.

Front Neuroendocrinol ; 29 : — Minireview: rapid glucocorticoid signaling via membrane-associated receptors. Endocrinology ; : — Buttgereit F , Scheffold A. Rapid glucocorticoid effects on immune cells. Steroids ; 67 : — Oxidative stress-associated mitochondrial dysfunction in corticosteroid-treated muscle cells. Muscle Nerve ; 30 : 49 — Chronic corticosteroid administration causes mitochondrial dysfunction in skeletal muscle.

J Neurol ; : — 9. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Skip Nav Destination Article Navigation.

Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Patients and methods. Report of cases. Urine myoglobin results were negative. He was seen again 30 days after initial presentation and was feeling fine and had resumed his normal active lifestyle, farming. He continues to complain of intermittent foot pain, which is worse with activity, and he takes ibuprofen mg as needed for relief.

ASM is rare and poorly understood. Several theories have been proposed to explain the pathogenesis of this condition. One model proposes activation of ubiquitin-dependent proteolytic systems [ 8 ]. Another model suggests that insulin-like growth factor-1, which may act as anti-apoptotic, is inhibited by steroids, thus allowing increased muscle apoptosis [ 9 ]. Askari et al. One patient developed symptoms of ASM within a few days of starting therapy.

Five patients tolerated a low maintenance dose of prednisone 15 to 60 mg for a duration of 60 to days without any signs or symptoms of myopathy. However, increasing the maintenance dose resulted in the appearance of symptoms of corticosteroid myopathy within 30 days in four of five patients. The group concluded that the development of myopathy in patients receiving corticosteroid therapy is not related to the age of the patient, the magnitude of the dose given or the duration of maintenance therapy [ 10 ].

Typical presentations include diffuse myalgias and muscle weakness. Pelvic girdle muscle involvement is most consistently seen [ 10 ]. Some patients present with difficulty weaning from mechanical ventilators [ 5 , 6 ].

Our patient received methylprednisolone, and he was not on any maintenance corticosteroid therapy. He did have pelvic girdle muscle weakness, but his symptoms were not limited to these muscle groups. A number of laboratory investigations may aid in the diagnosis of ASM. EMG and muscle biopsy may also be helpful. No single test is diagnostic for this condition. The diagnosis always involves a high degree of clinical suspicion with diagnostic tests as an adjunct.

Serum marker elevation is an inconsistent finding. They did find increased urinary creatinine excretion to be more consistently abnormal than elevated CPK [ 10 ]. EMG may be normal, but abnormal EMG findings classically include normal sensory and motor conduction velocities with decreased amplitude of muscle action potential [ 11 ]. We did not obtain EMG in our patient. Typically, muscle biopsy shows diffuse necrosis of both type I and type II fibers [ 6 , 11 ]; however, muscle biopsy is often diagnostically unhelpful [ 10 ].

Currently, there are no dosing recommendations for steroids that could decrease the likelihood of developing myopathy. Our patient received two doses of methylprednisolone, 24 mg and 20 mg. The only similar report involved a patient taking 40 mg of prednisone [ 7 ].

We were unable to find literature reports of patients developing myopathy while taking doses less than 40 mg of prednisone. There is no specific treatment available for this condition. The most consistent finding on literature review is the fact that myopathy resolves without any intervention with discontinuation of steroid therapy. Steroids, as a class, are well recognized as a critical treatment modality for a number of conditions.

They are prescribed by physicians belonging to almost all areas of medicine. Although very rare, ASM needs to be recognized early to ameliorate its significant effects. Written informed consent was obtained from the patient for publication of this case report. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Cushing H: The basophil adenomas of the pituitary body and their clinical manifestations. Bull Hopkins Hosp. Google Scholar. Dubois EL: Triamcinolone in the treatment of systemic lupus erythematosus. J Am Med Assoc. Ann Phys Med. J Rheumatol. Br Med J. Kumar S: Steroid-induced myopathy following a single oral dose of prednisolone. Neurol India. The role of the ubiquitin-proteasome pathway. N Engl J Med. Am J Med.

Muscle Nerve. Download references. The authors would like to acknowledge Robert C. You can also search for this author in PubMed Google Scholar. Correspondence to Muhammad A Khan. MAK wrote the case report and searched the literature. EL is the primary care physician of the patient. EL carried out the final revision of the manuscript. Both are involved in patient management. Both authors read and approved the final manuscript.

This article is published under license to BioMed Central Ltd. Reprints and Permissions. Khan, M. Acute myopathy secondary to oral steroid therapy in a year-old man: a case report. J Med Case Reports 5, 82 Download citation. Received : 26 April

ARNOLD SCHWARZENEGGER TALKS ABOUT STEROIDS

The catabolic effect of glucocorticoids on muscle proteolysis results from the activation of the major cellular proteolytic systems,[ 8 ] namely. Primarily, myofibrillar proteins are degraded. The ubiquitin-proteasome system is considered to play a major role in the catabolic action of glucocorticoids. It is thought that actin and myosin are dissociated probably by calpains, before they can be degraded by the UPS. There are mechanisms proposed on inhibitory effects of glucocorticoids on protein synthesis.

First, glucocorticoids inhibit the transport of amino acids into the muscle, which could limit the protein synthesis[ 10 ]. Secondly, glucocorticoids inhibit the stimulatory action of insulin, insulin-like growth factor-1, and amino acids leucine in particular on the phosphorylation of two key factors 4E-BP1 and S6K1. These two factors play a key role in the protein synthesis machinery by controlling the initiation step of mRNA translation[ 11 , 12 ].

Thirdly, there is evidence that glucocorticoids cause muscle atrophy by inhibiting myogenesis through the down-regulation of myogenin, a transcription factor mandatory for differentiation of satellite cells into muscle fibers. Glucocorticoids can also cause muscle atrophy by altering the production of growth factors that control locally the muscle mass development. They inhibit the production of IGF-1 by muscle. IGF-1 stimulates the development of muscle mass by increasing protein synthesis and myogenesis while decreasing proteolysis and apoptosis.

Glucocorticoids also stimulate production of myostatin by the muscles. Myostatin inhibits the muscle mass development by down-regulating the proliferation and differentiation of satellite cells and protein synthesis. For these reasons, decreased muscle IGF-1 and increased muscle myostatin play a key role in glucocorticoid-induced muscle atrophy[ 6 ]. Another mechanism of glucocorticoid-induced myopathy is mitochondrial dysfunction. The mitochondria are enlarged or aggregated, and their oxidative capacity is decreased due to glucocorticoids action[ 14 ].

Glucocorticoids also produce muscle weakness by lowering serum potassium and phosphate. Excessive amounts of ACTH can impair neuro-muscular transmission by decreasing the quantal content of the end-plate potential. The ACTH excess, therefore, may have myopathic actions that are separate from those of glucocorticoids. Hypokalemic myopathy is induced by glucocorticoids with high mineralocorticoid activity.

Glucocorticoids produce transient hypophosphatemia due to increased renal clearance of phosphate, and severe phosphate depletion can result in muscle necrosis. However, potassium and phosphate depletion do not play an important role in steroid myopathy.

Cushing first noted that patients with endogenous glucocorticoid excess developed proximal muscle wasting and weakness. Glucocorticoid-induced myopathy can occur in an acute or chronic form. The acute form most often occurs in the intensive care unit setting. It is characterized by rapidly progressive weakness of the proximal and distal muscle groups. Immobility, curare-like agents for neuromuscular blockade, high dose of steroid, nutritional deficiencies, and concurrent sepsis contribute to the rapid onset of weakness and wasting, sometimes referred to acute illness myopathy.

Rarely, the distal muscles are affected. Inhaled corticosteroids are rarely associated with myopathy; if such myopathy occurs, it can be quickly reversed by interrupting the steroid treatment. The diagnostic approach to patient with glucocorticoid-induced myopathy involves evaluation for endogenous hypercortisolism or exogenous glucocorticoid use.

Serum levels of muscle associated enzymes like creatine kinase, lactate dehydrogenase LDH , and aldose are usually normal. However, in acute phase, the levels of creatine kinase and aldose may be quite high. EMG results are typically normal in the early stages of the disease. The treatment of underlying etiology for glucocorticoid excess state is important. For exogenous cause, reducing steroid dose, alternate day treatment regimen, and switching to a non-fluorinated agent are associated with improvement in muscle weakness.

An adequate protein intake is helpful in preventing rapid acceleration of symptoms. The summary of the review is tabulated in Table 1. Source of Support: Nil. Conflict of Interest: No. National Center for Biotechnology Information , U. Indian J Endocrinol Metab. Anu Gupta and Yashdeep Gupta 1. Author information Copyright and License information Disclaimer. Corresponding Author: Dr. E-mail: ni. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.

This article has been cited by other articles in PMC. Abstract Glucocorticoid-induced myopathy is the most common type of drug-induced myopathy. Keywords: Glucocorticoid, myopathy, steroid. Mechanism of muscle proteolysis The catabolic effect of glucocorticoids on muscle proteolysis results from the activation of the major cellular proteolytic systems,[ 8 ] namely The ubiquitin-proteasome system UPS The lysosomal system cathepsins The calcium-dependent system calpains.

Mechanism of inhibition of muscle protein synthesis There are mechanisms proposed on inhibitory effects of glucocorticoids on protein synthesis. First, glucocorticoids inhibit the transport of amino acids into the muscle, which could limit the protein synthesis[ 10 ] Secondly, glucocorticoids inhibit the stimulatory action of insulin, insulin-like growth factor-1, and amino acids leucine in particular on the phosphorylation of two key factors 4E-BP1 and S6K1.

These two factors play a key role in the protein synthesis machinery by controlling the initiation step of mRNA translation[ 11 , 12 ] Thirdly, there is evidence that glucocorticoids cause muscle atrophy by inhibiting myogenesis through the down-regulation of myogenin, a transcription factor mandatory for differentiation of satellite cells into muscle fibers.

Other proposed mechanisms for muscle atrophy Glucocorticoids can also cause muscle atrophy by altering the production of growth factors that control locally the muscle mass development. His gait was normal. Normal deep tendon reflexes were noted. Babinski's sign was absent.

He had normal cardiovascular, respiratory and abdominal examination results. Muscle biopsy and electromyography EMG were not performed. A basic metabolic panel and complete blood count results were normal. He was sent home with ibuprofen mg every six hours as needed for myalgias and instructions to call if his symptoms worsened.

He was seen at a one-week scheduled return visit and reported significant improvement in muscle strength and decreased pain. Examination showed muscle strength of 5 of 5 in all muscle groups. Urine myoglobin results were negative. He was seen again 30 days after initial presentation and was feeling fine and had resumed his normal active lifestyle, farming.

He continues to complain of intermittent foot pain, which is worse with activity, and he takes ibuprofen mg as needed for relief. ASM is rare and poorly understood. Several theories have been proposed to explain the pathogenesis of this condition. One model proposes activation of ubiquitin-dependent proteolytic systems [ 8 ]. Another model suggests that insulin-like growth factor-1, which may act as anti-apoptotic, is inhibited by steroids, thus allowing increased muscle apoptosis [ 9 ].

Askari et al. One patient developed symptoms of ASM within a few days of starting therapy. Five patients tolerated a low maintenance dose of prednisone 15 to 60 mg for a duration of 60 to days without any signs or symptoms of myopathy.

However, increasing the maintenance dose resulted in the appearance of symptoms of corticosteroid myopathy within 30 days in four of five patients. The group concluded that the development of myopathy in patients receiving corticosteroid therapy is not related to the age of the patient, the magnitude of the dose given or the duration of maintenance therapy [ 10 ].

Typical presentations include diffuse myalgias and muscle weakness. Pelvic girdle muscle involvement is most consistently seen [ 10 ]. Some patients present with difficulty weaning from mechanical ventilators [ 5 , 6 ]. Our patient received methylprednisolone, and he was not on any maintenance corticosteroid therapy. He did have pelvic girdle muscle weakness, but his symptoms were not limited to these muscle groups.

A number of laboratory investigations may aid in the diagnosis of ASM. EMG and muscle biopsy may also be helpful. No single test is diagnostic for this condition. The diagnosis always involves a high degree of clinical suspicion with diagnostic tests as an adjunct.

Serum marker elevation is an inconsistent finding. They did find increased urinary creatinine excretion to be more consistently abnormal than elevated CPK [ 10 ]. EMG may be normal, but abnormal EMG findings classically include normal sensory and motor conduction velocities with decreased amplitude of muscle action potential [ 11 ]. We did not obtain EMG in our patient. Typically, muscle biopsy shows diffuse necrosis of both type I and type II fibers [ 6 , 11 ]; however, muscle biopsy is often diagnostically unhelpful [ 10 ].

Currently, there are no dosing recommendations for steroids that could decrease the likelihood of developing myopathy. Our patient received two doses of methylprednisolone, 24 mg and 20 mg. The only similar report involved a patient taking 40 mg of prednisone [ 7 ]. We were unable to find literature reports of patients developing myopathy while taking doses less than 40 mg of prednisone.

There is no specific treatment available for this condition. The most consistent finding on literature review is the fact that myopathy resolves without any intervention with discontinuation of steroid therapy. Steroids, as a class, are well recognized as a critical treatment modality for a number of conditions.

They are prescribed by physicians belonging to almost all areas of medicine. Although very rare, ASM needs to be recognized early to ameliorate its significant effects. Written informed consent was obtained from the patient for publication of this case report. A copy of the written consent is available for review by the Editor-in-Chief of this journal. Cushing H: The basophil adenomas of the pituitary body and their clinical manifestations.

Bull Hopkins Hosp. Google Scholar. Dubois EL: Triamcinolone in the treatment of systemic lupus erythematosus. J Am Med Assoc. Ann Phys Med. J Rheumatol. Br Med J. Kumar S: Steroid-induced myopathy following a single oral dose of prednisolone. Neurol India. The role of the ubiquitin-proteasome pathway. N Engl J Med. Am J Med. Muscle Nerve. Download references. The authors would like to acknowledge Robert C. You can also search for this author in PubMed Google Scholar. Correspondence to Muhammad A Khan.

MAK wrote the case report and searched the literature. EL is the primary care physician of the patient. EL carried out the final revision of the manuscript.

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I have a blood test Tuesday so I think I'll stay on 9. We're going away for a few days on the Wednesday and will have a 3 hour car journey - longer by the time we've had breaks. Would it be a good idea may be to actually go up to 12 for the journey and then reduce down to 10 over the next couple of days? I'll be relaxing in an empty house while my husband's out walking so it won't be stressful while we're there.

I haven't actually raised my dose for travelling ever - though if rounding up the dose for long haul flights means a bit extra I don't complain. I think some people do - but I don't know by how much. I found travelling back from the same place a couple of weeks ago absolutely exhausting evan though I'd been ok going down so I may give it a go.

I've not increased my dose while travelling before either so I'll see what happens this time. Didn't say WHO washes brains Really no problem. Makes such a difference. How long have you had PMR? Mine's been making its presence felt for over 15 years and been on pred for heading for 10 years. Getting bored now I remember how bad I was, kept falling over for no reason.

Was high as a kite and stared living again. My bottom is 5. I live at 7 a day. Always taken last thing at night to be ready for the 4. It's been a bit mixed up for the last year or so - looking forward to seeing if I can get back down to the 7mg I was very happy at this time last year. Time will tell.

Mostly it is like you say Most of the medications I take are solely to counteract the effects of prednisone. It does make me tired of it all but I have survived. I needed to dodge a few bullets along the way. I'm actually thinking I've gotten past PMR after years. It is hard to know when other things get uncovered.

Makes it impossible to know what causes what. I'm excited about Actemra but probably just wishful thinking. The problem is finding the lowest dose to achieve the highest result. Go too low and disaster strikes. I started at Looking back and realising it was possible for life, did not really matter. I started with GCA hence the high dose. I will never get used to this but am determined to have some fun. I have weak legs caused by steroids I am told. I have been on them for 5.

I'm also on methotrexate and humira. According to my gp my legs will never get back to normal. A physiotherapist said the ligaments are stretched due to pred, they certainly are wobbley and I wear knee supports. I know steroids would make it a lot better but I have had so many other conditions develop because of them that I dare not raise them again.

It would only be a temporary relief. I wouldn't agree with your GP - if you go about it right you probably could improve. I had quite severe steroid myopathy after about 4 months on methyl prednisolone. I was switched to a different form of steroid and started walking the way I have described a few times in the last few days.

At first I was on crutches. It took some months - but I got from 5 mins and struggling to being able to walk for up to 45 mins at a time, and again after a leisurely lunch rest! Since that time I was able to walk for a couple of hours at my own pace and with some rests. I can't at present but for another reason - it is time to start again once this sore knee calms down!

I am only on 5. I also get horrible pins and needles and numbness down the outside of my legs from the knee to my toes. Wearing the knee support alters that and makes it more bearable. Myostatin inhibits the muscle mass development by down-regulating the proliferation and differentiation of satellite cells and protein synthesis. For these reasons, decreased muscle IGF-1 and increased muscle myostatin play a key role in glucocorticoid-induced muscle atrophy[ 6 ].

Another mechanism of glucocorticoid-induced myopathy is mitochondrial dysfunction. The mitochondria are enlarged or aggregated, and their oxidative capacity is decreased due to glucocorticoids action[ 14 ]. Glucocorticoids also produce muscle weakness by lowering serum potassium and phosphate. Excessive amounts of ACTH can impair neuro-muscular transmission by decreasing the quantal content of the end-plate potential.

The ACTH excess, therefore, may have myopathic actions that are separate from those of glucocorticoids. Hypokalemic myopathy is induced by glucocorticoids with high mineralocorticoid activity. Glucocorticoids produce transient hypophosphatemia due to increased renal clearance of phosphate, and severe phosphate depletion can result in muscle necrosis. However, potassium and phosphate depletion do not play an important role in steroid myopathy.

Cushing first noted that patients with endogenous glucocorticoid excess developed proximal muscle wasting and weakness. Glucocorticoid-induced myopathy can occur in an acute or chronic form. The acute form most often occurs in the intensive care unit setting. It is characterized by rapidly progressive weakness of the proximal and distal muscle groups.

Immobility, curare-like agents for neuromuscular blockade, high dose of steroid, nutritional deficiencies, and concurrent sepsis contribute to the rapid onset of weakness and wasting, sometimes referred to acute illness myopathy. Rarely, the distal muscles are affected. Inhaled corticosteroids are rarely associated with myopathy; if such myopathy occurs, it can be quickly reversed by interrupting the steroid treatment. The diagnostic approach to patient with glucocorticoid-induced myopathy involves evaluation for endogenous hypercortisolism or exogenous glucocorticoid use.

Serum levels of muscle associated enzymes like creatine kinase, lactate dehydrogenase LDH , and aldose are usually normal. However, in acute phase, the levels of creatine kinase and aldose may be quite high. EMG results are typically normal in the early stages of the disease. The treatment of underlying etiology for glucocorticoid excess state is important.

For exogenous cause, reducing steroid dose, alternate day treatment regimen, and switching to a non-fluorinated agent are associated with improvement in muscle weakness. An adequate protein intake is helpful in preventing rapid acceleration of symptoms. The summary of the review is tabulated in Table 1. Source of Support: Nil. Conflict of Interest: No. National Center for Biotechnology Information , U. Indian J Endocrinol Metab. Anu Gupta and Yashdeep Gupta 1.

Author information Copyright and License information Disclaimer. Corresponding Author: Dr. E-mail: ni. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3. This article has been cited by other articles in PMC. Abstract Glucocorticoid-induced myopathy is the most common type of drug-induced myopathy. Keywords: Glucocorticoid, myopathy, steroid. Mechanism of muscle proteolysis The catabolic effect of glucocorticoids on muscle proteolysis results from the activation of the major cellular proteolytic systems,[ 8 ] namely The ubiquitin-proteasome system UPS The lysosomal system cathepsins The calcium-dependent system calpains.

Mechanism of inhibition of muscle protein synthesis There are mechanisms proposed on inhibitory effects of glucocorticoids on protein synthesis. First, glucocorticoids inhibit the transport of amino acids into the muscle, which could limit the protein synthesis[ 10 ] Secondly, glucocorticoids inhibit the stimulatory action of insulin, insulin-like growth factor-1, and amino acids leucine in particular on the phosphorylation of two key factors 4E-BP1 and S6K1.

These two factors play a key role in the protein synthesis machinery by controlling the initiation step of mRNA translation[ 11 , 12 ] Thirdly, there is evidence that glucocorticoids cause muscle atrophy by inhibiting myogenesis through the down-regulation of myogenin, a transcription factor mandatory for differentiation of satellite cells into muscle fibers.

Other proposed mechanisms for muscle atrophy Glucocorticoids can also cause muscle atrophy by altering the production of growth factors that control locally the muscle mass development. For these reasons, decreased muscle IGF-1 and increased muscle myostatin play a key role in glucocorticoid-induced muscle atrophy[ 6 ] Another mechanism of glucocorticoid-induced myopathy is mitochondrial dysfunction. The mitochondria are enlarged or aggregated, and their oxidative capacity is decreased due to glucocorticoids action[ 14 ] Glucocorticoids also produce muscle weakness by lowering serum potassium and phosphate.

Table 1 Summary of Glucocorticoid induced myopathy. Open in a separate window. Cushing H. The basophil adenoma of the pituitary body and their clinical manifestation. Johns Hopkins Med J. The Adrenal Cortex. Williams Textbook of Endocrinology. Philadelphia: Elsevier Saunders; Glucocorticoid-induced myopathy. Joint Bone Spine. Endocrine myopathies.

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