Steroid induced myopathy

Myopathies in systemic disease results from several different disease processes including endocrine, inflammatory, paraneoplastic, infectious, drug- and toxin-induced, critical illness myopathy, metabolic, collagen related, [2] and myopathies with other systemic disorders. Patients with systemic myopathies often present acutely or sub acutely. On the other hand, familial myopathies or dystrophies generally present in a chronic fashion with exceptions of metabolic myopathies where symptoms on occasion can be precipitated acutely. Most of the inflammatory myopathies can have a chance association with malignant lesions; the incidence appears to be specifically increased only in patients with dermatomyositis. [3]

Neuroactive steroids are also called as neurosteroids . They are endogenous steroids that rapidly alter neuronal excitability through interaction with ligand-gated ion channels and other cell surface receptors. Neuroactive steroid refers to steroids that are synthesized by an endocrine gland that reach the brain through the bloodstream and have effects on brain function. Neurosteroids have a wide range of potential clinical applications from sedation to treatment of epilepsy and traumatic brain injury. Ganaxolone is a synthetic analog of the endogenous neurosteroid. Allopregnanolone is under investigation for the treatment of epilepsy.

Glucocorticoid-induced myopathy, characterized by muscle weakness without pain, fatigue and atrophy, is an adverse effect of glucocorticoid use and is the most common type of drug-induced myopathy. This muscle disturbance has a frequency of 60%, and it has been most often associated with fluorinated glucocorticoid preparations. Glucocorticoids have a direct catabolic effect on muscle, decreasing protein synthesis and increasing the rate of protein catabolism leading to muscle atrophy. In clinical practice, it is important to differentiate myopathy due to glucocorticoid from muscle inflammatory diseases. The treatment is based on reduction or, if possible, on discontinuation of the steroid. Fluorinated glucocorticoids such as dexamethasone should be replaced with nonfluorinated glucocorticoids such as prednisone. Other experimental treatments may be tried such as IGF-I, branched-chain amino acids, creatine, androgens such as testosterone, nandrolone and dehydroepiandrosterone (DHEA), and glutamine.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses , as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails ). [15] [16] While only a small number of skin diseases account for most visits to the physician , thousands of skin conditions have been described. [14] Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. [17] [18] Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane ), morphology ( chronic blistering conditions ), etiology ( skin conditions resulting from physical factors ), and so on. [19] [20] Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion (s), including the location (such as arms, head, legs), symptoms ( pruritus , pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology ( macules , papules , vesicles ), and color (red, blue, brown, black, white, yellow). [21] Diagnosis of many conditions often also requires a skin biopsy which yields histologic information [22] [23] that can be correlated with the clinical presentation and any laboratory data. [24] [25] [26]

Steroid induced myopathy

steroid induced myopathy

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses , as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails ). [15] [16] While only a small number of skin diseases account for most visits to the physician , thousands of skin conditions have been described. [14] Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. [17] [18] Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane ), morphology ( chronic blistering conditions ), etiology ( skin conditions resulting from physical factors ), and so on. [19] [20] Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion (s), including the location (such as arms, head, legs), symptoms ( pruritus , pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology ( macules , papules , vesicles ), and color (red, blue, brown, black, white, yellow). [21] Diagnosis of many conditions often also requires a skin biopsy which yields histologic information [22] [23] that can be correlated with the clinical presentation and any laboratory data. [24] [25] [26]

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