Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myopathies produced by drugs are of vital concern and often confused with other more frequently diagnosed causes, such as the inflammatory myopathies of polymyositis/dermatomyositis and myositis secondary to toxic agents, metabolic and endocrine abnormalities, genetic predisposition, malignancies, and infections, particularly viruses. The drug-induced causes of myopathy warrant special emphasis because they are often overlooked, resulting in misdiagnosis and improper care.
 ...
PMID:Drug-related myopathies. 785 22

Plasma CK concentrations have been widely used as the primary muscle enzyme marker for diagnosis and progression of myositis. Recently, total CK and CK-MB serum concentrations have been compared to, and used in conjunction with, serum concentrations of aspartate aminotransferase in diagnosis of myositis. The algorithmic use of CK, AST, and aldolase plasma concentrations to diagnose and categorize patients with myopathy may be a useful method of diagnosing specific muscle disease without invasive procedures. CAIII, as a specific marker for skeletal muscle damage, may replace CK as the enzyme of choice in diagnosis and progression of myositis and other muscle disease. Additional studies are required to determine the usefulness of carbonic anhydrase for the diagnosis and assessment of myositis.
 ...
PMID:Evaluation of laboratory tests as a guide to diagnosis and therapy of myositis. 785 25

Among the main concerns regarding the current therapy for the inflammatory myopathies are a lack of adequate controlled trials, a lack of objective means to reliably measure muscle strength, lack of natural history data, consideration of polymyositis, dermatomyositis, and inclusion-body myositis as a homogeneous group of inflammatory myopathies, and reliance on nonspecific markers for determining prognosis and assessing response to therapies. Prednisone remains the drug of choice in treating these disorders, although a controlled trial has never been undertaken to study its efficacy. Among the steroid-sparing agents, azathioprine, methotrexate, cyclosporine, and chlorambucil are used with invariably low to moderate success. There are no results of controlled trials to indicate whether one of these drugs is superior to another. Intravenous immunoglobulin, which is very expensive, was shown in a controlled trial to be effective in steroid-resistant dermatomyositis not only in dramatically improving muscle strength and skin rash but also in resolving the underlying immunopathology. Controlled trials of intravenous immunoglobulin in patients with polymyositis and inclusion-body myositis are under way. Inclusion-body myositis has emerged as a common inflammatory myopathy that is predictably disabling and resistant to most therapies.
 ...
PMID:Current treatment of the inflammatory myopathies. 786 79

A 24-year-old black woman developed polymyositis with autoantibodies to threonyl-tRNA synthetase in the 2nd trimester of her 3rd pregnancy. This was complicated by fetal loss and the development of severe relapsing myositis resistant to corticosteroid and azathioprine therapy. These features were also common in other cases in the literature. Antisynthetase antibodies had not been reported in myositis occurring during pregnancy and may be of interest regarding the pathogenesis of inflammatory myopathy complicating pregnancy.
 ...
PMID:Onset of polymyositis with autoantibodies to threonyl-tRNA synthetase during pregnancy. 798 66

Sporadic inclusion-body myositis is the most common progressive muscle disease of older patients. The muscle biopsy demonstrates mononuclear cell inflammation and vacuolated muscle fibers containing paired helical filaments and 6 to 10-nm fibrils, both resembling those of Alzheimer brain, and Congo-red positivity. Hereditary inclusion-body myopathy designates patients cytopathologically similar but without inflammation. In both muscle diseases, prion, and several proteins characteristic of Alzheimer brain--eg, beta-amyloid protein and hyperphosphorylated tau (which normally are expressed mainly in neurons), and apolipoprotein E--are abnormally accumulated in vacuolated muscle fibers, by unknown mechanisms. We now demonstrate in both muscle diseases that prion mRNA is strongly expressed in the vacuolated muscle fibers, which suggests that their accumulated prion protein results, at least partly, from increased gene expression. This, to our knowledge, is the first demonstration of abnormally increased prion mRNA in human disease. Another novel finding is the increased prion mRNA in human muscle macrophages, and both increased prion protein and prion mRNA in regenerating muscle fibers. The latter indicates that prion may play a role in human muscle development.
 ...
PMID:Abnormal accumulation of prion protein mRNA in muscle fibers of patients with sporadic inclusion-body myositis and hereditary inclusion-body myopathy. 799 30

Methionine sulphoximine (MSO) is a centrally acting neurotoxin which inhibits the glutamate metabolism enzymes and has convulsive properties. Small doses of MSO were administered to rabbits, either intravenously (i.v.) or intracerebroventricularly (ICV), and electron microscopic examination of the cerebellum, the spinal cord and the sciatic nerve was performed on the first day of rabbit hind leg rigid paralysis (myopathy with histological findings resembling myositis), which set in by the 2nd to 4th day after MSO administration. In the cerebellum focal minor alterations were found in the astrocytes (swelling and lucidity, diminution of glycogen granules) and sparsely in the presynaptic terminals (lucidity and clumping), whereas most of the neuron presented a normal appearance. In the spinal cord and in the sciatic nerve a dissociation of the axon from the myelin sheath was evident in a small number of myelinated nerve fibres, along with the appearance of vacuolated spaces. Mitochondrial disorganisation in the axons, as well as glial cell alterations, were also seen. The ultrastructural alterations were non specific, and since they were induced 2 to 4 days after the administration of either minimum doses (i.v.) or of extremely low doses (ICV) of MSO, they may be attributed to the inordinate increase of metabolism during the period of convulsions.
 ...
PMID:Ultrastructural alterations of the rabbit sciatic nerve, spinal cord and cerebellum, following methionine sulphoximine administration. 800 5

Congenital myopathies are developmental disorders of muscle that are best understood in the context of ontogenesis. Segmental amyoplasia results from a defective somite, usually because of lack of induction by the notochord and neural tube; the connective tissue matrix of the muscle is derived from lateral mesoderm and is present, but the myocytes are derived from somitic mesoderm and are replaced by adipose cells. Generalized amyoplasia is due to defective myogenic regulatory genes. X-linked recessive myotubular myopathy is associated with overexpression of vimentin and desmin, fetal intermediate filaments that attach to nuclear, mitochondrial, and inner sarcolemmal membranes and Z-bands of sarcomeres to preserve the morphologic organization of the myotube. Neonatal myotonic dystrophy is a true maturational delay in muscle development. Congenital muscle fiber-type disproportion is a syndrome of multiple etiologies but in some cases is associated with cerebellar hypoplasia and may be the result of abnormal suprasegmental stimulation of the developing motor unit at 20 to 28 weeks' gestation, mediated through bulbospinal pathways but not the corticospinal tract. Maturational delay of muscle in late developmental stages is less specific than in stages before midgestation. The Proteus syndrome is a muscular dysgenesis; abnormal paracrine growth factors and perhaps altered genes that regulate muscle differentiation and growth, such as myoD and myogenin, are the suspected cause. Focal proliferative myositis may be another example of a "paracrine myopathy."
 ...
PMID:New insights into the pathogenesis of congenital myopathies. 800 74

Seventy-four patients with plasma low-density lipoprotein cholesterol levels > or = 160 mg/dl after an American Heart Association phase 1 diet were randomized to double-blind treatment with fluvastatin, 20 mg/day, or placebo for 6 weeks. Immediate-release niacin was then added to both treatment regimens and titrated to a maximum of 3 g/day for a further 9 weeks. After 6 weeks of fluvastatin monotherapy, low-density lipoprotein cholesterol levels decreased by 21% (p < 0.001 vs placebo), and after the addition of niacin, response was potentiated to 40% compared with 25% for the niacin control group at study end point (p < 0.001). Fluvastatin, alone and in combination with niacin, also significantly improved high-density lipoprotein cholesterol (increases of about 30%) and triglyceride profiles (decreases of approximately 28%) from baseline. Lipoprotein(a) decreased by 37% in those receiving fluvastatin-niacin but was unaltered in those receiving fluvastatin alone. No serious adverse events were ascribed to fluvastatin, and no cases of myositis were observed. Small, transient, asymptomatic increases in aspartate aminotransferase were noted with fluvastatin-niacin treatment but were not considered clinically relevant. Although the fluvastatin-niacin combination in this study was without evidence of significant transaminitis, myopathy, or rhabdomyolysis, it would seem prudent to continue to monitor its safety with longer term use. In conclusion, fluvastatin, both as monotherapy and in combination with niacin, proved to be an effective, safe, and well-tolerated therapeutic alternative for hypercholesterolemia.
 ...
PMID:Fluvastatin with and without niacin for hypercholesterolemia. 802 79

The major new advances in seeking the pathogenic mechanisms of sporadic inclusion-body myositis and hereditary inclusion-body myopathy are discussed. Hypotheses are presented regarding the possible causes and significance of amyloid deposits in sporadic inclusion-body myositis and the roles of abnormally accumulated ubiquitin, beta-amyloid protein, beta-amyloid precursor protein, alpha 1-antichymotrypsin, hyperphosphorylated tau, and prion protein in the vacuolated muscle fibers in both sporadic inclusion-body myositis and hereditary inclusion-body myopathy. Because hereditary inclusion-body myopathy is virtually free of Congophilic amyloid deposits but, like sporadic inclusion-body myositis, contains large accumulations of beta-amyloid protein, it is possible that the lesions in hereditary inclusion-body myopathy may represent "early" changes. There are striking similarities between the pathology of inclusion-body myositis muscle and brains affected by Alzheimer's disease in regard to accumulation of ubiquitin, beta-amyloid protein and its precursor protein, alpha 1-antichymotrypsin, and hyperphosphorylated tau.
 ...
PMID:New advances in inclusion-body myositis. 811 35

The management of inflammatory myopathy is a challenge. Although corticosteroids remain the initial therapeutic choice in most instances, their side effects and lack of efficacy are such that alternative modes of therapy are frequently sought. The identification of serum autoantibodies associated with more severe forms of myositis has prompted new classification schemes and has led to more aggressive approaches with combination therapy, using corticosteroids, immunosuppressive drugs, or other immune-modulating agents. Non-corticosteroid agents that provide some benefit include methotrexate, azathioprine, chlorambucil, and perhaps cyclophosphamide. Cyclosporine has been increasingly studied with encouraging results, and intravenous immunoglobulin has demonstrated some benefit for myositis patients. Plasma exchange and leukapheresis were of no proven benefit in a randomized, double-blind trial.
 ...
PMID:Therapy for myositis. 811 36


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>