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

Animal models have proven very useful in furthering insight into a number of muscle diseases. Studies of ethanol-fed rats are being used to understand the pathogenetic mechanisms underlying acute and chronic myopathy induced by ethanol. Several animal species, including mice, dogs, and cats, develop X-linked muscular dystrophies, which have genetic defects identical to those of Duchenne muscular dystrophy. As in the human disease, these animals lack dystrophin. They are being used to investigate the mechanisms by which lack of dystrophin results in weakness and to examine myoblast transfer as a treatment modality. A model of eosinophilia-myalgia syndrome has recently been induced in Lewis rats by the feeding of L-tryptophan samples that were implicated in the clinical syndrome in humans, making possible studies of the pathogenesis of this interesting new entity. A dermatomyositis-like syndrome occurs spontaneously in dogs, and polymyositis-like illnesses can be induced in mice by immunization with muscle or following infection with selected viruses, especially enteroviruses. Study of the latter is helping us understand mechanisms in the etiology and pathogenesis of inflammatory myositis and virus-induced autoimmunity.
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PMID:Animal models of myopathy. 177 47

Twenty-two chronic alcoholic patients were assessed by neurologic examination and muscle biopsy. The patients manifested proximal muscular weakness to a variable extent. One case presented as an acute bout of myopathy, according to the Manual Muscle Test, MMT. The most prominent histologic feature observed was muscle atrophy (95.3%) better evidenced through the ATPase stain with the predominance of type II A fibers (71.4%). Lack of the mosaic pattern (type grouping) seen in 76% of the cases and an important mitochondrial proliferation with intrasarcoplasmatic lipid accumulation in 63% of the patients. In case of acute presentation of muscle weakness the pathological substrate is quite different, i.e. presence of myositis mainly interstitial characterized by lymphoplasmocytic infiltrate and several spots of necrosis like Zencker degeneration. Based on histologic criteria, our data suggest that: the main determinant of muscle weakness seen in chronic alcoholic patients is neurogenic in origin (alcoholic polyneuropathy); the direct toxic action of ethanol under the skeletal muscle is closely related to the mitochondrial metabolism; the so-called acute alcoholic myopathy has probably viral etiology.
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PMID:[Histochemical study of the skeletal muscle in chronic alcoholism]. 248 Jul 68

The effect of chronic ethyl alcohol intoxication on the evolution of Trypanosoma cruzi infection in mice was studied by two experimental procedures: (1) mice after 60 days of infection with a myotropic strain of T. cruzi were submitted to chronic alcoholic intoxidation receiving a 7% ethanol solution as only liquid source for six months; (2) mice chronically intoxicated with ethanol during five months were infected with the same strain of T. cruzi and were followed up for 45 days drinking the 7% alcoholic solution. In comparison with the infected group, not treated with ethanol, the infected mice that received the ethanol showed: a) similar mortality in the two experiments; (b) higher parasitemia in the acute phase and more frequent blood parasites in the chronic phase; (c) myocarditis with less severe cellular exudation but with increased fibrosis; (d) in the skeletal muscle, milder myositis and low frequency of arteritis and hyaline thrombi.
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PMID:[Effects of chronic ethanol intoxication on the evolution of experimental trypanosomiasis cruzi in mice]. 251 67

A procedure for the isolation and partial purification of three hydroxymethylglutaryl coenzyme A reductase phosphatases in their native high molecular weight form from rat liver microsomes is described for the first time. Reductase phosphatase Ex (Mr 90,000), IM (Mr 75,000), and IIM (Mr 180,000) were purified 132-, 55-, and 98-fold, respectively. Treatment with 80% ethanol irreversibly inactivated the three enzymes contrary to what is found for cytosolic reductase phosphatases. The three microsomal reductase phosphatases differ among themselves and with respect to the cytosolic reductase phosphatases in molecular weight, response to inhibitors, thermal stability, and optimum pH. Indirect evidence that these three proteins are phosphatases includes their inhibition by inhibitors of phosphatase activity, such as KF, Pi, and PPi. Direct evidence includes their ability to release 32P from highly radioactive homogeneous 32P-labeled HMG-CoA reductase, this dephosphorylation being concomitant with activation of HMG-CoA reductase. The three phosphatases dephosphorylate 32P-labeled phosphorylase a, but only reductase phosphatase IIM shows glycogen synthase phosphatase activity.
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PMID:Partial purification from rat liver microsomes of three native protein phosphatases with activity towards HMG-CoA reductase. 633 Feb 55

The use of lipid-altering drugs has been shown to reduce the progression of atherosclerotic lesions and reduce the risk of atherosclerotic events (such as myocardial infarction and stroke). In general, these lipid-altering drugs are well tolerated but there is the potential for drug interactions. For example, HMG-CoA reductase inhibitors may interact with macrolides, azalides, azole antifungals and cyclosporin. Resins (such as cholestyramine and colestipol) may impair the absorption of many concurrent medications. Fibrates have potential drug interactions with warfarin, furosemide (frusemide), oral hypoglycaemics and probenecid. Nicotinic acid (niacin) may have potential drug interactions with high dose aspirin (acetylsalicylic acid), uricosuric agents (such as sulfapyrazone) and alcohol (ethanol). Finally, probucol may have potential drug interactions with antidysrhythmics, tricyclic antidepressants and phenothiazines. In addition, lipid-altering drugs, used in combination, may have the potential for drug interactions, enhancing some of the risks of adverse effects, such as myositis and hepatotoxicity. Therefore, in order to use lipid-altering drugs in the most effective, and safest manner, it is important for the clinician to have an understanding of the mechanisms of potential drug interactions, which drug interactions may theoretically occur, and specifically, which spe cific drug interactions have already been described.
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PMID:Drug interactions of lipid-altering drugs. 982 49

The effect of an ethanol extract of Commiphora myrrha oleo-gum resin on hematological and pathophysiological parameters of male Wistar rats was examined. The extract was given daily for 2 w at 1000 mg/kg bw per os, 500 mg/kg bw i.m. or 250 mg/kg bw i.p. Depression, huddling together, soft feces, jaundice, ruffled hair, hepatonephropathy, hemorrhagic myositis and patchy peritonitis (at the injection site) and death were accompanied by increases in serum ALP and ALT activities, bilirubin, cholesterol and creatinine concentrations, and decreases in total protein and albumin levels, and macrocytic anemia and leucopenia. When administered at 500 mg extract/kg bw/d per os or 250 mg extract/kg bw/d i.m. for 2 w it was not lethal, and when given daily for 1 w the effect was less marked.
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PMID:Effects on rats of Commiphora myrrha extract given by different routes of administration. 1043 69

"A propensity to bend the trunk forward" and "the chin is now almost immovably bent down upon the sternum" were described by James Parkinson in patients with Parkinson's disease (PD). The term "dropped head" was first reported in "Gerlier disease" in Switzerland and 'kubisagari' in Japan and since then also reported in myositis, myopathy, myasthenia gravis, amyotrophic lateral sclerosis, neuropathy, and hypothyroidism. Disproportionate antecollis occurs in about half cases of multiple system atrophy (MSA) and is considered dystonic in nature. Dropped head is considered rare in PD, both in advanced and early stages of PD. However, it is known to progress subacutely over a period of several days. In my experience, dropped head is relatively common in PD. The mechanism of dropped head in PD is either dystonia of flexor neck muscles or weakness of extensor neck muscles. The response of dropped head to various anti-parkinsonian medications is rather inconsistent. Levodopa is reported to induce amelioration in some patients while dopamine agonists can cause deterioration. Muscle afferent block with lidocaine and ethanol is reported to be effective, while the effect of botulinum toxin injection into the affected muscles is limited. The effect of stereotaxic neurosurgery on dropped head is controversial. Early diagnosis and prompt treatment is necessary to prevent muscle damage associated with longterm overstretch of extensor neck muscles.
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PMID:Dropped head in Parkinson's disease. 1713 Dec 24

Although muscle diseases are relatively rare, several treatable myopathies must be recognized by the clinician to maximize the possibility of restoring strength in affected patients. The inflammatory myopathies, including polymyositis, dermatomyositis, inflammatory necrotizing myopathy, and myositis in association with mixed connective tissue disease, typically respond well to immunosuppressive treatment. Inclusion body myositis, a myopathy that has features of both inflammation and primary degeneration, may not be treatable at this time, but treatments are actively being sought. Muscle dysfunction caused by toxins must also be recognized because removal of the offending toxin usually results in restoration of normal muscle function. Important muscle toxins include cholesterol-lowering medications, colchicine, zidovudine, corticosteroids, emetine, and ethanol.
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PMID:Inflammatory and toxic myopathy. 2367 56

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the least deadly but most infectious coronavirus strain transmitted from wild animals. It may affect many organ systems. Aim of the current guideline is to delineate the effects of SARS-CoV-2 on the liver. Asymptomatic aminotransferase elevations are common in coronavirus disease 2019 (COVID-19) disease. Its pathogenesis may be multifactorial. It may involve primary liver injury and indirect effects such as "bystander hepatitis," myositis, toxic liver injury, hypoxia, and preexisting liver disease. Higher aminotransferase elevations, lower albumin, and platelets have been reported in severe compared with mild COVID-19. Despite the dominance of respiratory disease, acute on chronic liver disease/acute hepatic decompensation have been reported in patients with COVID-19 and preexisting liver disease, in particular cirrhosis. Metabolic dysfunction-associated fatty liver disease (MAFLD) has a higher risk of respiratory disease progression than those without MAFLD. Alcohol-associated liver disease may be severely affected by COVID-19-such patients frequently have comorbidities including metabolic syndrome and smoking-induced chronic lung disease. World Gastroenterology Organization (WGO) recommends that interventional procedures such as endoscopy and endoscopic retrograde cholangiopancreatography should be performed in emergency cases or when they are considered strictly necessary such as high risk varices or cholangitis. Hepatocellular cancer surveillance may be postponed by 2 to 3 months. A short delay in treatment initiation and non-surgical approaches should be considered. Liver transplantation should be restricted to patients with high MELD scores, acute liver failure and hepatocellular cancer within Milan criteria. Donors and recipients should be tested for SARS-CoV-2 and if found positive donors should be excluded and liver transplantation postponed until recovery from infection.
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PMID:WGO Guidance for the Care of Patients With COVID-19 and Liver Disease. 3323 11