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)

The following findings were obtained from pathomorphological examination of the myocardium of 100 pigs which had died on transport: Degenerative or necrobiotic changes of certain myocardial fibres were recorded from 73 per cent of all cases, usually in the form of granular degeneration (60 per cent). They were "scattered" in 33 per cent of all cases, "multiple" in 22 per cent, and "frequent" in five per cent. In 26 per cent, the myocardial fibres had undergone coarse granular or hyalin plaque-type decomposition, among them with "scattered" manifestation in 15 per cent, "multiple" in four per cent, "frequent" in five per cent, and "massive" in two per cent. Moderate focal resorptive myositis was recorded from eight per cent, while earlier myocardial scars were exhibited by four per cent. The figure for reactive inflammatory processes was twelve per cent. Prestatic hyperaemia of different degrees had taken place in 75 per cent of all animals, and it had been accompanied by varied congestion. The following results were obtained from comparative checks of 100 hearts of clinically intact pigs after slaughter under normal conditions: Granular degeneration was recorded only from 18 per cent of all cases, with actual manifestations "scattered" in 16 per cent and "multiple" in two per cent. Their myocardial fibres had undergone coarse granular or hyalin plaque-type decomposition of moderate intensity in three per cent only, all of them having been "scattered". Reactive inflammatory changes were not recorded at all and signs of prestatic hyperaemia only in 46 per cent. The degenerative-necrobiotic alterations of myocardial fibres which had been observed in the context of death on transport are interpreted as a result of hypoxaemic or hypoxic conditions accompanying acute shock-type circulatory failure in pigs.
 ...
PMID:[Studies of cardiac pathomorphology in swine which died during transport]. 53 38

Twenty-seven cases of linear morphoea are reported and compared with 218 cases collected from the literature. The various parameters studied, including clinical features and laboratory results, were identical in both series. The aetiology of linear morphoea is unknown, even though injuries or fever have been noted as triggering factors in 20 p. 100 of the cases. Linear morphoea is a childhood disease: it begins at the age of 7 or 8 and predominates in females (63 p. 100 of the cases). Its onset is marked by the abrupt occurrence of sclerosis in most cases, although a solitary morphoea or a trophic plaque may precede the disease proper. In our series, muscular or articular involvement appeared from the start in 40 p. 100 of the patients at the same time as the initial cutaneous lesions. The active stage lasts 3 years and sometimes longer. It is characterized by extension (37 p. 100) or both extension and multiplication (63 p. 100) of the initial lesions. Regional complications aggravate linear morphoea and are more frequent in patients whose lesions extend and multiply. Their incidence was lower among the published cases than in our series. Depending on the author, retractile myositis is present in 37 to 59 p. 100 of the cases, joint stiffness in 18 to 40 p. 100 and shortening of a limb in 10 to 22 p. 100. These complications often regress incompletely, leaving sequelae which persist in the steady state in 75 p. 100 of the patients. Antinuclear antibodies, present in 37 p. 100 of the cases, are either of the homogeneous or of the speckled type. Jablonska has met them more frequently (50 p. 100), and they were often of the speckled type. The significance of these antibodies in linear morphoea is unclear since they appear inconstantly and later than clinical signs. The skin lesions associated with linear morphoea show that the other forms of scleroderma--i.e. plaque morphoea, erythematous atrophic or dyschromic plaques and guttate scleroderma--belong to the same family. The same associations are found in frontoparietal "coup de sabre" scleroderma. The treatment of linear morphoea is not yet standardized. At the moment, the best and most regular results are obtained with systemic corticosteroids and local physiotherapy.
 ...
PMID:[Linear scleroderma in children (apropos of 27 cases)]. 375 60

Intracompartmental muscle pressures were recorded from the right and left forelimbs (extensor carpi radialis, triceps brachii) of healthy horses maintained in left lateral recumbency while under deep halothane anesthesia for 180 to 240 minutes. Cardiac output, blood pressure, blood gases, and acid-base status were monitored throughout the anesthesia, and electrolyte levels (Ca2+, P+, K+, Cl-, Na+) and enzyme activities (aspartate aminotransferase (AST), creatine phosphokinase (CPK), and blood lactate) were monitored for 7 days. Postanesthetic forelimb lameness was produced in 5 of the 6 horses with this prolonged anesthetic regime. This lameness was associated with muscle plaque formation and clinical signs which were similar to the forelimb lameness sometimes seen in horses after surgical anesthesia. Plasma protein, serum calcium, plasma sodium, and blood urea nitrogen concentrations did not change, whereas significantly increased hematocrit, plasma potassium, and serum inorganic phosphate values were seen at the end of anesthesia, along with a decrease in plasma chloride values. Blood lactate, serum AST, and serum CPK activities were significantly high in the postanesthetic period, although the sequence of the changes differed. Intracompartmental muscle pressures were higher in the left forelimb adjacent to the floor (contact limb), and in the instance of the triceps of the contact limb, the pressures were sufficiently high (greater than 30 mm of Hg) that they may have compromised capillary blood flow. However, these high intracompartmental muscle pressures did not persist when positional changes of the horses were introduced at the end of the anesthetic period. There was no correlation between the severity of postanesthetic lameness and any of the measured values. The results demonstrate an experimentally induced postanesthetic lameness which was primarily related to the development of a myositis. Although the causative factors of this myositis may be multiple, the present study implicates local hypoxia in that increased blood lactate and inorganic phosphate values preceded that increased CPK activity. Intracompartmental muscle pressure in the contact limb were possibly high enough to have restricted local capillary blood flow.
 ...
PMID:Equine postanesthetic forelimb lameness: intracompartmental muscle pressure changes and biochemical patterns. 721 25

Pathomorphological studies were conducted into seven different muscles of 50 pigs that had died on transport to slaughterhouses. Established was the following percentual presence of acute disseminated hyaline-plaque degeneration and necrosis of muscle fibres: Group 1 with high frequency of pathological findings: M. biceps femoris, bright portion positively affected in 72 per cent of all cases, dark portion in 68 per cent; M. semimembranosus affected in 64 per cent; M. longissimus dorsi affected in 56 per cent. Group 2 with low to medium frequency of pathological findings: M. Quadriceps femoris affected in 26 per cent; M. semitendinosus, bright portion affected in 26 per cent, dark portion in 16 per cent; M. psoas major affected in 18 per cent. Group 3 without myopathy frequency: M. masseter. The rare occurrence of resorptive myositis (between zero and six per cent of all cases, depending on affected muscles) seems to confirm the young age of that myopathy which usually develops only under transport stress. Hyaline transverse ligaments (supercontractures) were not observed at all in the context of transport deaths (M. longissimus dorsi, M. biceps femoris--bright portion, M. semitendinosus--bright portion, M. masseter) or only in rare cases (M. quadriceps femoris in two per cent of all cases, M. semimembranosus in six per cent, M. semitendinosus--dark portion in six per cent, M. biceps femoris in 18 per cent, M. psoas major in 24 per cent). A comparison with earlier results on the frequency of muscle damage showed that hyaline-plaque degeneration and necrosis of muscle fibres occurred much more often in the context of normal slaughter without any transport and with much graver severity following different modes of transport. These conclusions and results are all relating to pigs which died on transport. The results are discussed, with reference to aetiology and pathogenesis of myopathies in swine caused by stress.
 ...
PMID:[Pathomorphology of the skeletal musculature of swine dying during transportation]. 745 53

Inoculation of Coxsackie B1 virus (CB1) in newborn CD1 Swiss mice induces a chronic myositis of proximal hindlimb muscles (CB1 myositis). To study the possible role of the virus dose, and of antiviral antibodies in the development of CB1 myositis, we infected groups of newborn mice with six CB1 doses, ranging from 30 to 10,000 plaque forming units (pfu); after 4 and 8 weeks we determined morbidity and antiviral antibody titer, and quantified histopathological changes. At 4 weeks, morbidity and mononuclear cell infiltration differed significantly for the various groups, with the most prominent changes in 300 pfu animals. At 4 and 8 weeks diseased animals had significantly higher antibody titers than clinically unaffected animals, and at 4 weeks myopathic and infiltrative changes correlated positively with the serum antibody titer. Our data indicate that the virus dose plays a pathogenic role in CB1 myositis, and they suggest further study on the role of humoral immune mechanisms in the early phase of CB1 myositis.
 ...
PMID:Coxsackie B1 virus-induced murine myositis: relationship of disease severity to virus dose and antiviral antibody response. 817 48

BACE1 and BACE2 are recently discovered enzymes participating in processing of amyloid beta precursor protein (AbetaPP). Their discovery is contributing importantly to understanding the mechanism of amyloid-beta generation, and hence the pathogenesis of Alzheimer's disease (AD). Sporadic inclusion-body myositis (s-IBM) and hereditary inclusion-body myopathy (h-IBM) are progressive muscle diseases in which overproduction of AbetaPP and accumulation of its presumably toxic proteolytic product amyloid-beta (Abeta) in abnormal muscle fibers appear to play an important upstream role in the pathogenic cascade. In normal human muscle AbetaPP was also shown to be present and presumably playing a role (a) at neuromuscular junctions and (b) during muscle development. To investigate whether BACE1 and BACE2 play a role in normal and diseased human muscle, we have now studied them by immunocytochemistry and immunoblotting in 35 human muscle biopsies, including: 5 s-IBM; 5 chromosome-9p1-linked quadriceps-sparing h-IBM; and 25 control muscle biopsies. In addition, expression of BACE1 and BACE2 was studied in normal cultured human muscle. Our studies demonstrate that BACE1 and BACE2 (a) are expressed in normal adult muscle at the postsynaptic domain of neuromuscular junctions, and in cultured human muscle; (b) are accumulated in the form of plaque-like inclusions in both s-IBM and h-IBM vacuolated muscle fibers; and (c) are immunoreactive in necrotizing muscle fibers. Accordingly, BACE1 and BACE2 participate in normal and abnormal processes of human muscle, suggesting that their functions are broader than previously thought.
 ...
PMID:BACE1 and BACE2 in pathologic and normal human muscle. 1261 21

Sporadic inclusion-body myositis (s-IBM) is the only muscle disease in which accumulation of amyloid-beta (Abeta) in abnormal muscle fibers appears to play a key pathogenic role. Increased amyloid-beta precursor protein (AbetaPP) and Abeta accumulation have been reported to be upstream steps in the development of the s-IBM pathologic phenotype, based on cellular and animal models. Abeta is released from AbetaPP as a 40 or 42 aminoacid peptide. Abeta42 is considered more cytotoxic than Abeta40, and it has a higher propensity to aggregate and form amyloid fibrils. Using highly specific antibodies, we evaluated in s-IBM muscle biopsies intra-muscle fiber accumulation of Abeta40 and Abeta42-immunoreactive aggregates by light- and electron-microscopic immunocytochemistry, and quantified their amounts by ELISA. In s-IBM, 80-90% of the vacuolated muscle fibers and 5-20% of the non-vacuolated muscle fibers contained plaque-like Abeta42-immunoreactive inclusions, while only 69% of those fibers also contained Abeta40 deposits. By immuno-electronmicroscopy, Abeta42 was associated with 6-10 nm amyloid-like fibrils, small electron-dense floccular clumps and larger masses of amorphous material. Abeta40 was present only on small patches of floccular clumps and amorphous material; it was not associated with 6-10 nm amyloid fibrils. By ELISA, in s-IBM muscle biopsies Abeta42 was present in values 8.53-44.7 pg/ml, while Abeta40 was not detectable; normal age-matched control biopsies did not have any detectable Abeta42 or Abeta40. Thus, in s-IBM muscle fibers, Abeta42 is accumulated more than Abeta40. We suggest that Abeta42 oligomers and their cytotoxicity may play an important role in the s-IBM pathogenesis.
 ...
PMID:Amyloid-beta42 is preferentially accumulated in muscle fibers of patients with sporadic inclusion-body myositis. 1928 Feb 2

A 30-year-old woman was referred on April 2002 for a plaque that involved the internal aspect of the right leg, an erythema nodosum-like lesion on the lower extremities, and periarthritis on her left ankle. Subsequently, the patient developed anular, atrophic, growing, porcelain-white papules, with a thin rim of erythema and telangiectases over her upper and lower extremities. Clinically and histologically, these lesions were the characteristics of Degos disease. Despite arthritis and myositis that required treatment, low level C3 and C4, positive antinuclear antibodies, and elevated anticardiolipin antibodies only once, in a follow-up of 6 years the patient never developed a specific connective tissue disease or other systemic involvement. In conclusion, because clinical and histological findings of Degos disease might mimic connective tissue diseases, rheumatologists must be aware that this reaction pattern can be seen in a wide clinical spectrum of diseases.
 ...
PMID:Degos cutaneous disease with features of connective tissue disease. 2037 24

Currently the world faces epidemic of several closely related conditions: obesity, metabolic syndrome and type 2 diabetes (T2DM). The lipid profile of these patients and those with metabolic syndrome is characterized by the concurrent presence of qualitative as well as quantitative lipoprotein abnormalities: low levels of HDL, increased triglycerides, and prevalence of LDL particles that are smaller and denser than normal. This lipid phenotype has been defined as atherogenic dyslipidemia. Overwhelming evidences demonstrate that all components of the atherogenic dyslipidemia are important risk-factors for cardiovascular diseases. Optimal reduction of cardiovascular risk through comprehensive management of atherogenic dyslipidemias basically depends of the presence of efficacious lipid-modulating agents (beyond statin-based reduction of LDL-C). The most important class of medications which can be effectively used nowadays to combat atherogenic dyslipidemias is the fibrates. From a clinical point of view, in all available 5 randomized control trials beneficial effects of major fibrates (gemfibrozil, fenofibrate, bezafibrate) were clearly demonstrated and were highly significant in patients with atherogenic dyslipidemia. In these circumstances, the main determinant of the overall results of the trial is mainly dependent of the number of the included appropriate patients with atherogenic dyslipidemia. In a meta-analysis of dyslipidemic subgroups totaling 4726 patients a significant 35% relative risk reduction in cardiovascular events was observed compared with a non significant 6% reduction in those without dyslipidemia. However, different fibrates may have a somewhat different spectrum of effects. Currently only fenofibrate was investigated and proved to be effective in reducing microvascular complications of diabetes. Bezafibrate reduced the severity of intermittent claudication. Cardinal differences between bezafibrate and other fibrates are related to the effects on glucose metabolism and insulin resistance. Bezafibrate is the only clinically available pan - (alpha, beta, gamma) PPAR balanced activator. Bezafibrate decreases blood glucose level, HbA1C, insulin resistance and reduces the incidence of T2DM compared to placebo or other fibrates. Among major fibrates, bezafibrate appears to have the strongest and fenofibrate the weakest effect on HDL-C. Current therapeutic use of statins as monotherapy is still leaving many patients with atherogenic dyslipidemia at high risk for coronary events because even intensive statin therapy does not eliminate the residual cardiovascular risk associated with low HDL and/or high triglycerides. As compared with statin monotherapy (effective mainly on LDL-C levels and plaque stabilization), the association of a statin with a fibrate will also have a major impact on triglycerides, HDL and LDL particle size. Moreover, in the specific case of bezafibrate one could expect neutralizing of the adverse pro-diabetic effect of statins. Though muscle pain and myositis is an issue in statin/fibrate treatment, adverse interaction appears to occur to a significantly greater extent when gemfibrozil is administered. However, bezafibrate and fenofibrate seems to be safer and better tolerated. Combined fibrate/statin therapy is more effective in achieving a comprehensive lipid control and may lead to additional cardiovascular risk reduction, as could be suggested for fenofibrate following ACCORD Lipid study subgroup analysis and for bezafibrate on the basis of one small randomized study and multiple observational data. Therefore, in appropriate patients with atherogenic dyslipidemia fibrates- either as monotherapy or combined with statins - are consistently associated with reduced risk of cardiovascular events. Fibrates currently constitute an indispensable part of the modern anti-dyslipidemic arsenal for patients with atherogenic dyslipidemia.
 ...
PMID:Fibrates are an essential part of modern anti-dyslipidemic arsenal: spotlight on atherogenic dyslipidemia and residual risk reduction. 2305 87

Purpose: Myasthenia gravis (MG) is an autoimmune disease and closely related to thymoma. Inflammatory myopathy may accompany with other autoimmune diseases. However, concurrence of inflammatory myopathy and MG is very rare. Necrotizing autoimmune myopathy (NAM), a rare form of inflammatory myopathy, is characterized by necrosis and regeneration of myocytes in proximal muscles without significant inflammation. The aim of the study was to report a rare case of NAM and concomitant thymoma-associated MG after thymectomy.Materials and methods/results: A 27-year-old female patient presented with muscle soreness and weakness in four limbs. Eyelid fatigue and neostigmine tests were negative, and no ptosis was found but the electromyographic examination (EMG) showed myogenic damage and a gradual decrease in the amplitude (20%) of EMG activities evoked by repetitive electrical stimulation. Antibodies against AChR and increased titer of creatine kinase were detected and plaque-like signals in both legs were found in magnetic resonance imaging. Myositis-related antibodies were negative but necrotic myocytes without inflammatory cell infiltration, and MHC-1 positive muscle fibers were found in muscle biopsy. Pathological examination confirmed anterior mediastinal B2 type thymoma. Five weeks after thymectomy, she started to show typical MG symptoms. No recurrence of thymoma was found but immunoassay showed a higher titer of AChR-Ab. Myositis-related antibodies negative necrotizing autoimmune myopathy (NAM) was reported to be associated with thymoma-associated MG.Conclusions: The patient showed symptoms related NAM but developed MG-related symptoms only after thymectomy. The mechanisms for the phenomena may be related to immune dysfunction associated with thymoma.
 ...
PMID:Report of a case of necrotizing autoimmune myopathy with thymoma-associated myasthenia gravis. 3207 78


1