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PubMed2002

A muscular lesion suggestive of focal myositis in a child with Proteus syndrome.

Proteus syndrome is a polymorphic hamartomatous disorder associated with a broad spectrum of rare congenital malformations. Many neoplasms have been linked to this condition, including lipomas, lymphangiomas, and hemangiomas. The authors describe a case of a congenital muscular lesion in a child with Proteus syndrome. This mass was painless but was growing out of proportion to her leg musculature. A magnetic resonance imaging scan and incisional biopsy showed findings consistent with focal myositis. The clinical, radiographic, and histologic characteristics of this previously undescribed lesion are discussed, with a brief review of the literature.

Child, Preschool↗
PubMedDate not supplied

Resolving eosinophilic myositis: MR features.

We describe MR findings in a case of idiopathic eosinophilic myositis presenting as painful swelling of the upper arm. Imaging revealed diffusely enlarged and edematous triceps muscle with an associated ill-defined heterogeneous mass in its midportion. Prominent edema was noted in adjacent fascia. The follow-up MR image showed complete resolution, though no specific treatment was given.

Adult↗
PubMed1994

Myofibers from Duchenne/Becker muscular dystrophy and myositis express the intermediate filament nestin.

The intermediate filament nestin is transiently expressed in developing skeletal muscle. In the present investigation, we analyzed by immunohistochemistry the presence of nestin, as well as vimentin and desmin, in skeletal muscle affected by two diseases characterized by various degrees of necrosis and muscle regeneration: Duchenne/Becker muscular dystrophy and myositis. Nestin-positive areas were found in all analyzed muscle biopsies of both diseases. The same areas were, in most cases, also positive for vimentin and stained more intensely for desmin than surrounding myofibers. Only nestin was found specifically in myopathic muscle fibers; vimentin was in addition present in muscle fibroblasts and desmin in all myofibers. The areas staining positive for nestin were typically basophilic, small-diameter myofibers, often with centrally located nuclei. With the interesting exception of a 73-year-old healthy control with abundant ring fibers, nestin was not detected in the muscle of healthy controls. The intracellular distribution of nestin in the myopathic muscle fibers, as well as in the ring fibers, was confined to the vicinity of Z-bands. The presence of nestin protein in myopathic regenerating areas and in ring fibers correlated more closely to the presence of desmin than to vimentin immunoreactivity. Our results suggest that nestin is specifically expressed in newly formed muscle fibers also during regeneration, and that nestin may serve as a useful marker of regenerating muscle fibers in pathological conditions.

Adolescent↗
PubMed1996

Difference in expression of phosphorylated tau epitopes between sporadic inclusion-body myositis and hereditary inclusion-body myopathies.

Sporadic inclusion-body myositis (s-IBM) and the hereditary inclusion-body myopathies (h-IBMs) are severe and progressive muscle diseases, characterized pathologically by vacuolated muscle fibers containing paired-helical filaments (PHFs). An interesting feature of the s- and h-IBM muscle phenotype is its striking similarity to Alzheimer-disease (AD) brain. We immunostained muscle biopsies of 9 s-IBM patients, 9 autosomal-recessive h-IBM patients, 1 autosomal-dominant h-IBM patients, and 18 normal and disease-controls with several antibodies known to react with the hyperphosphorylated tau of AD-PHFs. Those included SMI-31, SMI-310, PHF-1, and AT8. In both s- and h-IBM, virtually all vacuolated muscle fibers had strongly immunoreactive inclusions with SMI-31, and by immuno-electronmicroscopy SMI-31 was exclusively localized to PHFs. Approximately 40 to 50% of both s- and h-IBM vacuolated muscle fibers were also immunoreactive with AT8 antibody. To the contrary, in h-IBM, there was no immunoreactivity with SMI-310 and PHF-1 antibodies, whereas in s-IBM the vacuolated muscle fibers had strong immunoreactivity with those two antibodies. By immunoelectronmicorscopy, SMI-310 and PHF-1 also were localized to PHFs. Within s-IBM muscle fibers, the structures immunoreactive with SMI-310 were congophilic, whereas h-IBM muscle fibers did not have congophilia. Our studies: (a) demonstrate a distinct difference between s-IBM and the h-IBMs in regard to expression of immunoreactive phosphorylated tau and congophilia; (b) demonstrate a new "diagnostic duo" combination of SMI-31 and SMI-310 antibodies for identifying and distinguishing s-IBM and the h-IBMs; and (c) provide another close similarity of pathologic phenotypes between s-IBM muscle and AD brain, suggesting that similar cellular pathogenic mechanisms may be active in both diseases.

Adult↗
PubMed1996

MHC class I-mediated cytotoxicity does not induce apoptosis in muscle fibers nor in inflammatory T cells: studies in patients with polymyositis, dermatomyositis, and inclusion body myositis.

Apoptosis plays a crucial role in natural recovery from T cell-mediated autoimmune disorders of the nervous system. Whether apoptosis also occurs in human inflammatory myopathies is unclear. In this study we examined muscle biopsy specimens from untreated patients with polymyositis (n = 12), dermatomyositis (n = 12), and inclusion body myositis (n = 12) for the presence of apoptosis using morphological criteria and DNA fragmentation by in situ tailing. In all these disorders, only rare T cells exhibited signs of apoptosis by nuclear morphology and in situ labeling techniques. Although Fas-expression was upregulated in a few inflammatory cells, increased apoptosis of the surrounding T cells was not observed. Further, nuclei of degenerating muscle fibers did not show morphological signs of apoptosis and were not labeled by the tailing reaction. We conclude that in the inflammatory myopathies, T cell inflammation is not cleared by apoptosis and affected muscle fibers do not die by apoptosis. The observations are consistent with the non-self-limited nature of these disorders and suggest that, in contrast to the nervous system, the local microenvironment in muscle does not deliver pro-apoptotic stimuli.

Adult↗
PubMed1998

Characterization of the mitochondrial DNA abnormalities in the skeletal muscle of patients with inclusion body myositis.

Inclusion body myositis (IBM) is a late-onset inflammatory myopathy with distinctive clinical and histopathological features. The molecular basis for the disease remains unknown, but abnormal nuclear morphology and the accumulation of a protein that binds single-stranded DNA in a sequence-independent fashion suggest a nuclear defect. Evidence of mitochondrial respiratory chain dysfunction (ragged-red fibers, multiple mtDNA deletions) has been reported in IBM muscle. Here we have investigated the relationship of the mtDNA abnormalities in sporadic and familial IBM patients to the pathogenesis of the disease. In situ hybridization analysis with mtDNA probes revealed several different mtDNA abnormalities in cytochrome c oxidase-negative muscle fibers including large-scale mtDNA deletions and mtDNA depletion, but no evidence for nonspecific DNA binding. Contrary to previous reports, we did not observe mtDNA deletions on Southern blot analysis, consistent with the presence of multiple different deleted mtDNA species demonstrated by single fiber PCR. There was no consistent correlation between the mitochondrial abnormalities and markers of muscle regeneration, inflammation, or microscopically detectable pathological alterations of myonuclei in the same fibers. Thus, early molecular abnormalities in IBM may simply accelerate the accumulation of mtDNA abnormalities that occurs with natural aging.

Adult↗
PubMed2002

Myositis ossificans circumscripta of the sacrotuberous ligament: a case report and review of the literature.

Soft tissue ossification is a well-known phenomenon in various pathologic conditions. Myositis ossificans circumscripta refers to posttraumatic calcification of soft tissue, including various ligaments. However, posttraumatic calcification of ligaments in the pelvis is a rare complication described only anecdotally in the past. We present a rare case of posttraumatic calcification of the sacrotuberous ligament in a patient, several months after suffering a pelvic trauma. This is one of the differential diagnoses of soft tissue pain and tenderness after trauma.

Adult↗
PubMed1996

A curable cause of chronic idiopathic intestinal pseudo-obstruction in children: idiopathic myositis of the small intestine.

We report an intestinal pseudo-obstruction syndrome occurring in a 6-month-old infant girl suffering from acquired major and persistent abdominal distension, which 2 months later required ileostomy. Histologic examination of samples of the small intestine showed considerable inflammatory reaction in the muscular layers of the intestinal wall. Steroid therapy, begun as soon as the histologic results were known, resulted in recovery. In a similar case, reported previously, steroid therapy used after the lesions had already caused fibrosis and atrophy of the intestinal wall, proved ineffective. This particular form of pseudo-obstruction is classified as "idiopathic myositis of the small intestine." It is important to identify the condition because an early course of steroid therapy, before the appearance of fibrotic lesions, could improve the prognosis.

Female↗
PubMed1976

Treatment of traumatic myositis ossificans circumscripta; use of aspiration and steroids.

The classification, clinical presentation, forms of treatment, and theories of pathogenesis of traumatic myositis ossificans circumscripta are reviewed. A group of 7 patients with this lesion was treated with hematoma aspiration and injection of steroids, lysosomal enzymes, and xylocaine, resulting in significant limitation of disability. The determining factor in the development of this disorder seems to be the response of local soft tissues to trauma rather than the magnitude of the trauma itself which we feel accounts for the success of the form of treatment described.

Adolescent↗
PubMed1998

Dysphagia in patients with inclusion body myositis.

OBJECTIVES: Inclusion body myositis (IBM) is an inflammatory myopathy with a 40% reported incidence of dysphagia. A protracted course, refractory to medical therapy, frequently leads to consultation with an otolaryngologist for dysphagia management. We studied the incidence, symptoms, and mechanisms of dysphagia in patients with IBM. STUDY DESIGN: Retrospective study of medical records and self-reported follow-up survey; dysphagia is defined as difficulty in swallowing. MATERIALS: Twenty-two patients with biopsy-proven IBM. RESULTS: The rate of dysphagia was more than 80% (16 of 19), twice as high as previously reported. Progressive dysphagia was associated with a significantly worse functional class. Relevant management guidelines are established, including the timing for appropriate surgical intervention. CONCLUSION: Progressive dysphagia may signify more aggressive IBM or an episodic worsening in status. Recognition of the disease manifestations will afford proper patient management. Informed otolaryngologists can have a favorable impact on the dysphagia associated with IBM.

Activities of Daily Living↗
PubMedDate not supplied

Deep muscle contusion complicated by myositis ossificans (a.k.a. heterotopic bone).

One muscle trauma is a common injury in contact sports. The most extensively damaged muscle is that segment closest to the underlying bone. By an unknown mechanism, this injured muscle can become transformed into heterotopic bone, a complication also called myositis ossificans. It is best managed conservately and rarely requires surgery.

Adolescent↗
PubMed1997

Cellulitis and myositis caused by Agrobacterium radiobacter and Haemophilus parainfluenzae after influenza virus vaccination.

Agrobacterium radiobacter is a gram-negative aerobic bacillus that has been reported as a cause of disease only 36 times in the literature. More than half of the patients (25) have had bacteremia. Peritonitis, urinary tract infection, endocarditis, and one case of cellulitis associated with bacteremia have also been reported. Infection is often associated with immunosuppression and the presence of a plastic foreign body, such as central venous catheters, nephrostomy tubes, intraperitoneal catheters, and prosthetic cardiac valves. We present apparently the first case of A radiobacter causing myositis after influenza virus vaccination.

Adult↗
PubMed1997

Inclusion body myositis and myopathies.

Sporadic inclusion body myositis is a frequent, acquired, adult-onset vacuolar myopathy affecting proximal and distal muscles with a distinct, easily identifiable clinical pattern. Although its primary cause is still unknown, autoimmune, viral, and degenerative processes, alone or in combination, are being considered. A uniform and sustained therapeutic response using the currently available immunomodulatory agents has not yet been achieved. Hereditary, inherited noninflammatory rimmed vacuolar myopathies with similar histologic features, collectively called hereditary inclusion body myopathies, are being redefined with the use of molecular genetics. The implications of the recent advances in clinical and basic sciences are discussed in the present review.

Aged↗
PubMed1999

Inclusion body myositis.

Sporadic inclusion body myositis is a severely disabling muscle disease that mainly affects elderly individuals. The typical distribution of muscle weakness, poor response to immunosuppressive treatment, pathological accumulation of various proteins in vacuolated muscle fibres, inflammatory reaction and mitochondrial changes have all been subjects of recent research that has led to better understanding of the pathogenic events that leads to muscle degeneration and weakness.

Humans↗
PubMed2002

Inclusion-body myositis and myopathies: different etiologies, possibly similar pathogenic mechanisms.

PURPOSE OF REVIEW: Sporadic inclusion-body myositis (s-IBM) and hereditary inclusion body myopathies are progressive muscle diseases that lead to severe disability. We discuss recent advances in illuminating their pathogenic mechanism(s). RECENT FINDINGS: We emphasize how different etiologies might lead to the strikingly similar pathology and possibly similar pathogenic cascade. Our basic hypothesis is that over-expression of amyloid-beta precursor protein within aging muscle fibers is an early upstream event causing the subsequent pathogenic cascade. On the basis of our research, several processes seem to be important in relation to the still speculative pathogenesis: (a) increased transcription and accumulation of amyloid-beta precursor protein, and accumulation of its proteolytic fragment Abeta; (b) accumulations of phosphorylated tau and other Alzheimer-related proteins; (c) accumulation of cholesterol and low-density lipoprotein receptors, the cholesterol accumulation possibly due to its abnormal trafficking; (d) oxidative stress; and (e) a milieu of muscle cellular aging in which these changes occur. We discuss unfolded and/or misfolded proteins as a possible mechanism in formation of the inclusion bodies and their consequences. The remarkable pathologic similarities between s-IBM muscle and Alzheimer disease brain are discussed. SUMMARY: Unfolding knowledge of the various pathogenetic aspects of the s-IBMs and hereditary inclusion body myopathies may lead to new therapeutic avenues.

Aging↗
PubMed1983

Successful second bone marrow transplantation in a patient with myositis ossificans progressiva and aplastic anemia.

Bone marrow transplantation has become the treatment of choice for patients with severe aplastic anemia who are fortunate enough to have allogeneic sibling donors. As patients have been transplanted earlier in the course of their disease, significant improvements have been obtained in long-term survival. However, in patients who have been sensitized by previous blood product transfusions, graft rejection continues to be a significant problem and second transplants when performed are frequently unsuccessful. This case report deals with a patient with myositis ossificans progressiva (MOP) who developed severe idiopathic aplastic anemia. He rejected his first graft after 160 days. However, he was successfully reingrafted with marrow from the same donor using a different conditioning regimen.

Anemia, Aplastic↗
PubMed1998

Inclusion body myositis--a review.

Inclusion body myositis (IBM), a sporadic inflammatory myopathy, is the most frequently occurring progressive myopathy in adults older than 55 years. It more commonly affects men and usually is clinically and pathologically distinguishable from dermatomyositis or polymyositis. Muscle biopsy specimens will display inflammation in virtually all cases of sporadic IBM, along with rimmed vacuoles accompanied by the accumulation of beta-amyloid and other substances similar to those found in the degenerating neurons of Alzheimer's disease. The similarities between IBM and other inflammatory myopathies may contribute to its low level of diagnosis by pathologists. The proper recognition of IBM is important because, unlike other inflammatory myopathies, IBM is unresponsive to anti-inflammatory drugs.

Actin Cytoskeleton↗