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PubMed1993

Inclusion body myositis and renal cell carcinoma. Report of two cases and review of the literature.

OBJECTIVE: To describe the clinical course of 2 patients with concurrent inclusion body myositis and renal cell carcinoma and review published reports of inclusion body myositis associated with malignancy. METHODS: Prospective followup of 2 patients. Review of published case reports and series of patients with inclusion body myositis. RESULTS: Our 2 patients with inclusion body myositis and renal cell carcinoma had no improvement of strength following nephrectomy. Seven previously reported cases of inclusion body myositis and malignancy were identified and are discussed. CONCLUSION: Findings in our 2 patients suggest that there is no etiopathologic relationship between inclusion body myositis and malignancy.

Carcinoma, Renal Cell↗
PubMed1987

Aspergillus myositis in a patient with a myelodysplastic syndrome.

We present the case of an elderly man who, while being treated with corticosteroids for a myelodysplastic syndrome, developed myositis of the calf due to Aspergillus fumigatus. Despite therapy with amphotericin B the myositis failed to resolve and he died. At autopsy, a localized necrotizing myositis of the right calf was found with no evidence of disseminated Aspergillus infection. Myositis in the setting of disseminated candidiasis or cryptococcosis has been previously reported. This case is unique in that it is the first reported case of localized fungal myositis and of myositis caused by Aspergillus.

Adrenal Cortex Hormones↗
PubMed1993

Borrelia burgdorferi myositis: report of eight patients.

Myositis is a rare manifestation of Lyme disease of unknown pathogenesis. This study describes the course of disease in eight patients with Lyme disease, aged 37-70 years, all of whom were suffering from histologically proven myositis. The clinical, electrophysiological, and myopathological findings are reported. One patient showed signs and symptoms of myositis of all limbs. In six patients myositis was localized in the vicinity of skin lesions, arthritis or neuropathy caused by Borrelia burgdorferi. In another patient suffering from pronounced muscle weakness of the legs and cardiac arrest, inflammation of the myocardium, the conducting system and skeletal muscles was revealed at autopsy. Muscle biopsy revealed lymphoplasmocellular infiltrates combined with few fibre degenerations in three patients. The lymphoplasmocellular infiltrates were found predominantly in the vicinity of small vessels. Several spirochetes were stained in six of seven muscle biopsy samples by means of the immunogold-silver technique. Culturing of B. Burgdorferi from the muscle biopsy samples was, however, unsuccessful. Antibiotic treatment succeeded in curing the myositis in four of six patients. In one patients signs and symptoms improved. One patient died from cardiac arrest caused by myocarditis and Guillain-Barré syndrome. The outcome is unknown in one patient. Clinical and myopathological findings indicate that Lyme myositis can be caused either by local spreading of B. burgdorferi or an unknown antigen or toxin from adjacent tissues or haematogenously.

Adult↗
PubMed2005

Preservation of in vitro muscle fiber function in dermatomyositis and inclusion body myositis: a single fiber study.

Five patients with untreated dermatomyositis, five with inclusion body myositis, and 16 healthy elderly volunteer subjects (controls) underwent open (dermatomyositis and inclusion body myositis) or percutaneous (controls) muscle biopsy. Biopsied muscles included deltoid, biceps and vastus lateralis. Chemically skinned single muscle fibers were activated with Ca(+2); the slack test was performed to determine maximal unloaded shortening velocity (Vo). Parameters measured include single fiber cross sectional area, maximal force, specific force and Vo. 429 Type I and 94 Type IIA fibers were studied. Cross sectional area and maximal force were greater in inclusion body myositis than dermatomyositis or control for Type I and IIA fibers. Specific force of Type I fibers was similar in inclusion body myositis and dermatomyositis but greater than in controls. Vo was greater in Type I, but not IIA, fibers in dermatomyositis compared with inclusion body myositis and controls. The force and velocity generating capacity of single muscle fibers is preserved in patients with dermatomyositis and inclusion body myositis suggesting that dysfunction of the contractile proteins does not contribute to clinical muscle weakness.

Adult↗
PubMed1997

Outcome of orbital myositis. Clinical features associated with recurrence.

PURPOSE: Although orbital myositis usually responds to prompt systemic therapy, recurrent or persistent episodes often require prolonged therapy. This study presents the clinical and radiologic features of 26 patients with orbital myositis and suggests a treatment regimen with special emphasis on recurrent or persistent orbital myositis. METHODS: Retrospective analysis and comparison of clinical and radiologic parameters with clinical outcome in 26 patients with strictly defined orbital myositis was performed. A consultant radiologist reviewed computed tomography studies without knowledge of the clinical data or outcome. The frequency of certain clinical and radiologic parameters among two outcome groups was analyzed using Fisher's exact test. RESULTS: Comparison of clinical and radiologic features of 20 patients with a single acute episode and 6 patients with recurrent episodes disclosed several characteristics associated with recurrence. Male gender, lack of proptosis, eyelid retraction, horizontal extraocular muscle (EOM) involvement, multiple or bilateral EOM involvement (P = 0.05), muscle tendon sparing, and lack of response to systemic corticosteroids (P = 0.01), or nonsteroidal anti-inflammatory agents (P = 0.01) were associated with recurrent orbital myositis. CONCLUSIONS: A treatment algorithm is suggested for patients with orbital myositis. Those patients whose clinical or radiologic features are associated with recurrence may benefit from early systemic steroid therapy.

Acute Disease↗
PubMed1997

Myositis-induced functional reorganisation of the rat dorsal horn: effects of spinal superfusion with antagonists to neurokinin and glutamate receptors.

The study aimed at identifying some of the receptors for neurotransmitters/neuromodulators that are involved in the myositis-induced neuroplastic changes in spinal neurones. In anaesthetised rats, an experimental myositis was induced in the gastrocnemius-soleus muscle and the activity of single dorsal horn neurones recorded in the segment L3, just rostral to the main input region from that muscle. During the development of the myositis, the segment L3 was continuously superfused with antagonists to neurokinin receptors (GR 82.334, Spantide II), NMDA receptors (MK-801, AP 5) or AMPA/kainate receptors (CNQX). Each of the antagonists reduced the myositis-induced increase in excitability, but acted on different aspects of the hyperexcitability. GR 82.334 was most effective in preventing the expansion of the neurone population that responded to A-fibre input from the inflamed muscle, which was the main myositis effect in the present study. None of the antagonists influenced the background activity of the neurones. The results show that in the myositis-induced hyperexcitability of dorsal horn neurones all of the above receptors are involved. Excitability by peripheral input and background activity of the neurones are probably controlled by different mechanisms.

Animals↗
PubMed2002

Idiopathic inflammatory myopathies - myositis.

The inflammatory myopathies - myositis - encompass a heterogeneous group of chronic muscle disorders of unknown origin and with varying prognoses. New clinical phenotypes of myositis have been identified since the most widely used classification criteria were proposed in 1975. Based on clinical and histopathological features, inclusion body myositis was identified. Furthermore, the myositis-specific autoantibodies may also identify different clinical phenotypes and serve as prognostic markers. The different classifications and inclusion criteria that have been used in different studies make some epidemiological data uncertain. In order to improve our knowledge of causative factors, as well as of pathogenic mechanisms, there is a need for revision and also for an international acceptance of the classification criteria. During recent years, our knowledge has increased regarding the role of some genetic and environmental factors that could affect susceptibility for developing myositis as well as the prognosis. Whether there is an association between myositis and malignancies has been a subject of controversy for many years and recent epidemiological data have brought some clarification on this issue.

Adult↗
PubMed1998

Sporadic inclusion-body myositis and its similarities to Alzheimer disease brain. Recent approaches to diagnosis and pathogenesis, and relation to aging.

Sporadic inclusion-body myositis (s-IBM) is the most common, debilitating and progressive muscle disease beginning at the age 50 or later. The most characteristic pathologic feature is vacuolar degeneration of muscle fibers accompanied by intrafiber congophilia and clusters ("tangles") of paired-helical filaments, containing phosphorylated tau. An unusual feature of sporadic inclusion-body myositis is accumulation within its abnormal muscle fibers of several proteins that are characteristic of Alzheimer disease brain, including epitopes of beta-amyloid precursor protein (betaAPP), phosphorylated tau, alpha-1-antichymotrypsin, apolipoprotein E, and presenilin-1. Indicators of oxidative stress are also present within abnormal s-IBM muscle fibers. In this review, we describe new advances seeking the pathogenic mechanism of sporadic inclusion-body myositis. We hypothesize on the possible pathogenic role of abnormally accumulated proteins, and we propose that important contributory factors leading to inclusion-body myositis are the milieu of muscle-fiber aging and oxidative stress. In addition, we present evidence that overexpression of adenovirus-transferred betaAPP gene in cultured human muscle fibers induces aspects of the inclusion-body myositis phenotype, and suggest that betaAPP-overexpression is an early event in the pathogenic cascade causing inclusion-body myositis.

Alzheimer Disease↗
PubMed1998

Absence of characteristic features in two patients with inclusion body myositis.

According to recently published criteria a diagnosis of definite sporadic inclusion body myositis is made if the typical histopathological abnormalities (rimmed vacuoles and abnormal accumulations of proteins, in addition to mononuclear cell infiltrates) are present. The two women described here presented with myositis which was unresponsive to treatment. Patient 1 had features of non-progressive sporadic inclusion body myositis clinically, whereas patient 2 had a very slowly progressive limb girdle syndrome. The cryostat sections of the first biopsies did not show rimmed vacuoles, even in retrospect. Only a repeated biopsy, 12 years after presentation in one patient and 18 years after presentation in the other, disclosed the typical features of sporadic inclusion body myositis. The initial absence of abnormal fibres probably represents a real absence or scarcity rather then a sampling error due to a multifocal nature of the histological abnormalities. It is of importance for the clinician to realise that some patients with myositis unresponsive to treatment, even if both clinical and histological features do not suggest sporadic inclusion body myositis, may prove to have the disease on repeated histopathological examination.

Adult↗
PubMed2000

[Myositis and rhabdomyolysis with influenza infection].

Myositis and rhabdomyolysis with influenza are rare, but sometimes serious complications. Patients with myositis more commonly have influenza B infection than influenza A. On the other hand, rhabdomyolysis are more frequently recognized in patients with influenza A infection than those with influenza B. Upper respiratory symptoms usually precede myositis, while rhabdomyolysis occurs simultaneously or shortly after the respiratory symptoms. Creatine kinase levels are elevated in myositis mildly and in rhabdomyolysis markedly. Influenza myositis improve spontaneously within 6 weeks, but influenza rhabdomyolysis sometimes induce renal failure with fatal outcome. Although the true incidence of myositis and rhabdomyolysis in the influenza infection remains unknown, careful medical care is necessary when patients have muscle pain and weakness.

Adolescent↗
PubMed1987

Streptococcal necrotizing myositis: a rare entity. A report of two cases.

Deep muscle abscess or bacterial myositis is not an uncommon disease in the tropics. The commonest pathogen involved is Staphylococcus aureus. However, streptococcal myositis is rare. Only a few cases have been reported in literature. Furthermore, streptococcal myositis with extensive necrosis of muscles has not been reported. In two cases of streptococcal myositis with extensive muscle necrosis, both developed severe acute infection with septicaemia. Histologic observations revealed massive necrosis of muscle tissue with acute inflammatory infiltration. This condition, which we designate streptococcal necrotizing myositis should be treated as a separate disease entity. It requires not just incision and drainage, as in bacterial myositis, but radical excision of all the necrotic muscles in addition to appropriate antibiotics. Unless it is recognized, the treatment will be inadequate and un-necessarily prolonged. Intramuscular pressure may contribute to the pathogenesis of muscle necrosis and may stimulate compartmental syndrome.

Acute Disease↗
PubMed2005

Orbital myositis following streptococcal pharyngitis in a pediatric patient.

BACKGROUND: Orbital myositis is a relatively rare ocular inflammatory disease. It is currently classified as an idiopathic orbital inflammatory disease, but has been associated with ocular and systemic disorders, including scleritis, rheumatoid arthritis, Crohn's disease, and systemic lupus erythematosis. Orbital myositis has also been associated with infectious disease such as streptococcal pharyngitis, viral upper respiratory infection, and Borrelia burgdorferi infection. CASE REPORT AND DISCUSSION: This report documents treatment and imaging of a 13-year-old boy who had an episode of right-sided orbital myositis following streptococcal pharyngitis with anti-streptolysin-o (ASO) titer elevation to 1,188 IU/ml. Clinically, this patient demonstrated acute onset of marked restriction and mild under-action of the lateral rectus muscle of the right eye. Thickening of the lateral and medial recti was demonstrated on computed tomography. The mild orbital myositis was treated with oral nonsteroidal anti-inflammatory drug therapy. The nonconcomitant strabismus resolved approximately 7 weeks after initial presentation. General orbital inflammatory disease management and the association of upper respiratory tract infection with orbital myositis are discussed. CONCLUSION: Orbital myositis is a distinct clinical entity that can occur after streptococcal upper respiratory infection, consisting of pain on ocular movement, localized swelling, restrictive strabismus, and inflammatory signs of the involved muscle(s).

Adolescent↗
PubMed2006

Cancer and myositis: new insights into an old association.

PURPOSE OF REVIEW: The association between the idiopathic inflammatory myopathies and the development of malignancy has been appreciated for nearly a century, but its meaning and significance have remained unclear. Significant advances in our understanding of the epidemiology and pathophysiology of this association have recently been made. This review will describe the major epidemiological evidence linking inflammatory myopathies with cancer, and will use this evidence to highlight a recently proposed model for the development of cancer-associated myositis. RECENT FINDINGS: The temporal relationship between the development of cancer and myositis is reminiscent of that seen in neurological paraneoplastic disorders, in which antigens targeted for an immune response are expressed at high levels in the inciting tumor and the affected neuronal tissue. It has also recently been observed that regenerating cells in myositis muscle, but not its normal counterpart, express high levels of myositis-specific autoantigens. These same antigens are expressed at high levels in several cancers known to be associated with the development of myositis, but not in corresponding normal tissue. SUMMARY: These observations suggest a model of paraneoplasia focusing on common autoantigen expression and immune targeting between cancer tissues and muscle tissue in myositis.

Dermatomyositis↗
PubMed2000

The inhibition of apoptosis in myositis and in normal muscle cells.

The mechanism of injury and death of muscle cells in the inflammatory myopathies (dermatomyositis, polymyositis, and inclusion body myositis) remains obscure. We and others have not detected apoptosis in the muscle biopsies from patients with myositis despite clear evidence of cell damage and loss. We provide evidence in this study that Fas ligand (FasL) as well as Fas is present on muscle cells and inflammatory cells in myositis biopsies: Fas is present on most muscle cells and lymphocytes, and FasL is present on degenerating muscle cells and many infiltrating mononuclear cells. The expression of both Fas and FasL in the inflamed tissue makes the absence of apoptosis more striking. To address the mechanisms of this resistance to classical apoptosis in muscle cells, we have investigated the expression of the antiapoptotic molecule FLICE (Fas-associated death domain-like IL-1-converting enzyme)-inhibitory protein (FLIP) in muscle biopsies of myositis patients and in cultured human skeletal muscle cells. Using laser capture microscopy, we have shown that FLIP is expressed in the muscle fibers and on infiltrating lymphocytes of myositis biopsies. Furthermore, we have shown that FLIP, but not Bcl-2, is expressed in cultured human skeletal muscle cells stimulated with proinflammatory cytokines, and inhibition of FLIP with antisense oligonucleotides promotes significant cleavage of poly(ADP-ribose) polymerase autoantigen, a sensitive indicator of apoptosis. These studies strongly suggest that the resistance of muscle to Fas-mediated apoptosis is due to the expression of FLIP in muscle cells in the inflammatory environment in myositis.

Apoptosis↗
PubMed1992

[Clinical and neuroradiological studies on orbital myositis and Tolosa-Hunt syndrome].

Tolosa-Hunt syndrome and orbital myositis have common features such as ocular pain, ophthalmoplegia and exophthalmos. Both syndromes are thought to be caused by a granulomatous inflammation involving the cavernous sinus area in the former and the orbital cavity in the latter. The question whether these two conditions represent different presentations of a single disease, or they belong to different entities has not been settled. To address this question, we reviewed our cases having clinical diagnosis of either Tolosa-Hunt syndrome or orbital myositis. Six cases were diagnosed as Tolosa-Hunt syndrome, and 7 orbital myositis. In the thin-slice enlarged orbital CT, hypertrophic and high-density changes of at least one of the extraocular muscles were found in all cases with orbital myositis, but in none of the patients with Tolosa-Hunt syndrome. The age of onset was younger and the duration of the disease before admission was shorter in Tolosa-Hunt syndrome. They responded to steroid therapy better than those with orbital myositis. These findings lead us to conclude that Tolosa-Hunt syndrome and orbital myositis belong to different syndromes, although clinical manifestations have many similarities. Then we studied the relationship between the hypertrophic change of the extraocular muscle and the direction of the oculomotor restriction. For this purpose four additional cases with dysthyroid ophthalmopathy were also studied. We found that the presence of hypertrophic change was frequently associated with the restriction of ocular movement to the direction not only of the hypertrophic muscle but also of the opposite muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Apolipoprotein E and apolipoprotein E messenger RNA in muscle of inclusion body myositis and myopathies.

Sporadic inclusion body myositis and the hereditary inclusion body myopathies are severe, progressive muscle diseases, characterized pathologically by vacuolated muscle fibers containing paired helical filaments. We immunostained muscle biopsy specimens from sporadic inclusion body myositis, hereditary inclusion body myopathy, disease control, and normal patients with several antibodies against apolipoprotein E (ApoE). Approximately 80 to 90% of the vacuolated muscle fibers of sporadic inclusion body myositis contained well-defined, strongly immunoreactive ApoE inclusions. In hereditary inclusion body myopathy, only rare vacuolated fibers had immunoreactive inclusions, whereas most had diffuse cytoplasmic ApoE immunoreactivity. Ultrastructurally, ApoE immunoreactivity in sporadic myositis was localized mainly to the paired helical filaments. By contrast, in the hereditary form, ApoE immunoreactivity occurred on material in close proximity to the paired helical filaments, but never was on the paired helical filaments. In both muscle diseases, ApoE was also on the 6- to 10-nm filaments and amorphous material. In the sporadic form, ApoE-immunoreactive deposits colocalized with Congo red-positive deposits; however, in muscle fibers from patients with hereditary disease there was no congophilia. ApoE messenger RNA was not detectable in muscle fibers from patients with hereditary or sporadic disease but was expressed abundantly in muscle macrophages. In all control and inclusion body myositis or myopathy biopsy specimens, ApoE immunoreactivity was strong at the postsynaptic domain of neuromuscular junctions; nonjunctional regions of normal fibers were negative for ApoE. ApoE immunoreactivity occurred diffusely in regenerating muscle fibers, a subset of which had detectable ApoE messenger RNA.

Amyotrophic Lateral Sclerosis↗
PubMed2003

[Idiopathic myositis].

The idiopathic myositis, dermatomyositis, polymyositis and inclusion body myositis are recognized by their clinical and laboratory presentation, and by morphological changes in the muscle biopsy. A rapid diagnostic process is important, in order to start early treatment, which will be more effective and to direct further investigations and management. In the presence of dermatomyositis a precise investigation of neoplasia is important because they are often associated, which is not the case with inclusion body myositis. Symptoms in dermatomyositis and polymyositis respond sometimes quite well to immunomodulatory therapy but not in inclusion myositis. Controlled muscle training may sometimes slow progression in inclusion myositis.

Biopsy↗
PubMedDate not supplied

[Post-influenza viral myositis: report of a case].

The inflammatory myopathies are a heterogeneous group of diseases due to autoimmunitary or infective causes. They are diagnosed by clinical electrophysiological features, and muscle biopsy. The autoimmunity group is subdivided in dermatomyositis, polimyositis and inclusion body myositis. The second group caused by viral genesis are called generally "myositis". The two groups have a different prognosis and therapy. The infective group denominated myositis have usually a viral etiology. We have evaluated 6 patients with viral myositis that are studied by physical examination, blood test (CK included), electromyographic pattern and muscle biopsy. The Authors emphasized the role of muscle biopsy for the diagnosis of this pathology and in particular for the myositis.

Biopsy↗