Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “MYOSITIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMed2002

Dermatomyositis sine myositis and antisynthetase syndrome.

We describe a 66-year-old woman with cutaneous lesions typical of classic dermatomyositis, clinical evidence of antisynthetase syndrome (arthritis, Raynaud's phenomenon, mechanic's hands and interstitial lung disease with anti-Jo-1 autoantibody) and lack of muscle disease after a full muscle evaluation that included clinical, enzymatic, electromyographic, magnetic resonance imaging and histological studies. The patient did not develop myositis after 9 years of clinical disease. The association of dermatomyositis sine myositis with antisynthetase antibodies suggests that the characteristic skin lesions are closely linked with dermatomyositis on the basis of the similar clinical and serological features of both dermatomyositis sine myositis and classic dermatomyositis.

Aged↗
PubMed2000

Inclusion body myositis masquerading as polymyositis: a case study.

A case of inclusion body myositis masquerading as unresponsive polymyositis is presented. A 56-year-old woman diagnosed with "biopsy-proven" polymyositis in 1991 was referred to our clinic in 1997 with progressive, painless weakness that was unresponsive to steroid therapy. Further evaluation, including electromyography and review of the original muscle biopsy specimen, found a diagnosis of inclusion body myositis, leading to a change in the patient's prognosis and management. Inclusion body myositis is frequently mistaken for polymyositis, despite the fact that it is now the most common inflammatory myopathy affecting people older than 50 years. The purpose of this report is to increase awareness of this disease, to enhance early diagnosis, and to ensure appropriate management. We discuss the clinical findings, pathogenesis, and physiatric management, as well as compare this disease with other idiopathic inflammatory myopathies.

Creatine Kinase↗
PubMed2002

Nontraumatic myositis ossificans with an unusual location: case report.

Myositis ossificans is a pathologic entity rarely met, but still it must be kept in mind in differential diagnosis of a tender soft tissue swelling. The authors present an 8-year old boy with nontraumatic myositis ossificans circumscripta in the left paravertebral muscle. In diagnostic workup, ultrasonography and computed tomography (CT)-scan showed a well marginated, regular, ossified mass in the paravertebral muscle, but we were not able to exclude malignancy on the clinical grounds. The mass was excised totally, and the histopathologic examination found myositis ossificans. The authors suggest that surgical intervention may be an option for diagnosis and treatment in unusual cases when diagnosis is not certain.

Child↗
PubMed1977

[Difficulties in the differential diagnosis of a non-traumatic, active myositis ossificans during pregnancy (author's transl)].

A 28 year old patient complained of sensory disturbances and pain in the right upper arm during pregnancy. During the 32nd week of her pregnancy, a large painful mass developed in the flexor muscles which, radiographically, showed some calcification. A diagnosis of a parosseous sarcoma was made; biopsy, however, indicated a diagnosis of non-traumatic myositis ossificans. Since the histological appearances of active myositis may be vary difficult to distinguish from a juxtacortical sarcoma, a right brachial angiogram and scintiscan were obtained. The angiographic and scintigraphic findings were erroneously considered to suggest malignancy. Following delivery, the tumour was removed. Futher histology confirmed the diagnosis of localised, non-traumatic myositis ossificans. The value of radiology, biopsy, angiography and scintigraphy are discussed with reference to our experience.

Adult↗
PubMed2006

Focal myositis of the iliopsoas muscle--a benign pseudotumour: ultrasound appearance in correlation with CT and MRI.

OBJECTIVE: Focal myositis of the iliopsoas muscle is a rare condition. A case is presented, emphasizing the value of ultrasound for detection, localisation, image-guided biopsy and follow-up in correlation with CT and MRI findings. MATERIAL AND METHODS: A 58-year-old woman was referred to our clinic with strong left sided inguinal pain, which radiated to the thigh and had lasted for four days. Ultrasound, CT and MRI were performed. Ultrasound-guided biopsy with histological correlation was obtained and US-follow-ups were available. RESULTS: CT showed an enlarged iliopsoas muscle on the left side without any focal pathology or enhancement. MRI revealed a sharpely delineated lesion, which was hypointense to muscle in fat-suppressed T1 w images with circumferential enhancement and showed a hyperintense appearance in T2 w images. Ultrasound displayed a polylobulated, inhomogeneous and hypoechoic tumour within the iliopsoas muscle. Ultrasound-guided biopsy was found to be compatible with myositis. After oral therapy with steroids, improvement could be documented by serial ultrasound follow-up as the size of the tumour was definitely regressing. CONCLUSION: Focal myositis of the iliopsoas muscle is a rare entity which may mimic a tumoural lesion. Imaging findings may not be conclusive, and US-guided biopsy is recommended to rule out a malignant mass. Ultrasound seems to be the most cost-effective method for diagnosis, image guided biopsy and follow-up.

Adrenal Cortex Hormones↗
PubMed2004

Myositis ossificans of psoas muscle: magnetic resonance imaging findings.

Myositis ossificans is a benign, localized, self-limiting ossifying soft tissue mass with unknown pathogenesis. It may be confused with a malignant tumor of bone or soft tissues, especially in the early stages of the disease. In this report, we present a case of myositis ossificans affecting unilateral psoas muscle, which to our knowledge is a very uncommon location. There was no history of trauma. We describe the imaging findings and clues to early diagnosis of myositis ossificans.

Adult↗
PubMed2005

Acquired retraction of the eye as the first sign of myositis.

The authors report a patient who was diagnosed with idiopathic orbital myositis based on the findings of diplopia, worse on right gaze, globe retraction on adduction and injection at the lateral muscle tendon insertion of the left eye. Although orbital myositis as a cause of acquired retraction of the eye is rare, they wish to emphasize the importance of globe retraction with injection over the recti as an important clue for the diagnosis of orbital myositis.

Adrenal Cortex Hormones↗
PubMed1999

Granulomatous myositis. Clinicopathologic study of 12 cases.

Granulomatous inflammation is infrequently encountered in skeletal muscle biopsy material. Of 2,985 muscle biopsy specimens reviewed over 12 years, 12 (0.4%) with granulomatous inflammation were identified. The patients included 9 women who ranged in age from 24 to 76 years (mean 50.3 years). The most common clinical findings included decreased strength or weakness in the extremities (n = 8), muscle pain (n = 5), and weight loss (n = 3). All muscles exhibited nonnecrotizing granulomas; an associated vasculitic process was identified in 2. Endomysial chronic inflammation consisting primarily of lymphocytes and plasma cells was present in 10 muscles, and perivascular chronic inflammation in 8. Degenerating muscle fibers were noted in 10 cases, and regenerating fibers in 11. Evidence of neurogenic atrophy was seen in 8 muscles. Increased endomysial fibrosis was observed in 5 muscles, and type II muscle fiber atrophy in 5 muscles. Stains for acid-fast bacilli and Gomori methenamine silver stain were performed in all but 2 cases and failed to demonstrate organisms. In 3 cases, concomitant sural nerve biopsies were performed, and granulomas were identified in 2 of those cases. Clinicopathologic diagnoses included sarcoidosis (n = 6), vasculitis (n = 2), and granulomatous myositis not otherwise specified (n = 2). In 2 cases, there was insufficient clinical information or follow-up data to determine a cause. In conclusion, granulomatous myositis is infrequently found in muscle biopsy specimens (0.5% of all biopsies in this series); most muscles demonstrate evidence of chronic endomysial or perivascular inflammation accompanied by muscle fiber degeneration and regeneration; and the most common cause for granulomatous myositis was sarcoidosis in this series.

Adult↗
PubMed1993

Mitochondrial DNA deletions in inclusion body myositis.

Skeletal muscle specimens from three patients with inclusion body myositis, aged 39, 60 and 71 years, respectively, were investigated. Enzyme histochemical staining of cytochrome c oxidase (COX), succinate dehydrogenase and myofibrillar ATPase, and in situ hybridization of transcripts of mitochondrial DNA (mtDNA) were performed on consecutive sections. In all three cases a proportion of muscle fibres (2-5%) showed low or absent COX activity in spite of medium or high succinate dehydrogenase activity (COX deficient muscle fibres). Two probes detecting transcripts of different segments of mtDNA were used for the in situ hybridization. One of the probes (ND4 probe) detected transcripts of a segment of the NADH dehydrogenase subunit 4 gene, which is known to be affected in most cases of mitochondrial myopathy with large deletions of mtDNA. There was reduced hybridization of the ND4 probe in many COX deficient muscle fibres compared with adjacent normal fibres. The other probe (ND2 probe) detected transcripts of a segment of the NADH dehydrogenase subunit 2 gene, which usually is not included in mtDNA deletions. There was accumulation of transcripts corresponding to the ND2 probe in COX deficient fibres in all three cases. These findings demonstrate that deleted mtDNA had accumulated in COX deficient muscle fibres in patients with inclusion body myositis. Southern blot analysis of mtDNA in muscle revealed a 16.6 kb fragment corresponding to normal mtDNA in all three cases. In one case two additional less abundant fragments of smaller size, corresponding to deleted mtDNA, were detected. Ultrastructural investigation showed abnormal mitochondria in all three cases. Control muscle specimens were obtained from nine patients, aged 63-71 years, with muscle pain but without morphological evidence of muscle disease. Occasional COX deficient fibres (< 1%) were found in three of the control cases. The other six control cases showed no COX deficient fibres. Our results show that mtDNA deletions may be involved in the pathogenesis of inclusion body myositis and cause respiratory chain dysfunction in muscle fibre segments.

Adult↗
PubMed1995

Fracture of a supracondylar humeral myositis ossificans.

Although myositis ossificans is a well-known sequela of elbow trauma, reinjury to the affected region can also occur, resulting in acute symptoms from a fracture of the myositis ossificans. An 18-year-old man presented with localized pain, soft-tissue swelling, and a bony mass along the anterolateral distal humerus with restricted elbow range of motion after injury to his elbow during football. One year earlier he had sustained a similar crush injury to his elbow that resulted in a limited, although painless, arc of motion. Radiographs and tomograms established the diagnosis of a fractured supracondylar humeral myositis ossificans. Surgical excision of the large mature ossified fragment confirmed the diagnosis and restored a full range of motion of the elbow.

Adolescent↗
PubMed2004

Is it really myositis? A consideration of the differential diagnosis.

PURPOSE OF REVIEW: The idiopathic inflammatory myopathies are an important and treatable group of disorders. However, the potential toxicity associated with the immune therapeutic regimens used to treat these disorders may be significant; therefore, accurate diagnosis before such treatment is essential. The differential diagnosis is potentially large. Accurate diagnosis usually depends on a combination of careful clinical assessment in conjunction with detailed laboratory investigations. Muscle biopsy remains essential in achieving an accurate diagnosis that will then guide treatment. This review describes the diagnostic approach used. RECENT FINDINGS: There has been debate over the requirements for an accurate diagnosis of inflammatory myopathy (i.e., polymyositis and dermatomyositis). It is increasingly recognized that there can be clinical and muscle histopathologic overlap between the features of inflammatory myopathies and those of other muscle disorders, in particular, the genetic muscular dystrophies. Pathologic findings of inflammation and major histocompatibility complex upregulation, although typical of inflammatory myopathies, have been shown to occur in some muscular dystrophies, complicating the diagnostic process. Inclusion body myositis is much less responsive to immunotherapy and is now recognized as the most common acquired muscle disease in those older than 50 years of age. It is likely that genetic muscular dystrophies and inclusion body myositis account for some cases of apparently "treatment-resistant" myositis. SUMMARY: A thorough clinical assessment, including a detailed family history, complemented by electromyography and creatine kinase measurements, should be undertaken in any patient with presumed idiopathic inflammatory myopathy. In addition, a muscle biopsy remains essential in all cases. A precise tissue diagnosis confirming features of an active inflammatory process should be achieved before immunosuppressive treatment is commenced. An increasing array of immunocytochemical and histioenzymatic stains now allows a full analysis and will help to confirm or exclude virtually all the differential diagnostic possibilities considered in this review. Electron microscopy may also be valuable in selected cases. Close collaboration between clinicians and muscle pathologists is essential in allowing the most accurate interpretation of myopathologic findings in the clinical context.

Diagnosis, Differential↗
PubMed1993

Coxsackievirus B1-induced murine myositis: no evidence for viral persistence.

The persistence of coxsackievirus B1 in the muscles of mice with coxsackievirus B1-induced chronic myositis was investigated. Neonatal CD1 Swiss mice were inoculated with a myositis-causing variant of coxsackievirus B1 (Tucson strain). Hamstring muscle samples of diseased mice obtained at various times after inoculation were examined for the presence of infectious virus, viral RNA and histological abnormalities. Viral RNA was detected up to 4 weeks after initiation of infection, whereas virus could be isolated from hamstring muscles for up to 2 weeks. Thereafter no sign of infection was demonstrated although histological abnormalities remained present for the entire observation period of 16 weeks. That viral RNA was detectable for only 2 weeks after tissues became negative for infectious virus suggests that the infection slowly waned rather than the viral RNA persisting. Hence, it is concluded that coxsackievirus B1 plays an essential role in the initiation of myositis but not in the maintenance of the chronic phase.

Animals↗
PubMed1986

Proliferative myositis and fasciitis. Report of five cases with an ultrastructural and immunohistochemical study.

Cases of proliferative myositis and fasciitis were studied immunohistochemically and ultrastructurally for further understanding of the nature of ganglion cell-like giant cells. Blood coagulation factor XIIIa, fibronectin, myoglobin, myosin, CPK MM, and alpha-1-antichymotrypsin were detected in three cases of proliferative myositis and two cases of proliferative fasciitis by the avidin-biotin-peroxidase complex method. Factor XIIIa (a fibrin-stabilizing factor) and fibronectin were strongly positive in the giant cells, but not in striated muscle fibers. A small quantity of myosin was demonstrated in the giant cells, but myoglobin and CPK MM were never demonstrated in these cells. No alpha-1-antichymotrypsin was demonstrated in the giant cells. One case of proliferative myositis showed ultrastructural features suggestive of fibroblast rather than muscle cell or histiocytic origin. Strongly positive factor XIIIa in the giant cells is suggestive of the fact that they are active fibroblasts.

Aged↗
PubMed1992

Idiopathic myositis: a rheumatological view.

Twenty five patients with idiopathic myositis attended this department for long term follow up from 1980 to 1989. Twelve patients had primary polymyositis (four men, eight women) and six had primary dermatomyositis (three men, three women); five women had an overlap syndrome. Two patients had a malignant condition associated with the myositis. The mean age at diagnosis was 40 years. All of the patients had proximal muscle weakness, 18/25 had a raised creatine kinase value (mean 2325 IU/l), 19/20 had an abnormal electromyogram, and 19/24 had positive muscle biopsy samples. Of the disease specific antibodies, anti-Jo-1 was detected in only 1/21 patients tested (three patients with fibrosing alveolitis were negative for this antibody), but the 56 kDa antibody was detected in 12/17 patients. The HLA data analysed in the white patients (17/25) showed that 6/8 of those tested were HLA-DR3 positive. All patients were treated with prednisolone and azathioprine was used for 14/25 patients. Only three deaths occurred during the eight year follow up, but there was a substantial morbidity, which may reflect the referral pattern. Muscle strength tests and creatine kinase levels were useful in recording the response to treatment in some patients. These data emphasise that careful long term follow up of patients with myositis is mandatory and that although the present treatment strategy has substantially reduced the death rate, morbidity associated with the disease remains a major problem.

Adolescent↗
PubMed1993

Inclusion body myositis: an underdiagnosed condition?

Inclusion body myositis is an increasingly recognised form of inflammatory myopathy with characteristic clinical and histopathological features which has seldom been reported in the United Kingdom. This paper presents the clinicopathological features of a series of patients diagnosed in Nottingham from 1986 to 1990. During this period, 1319 muscle biopsy samples were processed by this laboratory and rimmed vacuoles were seen in 17 patients. Eleven patients had definite or probable inclusion body myositis according to published criteria. The mean age of the group was 69.4 years with a male to female ratio of 8:3. Typical clinical features were a slowly progressive painless, proximal lower limb weakness, with muscle wasting and early loss of reflexes. The median duration of illness from first symptom to presentation was five years (range 2-18 years). Falls were a prominent symptom in six patients and distal weakness occurred in nine patients. Creatine kinase was increased in 10 patients but only one had a level > 1000 IU/l; the erythrocyte sedimentation rate was normal in five patients. Treatment with steroids or cytotoxic drugs, or both, did not prevent disease progression. It is confirmed that inclusion body myositis is a distinct cause of inflammatory myopathy which is probably underdiagnosed in the United Kingdom. Clinically, it should be suspected in older patients presenting with muscle weakness of insidious onset. Pathologically, a careful search should be made for rimmed vacuoles and inflammation; ultrastructurally, the presence of inclusions will confirm the diagnosis.

Aged↗
PubMed1990

Contracturing granulomatous myositis: a separate entity.

Granulomatous muscle disease is most commonly seen in sarcoidosis, but may be seen in association with a wide variety of other disorders or in isolation. Patients with granulomatous myositis usually present with slowly progressive muscle pain and weakness affecting mainly proximal muscles. There are, however, a few reports of granulomatous muscle disease presenting with flexion contractures of the limbs. Two further patients with granulomatous muscle disease and flexion contractures of the limbs, but with no evidence of systemic granulomatous disease, is presented. It is suggested that such patients represent a separate clinical entity that is distinct from idiopathic granulomatous myositis presenting with muscle pain and weakness. The association of contracturing granulomatous myositis with a long-standing vasculitis in one patient suggests that the two conditions may be related.

Aged↗
PubMed2000

A case of inclusion body myositis with benign monoclonal gammopathy successfully responding to repeated immunoabsorption.

A 69 year old woman with inclusion body myositis is described. She presented with benign monoclonal gammopathy. She was resistant to steroid therapy, but responded to repeated immunoabsorption. Up to now, there has been no established therapy for inclusion body myositis, including IVIg. It is suggested that immunoabsorption could be an alternative therapy for inclusion body myositis, when it was accompanied by immunological abnormality.

Aged↗
PubMed1991

Differential diagnosis of bacterial myositis in AIDS: evaluation with MR imaging.

Magnetic resonance (MR) imaging was used to assess for the presence of bacterial myositis, rare outside the tropics, in 13 patients with either the acquired immunodeficiency syndrome (AIDS) (n = 11) or positive results of serologic tests for the human immunodeficiency virus but without other evidence of AIDS (n = 2). Bacterial myositis was diagnosed in six patients: in five it was caused by pyogenic bacteria, and in the other, by Mycobacterium tuberculosis; in each patient, little or no subcutaneous tissue alteration occurred. On T1-weighted images in three patients, muscle abscesses showed a rim of increased signal intensity corresponding to margins between drainable pus and edematous muscle. Subcutaneous tissues appeared normal in patients with bacterial myositis but was not in the others, in whom muscle abnormalities tended to be less prominent. The latter group included patients with lymphoma (n = 1), Kaposi sarcoma (n = 2), and carbunculosis (n = 1), and three patients in whom no diagnosis was made; lymphedema was presumed to account for imaging abnormalities in four of the latter group.

Acquired Immunodeficiency Syndrome↗