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At least 811 records · Page 45Linked to original sources

PubMed2001

Presence of BACE1 and BACE2 in muscle fibres of patients with sporadic inclusion-body myositis.

Sporadic inclusion-body myositis (IBM) is the most common, progressive muscle disease of older individuals. We investigated the presence of BACE1 and BACE2-two beta secretases that cleave amyloid-beta-precursor protein-in muscle-biopsy samples from patients with IBM and from controls. On immunofluorescence, BACE1 and BACE2 co-localised with amyloid beta in IBM vacuolated muscle fibres, but were not found in controls. Immunoblotting showed increased BACE2 but not BACE1 in patients with IBM compared with controls. Our study suggests that both of these proteases might participate in processing of amyloid-beta-precursor protein in IBM muscle fibres.

Amyloid Precursor Protein Secretases↗

PubMed1984

Trochleitis with superior oblique myositis.

Thirteen patients complained of recent fluctuating aching of one orbit, punctuated by stabbing pains. All had exquisite point tenderness over the trochlea and in half of the patients the pain was aggravated by eye movement. Standardized A-scan echography demonstrated swelling of the peritrochlear tissue and thickening of the superior oblique muscle with low internal acoustic reflectivity, typical of myositis. CT scan showed a soft tissue density in the region of the trochlea. Biopsy, performed on two patients, revealed peri-trochlear inflammation. In all patients the symptoms resolved within a period of weeks or months: indomethacin or naproxen were not effective, but oral or locally injected corticosteroids shortened the course compared to no treatment. None of the patients had ptosis, proptosis, Brown's syndrome, or a click, nor did they have echographic or radiographic signs of sinusitis or inflammation away from the trochlea. This probably represents a highly localized subtype of idiopathic orbital inflammation ("pseudotumor").

Adult↗

PubMed2002

Evidence for heterogeneity of T cell expansion in polymyositis and inclusion body myositis.

Vbeta usage of muscle-infiltrating T lymphocytes in polymyositis (PM) and sporadic inclusion body myositis (s-IBM) was correlated with clinical and histopathological features. Immunohistochemical analysis was combined with complementarity-determining region 3 (CDR3) length analysis in nine muscle biopsies of eight PM patients and six biopsies of five s-IBM patients. Vbeta usage was heterogeneous in seven patients. Four of these patients had definite PM with endomysial located T cell infiltrates, but T cells specifically surrounding and invading individual non-necrotic fibers were not found. In two s-IBM patients, Vbeta 2 usage was increased. In one of them, a repeat biopsy showed a heterogeneous Vbeta usage. We conclude that clonal expansion of muscle-infiltrating T cells could only be detected in part of the patients. Explanations may be that clonal expansion does not take place in all disease phases and that PM is a heterogeneous disease with respect to pathogenesis.

Adult↗

PubMed2003

Expression of IFN-gamma-inducible chemokines in inclusion body myositis.

Because IFN-gamma-inducible chemokines, Mig (CXCL9), IP-10 (CXCL10), I-TAC (CXCL11) and their receptor, CXCR3, are critical molecules in T cell trafficking and generation of effector T cells, we examined their expression in the muscle biopsies of patients with sporadic inclusion body myositis (s-IBM) and disease controls. The functional role of these molecules was also studied by examining the effect and time kinetics of IFN-gamma in inducing Mig and IP-10 expression in human myotubes in vitro. We found significantly high levels of Mig and IP-10 mRNA expression in s-IBM muscles compared to controls. IFN-gamma upregulated the mRNA expression of Mig and IP-10 by human myotubes in a dose-dependent manner. By double-label immunohistochemistry, Mig was expressed on a subset of CD8(+) cells and the areas of the muscle fiber in contact or contiguous to the T cells; CXCR3 was expressed only on a subset of the autoinvasive CD8(+) T cells but not the myofibers. IP-10 and I-TAC were not detected by immunocytochemistry. The findings indicate that in s-IBM, IFN-gamma is involved in the upregulation and in situ production of proinflammatory chemokines, which, in turn, participate in the recruitment of activated T cells and contribute to the self-sustaining nature of endomysial inflammation.

Chemokine CXCL10↗

PubMed1997

Oligoclonal expansion of muscle infiltrating T cells in inclusion body myositis.

Inclusion body myositis (IBM) is the most common muscle disease affecting individuals over 50 years of age. An important feature of IBM is invasion of muscle fibers by T cells. The muscle infiltrating T cells show a restricted usage of variable (V) alpha/beta gene families. In this study we have investigated the clonality of T cells using two of the predominant V beta families i.e. V beta 3 and V beta 8 in three patients with IBM. The study was performed by reverse transcription and polymerase chain reaction (RT-PCR) analysis, followed by cloning and sequencing of the T cell receptor complementarity determining region 3. We found oligoclonal expansion of V beta 3 bearing muscle infiltrating T cells in two patients and of V beta 8 in one patient, supporting the concept that antigen stimulated T cells are important in the pathogenesis of IBM. Results of HLA typing indicated a genetic predisposition for the disease by the presence of DR3, DR52 and DQB1*0201/0202 in all three patients.

Aged↗

PubMed1998

HLA allele distribution distinguishes sporadic inclusion body myositis from hereditary inclusion body myopathies.

We studied the HLA class II associations in patients with sporadic inclusion body myositis (s-IBM) and hereditary inclusion body myopathies (h-IBM) and attempted to distinguish these myopathies on the basis of HLA allele assignments. Forty-five patients, 30 with s-IBM and 15 with h-IBM, underwent HLA class II allele-specific typing using polymerase chain reaction sequence-specific primers for 71 alleles contained in the DRbeta1, DRbeta3-5, and DQbeta1 loci. In s-IBM, we found a high (up to 77%) frequency of DRbeta1*0301, DRbeta3*0101 (or DRbeta3*0202) and DQbeta1*0201 alleles. No significant association with alleles in the DR and DQ haplotypes was found among the 15 h-IBM patients. The strong association of prominent alleles with s-IBM, but not h-IBM, suggests that s-IBM is a distinct disorder with an immunogenetic background that differs from h-IBM.

Aged↗

PubMed1998

T-cell heterogeneity in muscle lesions of inclusion body myositis.

In the muscle lesions of inclusion body myositis (IBM), two populations of T cells can morphologically be distinguished, T cells that invade muscle fibers and T cells that remain in interstitial areas. Using combined immunohistochemistry and RT-PCR, we analysed the TCR expressed by these distinct T cell populations. In three of eight IBM muscle specimens, the autoinvasive T cells were stained with one of the available mAbs: anti-Vbeta5.3 in patient 1, anti-Vbeta5.2 in patient 2, and anti-Vbeta3 in patient 3. The corresponding TCR Vbeta mRNAs were amplified by RT-PCR and the PCR products were cloned and sequenced. In all three specimens, the TCRs expressed by the autoinvasive T cells were clonally restricted. Furthermore, in patient 1 two different mAbs labelled two distinct populations of T cells: an autoaggressive population of CD8 + Vbeta5.3 + cells that invaded muscle fibers and a noninvasive interstitial population of CD8 - Vbeta5.1 + cells. TCR sequence analysis revealed that the noninvasive Vbeta5.1 + T cells were clonally diverse, whereas the autoinvasive Vbeta5.3 + T cells were clonally restricted.

Antibodies, Monoclonal↗

PubMed1998

T cell receptor beta-chain repertoire in inclusion body myositis.

Inclusion body myositis (IBM) is the most common muscle disease affecting individuals over 50 years of age. The inflammatory reaction is characterized by cell infiltrates predominated by CD8+ cytotoxic T cells. To analyze clonality of muscle infiltrating lymphocytes, we studied the complementarity determining region 3 (CDR3) length distribution of the T cell receptor (TCR). Muscle infiltrating lymphocytes were studied in three IBM patients and compared with peripheral blood lymphocytes (PBL) in two of these patients. The study was performed by reverse transcription polymerase chain reaction (RT-PCR) of RNA extracted from muscle tissue and PBL followed by analysis of fragment length distribution of the CDR3 region in each of 24 different Vbeta families. There was a restricted usage of TCR Vbeta gene families in muscle infiltrating T cells in all three patients. Some of the TCR Vbeta gene families showed oligoclonal expansions but polyclonal patterns were dominating. The CDR3 distribution of most Vbeta families differed between muscle infiltrating lymphocytes and PBL indicating that T cells have expanded locally or selectively accumulated in muscle.

Aged↗

PubMed1996

Orbital myositis, vitiligo, and giant cell myocarditis.

Giant cell myocarditis is a rare idiopathic inflammatory heart disease characterized histologically by multinucleated giant cells, and clinically by rapid progressive heart failure, arrhythmias, or sudden death, often within hours to days of initial symptoms. There are two previously reported cases of giant cell myocarditis with idiopathic orbital myositis. We report a similar case in a patient who also had vitiligo, a diagnostic endomyocardial biopsy, and survival because of a cardiac transplant. Giant cell myocarditis should be monitored for in the course of inflammatory orbital myopathy because of its life-threatening fulminant course.

Adult↗

PubMed1985

Myositis ossificans in an adolescent following sports injury.

Myositis ossificans, an abnormal formation of new bone in an injured muscle, can occur in young athletes involved in contact sports. Recognition and appropriate therapy can reduce associated disability. This report illustrates the condition and reviews the clinical manifestations and available therapeutic modalities.

Adolescent↗

PubMed1999

First report of tropical myositis and crescentic glomerulonephritis in a renal transplant recipient.

We describe a renal transplant recipient who presented with tropical myositis and acute allograft dysfunction 2(1/2) years after transplantation. Graft biopsy showed immune-complex crescentic glomerulonephritis. He was receiving only 7.5 mg/d of prednisolone for more than 2 months before presentation. Renal function did not improve despite treatment with antibiotics, methylprednisolone pulse therapy, and cyclophosphamide. He died of septicemia.

Adult↗

PubMed1987

Ulcerative colitis and interstitial myositis.

Amongst the protean extra-intestinal manifestations of inflammatory bowel disease, scant mention is made of muscle involvement. This report outlines the clinical features, electrodiagnostic and muscle biopsy findings in a patient with ulcerative colitis who developed progressive proximal muscle weakness. The demonstration of interstitial myositis is discussed in relation to his underlying disease.

Adult↗

PubMed2000

Redox factor-1 in muscle biopsies of patients with inclusion-body myositis.

To determine whether redox factor-1 (Ref-1) participates in the pathogenesis of inclusion-body myositis (IBM), we immunolocalized Ref-1 in muscle biopsies of IBM patients by light- and electron-microscopy. Approximately 70-80% of the IBM vacuolated muscle fibers had focal inclusions strongly immunoreactive for Ref-1. By immunoelectronmicroscopy, Ref-1 was localized to paired-helical filaments, 6-10 nm amyloid-like fibrils and amorphous material. Virtually all regenerating and necrotic muscle fibers in various muscle biopsies had diffusely strong Ref-1 immunoreactivity. At all neuromuscular junctions, postsynaptically there was strong Ref-1 immunoreactivity. Our study suggests that Ref-1 plays a role in IBM pathogenesis, and in other pathologic and normal processes of human muscle.

Biopsy↗

PubMed2000

Cyclin-dependent kinase 5 colocalizes with phosphorylated tau in human inclusion-body myositis paired-helical filaments and may play a role in tau phosphorylation.

To investigate the possible role of cyclin-dependent kinase 5 (cdk5) in the formation of paired helical filaments (PHFs) in muscle of patients with inclusion-body myositis (IBM), we immunolocalized cdk5, by light- and electron- microscopy, in muscle biopsies of six IBM patients. Approximately 80-90% of IBM vacuolated muscle fibers, and 10-15% of nonvacuolated fibers, contained well defined cdk5-immunoreactive inclusions that colocalized with phosphorylated tau in 70-80% of those fibers. Immunoelectronmicroscopy revealed the association of cdk5 with tau-immunoreactive PHFs. In all biopsies that contained them, regenerating muscle fibers had diffuse, moderate to strong cdk5 immunoreactivity. At all neuromuscular junctions, there was strong cdk5 immunoreactivity postsynaptically. Our study suggests that cdk5: (1) plays a role in IBM pathogenesis, possibly mediating phosphorylation of PHF-related tau; (2) is involved in muscle regeneration; and (3) has a novel function at normal neuromuscular junctions.

Cyclin-Dependent Kinase 5↗

PubMed1998

Immunolocalization of transcription factor NF-kappaB in inclusion-body myositis muscle and at normal human neuromuscular junctions.

To investigate whether nuclear factor kappaB (NF-kappaB) is involved in the pathogenesis of inclusion-body myositis (IBM), we immunostained muscle biopsies of eight patients with IBM with specific antibodies against its p50 and p65 subunits. Approximately 70% of IBM vacuolated muscle fibers had strong focal accumulations of both NF-kappaB p50 and p65, which by immunoelectronmicroscopy, localized mainly to clusters of paired-helical filaments (PHFs). Virtually all necrotic fibers, in various muscle biopsies, had diffusely strong p50 immunoreactivity, whereas p65 immunoreactivity was present only in a small subset of necrotic fibers. At all neuromuscular junctions, postsynaptically there was strong p65 but no p50 immunoreactivity. Our data suggest that NF-kappaB plays a role in IBM pathogenesis. Different distributions of NF-kappaB subunits in necrotic fibers and at normal neuromuscular junctions (NMJs) suggests different roles of each subunit in human muscle pathology and physiology.

Humans↗

PubMed1987

Classification of myositis. Correlations between morphological and clinical classifications of inflammatory muscle disease.

Insufficient clinical data given to pathologists often hamper the differentiation of inflammatory muscle diseases. Thus we proved the value of a classification based only upon morphological criteria. Among 160 biopsies with myositic pattern (4.9% of a series of 3264 muscle biopsies) we could distinguish the following groups: Interstitial inflammation with only few fibre necroses (17.6%), predominance of fibre necroses with few inflammatory infiltrates (38.1%), small vessel vasculitis (20.0%), arteritis (13.1%), granulomatous myositis (8.8%) and polymorphonuclear leukocytic infiltrates (2.6%). This classification is compared with the used clinical diagnoses. Some special morphological aspects (histometric and immunocytologic examinations, tissue calcification, inclusion bodies, neurogenic atrophies) are analysed and so are some clinical peculiarities (e.g. malignoma-association, differentiation of mixed connective tissue syndrome, drug-induced reactions). The diagnostic value of purely morphologic criteria is restricted. For better diagnostic work a great number of clinical informations is required. Nevertheless, certain morphological patterns give important directions, e.g. to occult malignoma.

Adult↗

PubMed1982

Peripartum pseudomalignant myositis ossificans of the finger.

Two cases of pseudomalignant peripartum myositis ossificans of the finger are reported. The benign diagnosis is confirmed by the histologically characteristic zone phenomenon, consisting of a transition from an inner zone of proliferating spindle cells to a middle zone of well-oriented osteoid and finally to an outer zone of mature bone. In Case No. 1, because of the question of malignancy, a ray amputation was performed. In Case No. 2, the patient was observed during the peripartum period to show diminution in the size of the tumor. The lesion was eventually treated by local excision.

Adult↗

PubMed1987

Pseudomalignant myositis ossificans occurring in the hand.

This is a case report of a patient with pseudomalignant myositis ossificans of the hand. This entity is usually related to trauma, but there was no history of injury in this patient. Radiographic follow-up, histologic zone phenomena and computerized tomography are helpful in obtaining the correct diagnosis.

Adult↗