1/9. A case of polymyositis associated with hepatitis B infection.This report describes the case of a 47-year old man who developed myositis in association with hepatitis B surface antigen-positive hepatitis. Interestingly, the myositis repeatedly worsened 2 months after the exacerbation of hepatitis in this case, suggesting a close association between hepatitis B infection and myositis. The dose of prednisolone was increased twice in order to treat the exacerbating myositis, resulting in improvement of the muscle symptoms, but the patient eventually died of liver failure. Only 5 other myositis patients with hepatitis B antigenemia have been reported in the literature. We review these cases of the association between hepatitis B infection and myositis.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
2/9. Clonal expansion of limited T cell clonotypes in affected muscle from a patient with post-transplant polymyositis.Critical roles of T cells in idiopathic polymyositis have been suggested, but, those in polymyositis occurring as GVHD after BMT are poorly understood. We thus investigated T cell clonality in a patient with post- transplant polymyositis. As a result, T cell receptor beta chains used various BV families in peripheral blood, but only one BV family (BV7) in affected muscle. Importantly, T cells proliferated oligoclonally both in the peripheral blood and the muscle, however, the expanded clonotypes were completely different. Taken together, T cells expanded in the muscle, possibly stimulated by limited kinds of antigens, may drive myositis.- - - - - - - - - - ranking = 0.5keywords = antigen (Clic here for more details about this article) |
3/9. Acute polymyositis following renal transplantation.Myositis is a rare complication following renal transplantation and is most commonly the result of drug-mediated myotoxicity. Other causative disorders include viral infection, electrolyte imbalance and myositis of autoimmune origin. We describe a 60-year-old patient who developed acute polymyositis 4 weeks after a 000 human leukocyte antigen (HLA) mismatch cadaveric renal transplant. Following an uncomplicated transplant course with maintenance triple immunosuppression (prednisolone, mycophenolate mofetil and cyclosporine), the patient presented with severe symmetrical proximal muscle weakness associated with a rise in serum creatine kinase to 46800 U/L. electromyography confirmed myopathic changes and muscle biopsy demonstrated extensive muscle-fiber necrosis with an inflammatory infiltrate. There were no obviously culpable drugs and viral studies were negative. Prompt initiation of high-dose steroid therapy led to clinical and biochemical recovery. Acute polymyositis may occur following renal transplantation. Potential mechanisms include viral antigen transmission or a localized form of graft vs. host disease.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
4/9. polymyositis: rare complication of hepatitis B vaccination. An unusual cause of toxic shock syndrome.Transient weakness of the legs developed in a 17 year-old male high school student three weeks after the initial injection of a hepatitis B vaccine. Seventeen days after the second injection of the vaccine, low-grade fever, a pruritic maculopapular rash appeared and weakness of the legs recurred. This was associated with elevation of the creatinine kinase to 2,406 U/L. The day after admission he became afebrile and in the subsequent four days the rash improved but leg weakness persisted. One-month later, muscle strength had returned; and the creatinine kinase had returned to normal levels. The only case of dermatomyositis associated with hepatitis B vaccination and the findings in the six reported cases of surface antigen-positive hepatitis associated with polyomyositis or dermatomyositis are briefly reviewed. Hepatitis B vaccination should be encouraged, but it is important to be aware that, rarely, dermatomyositis, polymyositis or neurovascular complications may occur. polymyositis associated with the administration of the hepatitis B vaccine or with hepatitis b virus infection is a rare occurrence. A medline Search performed from 1960 to January 2002 associating hepatitis B vaccine or hepatitis b virus with myopathy, myositis, polymyositis and dermatomyositis, showed only one case of dermatomyositis related to the hepatitis B vaccine, and six case reports relating polymyositis to hepatitis b virus infection. We present a case where a causal relationship between polymyositis and hepatitis B vaccination appears quite likely.- - - - - - - - - - ranking = 0.5keywords = antigen (Clic here for more details about this article) |
5/9. polymyositis associated with Ki-1 lymphoma.We report here a case of acute polymyositis associated with a Ki-1 non-Hodgkin's lymphoma (NHL). This anaplastic large cell malignant lymphoma was a primary T-cell NHL lymphoma of the bone marrow. The malignant cells expressed the CD30 (Ki-1), CD3, and CD4 antigens, the beta chain of the interleukin 2 receptor (CD25), and the betaF1 antigen (alpha/beta T-cell receptor). Chemotherapy and high dose methylprednisolone pulse therapy were initiated. However, no clinical improvement was noticed, because the patient rapidly died of an acute respiratory distress syndrome. To our best knowledge, this represents the first case of Ki-1 lymphoma associated with polymyositis.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
6/9. Temporal alterations of immunohistochemical findings in polymyositis.To investigate the pathological mechanisms of polymyositis, we performed immunohistochemical analyses with biopsied muscles. Comparative studies using specimens obtained from the same patient enabled us to analyze the pathological alterations at different sequential clinical phases without taking into account each immunogenetic difference. Expression of MHC (major histocompatibility complex) antigens, especially ectopic MHC-class-II antigens, in muscle fibers and infiltrating T-cells were shown to increase concomitantly with the clinically observed exacerbation. Moreover, other observations seem to support the possibilities that 1) administration of steroids lowers the number of invading CD8-positive cells, 2) induction of MHC-class-I antigens in muscle fibers precedes the inflammatory cell infiltration and that 3) remaining MHC-class-I antigens in muscle fibers may explain the recurrence of myositis often observed in the follow up period.- - - - - - - - - - ranking = 2keywords = antigen (Clic here for more details about this article) |
7/9. Anterior horn cell degeneration in polymyositis associated with human T lymphotropic virus Type-1 in patients from barbados.Anterior horn cell degeneration has only occasionally been noted in patients with tropical spastic paraparesis associated with human T lymphotropic virus type-1 (HTLV-1) infection. We report on three adult patients with HTLV-1-associated polymyositis who had clinical evidence of anterior horn cell degeneration. One patient had moderate proximal weakness and muscle wasting in all four limbs, while two had mild upper limb weakness with more profound proximal weakness and wasting in the lower limbs. In all three patients, electromyographic findings were compatible with motor unit loss and muscle biopsies showed mononuclear inflammatory cell infiltration; muscle biopsies in two patients showed features of denervation. immunoglobulin g (IgG) antibodies to HTLV-1 were detected by enzyme-linked immunosorbent assay (ELISA) and confirmed by Western immunoblot in serum and cerebrospinal fluid in all three patients. In two, cell cultures were established from peripheral blood lymphocytes and HTLV-1 antigen was identified by immunofluorescence and the ELISA antigen-capture technique using an anti-p19 HTLV-1 mouse monoclonal antibody. The three cases illustrate the variety of neuromuscular disease, other than spastic paraparesis, that may occur in HTLV-1 infection. In some cases of HTLV-1-associated polymyositis, anterior horn cell degeneration may make a significant contribution to the muscle atrophy observed.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
8/9. Localized myofibroblastic proliferation in the neck of a patient with an IgG myeloma.We describe a myofibroblastic proliferation in the neck and lower part of the face involving skin and muscle of a 68-year-old female patient with an IgG kappa myeloma. Biopsies showed a fusocellular proliferation with scarce pseudoganglion cells involving the superficial fascia and the cutaneous muscle of the neck. The proliferative cells showed immunohistochemical and ultrastructural features characteristic of myofibrobasts with a proliferating cell nuclear antigen index of 48%; 42% of the cells displayed HLADR-positive membrane staining. Cellular proliferation subsided following the use of immunosuppressive drugs. Eight months after initial consultation, the patient developed polymyositis without a proliferative component and died of aplastic anemia.- - - - - - - - - - ranking = 0.5keywords = antigen (Clic here for more details about this article) |
9/9. Adhesion molecules in hiv-related and idiopathic polymyositis: immunohistochemical studies.Idiopathic polymyositis (IPM) and hiv polymyositis (hiv-PM) are considered to be related autoimmune diseases whose target is skeletal muscle. They have been associated to a T cell-mediated and MHC-I-restricted cytotoxic phenomenon, but both etiology and physiopathology remain incompletely understood. Their histological hallmarks are mononuclear leukocyte infiltrates as well as necrosis, degeneration, and regeneration of muscle fibers. In the present study, we have investigated the immunohistochemical expression of cell adhesion molecules, cytokines, and leukocyte surface antigens in biopsies of hiv-PM and IPM patients. The aim was to better define factors involved in lymphocyte recruitment and in inflammatory changes seen in PM. Notable upregulation of ICAM-1 and TNF-alpha was detected on capillary and venular endothelia and on inflammatory cells, whereas no significant VCAM-1 and ELAM-1 expression was present. LFA-1, the main ICAM-1 counter-receptor, was found to be highly expressed on lymphocytes and monocytes, especially at the vicinity of damaged fibers. The majority of infiltrating cells were CD8 CD45 RO-T cells, which are thought to have memory capacities. These findings suggest that in IPM and hiv-PM, enhanced ICAM-1 and LFA-1 expression possibly induced by TNF-alpha, may regulate the homing process of selected lymphocyte clones in muscle tissue. Lymphocyte proliferation and differentiation into memory subsets may further potentiate tissue-restricted homing capabilities.- - - - - - - - - - ranking = 0.5keywords = antigen (Clic here for more details about this article) |