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Query: UMLS:C0002736 (amyotrophic lateral sclerosis)
 19,048 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amyotrophic lateral sclerosis (ALS) is a fatal, progressive disease of the central nervous system. Its possible association with poliomyelitis was studied by measuring neutralizing antibodies against polio virus types 1, 2 and 3 in the sera and cerebrospinal fluids of 11 ALS-patients, but antibody titers did not markedly differ from those of the controls. The HLA antigens of 12 ALS patients were also determined, in order to reveal any possible genetically-determined susceptibility to the disease. Possible association of ALS with HLA-Bw40 was noted. In addition, the Bw40 antigen seemed to be associated with milder progression of the disease. The lymphocytes of the ALS patients seemed defective in their capacity to stimulate allogenic lymphocytes, possibly due to a relative decrease of B cells in the peripheral blood. Joint efforts of study groups of neuroepidemiology, immunology and genetics should be mobilized to reveal the true nature of these findings.
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PMID:Polio antibodies and HLA antigens in amyotrophic lateral sclerosis. 7 26

Cell-mediated immunity to poliovirus was demonstrated in 21 of 33 patients suffering from amyotrophic lateral sclerosis (ALS), whereas no response to poliovirus was found in patients suffering from other neurologic disorders or in healthy controls. Three of the severe bulbar cases produced a migration inhibition factor (MIF) in the presence of poliovirus, although skin tests to common antigens were negative. An increased incidence (46 percent) of HLA-A3 was found in patients with amytrophic lateral sclerosis. Nine of the 13 patients with HLA-A3 antigen also had a positive index of MIF to poliovirus. These findings suggest a strong linkage between HLA-A3 and poliovirus in the pathogenesis of amyotrophic lateral sclerosis.
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PMID:Cell-mediated immunity to polio and HLA antigens in amyotrophic lateral sclerosis. 22 41

52 patients with amyotrophic lateral sclerosis and 300 normal subjects were tested for 33 HLA-A, B, C antigens. We did not observe any statistically significant difference in antigenic frequencies between the two groups. The absence of association with HLA in amyotrophic lateral sclerosis is a distinction with multiple sclerosis, which is associated with several HLA antigens.
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PMID:[HLA and amyotrophic lateral sclerosis (author's transl)]. 22 16

To test the hypothesis that host resistance factors may be abnormal in Guamanians in whom amyotrophic lateral sclerosis and Parkinsonism-dementia develop, cellular immunity was evaluated in both diseases and compared to that of Guamanians with other nervous-system diseases, normal adult Guamanians and non-Guamanians with amyotrophic lateral sclerosis and Parkinsonism. Diminished responses to skin-test antigens, lymphopenia, diminished per cent and total T cells and, less frequently, decreased mitogen responses were seen in Guamanian patients with amytorophic lateral sclerosis and Parkinsonism-dementia but not in the other patient or normal groups. Guamanian patients with amyotrophic lateral sclerosis and diminished cellular immunity had an increased frequency of HLA-Bw35 (P less than 0.005) and shorter mean duration of disease (P less than 0.05) than those with normal cellular immunity. In Parkinsonism dementia diminished cellular immunity was less strongly associated with HLA-BW35 (P less than 0.05) and was not associated with differences in duration of disease. Normal Guamanians and those with other nervous-system diseases showed no association of diminished cellular immunity with HLA-Bw35. The association appeared disease-related, with onset concomitant with the neurologic expression of Guamanian amyotrophic lateral sclerosis and Parkinsonism-dementia.
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PMID:Cellular immunity in Guamanians with amyotrophic lateral sclerosis and Parkinsonism-dementia. 30 83

Twenty-five patients with a definite diagnosis of amyotrophic lateral sclerosis (ALS) were HLA-typed for the serologically detectable antigens A, B and C and MLC-typed for 7 HLA-D-determinants. No significant deviation was found neither in the A, B, and C-series nor in the HLA-D-series as compared to normal controls. The aetiological problem of ALS is discussed.
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PMID:HLA (SD and LD) in patients with amyotrophic lateral sclerosis (ALS). 84 14

Immunological capability is to a substantial extent genetically determined. Because genetic linkage exists between histocompatibility gene loci and certain immune response gene loci, histocompatibility specificities can serve as indicators for the presence of particular inherited immunological traits. In man, certain HLA antigens seem to be associated with immunogenetic traits which result in altered susceptibility to disease with known or suspected viral or autoimmune etiologies. We have found an association between HLA-A3 and "classic" cases of ALS. The A3 antigen was present in 49% of these cases, but not in the more chronic or benign form of the disease. Five out of six "benign" cases carried HLA-B12, suggesting perhaps the presence of a trait conferring resistance to the disease. Epidemiological surveys provide evidence both for and against a correlation between the incidence of ALS and that of HLA-A3 in various population groups. Because of the multiplicity of immune response genes, susceptibility or resistance to ALS in different populations may depend on different immune response genes. The association of a disease with selected HLA antigens or phenotypes might be suggestive of a viral-allergic etiology. Evidence that bears on this hypothesis has been reviewed.
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PMID:Immunogenetics and amyotrophic lateral sclerosis. 102 69

Muscle biopsy specimens from 15 autopsied patients with the isolated form of amyotrophic lateral sclerosis were examined by routine histological and immunocytochemical methods using a panel of monoclonal antibodies directed against differentiation and activation markers of immunocompetent cells. In 12 cases, cellular infiltrates consisting mainly of T-cells and macrophages were seen. Both CD8+ and CD3+ cells, in juxtaposition with OKM1+ macrophages, were particularly seen in the atrophied parts of muscle. The majority of the T-cells appeared to be of the CD4+ T-helper/inducer type, whereas the CD8+ T-suppressor/cytotoxic cells were only rarely and focally present. On the other hand, B-, NK- and K-cells were infrequently seen. Most of the T-cells and macrophages surrounding the atrophied muscle fibers were in an activated state, as indicated by their intense HLA DR expression. In addition, some angulated degenerated fibers showed strong endomysial positivity for HLA DR in the regions where T-cells and macrophages were present in clusters. The immunoreactive changes in ALS-associated muscle atrophy are very similar to those reported for exercise-induced damage and some forms of myositis. The present study shows that the expression of major histocompatibility complex products and the relative numbers of infiltrating immunocompetent cells are closely associated with the extent of destruction of muscle fibers in ALS.
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PMID:Immunohistological alterations in muscle of patients with amyotrophic lateral sclerosis: mononuclear cell phenotypes and expression of MHC products. 161 23

Since the introduction of CsA in 1983, several changes in SEOPF activity have been observed: 1. Organ recovery has increased at a rate slower than candidate registration, whereas the utilization rate has increased substantially. 2. Overall organ sharing has decreased for both CsA and non-CsA-treated patients. 3. The percentage of poor HLA-A,B matched recipients has increased for both CsA- and non-CsA-treated patients. 4. The use of cold storage preservation has increased for both CsA- and non-CsA-treated patients. 5. The use of ALS has decreased, predominantly in CsA-treated patients. 6. A majority of diabetics are being treated with CsA. 7. There is substantial individual variation in SEOPF center preferences for CsA use, HLA matching, and use of shared kidneys. In terms of graft outcome, the following associations have been observed: 1. The incidence of delayed graft function has increased with shared kidneys only, suggesting sharing of poorer quality as well as fewer kidneys. 2. First transplant recipients receiving CsA tend to have lower delayed graft function rates, possibly as a result of treatment selection. However, the risk of graft failure associated with delayed function is greater in patients receiving CsA. 3. By univariate analysis, there is an additive benefit of HLA-A,B matching and CsA use in patients receiving local kidneys with immediate function. 4. By multivariate analysis, there is a significant relative risk of graft rejection associated with poor HLA-A,B matching in patients receiving CsA. 5. By multivariate analysis, there is an apparent risk of graft loss associated with shared organs, but only in patients receiving CsA. One possible explanation is that poorer quality kidneys are being accepted for patients treated with CsA. 6. By multivariate subset analysis, there is a significant benefit of CsA use in patients whose HLA is poorly matched, but no observed benefit in well-matched patients. 7. Definitive evaluation of the relative effects of CsA and HLA matching on cadaver renal allograft survival must await long-term follow-up data on survival and function, and the ability to control for center bias in sharing, HLA matching, and CsA use.
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PMID:HLA matching for cadaver renal transplantation in SEOPF: the impact of cyclosporine. Southeastern Organ Procurement Foundation. 315 72

1. HLA matching is associated significantly with factors including CsA use, ALS use, recipient race, prior graft loss, presensitization, preservation time and most strongly, with organ sharing. However, HLA match is not directly associated with delayed graft function. 2. By univariate and multivariate analyses, good HLA matching provides significant benefits in graft survival regardless of CsA use, organ source or other potentially confounding factors. 3. HLA-A,B, and DR matching have independent and essentially equivalent benefits on graft survival in CsA-treated patients, whereas HLA-A,B matching has a greater benefit in non-CsA-treated patients. 4. Organ sharing, per se, provides no direct detrimental effect on graft survival by univariate or multivariate analysis. 5. By multivariate and univariate analyses, shared/well-matched kidneys provide significantly better graft survival than local/poorly matched kidneys. 6. Delayed graft function is associated in a complex relationship with organ sharing, prior graft failure, presensitization, and CsA use. 7. The increased rate of delayed graft function associated with organ sharing is overcome by the benefit of good HLA matching. 8. Since April 1986, purposeful organ sharing at SEOPF centers for good HLA matching has been associated with improved graft survival, especially in patients at high risk due to presensitization or prior graft failure.
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PMID:Organ sharing for good HLA-A,B, and DR matching improves cadaver renal graft survival in SEOPF: retrospective and prospective studies considering delayed graft function, race, center effects, cyclosporine, and other factors. 315 74

Histocompatibility antigen (HLA A, B and DR) serotyping was performed on 65 patients with motor neuron disease in the northern region of England and compared to a large control population from the Newcastle upon Tyne area. Thirty two patients had amyotrophic lateral sclerosis, 17 had progressive bulbar palsy and 16 had progressive muscular atrophy. Ten patients had a more slowly progressive course. No significant HLA associations were observed in the motor neuron disease patients. Subdivision of the patients by the clinical course of their disease did not reveal any significant associations. Forty six motor neuron disease patients from the Newcastle upon Tyne area had a reduced frequency of HLA DR4 compared to the local control population. The relevance of histocompatibility antigens to the pathogenesis of motor neuron disease is discussed.
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PMID:A study of histocompatibility antigens in patients with motor neuron disease in the northern region of England. 345 97


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