Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004364 (autoimmune disease)
 24,845 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of relapsing type of neuromyelitis optica following influenza-like illness treated successfully with steroids and corticotrophin has been described. Raised gamma-globulin in CSF was suggestive of an autoimmune disorder. Inspite of six relapses in 8 years she has minimal neurological deficit.
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PMID:Neuromyelitis optica (relapsing type). 18 Mar 5

Two cases of Vogt-Koyanagi-Harada disease with rare neurological complications were reported, which are one case with vestibular and cerebellar ataxia, and one with multiple cranial nerve palsies. The first case, a 32-year-old man, was admitted to our ophthalmologic department because of visual impairment. Two weeks later, he complained of gait disturbance. Limb and truncal ataxia, vestibular dysfunction and perceptive deafness were observed. Ophthalmologic examination revealed typical findings of Vogt-Koyanagi-Harada disease. CSF showed elevated protein and mononuclear pleocytosis. After treatment with oral steroid therapy, vestibular and cerebellar ataxia, and visual impairment improved. The second case, a 22-years-old man, showed the VIIth, VIIIth, IXth, and Xth cranial nerve palsies with visual impairment, and he was diagnosed to have cranial nerve palsies associated with Vogt-Koyanagi-Harada disease. After steroid therapy, there was a marked clinical improvement. Vogt-Koyanagi-Harada disease is an autoimmune disease against the melanocytes and involving tissues containing melanocytes such as uvea, meningea, skin and inner ear, etc.. Neurological complications except for meningitis and perceptive deafness have been rarely reported in Japan. Related to the present cases, possible pathogenesis was discussed.
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PMID:[Each one case of Vogt-Koyanagi-Harada disease with vestibular and cerebellar ataxia, and multiple cranial nerve palsies]. 266 96

A case of chronic polyneuropathy associated with ulcerative colitis was reported. The patient was 57-year-old man who developed sensory disturbances and muscle weakness in four extremities along with the digestive symptoms of ulcerative colitis. Neurological examination revealed that sensory impairment in all modalities, muscular atrophy and weakness in the distal portions of all extremities and decreased or absent muscle stretch reflexes. Laboratory data included sedimentation rate 119mm/hour, CRP 4+, increased IgG and IgM. Lumbar puncture revealed normal CSF pressures, increased protein and IgG content with almost normal cell count. Nerve conduction velocity was delayed dominantly in sensory nerves. Sural nerve biopsy demonstrated degeneration of myelin sheath and decreased number of large fibers. Teased nerve study showed shortened internodal distances with myelin ovoids. These data together with the clinical course of this patient suggested that this peripheral neuropathy might be resulted from the common pathogenesis for ulcerative colitis which is considered as autoimmune disease.
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PMID:Chronic polyneuropathy and ulcerative colitis. 272 50

Guillain-Barre syndrome is known as one of the autoimmune disease, but the etiology, pathophysiology relating immune reaction, as well as the treatment are not established. It still causes physical handicap although its rate is low. The causes, clinical symptoms and outcome of 132 cases of Guillain-Barre syndrome have been analyzed. The patients' ages ranged from 4 months to 15 years. The antecedent events for 56.1% of the patients were known. These were upper respiratory tract infection, unexplained fever, vomiting, diarrhea, vaccination, measles, german measles, shigellosis, mumps, hepatitis, pertussis and surgery in order of frequency. The CSF protein level reached a maximum at 12.3 +/- 9.5 days. Steroids did not influence the outcome of this disease. More studies are necessary to conquer the disease.
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PMID:Guillain-Barre syndrome in Korean children. 274 76

Lymphoid adenohypophysitis is an autoimmune disorder. Eighteen percent of the multipartums are reported to have autoantibodies to pituitary tissues. The symptoms in lymphoid adenohypophysitis, such as hypopituitarism and sellar tumors, exhibit spontaneous remission. The pituitary is a feasible target organ in other autoimmune diseases of the endocrine system. Of these patients, 19/287 showed a positive immune reaction with pituitary tissue antigens. Our three female patients with sellar and suprasellar mass were clinically diagnosed as having lymphoid adenohypophysitis, because of the spontaneous regression of tumors, or presence of immunologically and endocrinologically abnormal findings. The first case was a 31-year-old woman who had amenorrhea and galactorrhea syndrome for two years after delivery of her second child. CT scan revealed a supraseller enhanced mass lesion. She had concomitant signs of recurrent meningeal irritations. The number of cells in the CSF increased, though the protein concentration increased only slightly. During a one-year close observation, the suprasellar mass spontaneously regressed. The second patient was a 66-year-old woman. In 1945, she underwent hysterectomy and oophorectomy for appendicitis followed by adnexitis. She was admitted because of episodes of headache, vomiting and visual field defect in 1983. CT scan also showed a contrast enhanced mass in the suprasellar region. She had two episodes of high fever. After the treatment with antibiotics and anti-inflammatory agents for 4 months, the tumor disappeared. The third case was a 20-year-old female. She had neither neurological nor endocrinological abnormality, except for attacks of vertigo, nausea and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lymphoid adenohypophysitis, with special reference to 2 cases with sellar tumors spontaneously disappearing on the CT]. 377 4

We describe eosinophilic meningitis associated with ibuprofen therapy in a young woman who had no evidence of underlying illness. Discontinuation of ibuprofen was followed by prompt resolution of symptoms and disappearance of eosinophils from the CSF. Ibuprofen has been implicated previously in only five cases of aseptic meningitis--all in patients with an underlying autoimmune disease. No drug has been implicated previously as a cause of eosinophilic meningitis to our knowledge.
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PMID:Eosinophilic meningitis and ibuprofen therapy. 653 31

A patient with Felty's syndrome and rheumatoid arthritis was treated with recombinant granulocyte stimulating factor rhG-CSF (Neupogen) in view of severe neutropenia. He had a prompt rise in his neutrophil count and associated with this a severe flare of his arthritis and a skin rash. rhG-CSF was stopped, his neutrophil count fell rapidly and his symptoms resolved. rhG-CSF and the resulting rise in neutrophil count may be associated with flare of autoimmune disease in susceptible individuals.
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PMID:Felty's syndrome treated with rhG-CSF associated with flare of arthritis and skin rash. 754 May 27

Multiple sclerosis (MS), a putative autoimmune disease of unknown etiology, is characterized by CNS perivascular inflammation, foci of demyelination, and elevated intrathecal production of oligoclonal IgG's. T and B cells, macrophages, and microglia are all implicated in contributing to the initiation and perpetuation of the disease. In this brief review we discuss the possible role of T cells, B cells, macrophages, and microglia in contributing to the initiation and perpetuation of inflammation and demyelination in MS. Data from the rodent model of MS, experimental allergic encephalomyelitis (EAE) supporting a immunological basis for the pathology of MS is noted. This paper discusses recent data suggesting an interaction of the above-mentioned cells, as well as serum and CSF proteins including complement and anti-myelin/oligodendrocyte antibodies, in the pathogenesis of MS and EAE. Additionally, this review describes each cell type including the clinical and experimental evidence for their contribution to the immunologically mediated pathology of MS. Following the description of the role of individual cells, there is consideration of: the possible interaction of cells with the blood brain barrier (BBB) under normal and pathologic inflammatory conditions; the traffic of cells into the CNS in inflammation; and the role of antigen presentation within the CNS in the initiation, and perpetuation, of the CNS immune response. Finally, the review suggests a role for T cells in the initiation, amplification, and possibly the termination of CNS inflammatory events with particular attention paid to the pattern of T cell activation and T cell cytokine production.
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PMID:Immunology of multiple sclerosis. 774 93

To examine the complex role of cytokines in the pathogenesis of actively induced murine EAE we measured the levels of a number of cytokines (IL-6, IFN gamma and TNF) in the spinal cord and CSF of mice with active experimental autoimmune encephalomyelitis (EAE) and found them all to be elevated. We next treated mice with antibodies to these three cytokines, which were over expressed in the CNS, to determine if they would alter disease and found the following: anti-IL-6 had no significant effect on disease, anti-IFN gamma exacerbated disease, and anti-TNF either enhanced, had no effect or inhibited EAE depending on the antibody used. We then treated mice with exogenous cytokines, delivered using a recombinant vaccinia virus system, and found that the IL-6 and TNF virus constructs inhibited EAE whereas the IFN gamma construct had no effect on disease. Other cytokine recombinant viruses were also tested and it was found that the IL-1 beta, IL-2 and IL-10 viruses inhibited EAE while an IL-4 virus either had no effect or enhanced disease. We do not know the mechanism of action of the various cytokines in this system, but irrespective of the mechanism(s), this work clearly demonstrates that delivery of select cytokines using recombinant virus-cytokine constructs can provide a powerful means of down-regulating experimental organ-specific autoimmune disease.
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PMID:Cytokines and murine autoimmune encephalomyelitis: inhibition or enhancement of disease with antibodies to select cytokines, or by delivery of exogenous cytokines using a recombinant vaccinia virus system. 782 86

FN18-CRM9 is an anti-rhesus anti-CD3 immunotoxin that can transiently deplete T cells to 1% of initial values in both the blood and lymph node compartments and can induce long-term tolerance to mismatched renal allografts. We have investigated the ability of this immunotoxin to interdict the course of an experimental rhesus T-cell-driven autoimmune disease, experimental allergic encephalomyelitis (EAE) induced by myelin basic protein. Monkeys showing CSF pleocytosis were then treated with FN18-CRM9 alone or in combination with cranial irradiation (325 or 650 cGy). EAE in nontreated control monkeys progressed rapidly. Paralysis occurred 4-6 days after CSF pleocytosis. Paralysis was either delayed or never occurred in treated monkeys, and histopathology revealed few inflammatory plaques that were notable for their low or absent T cell content. While T cells repopulate in the periphery posttreatment, they do not return to the CNS in large numbers, suggesting that the newly repopulated T cells have lost their previously acquired CNS homing capability. Anti-CD3 immunotoxin may be useful in treating clinical T-cell-driven autoimmune diseases such as rheumatoid arthritis and multiple sclerosis.
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PMID:Depletion of T lymphocytes with immunotoxin retards the progress of experimental allergic encephalomyelitis in rhesus monkeys. 914 93


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