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)

Non-Hodgkin's lymphoma originating from mucosa-associated lymphoid tissue has been connected with autoimmune disease. These tumours often arise in gastric mucosa and are extremely rare in airway mucosa. Three cases of mucosa-associated lymphoid tissue lymphoma in the cavum have been reported in the literature. A 52-year-old male with rheumatoid arthritis presented with an 8-month history of nasal obstruction and recurrent nasal blood discharge. On physical examination a bulky mass was observed in the nasopharynx. CT demonstrated a soft tissue lesion in the nasopharynx without bone destruction. MRI showed a contrast-enhanced mass with extension to the left pterygoid muscle. Biopsy revealed a low-grade B-cell lymphoid tumour of the marginal zone. The patient received six cycles of cyclophosphamide, vincristine and prednisone with adriamycin treatment, together with intracranial methrotrexate as a prophylactic measure. After 48 months of follow-up there was no evidence of disease and a control MRI scan was normal. The prognosis of this type of tumour is unpredictable and there are too few cases to enable definitive conclusions to be drawn.
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PMID:Extranodal lymphoma originating from mucosa-associated lymphoid tissue of the nasopharynx. 1471 Sep 15

Relapsing polychondritis (RP), which shows pain, swelling and destruction of the affected parts, is a rare autoimmune disorder affecting cartilage. We report a patient with RP that affected skull cartilage, who subsequently developed multifocal meningoencephalitis. The patient presented with severe recent memory disturbance, anxiety and moderate depression. MRI study showed bilateral median temporal lobe lesions including hippocampi and amygdaloidal bodies, abnormal findings that disappeared after treatment with high-dose steroids. This is thought to be the first case of RP presenting amnesic syndrome and mental disorder associated with nonparaneoplastic limbic encephalitis involving bilateral hippocampi and amygdaloidal bodies detected by MRI.
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PMID:Nonparaneoplastic limbic encephalitis with relapsing polychondritis. 1514 Jun 11

Immunosuppressive therapy has been used to treat multiple sclerosis (MS) for over 30 years based on the hypothesis that MS is a T cell-mediated autoimmune disease. The most commonly used immunosuppressive agents in MS are azathioprine, cyclophosphamide, methotrexate, and mitoxantrone. Since the interferons and glatiramer acetate have become widely used in MS, immunosuppressive agents have found a role given as combination therapy or as monotherapy in instances where the interferons and glatiramer acetate are not effective in controlling the disease. Like the interferons and glatiramer acetate, immunosuppressive drugs are most efficacious in stages of MS that have an inflammatory component as evidenced by relapses and/or gadolinium-enhancing lesions on MRI or in patients in earlier stages of disease where inflammation predominates over degenerative processes in the CNS. There is no evidence of efficacy in primary progressive MS or later stages of secondary progressive MS. In our studies of cyclophosphamide, we have found that although it is a general immunosuppressant that affects both T cell and B cell functions, cyclophosphamide has selective immune effects in MS by suppressing IL-12- and Th1-type responses and enhancing Th2/Th3 responses (IL-4, IL-10, TGF-beta; eosinophils in peripheral blood). Cyclophosphamide and mitoxantrone are the most common immunosuppressive drugs used in patients with rapidly worsening MS whose disease is not controlled by beta-interferon or glatiramer acetate.
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PMID:Immunosuppressive treatment in multiple sclerosis. 1526 54

This study was conducted to clarify the clinical and neurophysiologic characteristics of patients with Morvan syndrome, and to compare and contrast this syndrome with other forms of autoimmune encephalitis. A retrospective chart review of the clinical features and neurophysiologic studies of two cases of Morvan syndrome seen at the Mayo Clinic was performed. Neurophysiologic studies included polysomnography, comprehensive autonomic testing, MRI, positron emission tomography, EEG, and single-photon emission computed tomography. In two cases of Morvan syndrome, the clinical features, electrophysiologic findings, and immunologic studies (high levels of voltage-gated potassium channel antibodies) were consistent with previously reported findings. Several novel observations were made. Autonomic testing demonstrated peripheral autonomic neuropathy in addition to autonomic hyperactivity. Polysomnography showed complete absence of sleep. Neuroimaging study findings were largely normal. Morvan syndrome is an autoimmune disorder affecting both the peripheral and central nervous system. Neurophysiologic studies demonstrate hyperexcitability of peripheral nerves, autonomic dysfunction, and severe insomnia. The absence of abnormalities on imaging studies suggests that central nervous system symptoms are related to functional rather than structural disruption of neural networks.
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PMID:Neurophysiologic studies in Morvan syndrome. 1562 31

Autoimmune diseases are characterized by infiltration of the target tissue with specific immune cells that ultimately leads to the destruction of normal tissue and the associated disease. There is a need for imaging tools that allow the monitoring of ongoing inflammatory disease as well as the response to therapy. We discuss new magnetic resonance imaging-based technologies that have been used to monitor inflammation and disease progression in animal models of type 1 diabetes, multiple sclerosis, and rheumatoid arthritis. Therapeutic strategies for these diseases include the transfer of immune cells, such as dendritic cells, with the aim of preventing or halting the disease course. We discuss several new MRI labeling techniques developed to allow tracking of immune cells in vivo. These include direct ex vivo labeling techniques as well as the genetic modification of cells to allow them to produce their own contrast agents. This is an area of intense recent research and can be expanded to other conditions such as cancer.
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PMID:In vivo imaging of autoimmune disease in model systems. 1633 43

There is convincing evidence that neurological relapses in multiple sclerosis (MS) are the clinical counterpart of acute focal inflammation of the central nervous system (CNS) whereas neurological progression is that of chronic diffuse neurodegeneration. The classical view is to consider that MS is an organ-specific autoimmune disease, i.e. that inflammation is the cause of the neurodegeneration. The succession of relapses eventually leads to accumulation of disability and clinical progression results from subclinical relapses. A series of recent observations tends to challenge this classical concept. Important observations have come from the study of the natural history of MS. In the Lyon MS cohort, accumulation of irreversible disability appeared not to be affected by clinically detectable neurological relapses. This has also been shown to be "amnesic" for the early clinical characteristics of the disease, and essentially age-dependent. Suppressing relapses by disease-modifying agents does not dramatically influence the progression of irreversible disability. Interferons beta reduce the relapse rate by 30% and conventional MRI activity by more than 50%. In spite of this effect on inflammation, the effect on disability is only marginal and possibly relapse-reduction-dependent. Administration of Campath-1H to patients with very active disease in terms of frequency of relapses, accumulation of disability and MRI activity, results in a profound, prolonged lymphopenia and the suppression of clinical and MRI activity, but in spite of this, clinical disability and cerebral atrophy still progress. The same experience has been reported with cladribine and autologous haematopoietic stem cell transplantation. All these observations give support to the fact that relapses do not essentially influence irreversible disability in the long term in MS. They are consistent with what has been shown at the individual level in the 1970s by performing serial quantitative neurological examinations over several years, and with what is currently emerging from early and serial structural brain MRI studies. These breakthroughs have immediate implications for the counselling of patients with MS. They suggest that MS is as much neurodegenerative as inflammatory, and should cause the modification of disease-modifying therapeutic strategies by focussing on the protection and repair of the nervous system and not only on the control of inflammation.
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PMID:Accumulation of irreversible disability in multiple sclerosis: from epidemiology to treatment. 1641 61

Multiple sclerosis (MS) is an inflammatory demyelinating autoimmune disease of the central nervous system. The disorder displays marked clinical heterogeneity. In certain cases, making diagnosis can be challenging. Diagnosis of MS has become more important in the era of treatments that change the natural history of the disease. Several general diagnostic principles are useful to guide the diagnostic approach to MS. Clinically, MS requires neurological problems associated with objective abnormalities. Certain basic principles, first outlined by Schumacher et al. (1965) are still pertinent. Poser et al. (1983) have further modified the criteria using data derived from clinical evaluation and laboratory studies, including cerebrospinal fluid analysis, evoked potentials, and imaging studies. Poser criteria have long been familial for most neurologists. The most recent addition to our diagnostic armamentarium are the McDonald criteria (2001), which are the first attempt to incorporate standardized MRI criteria into the MS diagnostic process. The most innovative use of MRI to support an MS diagnosis is dissemination of demyelination can be demonstrated by MRI alone, in the absence of any new clinical attacks. Diagnosing MS by such sensitive MRI criteria will occur more quickly than waiting for a second clinical event. This has added some sensitivity, some controversy, and a lot of confusion. The application of the new criteria on Asian MS patients remains to be validated. Each of the criteria will be discussed, with major emphasis on the McDonald criteria.
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PMID:[Diagnosis of multiple sclerosis]. 1642 50

Recently, limbic encephalitis (LE) associated with Voltage-gated potassium channel antibody (VGKC-Ab) has been postulated as a new autoimmune disorder. Most previously reported cases of VGKC-Ab-associated LE were non-paraneoplastic, and reports of a paraneoplastic type are rare. Here we describe a 59-year-old woman with paraneoplastic VGKC-Ab-associated LE preceding the recurrence of invasive thymoma. There was a close temporal relationship between the clinical course and the changes of the VGKC-Ab titer. Unlike many of the non-paraneoplastic VGKC-Ab-associated LE cases, our cases showed the more extensive high intensity lesions on MRI and the absence of seizure and hyponatremia.
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PMID:Voltage-gated potassium channel antibodies associated limbic encephalitis in a patient with invasive thymoma. 1702 29

We present a 31-year-old female patient with primary non-Hodgkin's lymphoma of the CNS after immunosuppressive therapy. Colitis ulcerosa had been diagnosed 2 years previously. Prophylactic therapy with azathioprine over 9 months was stopped after the development of listeria meningitis which was treated successfully with antibiotics. At this time native CCT was normal. Three months later the patient developed an epileptic seizure and multiple cerebral lesions were detected in CCT and MRI. Although antibiotic therapy was started, the cerebral lesions showed no regression. Stereotactic biopsy revealed immunochemical and histologic high-grade malignant B cell lymphoma. The risk of primary CNS lymphoma under azathioprine treatment for an autoimmune disease with a possible congenital immunodeficiency is presented and the literature is reviewed.
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PMID:[Primary CNS lymphoma in azathioprine therapy for autoimmune diseases: review of the literature and case report]. 1737 74

Atorvastatin and simvastatin (members of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor family) are widely prescribed as cholesterol-lowering agents. As they have been shown to exhibit potent immunomodulatory effects, they may become a future treatment option for autoimmune disease in general and multiple sclerosis (MS) in particular. Several recent reports have demonstrated that statins prevent and reverse chronic and relapsing experimental autoimmune encephalomyelitis, an animal model of MS. An open-label clinical trial assessing simvastatin in MS revealed a significant decrease in the number and volume of new MRI lesions and a favorable safety profile. The results of a large multicenter, placebo-controlled clinical trial assessing atorvastatin in patients with clinically isolated syndrome (a disease that predisposes to development MS) are expected soon. However, prospective placebo-controlled trials of atorvastatin or simvastatin in definite MS are difficult to perform due to ethical and financial objections. In this review, we discuss the backgrounds, mechanisms of action and future perspectives of atorvastatin and simvastatin as putative future treatment options in MS.
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PMID:Evaluation of atorvastatin and simvastatin for treatment of multiple sclerosis. 1749 4


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