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001 | 978-3-319-76496-2 | ||
003 | DE-He213 | ||
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007 | cr nn 008mamaa | ||
008 | 180403s2018 gw | s |||| 0|eng d | ||
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_a9783319764962 _9978-3-319-76496-2 |
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_aPSAN _2bicssc |
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_aNeuropsychiatric Systemic Lupus Erythematosus _h[electronic resource] : _bPathogenesis, Clinical Aspects and Treatment / _cedited by Shunsei Hirohata. |
250 | _a1st ed. 2018. | ||
264 | 1 |
_aCham : _bSpringer International Publishing : _bImprint: Springer, _c2018. |
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300 |
_aVIII, 189 p. 24 illus., 12 illus. in color. _bonline resource. |
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336 |
_atext _btxt _2rdacontent |
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337 |
_acomputer _bc _2rdamedia |
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338 |
_aonline resource _bcr _2rdacarrier |
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347 |
_atext file _bPDF _2rda |
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500 | _aAcceso multiusuario | ||
505 | 0 | _a1 Epidemiology -- 2 Genetics -- 3 Immunology and pathogenesis -- 4 Pathology -- 5 Clinical Features -- 6 Cytokine -- 7 Diagnosis and Differential diagnosis -- 8 Imaging of NPSLE -- 9 Psychiatric symptoms -- 10 Treatment -- 11 Promising treatment alternatives -- 12 Prognosis. | |
520 | _aNeuropsychiatric manifestation in systemic lupus erythematosus (NPSLE) is one of the most recalcitrant complications of the disease. According to the 1999 ACR nomenclature and case definitions, diffuse psychiatric/neuropsychological syndromes in NPSLE (anxiety disorder, acute confusional state, cognitive dysfunction, mood disorder, psychosis) (diffuse NPSLE) present psychiatric manifestations unlike neurologic syndromes (focal NPSLE) originating from focal CNS lesions, such as cerebrovascular disease, demyelinating syndrome, headache, aseptic meningitis, chorea, seizures and myelopathy. A number of studies have reported that diffuse NPSLE is usually associated with the presence of autoantibodies against neuronal cells in serum as well as in cerebrospinal fluid (CSF). Moreover, IL-6 has been shown to be elevated in CSF of patients with diffuse NPSLE. Recently, it has been demonstrated that the severity of blood-brain barrier damages plays a crucial role in the development of acute confusional state, the severest form of diffuse NPSLE through the accelerated entry of larger amounts of autoantibodies to NMDA receptor subunit NR2 into the CNS. Since the importance of autoantibodies in the NPSLE has been now evident, such an aggressive treatment, especially B cell depleting therapy, would make sense in that it would reduce the levels of pathogenic autoantibodies, leading to a better prognosis of NPSLE. As far as we know, no single book specifically dedicated to NPSLE alone has been published as yet. As mentioned above, NPSLE constitutes a vastly expanding field of research with increasing numbers of papers published annually. Therefore, we believe that an effort to collect and critically review these publications is invaluable. Such an effort will provide an important contribution to basic researchers as well as clinicians working in the field of neurology, rheumatology, psychiatry and internal medicine fields. | ||
541 |
_fUABC ; _cTemporal ; _d01/01/2021-12/31/2023. |
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650 | 0 | _aNeurosciences. | |
650 | 0 | _aImmunology. | |
650 | 1 | 4 |
_aNeurosciences. _0https://scigraph.springernature.com/ontologies/product-market-codes/B18006 |
650 | 2 | 4 |
_aImmunology. _0https://scigraph.springernature.com/ontologies/product-market-codes/B14000 |
700 | 1 |
_aHirohata, Shunsei. _eeditor. _4edt _4http://id.loc.gov/vocabulary/relators/edt |
|
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_iPrinted edition: _z9783319764955 |
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_iPrinted edition: _z9783319764979 |
776 | 0 | 8 |
_iPrinted edition: _z9783030095031 |
856 | 4 | 0 |
_zLibro electrónico _uhttp://148.231.10.114:2048/login?url=https://doi.org/10.1007/978-3-319-76496-2 |
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