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      A Case of Systemic Lupus Erythematosus Presenting as Guillain-Barré Syndrome

      case-report

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          Abstract

          Systemic lupus erythematosus (SLE) is an autoimmune systemic disease with multiple organ involvement with high morbidity and mortality rate. Among the severe potential fatal complications are those of the central and peripheral nervous system which usually develop during the course of the disease and very rarely from the outset of the disease. We are reporting a rare case of Miller-Fisher (MFS) variant of Guillain-Barré syndrome (GBS) as the first manifestation of SLE in a 41-year-old female who progressed to flaccid paralysis with no neurological improvement with initial immunosuppressive therapy, plasmapheresis, and first cycle of intravenous immunoglobulin (IVIG) but with remarkable and complete recovery after the second 5-day course of IVIG.

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          The American College of Rheumatology nomenclature and case definitions for neuropsychiatric lupus syndromes.

          David Isenberg (1999)
          To develop a standardized nomenclature system for the neuropsychiatric syndromes of systemic lupus erythematosus (NPSLE). An international, multidisciplinary committee representing rheumatology, neurology, psychiatry, neuropsychology, and hematology developed case definitions, reporting standards, and diagnostic testing recommendations. Before and after the meeting, clinician committee members assigned diagnoses to sets of vignettes randomly generated from a pool of 108 NPSLE patients. To assess whether the nomenclature system improved diagnostic agreement, a consensus index was developed and pre- and postmeeting scores were compared by t-tests. Case definitions including diagnostic criteria, important exclusions, and methods of ascertainment were developed for 19 NPSLE syndromes. Recommendations for standard reporting requirements, minimum laboratory evaluation, and imaging techniques were formulated. A short neuropsychological test battery for the diagnosis of cognitive deficits was proposed. In the postmeeting exercise, a statistically significant improvement in diagnostic agreement was observed. The American College of Rheumatology (ACR) Nomenclature for NPSLE provides case definitions for 19 neuropsychiatric syndromes seen in SLE, with reporting standards and recommendations for laboratory and imaging tests. It is intended to facilitate and enhance clinical research, particularly multicenter studies, and reporting. In clinical settings, consultation with other specialists may be required. It should be useful for didactic purposes but should not be used uncritically or as a substitute for a clinical diagnosis. The complete case definitions are available on the ACR World Wide Web site: http://www.rheumatology .org/ar/ar.html.
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            Guillain-Barré syndrome: epidemiology, pathophysiology and management.

            Satoshi Kuwabara (2003)
            Guillain-Barré syndrome (GBS) is clinically defined as an acute peripheral neuropathy causing limb weakness that progresses over a time period of days or, at the most, up to 4 weeks. GBS occurs throughout the world with a median annual incidence of 1.3 cases per population of 100 000, with men being more frequently affected than women. GBS is considered to be an autoimmune disease triggered by a preceding bacterial or viral infection. Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus and Mycoplasma pneumoniae are commonly identified antecedent pathogens. In the acute motor axonal neuropathy (AMAN) form of GBS, the infecting organisms probably share homologous epitopes to a component of the peripheral nerves (molecular mimicry) and, therefore, the immune responses cross-react with the nerves causing axonal degeneration; the target molecules in AMAN are likely to be gangliosides GM1, GM1b, GD1a and GalNAc-GD1a expressed on the motor axolemma. In the acute inflammatory demyelinating polyneuropathy (AIDP) form, immune system reactions against target epitopes in Schwann cells or myelin result in demyelination; however, the exact target molecules in the case of AIDP have not yet been identified. AIDP is by far the most common form of GBS in Europe and North America, whereas AMAN occurs more frequently in east Asia (China and Japan). The prognosis of GBS is generally favourable, but it is a serious disease with a mortality of approximately 10% and approximately 20% of patients are left with severe disability. Treatment of GBS is subdivided into: (i) the management of severely paralysed patients with intensive care and ventilatory support; and (ii) specific immunomodulating treatments that shorten the progressive course of GBS, presumably by limiting nerve damage. High-dose intravenous immunoglobulin (IVIg) therapy and plasma exchange aid more rapid resolution of the disease. The predominant mechanisms by which IVIg therapy exerts its action appear to be a combined effect of complement inactivation, neutralisation of idiotypic antibodies, cytokine inhibition and saturation of Fc receptors on macrophages. Corticosteroids alone do not alter the outcome of GBS.
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              Treatment related fluctuations in Guillain-Barré syndrome after high-dose immunoglobulins or plasma-exchange.

              R Kleyweg, Andor F. van den Hoven (1991)
              Since the introduction of plasma exchange as a treatment for Guillain-Barré syndrome (GBS) patients, treatment related fluctuations have been found to occur in about 10% of the patients. These fluctuations are considered additional evidence of the beneficial effect of plasma exchange. In this report the occurrence of such treatment related fluctuations is described in the 147 patients who took part in the Dutch Guillain-Barré trial comparing high dose intravenous immunoglobulin with plasma exchange. Six of 72 patients in the plasma exchange group and eight of 74 in the immunoglobulin group showed such fluctuation. These results support the biological effect of immunoglobulin. More general use of immunoglobulin should await the full analysis of the Dutch GBS trial which is in progress.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Case Rep Rheumatol
                Journal ID (iso-abbrev): Case Rep Rheumatol
                Journal ID (publisher-id): CRIRH
                Title: Case Reports in Rheumatology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-6889
                ISSN (Electronic): 2090-6897
                Publication date (Print): 2015
                Publication date (Electronic): 17 August 2015
                Volume: 2015
                Electronic Location Identifier: 528026
                Affiliations
                Icahn School of Medicine at Mount Sinai, Queens Hospital Center, Jamaica, NY 11432, USA
                Author notes
                *Helen Chioma Okoh: helenokohc@ 123456gmail.com

                Academic Editor: Suleyman Serdar Koca

                Article
                DOI: 10.1155/2015/528026
                PMC ID: 4553270
                PubMed ID: 26366317
                SO-VID: 78999812-f79c-408f-b862-0a2d82883df6
                Copyright © Copyright © 2015 Helen Chioma Okoh et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 17 June 2015
                Date accepted : 30 July 2015
                Categories
                Subject: Case Report

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