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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/cdn\/css\/http\/css_Xg7z6oCTVgud_Q0huYz9x9iiD5H_2YPSJ5z2ZViSWdY.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EFor a classification of systemic lupus erythematosus (SLE), patients must have at least one clinical and one immunologic criterion of the SLICC classification criteria, for a total of four, or must have biopsy-proven lupus nephritis. This article discusses prednisone for the treatment of SLE, the treatment of severe thrombocytopenia in SLE, severe cutaneous manifestations in patients with SLE, as well as subtypes of posterior reversible leukoencephalopathy syndrome, myelitis, and small-fiber neuropathies in SLE.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003ELupus\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ESystemic Connective Tissue Disorders\u003C\/li\u003E\u003C\/ul\u003E\u003Cul class=\u0022kwd-group clinical-trial\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003ERheumatology\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ELupus\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ESystemic Connective Tissue Disorders\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EFor a classification of systemic lupus erythematosus (SLE), patients must have at least one clinical and one immunologic criterion of the SLICC classification criteria, for a total of four, or must have biopsy-proven lupus nephritis. Clinical criteria include acute cutaneous lupus, chronic cutaneous lupus, oral ulcers, nonscarring alopecia, arthritis, serositus, neurologic lupus, proteinuria, and dytopenias [Petri M et al. \u003Cem\u003EArthritis Rheum\u003C\/em\u003E 2012]. Immunologic criteria include ANA, antids DNA, anti-Sm, antiphospholipid antibodies, low complement, and direct Coombs.\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003EMichelle Petri, MD, MPH, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, pointed out that prednisone is independently associated not just with non-life-threatening organ damage (cataracts, osteoporosis), but with cardiovascular events. [Madger LS, Petri M. \u003Cem\u003EAm J Epidem\u003C\/em\u003E 2012; Thamer M et al. \u003Cem\u003EJ Rheumatol\u003C\/em\u003E 2009]. She emphasized that even low doses of prednisone \u0026gt;6 mg daily increase permanent organ damage. Most mild to moderate flares will respond to intramuscular triamcinolone or to a methylprednisolone \u201cdose pack,\u201d helping to avoid maintenance prednisone [Danowski A et al. \u003Cem\u003EJ Rheumatol\u003C\/em\u003E 2006]. Dr. Petri recommends administering hydroxychloroquine to all patients; it reduces flares [Canadian Hydroxychloroquine Study Group. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 1991] and thrombosis [Petri M. \u003Cem\u003EScand J Rheumatol\u003C\/em\u003E 1996; Pierangeli SS, Harris EN. \u003Cem\u003ELupus\u003C\/em\u003E 1996] by half, reduces organ damage [Fessler BJ et al. \u003Cem\u003EArthritis Rheum\u003C\/em\u003E 2005] and lipids [Petri M. \u003Cem\u003ELupus\u003C\/em\u003E 1996; Wallace DJ et al. \u003Cem\u003EAm J Med\u003C\/em\u003E 1990], improves survival [Alarcon GS et al. \u003Cem\u003EArthritis Rheum\u003C\/em\u003E 2005; Ruiz-Irastorza G et al. \u003Cem\u003ELupus\u003C\/em\u003E 2005], prevents seizures [Hanly JG et al. \u003Cem\u003EAnn Rheum Dis\u003C\/em\u003E 2012], and triples the response to mycophenolate [Kasitanon N et al. \u003Cem\u003ELupus\u003C\/em\u003E 2006] in severe lupus nephritis. Vitamin D is also a safe immunomodulator for patients with SLE [Petri M. \u003Cem\u003EArthritis Rheum\u003C\/em\u003E 2013].\u003C\/p\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ETREATMENT OF THROMBOCYTOPENIA\u003C\/h2\u003E\n         \u003Cp id=\u0022p-4\u0022\u003EBrady L. Stein, MD, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA, discussed the treatment of severe thrombocytopenia in SLE. He agreed with Dr. Petri that long-term steroids have unacceptable adverse effects. Immune thrombocytopenia may result from impaired platelet production and\/or increased platelet destruction mediated by autoantibodies, with subsequent splenic clearance. The differential diagnosis for thrombocytopenia in SLE is broad and a suggested diagnostic workup is summarized in \u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigure 1\u003C\/a\u003E.\u003C\/p\u003E\n         \u003Cdiv id=\u0022F1\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/13\/18\/22\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Thrombocytopenia in SLE: Differential Diagnosis and Workup\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-1416379879\u0022 data-figure-caption=\u0022Thrombocytopenia in SLE: Differential Diagnosis and Workup\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/13\/18\/22\/F1.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/13\/18\/22\/F1.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/13\/18\/22\/F1.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/13839\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption attrib\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-5\u0022 class=\u0022first-child\u0022\u003EThrombocytopenia in SLE: Differential Diagnosis and Workup\u003C\/p\u003E\n            \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-1\u0022\u003EAb=antibody; DAT=direct antiglobulin testing; DIC=disseminated intravascular coagulation;\u003C\/q\u003E\u003Cq class=\u0022attrib\u0022 id=\u0022attrib-2\u0022\u003ELDH=lactate dehydrogenase; MDS=myelodysplastic syndrome; MMF=mycophenolate mofetil;\u003C\/q\u003E\u003Cq class=\u0022attrib\u0022 id=\u0022attrib-3\u0022\u003EMPV=mean platelet volume; MTX=methotrexate; NSAIDs=nonsteroidal anti-inflammatory drugs; PT=prothrombin time; PTT=partial thromboplastin time; retic=reticulocyte count;\u003C\/q\u003E\u003Cq class=\u0022attrib\u0022 id=\u0022attrib-4\u0022\u003ESLE=systemic lupus erythematosus; TTP=thrombotic thrombocytopenic purpura.\u003C\/q\u003E\u003Cq class=\u0022attrib\u0022 id=\u0022attrib-5\u0022\u003EReproduced with permission from M Petri, MD, MPH.\u003C\/q\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-6\u0022\u003EPatient factors affect the selection of therapy for thrombocytopenia. Younger patients may be better able to tolerate splenectomy. Comorbidities, cost, and SLE activity should also be considered. The typical threshold for therapy is a platelet count \u0026lt;20 to 30 \u00d7 10\u003Csup\u003E9\u003C\/sup\u003E\/L. For patients with antiphospholipid antibody syndrome who require anticoagulation, the threshold should be 50 \u00d7 10\u003Csup\u003E9\u003C\/sup\u003E\/L.\u003C\/p\u003E\n         \u003Cp id=\u0022p-7\u0022\u003ESplenectomy is an \u201cold\u201d treatment that yields high responses, although it has been analyzed in small numbers of patients with SLE [You YN. \u003Cem\u003EAnn Surgery\u003C\/em\u003E 2004]. Another option is rituximab to suppress antibody production by B cells. Rituximab has been effective in primary idiopathic thrombocytopenic purpura (ITP), but this is an off-label use, may not be durable, and may be associated with adverse reactions in SLE patients [Gudbtrandsdottir S et al. \u003Cem\u003EBlood\u003C\/em\u003E 2013; Jovancevic C et al. \u003Cem\u003ELupus\u003C\/em\u003E 2013; Neunert C et al. \u003Cem\u003EBlood\u003C\/em\u003E 2011; Zaja F et al. \u003Cem\u003EBlood\u003C\/em\u003E 2010; Godeau B et al. \u003Cem\u003EBlood\u003C\/em\u003E 2008]. Other options are thrombopoietin agonists, like romiplostim [Kuter DJ et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2010; \u003Cem\u003ELancet\u003C\/em\u003E 2008] and eltrombopag [Cheng G et al. \u003Cem\u003ELancet\u003C\/em\u003E 2011; Bussel JB et al. \u003Cem\u003ELancet\u003C\/em\u003E 2009], although results in SLE are anecdotal. These agents require long-term therapy and have potential side effects including thrombosis, a concern in SLE [Kuter DJ et al. \u003Cem\u003EBr J Haematol\u003C\/em\u003E 2013; Saleh MN et al. \u003Cem\u003EBlood\u003C\/em\u003E 2013].\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ETREATMENT OF NEUROLOGIC COMPLICATIONS\u003C\/h2\u003E\n         \u003Cp id=\u0022p-8\u0022\u003EJulius Birnbaum, MD, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, described subtypes of posterior reversible leukoencephalopathy syndrome (PRES), myelitis, and small-fiber neuropathies in SLE. PRES is associated with visual disturbances, encephalopathies, seizures, and headaches. Risk factors for PRES are similar in patients with or without SLE, and include hypertension, renal failure, immunosuppressant use, and thrombotic thrombocytopenic purpura (TTP). SLE is associated with many concomitant risk factors for PRES.\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003ESmall-fiber neuropathies are very painful, affect unmyelinated C-fiber nerve, and, although common, are underdiagnosed in SLE. Nerve conduction studies are normal, and small-fiber deficits appear on physical examination. A punch skin biopsy showing a decreased density of small-fiber nerves in the epidermal layer is diagnostic. There are two patterns of small-fiber neuropathies in SLE: length-dependent, affecting distal-most axons, and non-length-dependent, affecting proximal dorsal root ganglia.\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EThere are two types of myelitis in SLE: gray-matter myelitis and white-matter myelitis. The distinguishing characteristics are summarized in \u003Ca id=\u0022xref-table-wrap-1-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T1\u0022\u003ETable 1\u003C\/a\u003E.\u003C\/p\u003E\n         \u003Cdiv id=\u0022T1\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/13840\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/13840\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/13840\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-11\u0022 class=\u0022first-child\u0022\u003ESummary of Distinguishing Differences Between Gray-Matter and White-Matter Myelitis\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-13\u0022\u003EGray-matter myelitis is caused by catastrophic venous hypertension in which blood flow to the spinal cord is impaired and necrosis occurs. Dr. Birnbaum pointed out that 9 of 11 patients they identified had sought medical attention for the inability to void, and were ambulatory at the time. Many were sent home with a catheter. He emphasized that unexplained inability to void in patients with highly active SLE should be taken as a sign of impending spinal cord herniation; patients should be treated immediately with pulsed intravenous steroids to avoid irreversible paraplegia.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-3\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EMANAGING DERMATOLOGIC MANIFESTATIONS OF SLE\u003C\/h2\u003E\n         \u003Cp id=\u0022p-14\u0022\u003EM. Kari Connolly, MD, University of California, San Francisco, California, USA, described severe cutaneous manifestations in patients with SLE, pointing out that the presentations of skin complications may be atypical or suggest other diagnoses. The differential diagnosis should include infection, drug rash, erythema multiforme, small-vessel vasculitis, bullous LE, and acute flare of SLE. Skin biopsy cannot differentiate SLE subtypes, but can differentiate SLE from other diagnoses, distinguish inflammation from scarring, and detect the presence of microthrombi or leukocytic vasculitis.\u003C\/p\u003E\n         \u003Cp id=\u0022p-15\u0022\u003EWhen SLE is refractory to standard therapies like antimalarials, thalidomide may be effective [Cuadrado MJ et al. \u003Cem\u003EAm J Med\u003C\/em\u003E 2005]. It requires enrollment in a safety program due to its teratogenicity; it can also cause neuropathy [Bastuji-Garin S et al. \u003Cem\u003EJ Invest Dermatol\u003C\/em\u003E 2002]. Maintenance therapy is usually needed. Lenalidomide, a newer thalidomide analogue, is also effective; neutropenia is a significant toxicity and necessitates regular blood counts [Cort\u00e9s-Hernandez J et al. \u003Cem\u003EArthritis Res Ther\u003C\/em\u003E 2012]. Topical steroids, tacrolimus, pimicolimus, and retinoids, may also be effective.\u003C\/p\u003E\n         \u003Cp id=\u0022p-16\u0022\u003EBullous LE is rare, nonscarring, and involves neutrophils rather than leukocytes. The immunomodulator dapsone is effective, but may require combination therapy with prednisone, mycophenolate, azathioprine, or rituximab [Hall RP et al. \u003Cem\u003EAnn Intern Med\u003C\/em\u003E 1982; Ludgate MW Greig DE. \u003Cem\u003EAustralas J Dermatol\u003C\/em\u003E 2008]. Dapsone causes hemolytic anemia in 20% of patients and requires testing for glucose-6-dehydrogenase. LE panniculitis is also rare, and is associated with characteristic saucer-shaped deformities. The differential diagnosis includes subcutaneous T cell lymphoma. The associated deformities do not respond well to cosmetic surgery, lasers, or fillers, or to kenalog injections. Other SLE therapies may be effective.\u003C\/p\u003E\n         \u003Cp id=\u0022p-17\u0022\u003EDr. Connolly said that dermatologists can help other clinicians by determining what is scar tissue and what is active disease (eg, when areas of hair loss are no longer treatable). Dermatologists are good at performing biopsies and experienced in the use of agents with which rheumatologists may be less familiar.\u003C\/p\u003E\n         \u003Cp id=\u0022p-18\u0022\u003ESome complications of SLE can be managed, including thrombocytopenia. Gray-matter myelitis that may present as an inability to void should be treated immediately to prevent permanent paraplegia. Other complications of SLE, such as atherosclerosis, a major cause of death, does not respond to statin therapy, so other therapies are needed, as they are for other symptoms that are important to patients, including fatigue and cognitive impairment.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2013 MD Conference Express\u00ae\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/13\/18\/22.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_figures.js?nzo6ip\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzo6ip\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_tables.js?nzo6ip\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}