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its clinical manifestations&#44; definition&#44; pathogenesis&#44; diagnosis and management of this entity&#46; It is essential for dermatologists to know the different aspects of Sweet&#39;s syndrome as well as its proper diagnosis&#44; prevention and treatment&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Definition</span><p id="par0015" class="elsevierStylePara elsevierViewall">Clinically&#44; Sweet&#39;s syndrome presents in patients&#44; all of which show characteristic neutrophilic infiltrate in the upper dermis&#46;<a class="elsevierStyleCrossRef" href="#bib0515"><span class="elsevierStyleSup">3</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Sweet&#39;s syndrome can present as one of three clinical types&#58; classical &#40;or idiopathic&#41; Sweet&#39;s syndrome&#44; malignancy-associated Sweet&#39;s syndrome&#44; or drug-induced Sweet&#39;s syndrome&#46; Specific diagnostic criteria were proposed by Su and Liu<a class="elsevierStyleCrossRef" href="#bib0520"><span class="elsevierStyleSup">4</span></a> and subsequently revised and modified by von den Driesch&#46;<a class="elsevierStyleCrossRef" href="#bib0525"><span class="elsevierStyleSup">5</span></a> Laboratory abnormalities may be found and are included in the diagnostic criteria&#44; such as increased erythrocyte sedimentation rate &#40;ESR&#41;&#44; elevated C-reactive protein and leukocytosis &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Etiology</span><p id="par0025" class="elsevierStylePara elsevierViewall">Sweet&#39;s syndrome is an inflammatory skin disorder characterized by the extensive infiltration of neutrophils into the epidermis and dermis&#46; For a dermatologist&#44; understanding the pathophysiology of Sweet&#39;s syndrome is crucial for treatment&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">The underlining biological pathways responsible for this cutaneous neutrophilic dermatosis have remained elusive&#46; However&#44; the association of this disease with infection&#44; autoimmune diseases&#44; neoplasms and drugs suggests an unusual hypersensitivity that may be mediated by cytokines&#44; followed by infiltration of neutrophils that are probably activated by interleukin &#40;IL&#41;-1&#46; Circulating autoantibodies&#44; cytokines&#44; dermal dendrocytes&#44; HLA serotypes&#44; immune complexes and leukotactic mechanisms have been suggested as factors that contribute to the pathogenesis of this syndrome&#46; The presence of IL-1&#44; IL-2 and IFN-&#947; but not IL-4&#44; suggests that type 1T helper cells may play a role in the pathogenesis of idiopathic varieties of this syndrome&#46;<a class="elsevierStyleCrossRefs" href="#bib0530"><span class="elsevierStyleSup">6&#44;7</span></a> Inflammatory cell markers&#44; including CD3&#44; CD163&#44; myeloperoxidase&#44; metalloproteinases and vascular endothelial growth factors&#44; display significantly higher values in the lesioned skin of patients with Sweet&#39;s syndrome compared to non-Sweet&#39;s syndrome individuals or patients with other neutrophilic dermatoses&#46;<a class="elsevierStyleCrossRef" href="#bib0540"><span class="elsevierStyleSup">8</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">It has also been postulated that photosensitivity may play a role in the pathogenesis of Sweet&#39;s syndrome&#44; although the pathomechanism is unknown&#44; as Sweet&#39;s syndrome has been experimentally induced by phototesting&#46;<a class="elsevierStyleCrossRef" href="#bib0545"><span class="elsevierStyleSup">9</span></a> One theory suggests that an isomorphic Koebner reaction is at work&#59; another proposed mechanism associates ultraviolet B radiation with neutrophil activation and epidermal production of tumor necrosis factor-alpha and interleukin-8&#46;<a class="elsevierStyleCrossRef" href="#bib0550"><span class="elsevierStyleSup">10</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">In malignancy-associated Sweet&#39;s syndrome&#44; the most accepted theory of mechanism of pathogenesis is the overproduction and inappropriate regulation of inflammatory cytokines&#44; such as IL-1&#44; IL-3&#44; IL-6&#44; IL-8&#44; granulocyte colony stimulating factor &#40;G-CSF&#41; and granulocyte macrophage colony stimulating factor &#40;GM-CSF&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">11</span></a> This theory is supported by cases in which Sweet&#39;s syndrome patients received G-CSF&#47;GM-CSF&#44; interferon-&#947; and all-trans retinoic acid &#40;ATRA&#41; and subsequently developed Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">11</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Although there is no consistent evidence of a genetic predisposition for Sweet&#39;s syndrome&#44; a higher frequency of HLA-Bw54 was reported in Japanese patients with Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0530"><span class="elsevierStyleSup">6</span></a> However&#44; analysis of the HLA antigens in a Caucasian population showed no association between this syndrome and specific HLA-ABC antigens&#46;<a class="elsevierStyleCrossRef" href="#bib0560"><span class="elsevierStyleSup">12</span></a> Recent evidence based on animal models suggest that an alteration in the gene encoding protein tyrosine phosphatase non-receptor type 6 &#40;Ptpn6&#41; could be involved in the pathogenesis of Sweet&#39;s syndrome&#44;<a class="elsevierStyleCrossRef" href="#bib0565"><span class="elsevierStyleSup">13</span></a> as it encodes non-receptor protein tyrosine phosphatase Src homology region 2 &#40;SH2&#41; domain-containing phosphatase-1 &#40;SHP-1&#41;&#46; The malfunction of Ptpn6 results in unremitting footpad swelling&#44; suppurative inflammation&#44; and neutrophilia&#46; More studies are required to better understand the etiology of this disease&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Clinical manifestations</span><p id="par0050" class="elsevierStylePara elsevierViewall">Classical Sweet&#39;s syndrome has a worldwide distribution&#44; usually presenting in middle age women with a 4&#58;1 female to male ratio&#44; no racial disparity&#44; and recurrence in one-third of patients&#46;<a class="elsevierStyleCrossRef" href="#bib0515"><span class="elsevierStyleSup">3</span></a> It presents as an acute febrile neutrophilic dermatosis characterized by a constellation of clinical symptoms&#44; physical features&#44; and pathological findings that include fever&#44; neutrophilia&#44; asymmetrically distributed painful tender erythematous skin lesions&#44; consisting of papules&#44; nodules and plaques&#44; usually affecting face&#44; neck and upper extremities &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; Histology reveals a characteristic diffuse infiltrate predominantly consisting of mature neutrophils typically located in the upper dermis&#44; which tend to promptly improve after the initiation of treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> Atypical lesions&#44; characterized by erythematous plaques&#44; vesicles and bullous lesions&#44; have also been described&#46;<a class="elsevierStyleCrossRef" href="#bib0570"><span class="elsevierStyleSup">14</span></a> Typically&#44; classical or idiopathic Sweet&#39;s syndrome may be associated with infection&#44; usually of the upper respiratory &#40;streptococci&#41; or gastrointestinal tract &#40;salmonellosis and yersiniosis&#41;&#44; and inflammatory bowel disease&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> It can also occur during pregnancy&#44;<a class="elsevierStyleCrossRef" href="#bib0575"><span class="elsevierStyleSup">15</span></a> possibly related to the vascular&#44; cellular&#44; microbiological&#44; and immunological changes linked to increased estrogen and progestogen levels during pregnancy&#46;<a class="elsevierStyleCrossRef" href="#bib0580"><span class="elsevierStyleSup">16</span></a> The symptoms and clinical manifestations typically respond promptly to systemic corticosteroid therapy and recurrence occurs in one-third of patients&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a></p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0055" class="elsevierStylePara elsevierViewall">Malignancy-associated Sweet&#39;s syndrome was first described by Cohen et al&#46; <a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">17</span></a>&#46; In this subtype&#44; the clinical manifestations can precede&#44; follow&#44; or appear concurrent with the diagnosis of neoplasm in patients&#46; Indeed&#44; the dermatosis can be the cutaneous portent of either an undiagnosed visceral malignancy in a previously cancer-free individual or an unsuspected cancer recurrence in an oncology patient&#46;<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">11</span></a> Approximately 21&#37; of Sweet&#39;s syndrome patients have an associated malignancy&#59; 85&#37; of these are linked to hematological disorders&#44; most frequently to acute myelogenous leukemia &#40;AML&#41;&#46; Malignancy-associated Sweet&#39;s syndrome has also been described in patients with Hodgkin disease<a class="elsevierStyleCrossRef" href="#bib0590"><span class="elsevierStyleSup">18</span></a> and polycythemia vera<a class="elsevierStyleCrossRef" href="#bib0595"><span class="elsevierStyleSup">19</span></a> and in 15&#37; of patients with solid tumors&#44; principally adenocarcinomas of the breast&#44; genitourinary tract and gastrointestinal tract&#46;<a class="elsevierStyleCrossRef" href="#bib0600"><span class="elsevierStyleSup">20</span></a> Extracutaneous manifestations are present in 50&#37; of patients affected with malignancy-associated Sweet&#39;s syndrome<a class="elsevierStyleCrossRef" href="#bib0605"><span class="elsevierStyleSup">21</span></a> and are more frequently caused by a hematological malignancy than a solid tumor&#46; Therefore&#44; it is important to maintain rigorous a follow-up in these types of patients&#44; possibly contributing to the early detection and treatment of the underlining malignancy&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">The syndrome may occur as a paraneoplastic accompaniment&#44; appearing as a first sign of malignancy or its recurrence&#44; usually meaning a poor prognosis&#44;<a class="elsevierStyleCrossRef" href="#bib0610"><span class="elsevierStyleSup">22</span></a> as it has been reported in cases of myelodysplastic syndrome &#40;MDS&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0615"><span class="elsevierStyleSup">23</span></a> This last variant of Sweet&#39;s syndrome represents lot of controversies in the literature&#44; as it has been associated with autoimmune disorders and abnormalities in chemokines which leads to a pro-inflammatory state&#44;<a class="elsevierStyleCrossRef" href="#bib0620"><span class="elsevierStyleSup">24</span></a> leading these patients to an increased instance of autoimmune skin disease including vitiligo&#44; alopecia areata&#44; eczema&#44; vasculitis and pyoderma gangrenosum&#46;<a class="elsevierStyleCrossRef" href="#bib0625"><span class="elsevierStyleSup">25</span></a> It has also been suggested to consider <span class="elsevierStyleItalic">MEFV</span> gene analysis&#44; the gene that is responsible for familial Mediterranean fever&#44; in patients with MDS who have marked neutrophilia and antibiotic-resistant high fever or in those with Sweet&#39;s syndrome&#44;<a class="elsevierStyleCrossRef" href="#bib0630"><span class="elsevierStyleSup">26</span></a> although further evidence is required&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">Finally&#44; in drug-induced Sweet&#39;s syndrome&#44; there is nearly always a temporal relationship between medication administration and symptom development&#46; In 1996&#44; Walker and Cohen described the diagnostic criteria &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41; for drug-induced Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0635"><span class="elsevierStyleSup">27</span></a> The most commonly reported drug causing Sweet&#39;s syndrome is granulocyte-colony stimulating factor&#46; Several anticancer agents&#44; including all-trans-retinoic acid proteosome inhibitors&#44; hypomethylating agents&#44; tyrosine kinase inhibitors and lenalidomide are potential harbingers of Sweet&#39;s syndrome&#46; <a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a> summarizes the top 5 reports of drug-induced Sweet&#39;s syndrome available in PubMed&#46;</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><p id="par0070" class="elsevierStylePara elsevierViewall">Sweet&#39;s syndrome can affect individually other organs&#44; such as bones&#44; brain&#44; ears&#44; eyes&#44; kidneys&#44; intestines&#44; liver&#44; heart&#44; lung&#44; mouth&#44; muscles and spleen&#44; particularly when associated with a malignancy that includes an extracutaneous site&#44; which occurs in up to 50&#37; of reported cases&#44;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> or present in patients with multiorganic affection&#46;<a class="elsevierStyleCrossRef" href="#bib0640"><span class="elsevierStyleSup">28</span></a> Lungs are the most common extracutaneous site&#59; symptoms range from upper respiratory tract infection with flu-like symptoms in its early stages to acute respiratory distress syndrome&#44; and imaging demonstrates diffuse ground-glass opacities or consolidation&#46; Radiological changes in the lungs include the presence of nodular&#44; reticular or patchy infiltration&#44; with or without effusion&#46;<a class="elsevierStyleCrossRef" href="#bib0645"><span class="elsevierStyleSup">29</span></a> Bronchoalveolar lavage is characterized by neutrophilic predominance with negative cultures&#46;<a class="elsevierStyleCrossRef" href="#bib0650"><span class="elsevierStyleSup">30</span></a> Some patients have been confirmed to have pulmonary involvement based on transbronchial lung biopsies&#44; characterized by interstitial inflammation&#44; edema and mild fibrosis&#44; in which a large number of neutrophils and occasional lymphocytes&#44; macrophages and eosinophils infiltrate the alveoli&#46;<a class="elsevierStyleCrossRef" href="#bib0655"><span class="elsevierStyleSup">31</span></a> Aortic stenosis&#44; aortitis&#44; cardiomegaly&#44; coronary artery occlusion and myocardial infiltration with neutrophils have all been previously reported to occur in patients with heart involvement&#46;<a class="elsevierStyleCrossRef" href="#bib0605"><span class="elsevierStyleSup">21</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Different varieties and atypical cases of Sweet&#39;s syndrome can occur&#46; Neutrophilic dermatosis of the hands is currently considered to be a localized form that is capable of spreading to other locations and is not always accompanied by fever and neutrophilia&#46;<a class="elsevierStyleCrossRef" href="#bib0660"><span class="elsevierStyleSup">32</span></a> Another atypical localized form is neutrophilic dermatosis on the site of a lymphedema&#44; which has a milder course with fewer systemic symptoms&#44; fewer relapses&#44; and typically responds well to oral antibiotics&#44; anti-inflammatory drugs&#44; and topical corticosteroids&#44;<a class="elsevierStyleCrossRef" href="#bib0665"><span class="elsevierStyleSup">33</span></a> although its etiogenesis remains undefined&#46; Recently&#44; Kroshinsky et al&#46; described necrotizing Sweet&#39;s syndrome&#44; a new variant of neutrophilic dermatoses characterized by the rapid onset of edematous&#44; erythematous&#44; warm cutaneous lesions with deep tissue neutrophilic infiltration and soft tissue necrosis in the absence of an infection&#44; which tends to be cyclic with a high morbidity&#46;<a class="elsevierStyleCrossRef" href="#bib0670"><span class="elsevierStyleSup">34</span></a> Necrotizing Sweet&#39;s syndrome can occur as the first manifestation of HIV infection<a class="elsevierStyleCrossRef" href="#bib0675"><span class="elsevierStyleSup">35</span></a> or dermatomyositis<a class="elsevierStyleCrossRef" href="#bib0680"><span class="elsevierStyleSup">36</span></a> or in association with inflammatory bowel disease&#44; Beh&#231;et&#39;s disease&#44; relapsing polychondritis&#44; rheumatoid arthritis or thyroid disease&#44; including Graves&#8217; disease and Hashimoto thyroiditis&#46;<a class="elsevierStyleCrossRef" href="#bib0685"><span class="elsevierStyleSup">37</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">In some patients with classical Sweet&#39;s syndrome&#44; the symptoms and lesions of Sweet&#39;s syndrome are eventually resolved without any therapeutic intervention&#44; while in others&#44; symptoms and lesions can persist without treatment for weeks or months&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> Successful management of the cancer occasionally results after clearing the related dermatosis in patients with malignancy-associated Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">17</span></a> Similarly&#44; discontinuation of the associated medication in drug-induced Sweet&#39;s syndrome results in spontaneous improvement and subsequent resolution&#46;<a class="elsevierStyleCrossRef" href="#bib0635"><span class="elsevierStyleSup">27</span></a> Reports of fatal outcomes of Sweet&#39;s syndrome are uncommon&#44; as it has been describe as an idiopathic chronic systemic inflammatory response syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0690"><span class="elsevierStyleSup">38</span></a> Recurrence is very common and remission between episodes is variable&#44; occurring either after spontaneous remission or therapy-induced clinical resolution&#59;<a class="elsevierStyleCrossRef" href="#bib0510"><span class="elsevierStyleSup">2</span></a> therefore&#44; it is crucial conduct follow-ups&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Histopathology</span><p id="par0085" class="elsevierStylePara elsevierViewall">Histopathological analysis that characterizes a dense and diffuse dermal neutrophilic infiltrate is important for the diagnosis of the disease because the differential diagnosis of Sweet&#39;s syndrome is extensive&#46;</p><p id="par0090" class="elsevierStylePara elsevierViewall">Histopathological diagnostic criteria include the presence of diffuse neutrophilic infiltrate in the dermis&#44; edema&#44; and fragmentation of the nuclei of neutrophils &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#46; The predominant cells that comprise the infiltrate in the dermis of cutaneous Sweet&#39;s syndrome lesions are mature neutrophils&#59; however&#44; eosinophils have been observed within the dermal infiltrate in the skin lesions of some patients with either the classical or the drug-induced Sweet&#39;s syndrome&#46; Occasionally&#44; lymphocytes or histiocytes may also be present in the inflammatory infiltrate&#46;<a class="elsevierStyleCrossRefs" href="#bib0545"><span class="elsevierStyleSup">9&#44;39</span></a> The neutrophilic infiltrate may be perivascular&#44; leading to leukocytoclastic vasculitis&#46;<a class="elsevierStyleCrossRefs" href="#bib0535"><span class="elsevierStyleSup">7&#44;40</span></a> The signs of this perivascular neutrophilic infiltration&#44; which are not always seen on histopathological examination&#44; are inflammatory infiltrate around postcapillary venules&#44; with a predominance of neutrophils&#44; nuclear dust&#44; extravasation of erythrocytes&#44; fibrin deposition in vessel walls&#44; necrosis&#44; and granuloma formation&#46;<a class="elsevierStyleCrossRef" href="#bib0705"><span class="elsevierStyleSup">41</span></a> This infiltrate is usually localized to the papillary and upper reticular dermis&#59; however&#44; neutrophils can also be present in the epidermis as either neutrophilic spongiotic vesicles<a class="elsevierStyleCrossRef" href="#bib0710"><span class="elsevierStyleSup">42</span></a> or subcorneal pustules<a class="elsevierStyleCrossRef" href="#bib0525"><span class="elsevierStyleSup">5</span></a>&#59; the infiltrate can also extend into the subcutaneous tissue and the hypodermis&#44; affecting lobules of adipocytes and&#47;or septa&#44; recently reported as being associated with myeloid disorders&#46;<a class="elsevierStyleCrossRef" href="#bib0715"><span class="elsevierStyleSup">43</span></a> This subcutaneous infiltration&#44; referred to as &#8220;subcutaneous Sweet&#39;s syndrome&#8221;&#44; may lead to neutrophilic panniculitis in up to 38&#37; of cases&#46; However&#44; the necrosis of adipocytes is clearly absent&#44; even though a large number of neutrophils&#44; and lymphocytes&#44; monocytes&#44; and multinucleated giant cells may also be found&#46;<a class="elsevierStyleCrossRef" href="#bib0720"><span class="elsevierStyleSup">44</span></a> The presence of subcutaneous neutrophilic inflammation in Sweet&#39;s syndrome lesions may be a more common finding in patients with either an associated hematologic dyscrasia or a solid tumor&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0095" class="elsevierStylePara elsevierViewall">An unusual histopathologic variant that should be addressed is the histiocytoid Sweet syndrome&#46; In this variant&#44; fresh lesions are histopathologically characterized by an inflammatory infiltrate mostly composed of cells that may be misinterpreted as histiocytes&#44; when in fact immunohistochemical studies demonstrate that they are immature neutrophils&#46; These lesions probably result from the release of immature myeloid cells by the bone marrow in early acute stages of the disease&#44; and these immature myeloid cells are replaced by mature neutrophils in later stages of evolution&#46; Histopathologic differential diagnosis should be established with leukemia cutis and other inflammatory conditions characterized by histiocytes interstitially arranged between collagen bundles of the dermis&#46; The lesions show a benign biological behavior and respond promptly to low doses of oral corticosteroids or nonsteroidal anti-inflammatory drugs&#46;<a class="elsevierStyleCrossRef" href="#bib0725"><span class="elsevierStyleSup">45</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">In a few rare cases of MDS&#44; lymphocytic infiltrates are the presenting feature of Sweet&#39;s syndrome&#46; Initially lymphocytic infiltrates in this subset could be attributed either to an early timing of the biopsy concerning the age of the lesion or to the dysgranulopoiesis syndrome&#46; A possible relationship between the dysfunction of the receptor of the granulocyte-macrophage colony stimulating factor&#44; the gene of which is located on the pseudoautosomal X-Y region&#44; may exist in MDS patients with initially lymphocytic Sweet&#39;s syndrome&#46; This could explain the male gender of this subset and might establish initially lymphocytic Sweet&#39;s syndrome as a distinguished clinicopathological entity for predicting the occurrence and even the prognosis of MDS&#46;<a class="elsevierStyleCrossRef" href="#bib0730"><span class="elsevierStyleSup">46</span></a></p><p id="par0105" class="elsevierStylePara elsevierViewall">All of these characteristics of the infiltrate make a clinic-pathological correlation essential for confirming the diagnosis of Sweet&#39;s syndrome&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Management</span><p id="par0110" class="elsevierStylePara elsevierViewall">The management of patients with a Sweet&#39;s syndrome can be performed in 3 steps&#58; assessment&#44; workup&#44; and treatment&#46; Assessment includes the identification of the type of cutaneous lesion&#44; the existence of possible extracutaneous sites&#44; and the search for associated disease&#46; In every case&#44; it is important to rule out the presence of an infection and to have a precise drug-therapy history&#46; Also&#44; the potential presence of hematological diseases must be systematically investigated&#46; Furthermore&#44; a routine or targeted search for cancer is performed according to the age and symptoms of the patient&#46; In the absence of symptoms&#44; aggressive investigatory procedures are unwarranted&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">Laboratory evaluation should include a complete blood cell count with leukocyte differential and platelet counts&#46; Evaluation of acute phase reactants&#44; including the erythrocyte sedimentation rate or C-reactive protein&#44; serum chemistries for evaluating hepatic and renal function&#44; and a urinalysis should also be performed&#46; It may also be reasonable to perform a serologic evaluation for antistreptolysin-O antibody&#44; rheumatoid factor&#44; and thyroid function because streptococcal infection&#44; rheumatoid arthritis&#44; and thyroid disease have been found to have either a probable or bona fide association with Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0515"><span class="elsevierStyleSup">3</span></a> Although the most consistent laboratory abnormalities in Sweet&#39;s syndrome are peripheral leukocytosis with neutrophilia and an elevated erythrocyte sedimentation rate&#44;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> it is not always observed in all patients with biopsy-confirmed Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0605"><span class="elsevierStyleSup">21</span></a> For example&#44; some of the patients with malignancy-associated Sweet&#39;s syndrome may present with anemia&#44; neutropenia&#44; and&#47;or abnormal platelet counts&#46; A work-up diagram is presented in <a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0120" class="elsevierStylePara elsevierViewall">A lesional skin biopsy for routine histopathologic evaluation is a useful procedure to confirm a clinically suspected diagnosis of Sweet&#39;s syndrome&#46; A 4<span class="elsevierStyleHsp" style=""></span>mm wide punch can be performed in the most recent skin lesion&#46; The skin biopsy should present the pathologic features of Sweet&#39;s syndrome&#44; such as the diffuse inflammatory infiltrate of neutrophils in the dermis&#44; subcutaneous fat&#44; or both&#44; which can also be observed in cutaneous lesions caused by an infectious agent&#46; Therefore&#44; it may also be prudent to submit lesional tissue for bacterial&#44; fungal&#44; mycobacterial&#44; and possibly viral cultures&#46;<a class="elsevierStyleCrossRef" href="#bib0515"><span class="elsevierStyleSup">3</span></a></p><p id="par0125" class="elsevierStylePara elsevierViewall">If extracutaneous involvement of Sweet&#39;s syndrome needs to be ruled out&#44; chest radiographs&#44; SPECTs&#44; computerized axial tomography&#44; electroencephalograms&#44; magnetic resonance imaging and even cerebrospinal fluid analysis can be performed&#44; depending on the suspected location&#46; For instance&#44; urinalysis abnormalities&#44; such as hematuria and proteinuria&#44; may be observed in patients with kidney involvement&#44; and hepatic serum enzyme elevation may be present in patients with Sweet&#39;s syndrome-associated liver involvement&#46; Pleural effusions and corticosteroid-responsive culture-negative infiltrates may be present on chest roentgenograms in patients with Sweet&#39;s syndrome who have extracutaneous manifestations that involve their lungs&#46;<a class="elsevierStyleCrossRef" href="#bib0735"><span class="elsevierStyleSup">47</span></a></p><p id="par0130" class="elsevierStylePara elsevierViewall">Recommendations for the initial malignancy workup in newly diagnosed Sweet&#39;s syndrome patients without a prior cancer diagnosis were proposed by Cohen and Kurzrock in 1993&#46;<a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">17</span></a> Their recommendations are based on the neoplasms that were concurrently or subsequently discovered in previously cancer-free Sweet&#39;s syndrome patients and on the age-related recommendations of the American Cancer Society for the early detection of cancer in asymptomatic persons&#46;<a class="elsevierStyleCrossRef" href="#bib0740"><span class="elsevierStyleSup">48</span></a> They recommended the obtaining the following&#58; detailed medical history&#59; complete physical examination&#44; including an examination of the thyroid&#44; lymph nodes&#44; oral cavity&#44; and skin&#44; digital rectal examination&#44; breast&#44; ovary&#44; and pelvic examination in women&#44; and prostate and testicle examination in men&#59; laboratory evaluation&#44; including carcinoembryonic antigen levels&#44; complete blood cell count with leukocyte differential and platelet count&#44; pap test in women&#44; serum chemistries&#44; stool guaiac slide test&#44; urinalysis&#44; and urine culture&#59; and other screening tests such as chest roentgenograms&#44; endometrial tissue sampling in either menopausal women or women with a history of abnormal uterine bleeding&#44; estrogen therapy&#44; failure to ovulate&#44; infertility&#44; or obesity&#44; and sigmoidoscopy in patients over 50 years of age&#46; Cohen and Kurzrock also suggest performing a complete blood cell count with leukocyte differential and platelet count every 6&#8211;12 months because the initial appearance of dermatosis-related skin lesions may precede the diagnosis of a Sweet&#39;s syndrome-associated hematologic malignancy by as much as 11 years&#46;<a class="elsevierStyleCrossRef" href="#bib0515"><span class="elsevierStyleSup">3</span></a></p><p id="par0135" class="elsevierStylePara elsevierViewall">Sweet&#39;s syndrome lesions&#44; without any therapeutic intervention&#44; can remain for weeks to months but eventually resolve in some patients with classical Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0510"><span class="elsevierStyleSup">2</span></a> In malignancy associated Sweet&#39;s syndrome&#44; the remission of the related cancer is occasionally followed by resolution of the dermatoses&#46; In cases of drug-induced Sweet&#39;s syndrome&#44; improvement and subsequent clearing of the syndrome occurs after stopping the associated medication&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a></p><p id="par0140" class="elsevierStylePara elsevierViewall">Although there are no guidelines for the treatment of Sweet&#39;s syndrome&#44; systemic corticosteroids are the first-line of treatment in most cases&#59; oral therapy with either potassium iodide or colchicine in patients for whom corticosteroids are contraindicated also typically results in the rapid resolution of Sweet&#39;s syndrome symptoms and lesions&#46;<a class="elsevierStyleCrossRef" href="#bib0745"><span class="elsevierStyleSup">49</span></a> Cutaneous and extracutaneous manifestations tend to improve within the first 72<span class="elsevierStyleHsp" style=""></span>h of the start of therapy&#46;<a class="elsevierStyleCrossRef" href="#bib0750"><span class="elsevierStyleSup">50</span></a> Sweet&#39;s syndrome can be treated initially by general corticotherapy with prednisone or with an initial prednisone dosage of 30&#8211;60<span class="elsevierStyleHsp" style=""></span>mg&#47;day &#40;0&#46;5&#8211;1&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;kg&#47;day&#41;&#44; with subsequent gradual reduction&#46;<a class="elsevierStyleCrossRefs" href="#bib0535"><span class="elsevierStyleSup">7&#44;51</span></a> In localized lesions&#44; high-potency topical corticosteroids or intralesional corticosteroids may be used&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> Alternative treatments such as potassium iodide tablets &#40;900<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#41; or colchicine solution &#40;1&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#41; are also considered first-line agents&#46;</p><p id="par0145" class="elsevierStylePara elsevierViewall">Second-line systemic therapies include indomethacin &#40;50&#8211;150<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#41;&#44; clofazimine &#40;100&#8211;200<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#41;&#44; dapsone &#40;100&#8211;200<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#41; and cyclosporine &#40;2&#8211;4<span class="elsevierStyleHsp" style=""></span>mg&#47;kg&#47;day&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> Other drugs prescribed for treatment include doxycycline&#44; metronidazole&#44; etretinate&#44; chlorambucil&#44; cyclophosphamide&#44; methotrexate&#44; etanercept&#44; infliximab and thalidomide&#46; The efficacy of IL-1 blocking agents such as anakinra in refractory cases has been recently published&#46;<a class="elsevierStyleCrossRef" href="#bib0760"><span class="elsevierStyleSup">52</span></a></p><p id="par0150" class="elsevierStylePara elsevierViewall">In conclusion&#44; Sweet&#39;s syndrome is a complex global disease without racial disparity that occurs more frequently in middle age women&#46; Although the etiology of Sweet&#39;s syndrome is not completely understood&#44; it has an inflammatory component in all 3 of its varieties&#46; Importantly&#44; this syndrome could be the first manifestation of a malignancy&#44; so each case should include an individual work-up&#46; Corticosteroids are the main line of treatment&#44; as recurrence is very common&#46; Follow-up is crucial&#46; Although there is no consensus in the literature and the recommendations range from simple monitoring to follow-up care&#44; we should always endeavor to keep well informed of patient conditions&#46;</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Ethical disclosures</span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Protection of human and animal subjects</span><p id="par0155" class="elsevierStylePara elsevierViewall">The authors declare that no experiments were performed on humans or animals for this investigation&#46;</p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Confidentiality of data</span><p id="par0160" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appears in this article&#46;</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Right to privacy and informed consent</span><p id="par0165" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appears in this article&#46;</p></span></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Conflicts of interest</span><p id="par0170" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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            ]
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              "identificador" => "sec0050"
              "titulo" => "Right to privacy and informed consent"
            ]
          ]
        ]
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          "identificador" => "sec0055"
          "titulo" => "Conflicts of interest"
        ]
        12 => array:1 [
          "titulo" => "References"
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    ]
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    "fechaRecibido" => "2015-09-03"
    "fechaAceptado" => "2015-12-15"
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      "en" => array:1 [
        0 => array:4 [
          "clase" => "keyword"
          "titulo" => "Keywords"
          "identificador" => "xpalclavsec819486"
          "palabras" => array:4 [
            0 => "Sweet syndrome"
            1 => "Neutrophilic dermatoses"
            2 => "Malignancy-associated Sweet&#39;s syndrome"
            3 => "Drug-induced Sweet&#39;s syndrome"
          ]
        ]
      ]
      "es" => array:1 [
        0 => array:4 [
          "clase" => "keyword"
          "titulo" => "Palabras clave"
          "identificador" => "xpalclavsec819487"
          "palabras" => array:4 [
            0 => "S&#237;ndrome de Sweet"
            1 => "Dermatosis neutrof&#237;licas"
            2 => "S&#237;ndrome de Sweet asociado a malignidad"
            3 => "S&#237;ndrome de Sweet inducido por medicamentos"
          ]
        ]
      ]
    ]
    "tieneResumen" => true
    "resumen" => array:2 [
      "en" => array:2 [
        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Sweet syndrome is the most representative entity of febrile neutrophilic dermatoses&#46; It typically presents in patients with pirexya&#44; neutrophilia&#44; painful tender erytomatous papules&#44; nodules and plaques often distributed asymmetrically&#46; Frequent sites include the face&#44; neck and upper extremities&#46; Affected sites show a characteristical neutrophilic infiltrate in the upper dermis&#46; Its etiology remains elucidated&#44; but it seems that can be mediated by a hypersensitivity reaction in which cytokines&#44; followed by infiltration of neutrophils&#44; may be involved&#46; Systemic corticosteroids are the first-line of treatment in most cases&#46; We present a concise review of the pathogenesis&#44; classification&#44; diagnosis and treatment update of this entity&#46;</p></span>"
      ]
      "es" => array:2 [
        "titulo" => "Resumen"
        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">El s&#237;ndrome de Sweet es la entidad m&#225;s representativa de las dermatosis neutrof&#237;licas&#46; Por lo general se presenta en pacientes con fiebre&#44; neutrofilia&#44; p&#225;pulas erytomatosas dolorosas&#44; n&#243;dulos y placas&#46; Los sitios frecuentemente afectados incluyen la cara&#44; cuello y extremidades superiores los cuales caracter&#237;sticamente presentan un infiltrado neutrof&#237;lico en la dermis superior&#46; Su etiolog&#237;a no esta bien establecida&#44; pero parece que puede estar mediada por una reacci&#243;n de hipersensibilidad de las citocinas&#44; seguido por un infiltrado de neutr&#243;filos&#46; Los corticosteroides sist&#233;micos son la primera l&#237;nea de tratamiento en la mayor&#237;a de los casos&#46; Se presenta una revisi&#243;n actual de la patog&#233;nesis&#44; clasificaci&#243;n&#44; diagn&#243;stico y tratamiento de esta entidad&#46;</p></span>"
      ]
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">&#40;A&#8211;C&#41; Disseminated dermatosis affecting the face&#44; upper trunk and four limbs&#44; predominantly on sun-exposed areas&#44; bilateral and prone to symmetry&#44; polymorphous&#44; characterized by erythematous&#44; thick&#44; sharply demarcated nodules and plaques&#44; and some yellow pustules between them&#46; &#40;D&#41; Pathergy phenomenon&#46;</p>"
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">&#40;A&#41; A papulopustular lesion localizated on the head&#44; in the posterior region of the right ear&#44; a skin biopsy &#40;Punch 4&#41; was performed and stained with hematoxylin&#8211;eosin&#59; &#40;B&#41; Histopathology reveals diffuse neutrophilic infiltrate with significant papillary dermal edema&#44; 10&#215;&#59; &#40;C&#41; Papillary dermal edema&#44; perivascular and interstitial infiltrate composed predominately of neutrophils&#44; scattered lymphocytes&#44; histiocytes&#44; and eosinophils&#44; 20&#215;&#59; &#40;D&#41; The infiltration was predominantly composed of neutrophils and histiocytes&#44; 40&#215;&#46;</p>"
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          "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Recommendations algorithm for the initial workup in newly diagnosed Sweet&#39;s syndrome patients&#46;</p>"
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          "leyenda" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">In classical&#58; The presence of both major criteria &#40;1 and 2&#41; and two minor criteria &#40;3&#8211;6&#41; is needed to establish the diagnosis of classical Sweet&#39;s syndrome&#46; In malignancy-associated&#58; the patients must precede&#44; follow&#44; or appear concurrent with the diagnosis of the patient&#39;s neoplasm and classical Sweet&#39;s syndrome diagnostic criteria&#46; In drug-induced&#58; All five features should be present to diagnose Sweet&#39;s syndrome&#46; Adapted from Cohen et al&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a></p>"
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                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " colspan="3" align="left" valign="top"><span class="elsevierStyleItalic">Drug-related Sweet syndrome</span></td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Diagnostic criteria&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " colspan="2" align="left" valign="top">A&#46; Abrupt onset of painful erythematous plaques or nodules<br>B&#46; Histopathological findings of dense neutrophilic infiltrate without evidence of leukocytoclastic vasculitis<br>C&#46; Fever &#62;38<span class="elsevierStyleHsp" style=""></span>&#176;C<br>D&#46; Temporal relation between use of medication and clinical presentation or relapse with readministration<br>E&#46; Disappearance of lesions after drug discontinuation or treatment with systemic corticosteroids</td></tr></tbody></table>
                  """
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          "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Diagnostic criteria for sweet syndrome&#44; including classical&#44; drug-induced and malignancy-associated forms&#46;</p>"
        ]
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                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Tretinoin&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">8&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top"><a class="elsevierStyleCrossRefs" href="#bib0635">27&#44;58&#44;83&#8211;88</a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Bortezomib<a class="elsevierStyleCrossRef" href="#tblfn0005"><span class="elsevierStyleSup">a</span></a>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top"><a class="elsevierStyleCrossRefs" href="#bib0945">89&#8211;95</a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Azathioprine&nbsp;\t\t\t\t\t\t\n
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              "identificador" => "tblfn0005"
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              "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Information updated on August 1&#44; 2015&#59; Bortezomib&#58; antineoplastic&#44; proteasome inhibitor use for mantle cell lymphoma&#44; multiple myeloma and follicular non-Hodgkin lymphoma&#46;</p>"
            ]
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        ]
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          "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Top 5 drugs related to Sweet&#39;s syndrome&#44; based on case reports published on PubMed&#46;</p>"
        ]
      ]
    ]
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      "titulo" => "References"
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                    0 => array:2 [
                      "titulo" => "An acute febrile neutrophilic dermatosis"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:1 [
                            0 => "R&#46;D&#46; Sweet"
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                        ]
                      ]
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                    0 => array:1 [
                      "Revista" => array:4 [
                        "tituloSerie" => "Br J Dermatol"
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                      "titulo" => "Acute febrile neutrophilic dermatosis"
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                        0 => array:2 [
                          "etal" => false
                          "autores" => array:3 [
                            0 => "P&#46;R&#46; Cohen"
                            1 => "L&#46; Almeida"
                            2 => "R&#46; Kurzrock"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:1 [
                      "Revista" => array:4 [
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                    0 => array:2 [
                      "titulo" => "Sweet&#39;s syndrome revisited&#58; a review of disease concepts"
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                        0 => array:2 [
                          "etal" => false
                          "autores" => array:2 [
                            0 => "P&#46;R&#46; Cohen"
                            1 => "R&#46; Kurzrock"
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                        ]
                      ]
                    ]
                  ]
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                    0 => array:1 [
                      "Revista" => array:4 [
                        "tituloSerie" => "Int J Dermatol"
                        "fecha" => "2003"
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                        "paginaFinal" => "778"
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                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Diagnostic criteria for Sweet&#39;s syndrome"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:2 [
                            0 => "W&#46;P&#46; Su"
                            1 => "H&#46;N&#46; Liu"
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                        ]
                      ]
                    ]
                  ]
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                    0 => array:1 [
                      "Revista" => array:4 [
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              "referencia" => array:1 [
                0 => array:3 [
                  "comentario" => "quiz 557-560"
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Sweet&#39;s syndrome &#40;acute febrile neutrophilic dermatosis&#41;"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:1 [
                            0 => "P&#46; von den Driesch"
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                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:1 [
                      "Revista" => array:4 [
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                        "fecha" => "1994"
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              "etiqueta" => "6"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Sweet&#39;s syndrome&#58; is the pathogenesis mediated by helper T cell type 1 cytokines&#63;"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:4 [
                            0 => "A&#46;S&#46; Giasuddin"
                            1 => "A&#46;H&#46; El-Orfi"
                            2 => "M&#46;M&#46; Ziu"
                            3 => "N&#46;Y&#46; El-Barnawi"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:1 [
                      "Revista" => array:4 [
                        "tituloSerie" => "J Am Acad Dermatol"
                        "fecha" => "1998"
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                      ]
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                  ]
                ]
              ]
            ]
            6 => array:3 [
              "identificador" => "bib0535"
              "etiqueta" => "7"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Sweet&#39;s syndrome &#8211; a comprehensive review of an acute febrile neutrophilic dermatosis"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:1 [
                            0 => "P&#46;R&#46; Cohen"
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                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:1 [
                      "Revista" => array:3 [
                        "tituloSerie" => "Orphanet J Rare Dis"
                        "fecha" => "2007"
                        "paginaInicial" => "34"
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                    ]
                  ]
                ]
              ]
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            7 => array:3 [
              "identificador" => "bib0540"
              "etiqueta" => "8"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Inflammatory cells&#44; cytokines and matrix metalloproteinases in amicrobial pustulosis of the folds and other neutrophilic dermatoses"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => true
                          "autores" => array:6 [
                            0 => "A&#46;V&#46; Marzano"
                            1 => "M&#46; Cugno"
                            2 => "V&#46; Trevisan"
                            3 => "R&#46; Lazzari"
                            4 => "D&#46; Fanoni"
                            5 => "E&#46; Berti"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:1 [
                      "Revista" => array:4 [
                        "tituloSerie" => "Int J Immunopathol Pharmacol"
                        "fecha" => "2011"
                        "paginaInicial" => "451"
                        "paginaFinal" => "460"
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              "etiqueta" => "9"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Experimentally confirmed induction of Sweet&#39;s syndrome by phototesting"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:4 [
                            0 => "V&#46; Meyer"
                            1 => "S&#46;W&#46; Schneider"
                            2 => "G&#46; Bonsmann"
                            3 => "S&#46; Beissert"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:1 [
                      "Revista" => array:4 [
                        "tituloSerie" => "Acta Dermato-Venereol"
                        "fecha" => "2011"
                        "paginaInicial" => "720"
                        "paginaFinal" => "721"
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            9 => array:3 [
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              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
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Review
Sweet Syndrome: A Review and Update
Síndrome de Sweet: Revisión y puesta al día
C.D. Villarreal-Villarreal, J. Ocampo-Candiani, A. Villarreal-Martínez
Autor para correspondencia
dravillarrealmtz@yahoo.com.mx

Corresponding author.
Department of Dermatology, “Dr. José E. González” University Hospital of the School of Medicine of the “Universidad Autónoma de Nuevo León”, Monterrey, Mexico
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        "titulo" => "S&#237;ndrome de Sweet&#58; Revisi&#243;n y puesta al d&#237;a"
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          "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Recommendations algorithm for the initial workup in newly diagnosed Sweet&#39;s syndrome patients&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Since it was first described by Dr&#46; Robert Douglas Sweet&#44; originally known as Gomm-Button disease &#40;in reference to the first two patients&#41;&#44; Sweet&#39;s syndrome&#44; also referred to as febrile neutrophilic dermatosis&#44; has been reported in hundreds of patients worldwide&#46;<a class="elsevierStyleCrossRef" href="#bib0505"><span class="elsevierStyleSup">1</span></a> Neutrophilic dermatoses are a heterogeneous group of inflammatory skin disorders that include Sweet&#39;s syndrome&#44; pyoderma gangrenosum&#44; and subcorneal pustular dermatosis&#44;<a class="elsevierStyleCrossRef" href="#bib0510"><span class="elsevierStyleSup">2</span></a> the former being the most represented and the focus of this review&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The purpose of this article is to make a review of Sweet syndrome&#44; its clinical manifestations&#44; definition&#44; pathogenesis&#44; diagnosis and management of this entity&#46; It is essential for dermatologists to know the different aspects of Sweet&#39;s syndrome as well as its proper diagnosis&#44; prevention and treatment&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Definition</span><p id="par0015" class="elsevierStylePara elsevierViewall">Clinically&#44; Sweet&#39;s syndrome presents in patients&#44; all of which show characteristic neutrophilic infiltrate in the upper dermis&#46;<a class="elsevierStyleCrossRef" href="#bib0515"><span class="elsevierStyleSup">3</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Sweet&#39;s syndrome can present as one of three clinical types&#58; classical &#40;or idiopathic&#41; Sweet&#39;s syndrome&#44; malignancy-associated Sweet&#39;s syndrome&#44; or drug-induced Sweet&#39;s syndrome&#46; Specific diagnostic criteria were proposed by Su and Liu<a class="elsevierStyleCrossRef" href="#bib0520"><span class="elsevierStyleSup">4</span></a> and subsequently revised and modified by von den Driesch&#46;<a class="elsevierStyleCrossRef" href="#bib0525"><span class="elsevierStyleSup">5</span></a> Laboratory abnormalities may be found and are included in the diagnostic criteria&#44; such as increased erythrocyte sedimentation rate &#40;ESR&#41;&#44; elevated C-reactive protein and leukocytosis &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Etiology</span><p id="par0025" class="elsevierStylePara elsevierViewall">Sweet&#39;s syndrome is an inflammatory skin disorder characterized by the extensive infiltration of neutrophils into the epidermis and dermis&#46; For a dermatologist&#44; understanding the pathophysiology of Sweet&#39;s syndrome is crucial for treatment&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">The underlining biological pathways responsible for this cutaneous neutrophilic dermatosis have remained elusive&#46; However&#44; the association of this disease with infection&#44; autoimmune diseases&#44; neoplasms and drugs suggests an unusual hypersensitivity that may be mediated by cytokines&#44; followed by infiltration of neutrophils that are probably activated by interleukin &#40;IL&#41;-1&#46; Circulating autoantibodies&#44; cytokines&#44; dermal dendrocytes&#44; HLA serotypes&#44; immune complexes and leukotactic mechanisms have been suggested as factors that contribute to the pathogenesis of this syndrome&#46; The presence of IL-1&#44; IL-2 and IFN-&#947; but not IL-4&#44; suggests that type 1T helper cells may play a role in the pathogenesis of idiopathic varieties of this syndrome&#46;<a class="elsevierStyleCrossRefs" href="#bib0530"><span class="elsevierStyleSup">6&#44;7</span></a> Inflammatory cell markers&#44; including CD3&#44; CD163&#44; myeloperoxidase&#44; metalloproteinases and vascular endothelial growth factors&#44; display significantly higher values in the lesioned skin of patients with Sweet&#39;s syndrome compared to non-Sweet&#39;s syndrome individuals or patients with other neutrophilic dermatoses&#46;<a class="elsevierStyleCrossRef" href="#bib0540"><span class="elsevierStyleSup">8</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">It has also been postulated that photosensitivity may play a role in the pathogenesis of Sweet&#39;s syndrome&#44; although the pathomechanism is unknown&#44; as Sweet&#39;s syndrome has been experimentally induced by phototesting&#46;<a class="elsevierStyleCrossRef" href="#bib0545"><span class="elsevierStyleSup">9</span></a> One theory suggests that an isomorphic Koebner reaction is at work&#59; another proposed mechanism associates ultraviolet B radiation with neutrophil activation and epidermal production of tumor necrosis factor-alpha and interleukin-8&#46;<a class="elsevierStyleCrossRef" href="#bib0550"><span class="elsevierStyleSup">10</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">In malignancy-associated Sweet&#39;s syndrome&#44; the most accepted theory of mechanism of pathogenesis is the overproduction and inappropriate regulation of inflammatory cytokines&#44; such as IL-1&#44; IL-3&#44; IL-6&#44; IL-8&#44; granulocyte colony stimulating factor &#40;G-CSF&#41; and granulocyte macrophage colony stimulating factor &#40;GM-CSF&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">11</span></a> This theory is supported by cases in which Sweet&#39;s syndrome patients received G-CSF&#47;GM-CSF&#44; interferon-&#947; and all-trans retinoic acid &#40;ATRA&#41; and subsequently developed Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">11</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Although there is no consistent evidence of a genetic predisposition for Sweet&#39;s syndrome&#44; a higher frequency of HLA-Bw54 was reported in Japanese patients with Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0530"><span class="elsevierStyleSup">6</span></a> However&#44; analysis of the HLA antigens in a Caucasian population showed no association between this syndrome and specific HLA-ABC antigens&#46;<a class="elsevierStyleCrossRef" href="#bib0560"><span class="elsevierStyleSup">12</span></a> Recent evidence based on animal models suggest that an alteration in the gene encoding protein tyrosine phosphatase non-receptor type 6 &#40;Ptpn6&#41; could be involved in the pathogenesis of Sweet&#39;s syndrome&#44;<a class="elsevierStyleCrossRef" href="#bib0565"><span class="elsevierStyleSup">13</span></a> as it encodes non-receptor protein tyrosine phosphatase Src homology region 2 &#40;SH2&#41; domain-containing phosphatase-1 &#40;SHP-1&#41;&#46; The malfunction of Ptpn6 results in unremitting footpad swelling&#44; suppurative inflammation&#44; and neutrophilia&#46; More studies are required to better understand the etiology of this disease&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Clinical manifestations</span><p id="par0050" class="elsevierStylePara elsevierViewall">Classical Sweet&#39;s syndrome has a worldwide distribution&#44; usually presenting in middle age women with a 4&#58;1 female to male ratio&#44; no racial disparity&#44; and recurrence in one-third of patients&#46;<a class="elsevierStyleCrossRef" href="#bib0515"><span class="elsevierStyleSup">3</span></a> It presents as an acute febrile neutrophilic dermatosis characterized by a constellation of clinical symptoms&#44; physical features&#44; and pathological findings that include fever&#44; neutrophilia&#44; asymmetrically distributed painful tender erythematous skin lesions&#44; consisting of papules&#44; nodules and plaques&#44; usually affecting face&#44; neck and upper extremities &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; Histology reveals a characteristic diffuse infiltrate predominantly consisting of mature neutrophils typically located in the upper dermis&#44; which tend to promptly improve after the initiation of treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> Atypical lesions&#44; characterized by erythematous plaques&#44; vesicles and bullous lesions&#44; have also been described&#46;<a class="elsevierStyleCrossRef" href="#bib0570"><span class="elsevierStyleSup">14</span></a> Typically&#44; classical or idiopathic Sweet&#39;s syndrome may be associated with infection&#44; usually of the upper respiratory &#40;streptococci&#41; or gastrointestinal tract &#40;salmonellosis and yersiniosis&#41;&#44; and inflammatory bowel disease&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> It can also occur during pregnancy&#44;<a class="elsevierStyleCrossRef" href="#bib0575"><span class="elsevierStyleSup">15</span></a> possibly related to the vascular&#44; cellular&#44; microbiological&#44; and immunological changes linked to increased estrogen and progestogen levels during pregnancy&#46;<a class="elsevierStyleCrossRef" href="#bib0580"><span class="elsevierStyleSup">16</span></a> The symptoms and clinical manifestations typically respond promptly to systemic corticosteroid therapy and recurrence occurs in one-third of patients&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a></p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0055" class="elsevierStylePara elsevierViewall">Malignancy-associated Sweet&#39;s syndrome was first described by Cohen et al&#46; <a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">17</span></a>&#46; In this subtype&#44; the clinical manifestations can precede&#44; follow&#44; or appear concurrent with the diagnosis of neoplasm in patients&#46; Indeed&#44; the dermatosis can be the cutaneous portent of either an undiagnosed visceral malignancy in a previously cancer-free individual or an unsuspected cancer recurrence in an oncology patient&#46;<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">11</span></a> Approximately 21&#37; of Sweet&#39;s syndrome patients have an associated malignancy&#59; 85&#37; of these are linked to hematological disorders&#44; most frequently to acute myelogenous leukemia &#40;AML&#41;&#46; Malignancy-associated Sweet&#39;s syndrome has also been described in patients with Hodgkin disease<a class="elsevierStyleCrossRef" href="#bib0590"><span class="elsevierStyleSup">18</span></a> and polycythemia vera<a class="elsevierStyleCrossRef" href="#bib0595"><span class="elsevierStyleSup">19</span></a> and in 15&#37; of patients with solid tumors&#44; principally adenocarcinomas of the breast&#44; genitourinary tract and gastrointestinal tract&#46;<a class="elsevierStyleCrossRef" href="#bib0600"><span class="elsevierStyleSup">20</span></a> Extracutaneous manifestations are present in 50&#37; of patients affected with malignancy-associated Sweet&#39;s syndrome<a class="elsevierStyleCrossRef" href="#bib0605"><span class="elsevierStyleSup">21</span></a> and are more frequently caused by a hematological malignancy than a solid tumor&#46; Therefore&#44; it is important to maintain rigorous a follow-up in these types of patients&#44; possibly contributing to the early detection and treatment of the underlining malignancy&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">The syndrome may occur as a paraneoplastic accompaniment&#44; appearing as a first sign of malignancy or its recurrence&#44; usually meaning a poor prognosis&#44;<a class="elsevierStyleCrossRef" href="#bib0610"><span class="elsevierStyleSup">22</span></a> as it has been reported in cases of myelodysplastic syndrome &#40;MDS&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0615"><span class="elsevierStyleSup">23</span></a> This last variant of Sweet&#39;s syndrome represents lot of controversies in the literature&#44; as it has been associated with autoimmune disorders and abnormalities in chemokines which leads to a pro-inflammatory state&#44;<a class="elsevierStyleCrossRef" href="#bib0620"><span class="elsevierStyleSup">24</span></a> leading these patients to an increased instance of autoimmune skin disease including vitiligo&#44; alopecia areata&#44; eczema&#44; vasculitis and pyoderma gangrenosum&#46;<a class="elsevierStyleCrossRef" href="#bib0625"><span class="elsevierStyleSup">25</span></a> It has also been suggested to consider <span class="elsevierStyleItalic">MEFV</span> gene analysis&#44; the gene that is responsible for familial Mediterranean fever&#44; in patients with MDS who have marked neutrophilia and antibiotic-resistant high fever or in those with Sweet&#39;s syndrome&#44;<a class="elsevierStyleCrossRef" href="#bib0630"><span class="elsevierStyleSup">26</span></a> although further evidence is required&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">Finally&#44; in drug-induced Sweet&#39;s syndrome&#44; there is nearly always a temporal relationship between medication administration and symptom development&#46; In 1996&#44; Walker and Cohen described the diagnostic criteria &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41; for drug-induced Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0635"><span class="elsevierStyleSup">27</span></a> The most commonly reported drug causing Sweet&#39;s syndrome is granulocyte-colony stimulating factor&#46; Several anticancer agents&#44; including all-trans-retinoic acid proteosome inhibitors&#44; hypomethylating agents&#44; tyrosine kinase inhibitors and lenalidomide are potential harbingers of Sweet&#39;s syndrome&#46; <a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a> summarizes the top 5 reports of drug-induced Sweet&#39;s syndrome available in PubMed&#46;</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><p id="par0070" class="elsevierStylePara elsevierViewall">Sweet&#39;s syndrome can affect individually other organs&#44; such as bones&#44; brain&#44; ears&#44; eyes&#44; kidneys&#44; intestines&#44; liver&#44; heart&#44; lung&#44; mouth&#44; muscles and spleen&#44; particularly when associated with a malignancy that includes an extracutaneous site&#44; which occurs in up to 50&#37; of reported cases&#44;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> or present in patients with multiorganic affection&#46;<a class="elsevierStyleCrossRef" href="#bib0640"><span class="elsevierStyleSup">28</span></a> Lungs are the most common extracutaneous site&#59; symptoms range from upper respiratory tract infection with flu-like symptoms in its early stages to acute respiratory distress syndrome&#44; and imaging demonstrates diffuse ground-glass opacities or consolidation&#46; Radiological changes in the lungs include the presence of nodular&#44; reticular or patchy infiltration&#44; with or without effusion&#46;<a class="elsevierStyleCrossRef" href="#bib0645"><span class="elsevierStyleSup">29</span></a> Bronchoalveolar lavage is characterized by neutrophilic predominance with negative cultures&#46;<a class="elsevierStyleCrossRef" href="#bib0650"><span class="elsevierStyleSup">30</span></a> Some patients have been confirmed to have pulmonary involvement based on transbronchial lung biopsies&#44; characterized by interstitial inflammation&#44; edema and mild fibrosis&#44; in which a large number of neutrophils and occasional lymphocytes&#44; macrophages and eosinophils infiltrate the alveoli&#46;<a class="elsevierStyleCrossRef" href="#bib0655"><span class="elsevierStyleSup">31</span></a> Aortic stenosis&#44; aortitis&#44; cardiomegaly&#44; coronary artery occlusion and myocardial infiltration with neutrophils have all been previously reported to occur in patients with heart involvement&#46;<a class="elsevierStyleCrossRef" href="#bib0605"><span class="elsevierStyleSup">21</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Different varieties and atypical cases of Sweet&#39;s syndrome can occur&#46; Neutrophilic dermatosis of the hands is currently considered to be a localized form that is capable of spreading to other locations and is not always accompanied by fever and neutrophilia&#46;<a class="elsevierStyleCrossRef" href="#bib0660"><span class="elsevierStyleSup">32</span></a> Another atypical localized form is neutrophilic dermatosis on the site of a lymphedema&#44; which has a milder course with fewer systemic symptoms&#44; fewer relapses&#44; and typically responds well to oral antibiotics&#44; anti-inflammatory drugs&#44; and topical corticosteroids&#44;<a class="elsevierStyleCrossRef" href="#bib0665"><span class="elsevierStyleSup">33</span></a> although its etiogenesis remains undefined&#46; Recently&#44; Kroshinsky et al&#46; described necrotizing Sweet&#39;s syndrome&#44; a new variant of neutrophilic dermatoses characterized by the rapid onset of edematous&#44; erythematous&#44; warm cutaneous lesions with deep tissue neutrophilic infiltration and soft tissue necrosis in the absence of an infection&#44; which tends to be cyclic with a high morbidity&#46;<a class="elsevierStyleCrossRef" href="#bib0670"><span class="elsevierStyleSup">34</span></a> Necrotizing Sweet&#39;s syndrome can occur as the first manifestation of HIV infection<a class="elsevierStyleCrossRef" href="#bib0675"><span class="elsevierStyleSup">35</span></a> or dermatomyositis<a class="elsevierStyleCrossRef" href="#bib0680"><span class="elsevierStyleSup">36</span></a> or in association with inflammatory bowel disease&#44; Beh&#231;et&#39;s disease&#44; relapsing polychondritis&#44; rheumatoid arthritis or thyroid disease&#44; including Graves&#8217; disease and Hashimoto thyroiditis&#46;<a class="elsevierStyleCrossRef" href="#bib0685"><span class="elsevierStyleSup">37</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">In some patients with classical Sweet&#39;s syndrome&#44; the symptoms and lesions of Sweet&#39;s syndrome are eventually resolved without any therapeutic intervention&#44; while in others&#44; symptoms and lesions can persist without treatment for weeks or months&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> Successful management of the cancer occasionally results after clearing the related dermatosis in patients with malignancy-associated Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">17</span></a> Similarly&#44; discontinuation of the associated medication in drug-induced Sweet&#39;s syndrome results in spontaneous improvement and subsequent resolution&#46;<a class="elsevierStyleCrossRef" href="#bib0635"><span class="elsevierStyleSup">27</span></a> Reports of fatal outcomes of Sweet&#39;s syndrome are uncommon&#44; as it has been describe as an idiopathic chronic systemic inflammatory response syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0690"><span class="elsevierStyleSup">38</span></a> Recurrence is very common and remission between episodes is variable&#44; occurring either after spontaneous remission or therapy-induced clinical resolution&#59;<a class="elsevierStyleCrossRef" href="#bib0510"><span class="elsevierStyleSup">2</span></a> therefore&#44; it is crucial conduct follow-ups&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Histopathology</span><p id="par0085" class="elsevierStylePara elsevierViewall">Histopathological analysis that characterizes a dense and diffuse dermal neutrophilic infiltrate is important for the diagnosis of the disease because the differential diagnosis of Sweet&#39;s syndrome is extensive&#46;</p><p id="par0090" class="elsevierStylePara elsevierViewall">Histopathological diagnostic criteria include the presence of diffuse neutrophilic infiltrate in the dermis&#44; edema&#44; and fragmentation of the nuclei of neutrophils &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#46; The predominant cells that comprise the infiltrate in the dermis of cutaneous Sweet&#39;s syndrome lesions are mature neutrophils&#59; however&#44; eosinophils have been observed within the dermal infiltrate in the skin lesions of some patients with either the classical or the drug-induced Sweet&#39;s syndrome&#46; Occasionally&#44; lymphocytes or histiocytes may also be present in the inflammatory infiltrate&#46;<a class="elsevierStyleCrossRefs" href="#bib0545"><span class="elsevierStyleSup">9&#44;39</span></a> The neutrophilic infiltrate may be perivascular&#44; leading to leukocytoclastic vasculitis&#46;<a class="elsevierStyleCrossRefs" href="#bib0535"><span class="elsevierStyleSup">7&#44;40</span></a> The signs of this perivascular neutrophilic infiltration&#44; which are not always seen on histopathological examination&#44; are inflammatory infiltrate around postcapillary venules&#44; with a predominance of neutrophils&#44; nuclear dust&#44; extravasation of erythrocytes&#44; fibrin deposition in vessel walls&#44; necrosis&#44; and granuloma formation&#46;<a class="elsevierStyleCrossRef" href="#bib0705"><span class="elsevierStyleSup">41</span></a> This infiltrate is usually localized to the papillary and upper reticular dermis&#59; however&#44; neutrophils can also be present in the epidermis as either neutrophilic spongiotic vesicles<a class="elsevierStyleCrossRef" href="#bib0710"><span class="elsevierStyleSup">42</span></a> or subcorneal pustules<a class="elsevierStyleCrossRef" href="#bib0525"><span class="elsevierStyleSup">5</span></a>&#59; the infiltrate can also extend into the subcutaneous tissue and the hypodermis&#44; affecting lobules of adipocytes and&#47;or septa&#44; recently reported as being associated with myeloid disorders&#46;<a class="elsevierStyleCrossRef" href="#bib0715"><span class="elsevierStyleSup">43</span></a> This subcutaneous infiltration&#44; referred to as &#8220;subcutaneous Sweet&#39;s syndrome&#8221;&#44; may lead to neutrophilic panniculitis in up to 38&#37; of cases&#46; However&#44; the necrosis of adipocytes is clearly absent&#44; even though a large number of neutrophils&#44; and lymphocytes&#44; monocytes&#44; and multinucleated giant cells may also be found&#46;<a class="elsevierStyleCrossRef" href="#bib0720"><span class="elsevierStyleSup">44</span></a> The presence of subcutaneous neutrophilic inflammation in Sweet&#39;s syndrome lesions may be a more common finding in patients with either an associated hematologic dyscrasia or a solid tumor&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0095" class="elsevierStylePara elsevierViewall">An unusual histopathologic variant that should be addressed is the histiocytoid Sweet syndrome&#46; In this variant&#44; fresh lesions are histopathologically characterized by an inflammatory infiltrate mostly composed of cells that may be misinterpreted as histiocytes&#44; when in fact immunohistochemical studies demonstrate that they are immature neutrophils&#46; These lesions probably result from the release of immature myeloid cells by the bone marrow in early acute stages of the disease&#44; and these immature myeloid cells are replaced by mature neutrophils in later stages of evolution&#46; Histopathologic differential diagnosis should be established with leukemia cutis and other inflammatory conditions characterized by histiocytes interstitially arranged between collagen bundles of the dermis&#46; The lesions show a benign biological behavior and respond promptly to low doses of oral corticosteroids or nonsteroidal anti-inflammatory drugs&#46;<a class="elsevierStyleCrossRef" href="#bib0725"><span class="elsevierStyleSup">45</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">In a few rare cases of MDS&#44; lymphocytic infiltrates are the presenting feature of Sweet&#39;s syndrome&#46; Initially lymphocytic infiltrates in this subset could be attributed either to an early timing of the biopsy concerning the age of the lesion or to the dysgranulopoiesis syndrome&#46; A possible relationship between the dysfunction of the receptor of the granulocyte-macrophage colony stimulating factor&#44; the gene of which is located on the pseudoautosomal X-Y region&#44; may exist in MDS patients with initially lymphocytic Sweet&#39;s syndrome&#46; This could explain the male gender of this subset and might establish initially lymphocytic Sweet&#39;s syndrome as a distinguished clinicopathological entity for predicting the occurrence and even the prognosis of MDS&#46;<a class="elsevierStyleCrossRef" href="#bib0730"><span class="elsevierStyleSup">46</span></a></p><p id="par0105" class="elsevierStylePara elsevierViewall">All of these characteristics of the infiltrate make a clinic-pathological correlation essential for confirming the diagnosis of Sweet&#39;s syndrome&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Management</span><p id="par0110" class="elsevierStylePara elsevierViewall">The management of patients with a Sweet&#39;s syndrome can be performed in 3 steps&#58; assessment&#44; workup&#44; and treatment&#46; Assessment includes the identification of the type of cutaneous lesion&#44; the existence of possible extracutaneous sites&#44; and the search for associated disease&#46; In every case&#44; it is important to rule out the presence of an infection and to have a precise drug-therapy history&#46; Also&#44; the potential presence of hematological diseases must be systematically investigated&#46; Furthermore&#44; a routine or targeted search for cancer is performed according to the age and symptoms of the patient&#46; In the absence of symptoms&#44; aggressive investigatory procedures are unwarranted&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">Laboratory evaluation should include a complete blood cell count with leukocyte differential and platelet counts&#46; Evaluation of acute phase reactants&#44; including the erythrocyte sedimentation rate or C-reactive protein&#44; serum chemistries for evaluating hepatic and renal function&#44; and a urinalysis should also be performed&#46; It may also be reasonable to perform a serologic evaluation for antistreptolysin-O antibody&#44; rheumatoid factor&#44; and thyroid function because streptococcal infection&#44; rheumatoid arthritis&#44; and thyroid disease have been found to have either a probable or bona fide association with Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0515"><span class="elsevierStyleSup">3</span></a> Although the most consistent laboratory abnormalities in Sweet&#39;s syndrome are peripheral leukocytosis with neutrophilia and an elevated erythrocyte sedimentation rate&#44;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> it is not always observed in all patients with biopsy-confirmed Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0605"><span class="elsevierStyleSup">21</span></a> For example&#44; some of the patients with malignancy-associated Sweet&#39;s syndrome may present with anemia&#44; neutropenia&#44; and&#47;or abnormal platelet counts&#46; A work-up diagram is presented in <a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0120" class="elsevierStylePara elsevierViewall">A lesional skin biopsy for routine histopathologic evaluation is a useful procedure to confirm a clinically suspected diagnosis of Sweet&#39;s syndrome&#46; A 4<span class="elsevierStyleHsp" style=""></span>mm wide punch can be performed in the most recent skin lesion&#46; The skin biopsy should present the pathologic features of Sweet&#39;s syndrome&#44; such as the diffuse inflammatory infiltrate of neutrophils in the dermis&#44; subcutaneous fat&#44; or both&#44; which can also be observed in cutaneous lesions caused by an infectious agent&#46; Therefore&#44; it may also be prudent to submit lesional tissue for bacterial&#44; fungal&#44; mycobacterial&#44; and possibly viral cultures&#46;<a class="elsevierStyleCrossRef" href="#bib0515"><span class="elsevierStyleSup">3</span></a></p><p id="par0125" class="elsevierStylePara elsevierViewall">If extracutaneous involvement of Sweet&#39;s syndrome needs to be ruled out&#44; chest radiographs&#44; SPECTs&#44; computerized axial tomography&#44; electroencephalograms&#44; magnetic resonance imaging and even cerebrospinal fluid analysis can be performed&#44; depending on the suspected location&#46; For instance&#44; urinalysis abnormalities&#44; such as hematuria and proteinuria&#44; may be observed in patients with kidney involvement&#44; and hepatic serum enzyme elevation may be present in patients with Sweet&#39;s syndrome-associated liver involvement&#46; Pleural effusions and corticosteroid-responsive culture-negative infiltrates may be present on chest roentgenograms in patients with Sweet&#39;s syndrome who have extracutaneous manifestations that involve their lungs&#46;<a class="elsevierStyleCrossRef" href="#bib0735"><span class="elsevierStyleSup">47</span></a></p><p id="par0130" class="elsevierStylePara elsevierViewall">Recommendations for the initial malignancy workup in newly diagnosed Sweet&#39;s syndrome patients without a prior cancer diagnosis were proposed by Cohen and Kurzrock in 1993&#46;<a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">17</span></a> Their recommendations are based on the neoplasms that were concurrently or subsequently discovered in previously cancer-free Sweet&#39;s syndrome patients and on the age-related recommendations of the American Cancer Society for the early detection of cancer in asymptomatic persons&#46;<a class="elsevierStyleCrossRef" href="#bib0740"><span class="elsevierStyleSup">48</span></a> They recommended the obtaining the following&#58; detailed medical history&#59; complete physical examination&#44; including an examination of the thyroid&#44; lymph nodes&#44; oral cavity&#44; and skin&#44; digital rectal examination&#44; breast&#44; ovary&#44; and pelvic examination in women&#44; and prostate and testicle examination in men&#59; laboratory evaluation&#44; including carcinoembryonic antigen levels&#44; complete blood cell count with leukocyte differential and platelet count&#44; pap test in women&#44; serum chemistries&#44; stool guaiac slide test&#44; urinalysis&#44; and urine culture&#59; and other screening tests such as chest roentgenograms&#44; endometrial tissue sampling in either menopausal women or women with a history of abnormal uterine bleeding&#44; estrogen therapy&#44; failure to ovulate&#44; infertility&#44; or obesity&#44; and sigmoidoscopy in patients over 50 years of age&#46; Cohen and Kurzrock also suggest performing a complete blood cell count with leukocyte differential and platelet count every 6&#8211;12 months because the initial appearance of dermatosis-related skin lesions may precede the diagnosis of a Sweet&#39;s syndrome-associated hematologic malignancy by as much as 11 years&#46;<a class="elsevierStyleCrossRef" href="#bib0515"><span class="elsevierStyleSup">3</span></a></p><p id="par0135" class="elsevierStylePara elsevierViewall">Sweet&#39;s syndrome lesions&#44; without any therapeutic intervention&#44; can remain for weeks to months but eventually resolve in some patients with classical Sweet&#39;s syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0510"><span class="elsevierStyleSup">2</span></a> In malignancy associated Sweet&#39;s syndrome&#44; the remission of the related cancer is occasionally followed by resolution of the dermatoses&#46; In cases of drug-induced Sweet&#39;s syndrome&#44; improvement and subsequent clearing of the syndrome occurs after stopping the associated medication&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a></p><p id="par0140" class="elsevierStylePara elsevierViewall">Although there are no guidelines for the treatment of Sweet&#39;s syndrome&#44; systemic corticosteroids are the first-line of treatment in most cases&#59; oral therapy with either potassium iodide or colchicine in patients for whom corticosteroids are contraindicated also typically results in the rapid resolution of Sweet&#39;s syndrome symptoms and lesions&#46;<a class="elsevierStyleCrossRef" href="#bib0745"><span class="elsevierStyleSup">49</span></a> Cutaneous and extracutaneous manifestations tend to improve within the first 72<span class="elsevierStyleHsp" style=""></span>h of the start of therapy&#46;<a class="elsevierStyleCrossRef" href="#bib0750"><span class="elsevierStyleSup">50</span></a> Sweet&#39;s syndrome can be treated initially by general corticotherapy with prednisone or with an initial prednisone dosage of 30&#8211;60<span class="elsevierStyleHsp" style=""></span>mg&#47;day &#40;0&#46;5&#8211;1&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;kg&#47;day&#41;&#44; with subsequent gradual reduction&#46;<a class="elsevierStyleCrossRefs" href="#bib0535"><span class="elsevierStyleSup">7&#44;51</span></a> In localized lesions&#44; high-potency topical corticosteroids or intralesional corticosteroids may be used&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> Alternative treatments such as potassium iodide tablets &#40;900<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#41; or colchicine solution &#40;1&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#41; are also considered first-line agents&#46;</p><p id="par0145" class="elsevierStylePara elsevierViewall">Second-line systemic therapies include indomethacin &#40;50&#8211;150<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#41;&#44; clofazimine &#40;100&#8211;200<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#41;&#44; dapsone &#40;100&#8211;200<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#41; and cyclosporine &#40;2&#8211;4<span class="elsevierStyleHsp" style=""></span>mg&#47;kg&#47;day&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a> Other drugs prescribed for treatment include doxycycline&#44; metronidazole&#44; etretinate&#44; chlorambucil&#44; cyclophosphamide&#44; methotrexate&#44; etanercept&#44; infliximab and thalidomide&#46; The efficacy of IL-1 blocking agents such as anakinra in refractory cases has been recently published&#46;<a class="elsevierStyleCrossRef" href="#bib0760"><span class="elsevierStyleSup">52</span></a></p><p id="par0150" class="elsevierStylePara elsevierViewall">In conclusion&#44; Sweet&#39;s syndrome is a complex global disease without racial disparity that occurs more frequently in middle age women&#46; Although the etiology of Sweet&#39;s syndrome is not completely understood&#44; it has an inflammatory component in all 3 of its varieties&#46; Importantly&#44; this syndrome could be the first manifestation of a malignancy&#44; so each case should include an individual work-up&#46; Corticosteroids are the main line of treatment&#44; as recurrence is very common&#46; Follow-up is crucial&#46; Although there is no consensus in the literature and the recommendations range from simple monitoring to follow-up care&#44; we should always endeavor to keep well informed of patient conditions&#46;</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Ethical disclosures</span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Protection of human and animal subjects</span><p id="par0155" class="elsevierStylePara elsevierViewall">The authors declare that no experiments were performed on humans or animals for this investigation&#46;</p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Confidentiality of data</span><p id="par0160" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appears in this article&#46;</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Right to privacy and informed consent</span><p id="par0165" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appears in this article&#46;</p></span></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Conflicts of interest</span><p id="par0170" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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    "fechaRecibido" => "2015-09-03"
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            0 => "Sweet syndrome"
            1 => "Neutrophilic dermatoses"
            2 => "Malignancy-associated Sweet&#39;s syndrome"
            3 => "Drug-induced Sweet&#39;s syndrome"
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          "palabras" => array:4 [
            0 => "S&#237;ndrome de Sweet"
            1 => "Dermatosis neutrof&#237;licas"
            2 => "S&#237;ndrome de Sweet asociado a malignidad"
            3 => "S&#237;ndrome de Sweet inducido por medicamentos"
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        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Sweet syndrome is the most representative entity of febrile neutrophilic dermatoses&#46; It typically presents in patients with pirexya&#44; neutrophilia&#44; painful tender erytomatous papules&#44; nodules and plaques often distributed asymmetrically&#46; Frequent sites include the face&#44; neck and upper extremities&#46; Affected sites show a characteristical neutrophilic infiltrate in the upper dermis&#46; Its etiology remains elucidated&#44; but it seems that can be mediated by a hypersensitivity reaction in which cytokines&#44; followed by infiltration of neutrophils&#44; may be involved&#46; Systemic corticosteroids are the first-line of treatment in most cases&#46; We present a concise review of the pathogenesis&#44; classification&#44; diagnosis and treatment update of this entity&#46;</p></span>"
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      "es" => array:2 [
        "titulo" => "Resumen"
        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">El s&#237;ndrome de Sweet es la entidad m&#225;s representativa de las dermatosis neutrof&#237;licas&#46; Por lo general se presenta en pacientes con fiebre&#44; neutrofilia&#44; p&#225;pulas erytomatosas dolorosas&#44; n&#243;dulos y placas&#46; Los sitios frecuentemente afectados incluyen la cara&#44; cuello y extremidades superiores los cuales caracter&#237;sticamente presentan un infiltrado neutrof&#237;lico en la dermis superior&#46; Su etiolog&#237;a no esta bien establecida&#44; pero parece que puede estar mediada por una reacci&#243;n de hipersensibilidad de las citocinas&#44; seguido por un infiltrado de neutr&#243;filos&#46; Los corticosteroides sist&#233;micos son la primera l&#237;nea de tratamiento en la mayor&#237;a de los casos&#46; Se presenta una revisi&#243;n actual de la patog&#233;nesis&#44; clasificaci&#243;n&#44; diagn&#243;stico y tratamiento de esta entidad&#46;</p></span>"
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">&#40;A&#8211;C&#41; Disseminated dermatosis affecting the face&#44; upper trunk and four limbs&#44; predominantly on sun-exposed areas&#44; bilateral and prone to symmetry&#44; polymorphous&#44; characterized by erythematous&#44; thick&#44; sharply demarcated nodules and plaques&#44; and some yellow pustules between them&#46; &#40;D&#41; Pathergy phenomenon&#46;</p>"
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">&#40;A&#41; A papulopustular lesion localizated on the head&#44; in the posterior region of the right ear&#44; a skin biopsy &#40;Punch 4&#41; was performed and stained with hematoxylin&#8211;eosin&#59; &#40;B&#41; Histopathology reveals diffuse neutrophilic infiltrate with significant papillary dermal edema&#44; 10&#215;&#59; &#40;C&#41; Papillary dermal edema&#44; perivascular and interstitial infiltrate composed predominately of neutrophils&#44; scattered lymphocytes&#44; histiocytes&#44; and eosinophils&#44; 20&#215;&#59; &#40;D&#41; The infiltration was predominantly composed of neutrophils and histiocytes&#44; 40&#215;&#46;</p>"
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          "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Recommendations algorithm for the initial workup in newly diagnosed Sweet&#39;s syndrome patients&#46;</p>"
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          "leyenda" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">In classical&#58; The presence of both major criteria &#40;1 and 2&#41; and two minor criteria &#40;3&#8211;6&#41; is needed to establish the diagnosis of classical Sweet&#39;s syndrome&#46; In malignancy-associated&#58; the patients must precede&#44; follow&#44; or appear concurrent with the diagnosis of the patient&#39;s neoplasm and classical Sweet&#39;s syndrome diagnostic criteria&#46; In drug-induced&#58; All five features should be present to diagnose Sweet&#39;s syndrome&#46; Adapted from Cohen et al&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">7</span></a></p>"
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                  \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head  " colspan="3" align="center" valign="top" scope="col" style="border-bottom: 2px solid black">Classical</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Diagnostic criteria&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleItalic">Major</span><br>1&#46; Abrupt onset of painful erythematous nodules or plaques&#46;<br>2&#46; Histopathological findings of dense neutrophilic infiltrate without evidence of leukocytoclastic vasculitis&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleItalic">Minor</span><br>3&#46; Fever &#62;38<span class="elsevierStyleHsp" style=""></span>&#176;C<br>4&#46; Association with hematologic or visceral malignancy&#44; inflammatory disease or pregnancy&#44; or preceded by upper respiratory tract infection&#44; gastro-intestinal infection or vaccination<br>5&#46; Excellent response to treatment with systemic corticosteroids or potassium iodide<br>6&#46; Abnormalities in laboratory tests &#40;three of four&#41;&#58; erythrocyte sedimentation rate&#62; 20<span class="elsevierStyleHsp" style=""></span>mm&#47;h&#59; high C-reactive protein&#44; leukocytes &#62;8000&#44; with &#62;70&#37; neutrophils&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " colspan="3" align="left" valign="top"><span class="elsevierStyleItalic">Drug-related Sweet syndrome</span></td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Diagnostic criteria&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " colspan="2" align="left" valign="top">A&#46; Abrupt onset of painful erythematous plaques or nodules<br>B&#46; Histopathological findings of dense neutrophilic infiltrate without evidence of leukocytoclastic vasculitis<br>C&#46; Fever &#62;38<span class="elsevierStyleHsp" style=""></span>&#176;C<br>D&#46; Temporal relation between use of medication and clinical presentation or relapse with readministration<br>E&#46; Disappearance of lesions after drug discontinuation or treatment with systemic corticosteroids</td></tr></tbody></table>
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          "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Diagnostic criteria for sweet syndrome&#44; including classical&#44; drug-induced and malignancy-associated forms&#46;</p>"
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                  \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Drug&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">&#35; of times&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Reference&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Granulocyte colony-stimulating factor&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top"><a class="elsevierStyleCrossRefs" href="#bib0535">7&#44;53&#8211;71</a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Tretinoin&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">11&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top"><a class="elsevierStyleCrossRefs" href="#bib0860">72&#8211;82</a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Sulfamethoxazole<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>Trimethoprim&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">8&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top"><a class="elsevierStyleCrossRefs" href="#bib0635">27&#44;58&#44;83&#8211;88</a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Bortezomib<a class="elsevierStyleCrossRef" href="#tblfn0005"><span class="elsevierStyleSup">a</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">7&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top"><a class="elsevierStyleCrossRefs" href="#bib0945">89&#8211;95</a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Azathioprine&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">5&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top"><a class="elsevierStyleCrossRefs" href="#bib0980">96&#8211;100</a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
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              "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Information updated on August 1&#44; 2015&#59; Bortezomib&#58; antineoplastic&#44; proteasome inhibitor use for mantle cell lymphoma&#44; multiple myeloma and follicular non-Hodgkin lymphoma&#46;</p>"
            ]
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        ]
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          "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Top 5 drugs related to Sweet&#39;s syndrome&#44; based on case reports published on PubMed&#46;</p>"
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      ]
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