Estudio retrospectivo de pacientes diagnosticados de síndrome de Sweet en el área de un hospital terciario de la Comunidad Valenciana

Díaz-Corpas, T.; Mateu-Puchades, Almudena; Morales-Suárez-Varela, María; Castells‐Rodellas, A.

doi:10.1016/j.ad.2011.04.014

Cited by 8 publications

(3 citation statements)

References 12 publications

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“…PG ulcers also appear to preferentially avoid body areas devoid of follicular adnexal structures, e.g., the nipple-areolar complex and the palms and soles. This is in contrast to Sweet’s syndrome (a neutrophilic disease), scleroderma, discoid lupus, and other autoimmune diseases, which indeed can occur at these sites (16). …”

Section: Discussionmentioning

confidence: 88%

Classic Ulcerative Pyoderma Gangrenosum Is a T Cell-Mediated Disease Targeting Follicular Adnexal Structures: A Hypothesis Based on Molecular and Clinicopathologic Studies

et al. 2018

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Background: Pyoderma gangrenosum (PG) is a debilitating ulcerative skin disease that is one of the most common associated diseases seen in patients with inflammatory bowel disease and rheumatoid arthritis. Although PG is classified as a neutrophilic dermatosis, its pathophysiology is poorly understood.objective: Use data obtained from patient-reported histories, immunohistochemistry, and gene expression analysis to formulate a hypothesis on PG pathophysiology.Methods: Ten PG patients participated and answered questions about new ulcer formation. Skin biopsies of healed prior ulcers and adjacent normal skin were obtained from four patients for immunohistochemistry. Scars from healthy patients and patients with discoid lupus were used as additional controls. New onset PG papules were analyzed using immunohistochemistry and gene expression analysis via quantitative real-time PCR.results: All PG patients reported that healed sites of previous ulceration are refractory to re-ulceration. Simultaneous biopsies of healed and uninvolved skin triggered ulceration only in the latter. On immunohistochemistry, healed PG scars showed complete loss of pilosebaceous units, which were present in normal skin, and to a lesser extent in control scars, and discoid scars. Early PG papules showed perivascular and peripilosebaceous T cell infiltrates, rather than neutrophils. These early inflammatory events were dominated by increased gene expression of CXCL9, CXCL10, CXCL11, IFNG, and transcription factors consistent with Th1 phenotype.Limitations: Small sample size was the main limitation. Conclusion:We put forth the hypothesis that PG is a T cell response resulting in the destruction of pilosebaceous units.

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Section: Discussionmentioning

confidence: 88%

Classic Ulcerative Pyoderma Gangrenosum Is a T Cell-Mediated Disease Targeting Follicular Adnexal Structures: A Hypothesis Based on Molecular and Clinicopathologic Studies

et al. 2018

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“…59 The association of Sweet syndrome with SLE is most commonly reported; it has been reported in 28 cases, including 6 drug-induced cases (hydralazine, n = 4 60 – 63 ; acyclovir, n = 2 64 , 65 ) and 22 cases that often occurred simultaneously with the onset of LE. 10 , 21 , 51 , 58 , 66 – 78 The skin lesion features may not accurately meet the Sweet syndrome diagnostic criteria; in these cases, a diagnosis of Sweet-like ND has been proposed in the literature (see below).…”

Section: Results Discussion and Literature Reviewmentioning

confidence: 99%

Neutrophilic Skin Lesions in Autoimmune Connective Tissue Diseases

et al. 2014

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The pathophysiology of neutrophilic dermatoses (NDs) and autoimmune connective tissue diseases (AICTDs) is incompletely understood. The association between NDs and AICTDs is rare; recently, however, a distinctive subset of cutaneous lupus erythematosus (LE, the prototypical AICTD) with neutrophilic histological features has been proposed to be included in the spectrum of lupus. The aim of our study was to test the validity of such a classification. We conducted a monocentric retrospective study of 7028 AICTDs patients. Among these 7028 patients, a skin biopsy was performed in 932 cases with mainly neutrophilic infiltrate on histology in 9 cases. Combining our 9 cases and an exhaustive literature review, pyoderma gangrenosum, Sweet syndrome (n = 49), Sweet-like ND (n = 13), neutrophilic urticarial dermatosis (n = 6), palisaded neutrophilic granulomatous dermatitis (n = 12), and histiocytoid neutrophilic dermatitis (n = 2) were likely to occur both in AICTDs and autoinflammatory diseases. Other NDs were specifically encountered in AICTDs: bullous LE (n = 71), amicrobial pustulosis of the folds (n = 28), autoimmunity-related ND (n = 24), ND resembling erythema gyratum repens (n = 1), and neutrophilic annular erythema (n = 1). The improvement of AICTDS neutrophilic lesions under neutrophil targeting therapy suggests possible common physiopathological pathways between NDs and AICTDs.

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“…The symptoms appeared after the second intravenous infusion. The drug was withdrawn, and no further recurrences were observed [19]. Recently, there have been papers describing bortezomib-induced SS [13].…”

Section: Discussionmentioning

confidence: 99%

Sweet’s syndrome with idiopathic thrombocythemia

Kaszewski

Czajkowski

Protas-Drozd

et al. 2014

pdia

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Diagnosis of paraneoplastic skin syndromes associating neoplastic processes is assumed as the crucial aspect of dermatological practice. Knowledge of clinical findings of dermatoses suggesting coincidence of malignant proliferative processes facilitates diagnostic and therapeutic procedures. We would like to present a case of Sweet's syndrome, qualified for comparative paraneoplastic skin syndromes. Sweet's syndrome, acute, febrile neutrophilic dermatosis, was first described by Robert Douglas Sweet in 1964 as a disorder characterized by fever, skin lesions of erythematous-infiltrative character, leukocytosis with neutrophilia and dense infiltrations of dermis by mature neutrophils. Sweet's syndrome aetiology is not fully understood, although cytokine abnormalities suggest that Th1 lymphocytes play an important role in pathogenesis of the dermatosis. Factors inducing Sweet's syndrome include: haematopoietic hyperplasia; neoplasms: genitourinary, breast, gastrointestinal; infections of the respiratory and alimentary system; inflammatory bowel diseases; drugs; pregnancy and vaccinations. Systemic corticosteroids are the “gold standard” of Sweet's syndrome treatment; potassium iodide or colchicine may also be used. Indomethacin, clofazimine, cyclosporine A and sulfones are the second-line drugs.

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Estudio retrospectivo de pacientes diagnosticados de síndrome de Sweet en el área de un hospital terciario de la Comunidad Valenciana

Cited by 8 publications

References 12 publications

Classic Ulcerative Pyoderma Gangrenosum Is a T Cell-Mediated Disease Targeting Follicular Adnexal Structures: A Hypothesis Based on Molecular and Clinicopathologic Studies

Classic Ulcerative Pyoderma Gangrenosum Is a T Cell-Mediated Disease Targeting Follicular Adnexal Structures: A Hypothesis Based on Molecular and Clinicopathologic Studies

Neutrophilic Skin Lesions in Autoimmune Connective Tissue Diseases

Sweet’s syndrome with idiopathic thrombocythemia

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