Sweet’s syndrome with idiopathic thrombocythemia

Abstract

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.

Corticosteroid-resistant Sweet’s syndrome as the first manifestation of myelodysplastic/ myeloproliferative neoplasm-unclassifiable: a case report

“…[2–5] As summarized by Kaszewski, et al (p. 51), other systemic drugs are also effective for the treatment of SS as the firstline or second-line therapy (Table 2). [6]…”

“…[2][3][4][5] As summarized by Kaszewski,et al (p. 51), other systemic drugs are also effective for the treatment of SS as the firstline or second-line therapy (Table 2). [6] SS associated with hematological malignancies (SSAHMs) has been reported in approximately 80% of SS cases associated with malignant disorders. The most common causes of SS are AML and MDS.…”

“…[10,30] Intravenous pulse administration of methylprednisolone sodium succinate (≤1000mg/day) over one or more hours, daily for 3-5 days, maybe utilized for patients whose condition is refractory to other therapies. [6] SS-AHMs are more likely to be corticosteroid-resistant, showing that the skin lesions progressed rapidly after routine dose and full course of glucocorticoid treatment. Additional immuno-suppressive agents, including IVIG, should be considered to treat corticosteroid-resistant SS.…”

Úlceras orales: diagnóstico diferencial y tratamiento

“…Las características clínicas incluyen úlceras orales y genitales, inflamación ocular, lesiones en la piel, así como manifestaciones articulares, vasculares, neurológicas, pulmonares, gastrointestinales y genitourinarias 23 Síndrome de Sweet Trastorno caracterizado por fiebre, lesiones en piel de carácter eritematoso infiltrativo, leucocitosis con neutrofilia e infiltración densa de la dermis por neutrófilos maduros 24 El tratamiento a prescribir (que sería extrapolable en buena medida a otros tipos de úlceras, como las descritas con anterioridad) lo condicionan la gravedad y sintomatología dolorosa de la enfermedad, la frecuencia de los episodios con úlceras y la tolerancia del paciente a la medicación (tabla 2) 13 . Frecuentemente se empieza con tratamiento tópico; la primera línea de tratamiento incluye antisépticos y medicamentos antiinflamatorios/analgésicos.…”

Sweet’s syndrome with idiopathic epididymitis

“…Other agents that have been previously reported as effective in the treatment of SS are potassium iodide (900 mg daily) and colchicine (1.5 mg daily). Indomethacin, cyclosporine, dapsone, clofazimine, chlorambucil, cyclophosphamide may be considered as the second-line treatment [ 4 , 14 ].…”