2,131 research outputs found

    Sweet's syndrome – a comprehensive review of an acute febrile neutrophilic dermatosis

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    Sweet's syndrome (the eponym for acute febrile neutrophilic dermatosis) is characterized by a constellation of clinical symptoms, physical features, and pathologic findings which include fever, neutrophilia, tender erythematous skin lesions (papules, nodules, and plaques), and a diffuse infiltrate consisting predominantly of mature neutrophils that are typically located in the upper dermis. Several hundreds cases of Sweet's syndrome have been published. Sweet's syndrome presents in three clinical settings: classical (or idiopathic), malignancy-associated, and drug-induced. Classical Sweet's syndrome (CSS) usually presents in women between the age of 30 to 50 years, it is often preceded by an upper respiratory tract infection and may be associated with inflammatory bowel disease and pregnancy. Approximately one-third of patients with CSS experience recurrence of the dermatosis. The malignancy-associated Sweet's syndrome (MASS) can occur as a paraneoplastic syndrome in patients with an established cancer or individuals whose Sweet's syndrome-related hematologic dyscrasia or solid tumor was previously undiscovered; MASS is most commonly related to acute myelogenous leukemia. The dermatosis can precede, follow, or appear concurrent with the diagnosis of the patient's cancer. Hence, MASS can be the cutaneous harbinger of either an undiagnosed visceral malignancy in a previously cancer-free individual or an unsuspected cancer recurrence in an oncology patient. Drug-induced Sweet's syndrome (DISS) most commonly occurs in patients who have been treated with granulocyte-colony stimulating factor, however, other medications may also be associated with DISS. The pathogenesis of Sweet's syndrome may be multifactorial and still remains to be definitively established. Clinical and laboratory evidence suggests that cytokines have an etiologic role. Systemic corticosteroids are the therapeutic gold standard for Sweet's syndrome. After initiation of treatment with systemic corticosteroids, there is a prompt response consisting of dramatic improvement of both the dermatosis-related symptoms and skin lesions. Topical application of high potency corticosteroids or intralesional corticosteroids may be efficacious for treating localized lesions. Other first-line oral systemic agents are potassium iodide and colchicine. Second-line oral systemic agents include indomethacin, clofazimine, cyclosporine, and dapsone. The symptoms and lesions of Sweet's syndrome may resolved spontaneously, without any therapeutic intervention; however, recurrence may follow either spontaneous remission or therapy-induced clinical resolution

    Frictional alopecia of the distal legs: case series and review

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    BackgroundAcquired alopecia of the lower legs may occur secondary to friction due to socks, footwear, or both on the lower extremities. There is scant literature that reports on this phenomenon.Methods and MaterialsWe describe 5 patients who presented with alopecia of their lower legs induced by socks, footwear, or both.Methods and Materials: We reviewed PubMed for the following terms: ankle alopecia, friction alopecia, frictional alopecia, lower extremity alopecia, non-scarring leg alopecia, and sock alopecia. We also reviewed papers containing these terms and their references.ResultsAcquired frictional alopecia of the lower extremities is often an asymptomatic condition found incidentally on physical examination. The condition can persist for many years despite removal of the source of friction.ConclusionThe incidence of acquired frictional alopecia of the lower extremities may be greater than reflected in previously published reports. It is a non-scarring subtype of alopecia that was noted as an incidental finding during the patient’s dermatology appointment

    Merkel Cell Carcinoma with a Suppressor of Fused (SUFU) Mutation: Case Report and Potential Therapeutic Implications

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    The Author(s) 2015. This article is published with open access at Springerlink.com Introduction: Merkel cell carcinoma is a neuroendocrine malignancy. Suppressor of fused (SUFU) is a tumor suppressor oncogene that participates in the Hedgehog (Hh) signaling pathway. The aim of the study wa

    Warning signal: Unaware of an in absentia conviction, South African cancer specialist jailed on return to the United Arab Emirates.

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    In 2002, Dr. Cyril Karabus, a specialist in pediatric cancers and retired head of the Oncology and Hematology Unit of Red Cross Children\u27s Hospital in Capetown, South Africa, spent a brief locum at Sheikh Khalifa Medical City, a hospital in Abu Dhabi in the United Arab Emirates (UAE). He was there for only 5 weeks, during which time he treated a young girl who died of acute myeloblastic leukemia. After Karabus returned home, the girl\u27s father complained to police about his daughter\u27s death, and Karabus was convicted of murder in absentia. Karabus knew nothing of the charges or of the conviction. Widely respected for his expertise and compassion, Karabus had dedicated his life to treating children with malignancies. In South Africa, he was especially well known for his commitment to saving the lives of black children with cancer during the apartheid era.
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