Successive development of cutaneous polyarteritis nodosa, leucocytoclastic vasculitis and Sweet's syndrome in a patient with cervical lymphadenitis caused by Mycobacterium fortuitum
Department of Dermatology, National Taiwan University Hospital and National Taiwan University College of Medicine, 7 Chung-Shan South Road, Taipei, Taiwan.British Journal of Dermatology (Impact Factor: 4.28). 11/2004; 151(5):1096-100. DOI: 10.1111/j.1365-2133.2004.06201.x
Mycobacterium fortuitum is a rapidly growing mycobacterium found in soil and water throughout the world. It can cause diseases in immunocompetent patients, usually resulting in localized skin and soft tissue infections. Cervical lymphadenitis caused by M. fortuitum is rare. We report a 46-year-old woman in whom skin lesions of cutaneous polyarteritis nodosa, leucocytoclastic vasculitis and Sweet's syndrome had successively developed before the diagnosis of cervical lymphadenitis caused by M. fortuitum was made. The skin lesions responded to colchicine and systemic corticosteroids but recurred intermittently. After establishment of the diagnosis, she received treatment with clarithromycin and ciprofloxacin. The cervical lymph nodes decreased in size 6 months later and no more new skin lesions were found.
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ABSTRACT: In recent years, many investigators have focused on potential associations between infections and vascular inflammation. We review the principal pathogenic mechanisms that have been implicated for possible roles in the vascular inflammation initiated by infectious agents. We also summarize the most important literature related to this topic. A novel theory known as autoantigen complementarity suggests that an infectious agent could trigger antineutrophil cytoplasmic antibody-associated vasculitis. Several recent studies investigating the presence of parvovirus B19 and herpesviruses in temporal arteries with giant cell arteritis have yielded contradictory results. A recent study has identified higher frequency of a novel human virus, the 'New Haven coronavirus', in respiratory secretions of children with Kawasaki disease. Many case reports have suggested potential relationships between human pathogens and vasculitis. There remains considerable interest in the possibilities of primary vasculitic syndromes caused in some fashion by infection. With the exception of a few well sustained associations - for example hepatitis B or C with known vasculitic syndromes - most of the purported links between microbial agents and primary vasculitides remain speculative.
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ABSTRACT: 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.
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ABSTRACT: Sweet's syndrome (SS) is the prototypic neutrophilic dermatosis. First described in 1964, the characterization of new clinical associations, unique histopathological findings and clinical variants have stimulated much interest and discussion recently. However, the prevalence of these unusual variants and clinical associations within a single cohort of patients, has not been described. To describe and evaluate the prevalence of unusual clinical and histopathological features, as well as the clinical associations of SS seen in patients from the National Skin Centre, Singapore. This is a retrospective study of all consecutive cases of SS seen at our centre over a 5.5-year period (June 1999-December 2004). Data on associated systemic diseases was obtained from the medical records and matched with information from the National Cancer Registry, Singapore. Patients not actively followed up for more than 3 months were contacted for their updated health status. Thirty-seven patients were identified. Ten (27%) had non-idiopathic SS. These were associated with haematological disorders, connective tissue disorders, infections or a drug. Twenty-nine patients (78%) had at least one atypical clinical or histopathological feature. Atypical clinical features included bullous lesions, SS with hand involvement or neutrophilic dermatoses of the hands and the concomitant existence of subcutaneous SS with pyoderma gangrenosum. SS was the presenting feature in three patients with infections caused by atypical organisms, including Mycobacterium chelonae, Penicillium species and Salmonella type D. Unique histopathological variants included subcutaneous SS and lesions containing an admixture of mature and immature neutrophils. Subcutaneous neutrophilic inflammation seemed to be more common in patients with an underlying haematological disorder. This group of patients also had a lower mean haemoglobin level. Unusual clinical and histopathological variants of SS described in the literature are similarly encountered in our cohort of patients, with some features being more common than others. We highlight and discuss some unique clinical and histopathological observations seen in our patients with SS.
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