DermKnowledgeBASE: Cutaneous Leukocytoclastic Vasculitis

Cutaneous Leukocytoclastic Vasculitis

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The text is the summary of recent articles on Cutaneous Leukocytoclastic Vasculitis at 75 thresold from National Library of Medicine (NLM). This information is subject to NCBI's Disclaimer and Copyright notice.


T helper Cells and granzyme B seem to be involved in the inflammatory cutaneous process of CLV [1]. It can cause agranulocytosis and cutaneous Vasculitis that can possibly lead to cutaneous necrosis [2]. In all reported cases of levamisole-induced Vasculitis, it has been described as a clinical syndrome characterized by a constellation of typical clinical features and a positive serum serology for ANCA levels, especially very high-titer p-ANCA levels, in the background of cocaine abuse [3]. Ultimately, a final diagnosis was made by Skin Biopsy, which revealed findings suggestive of leukocytoclastic vasculitis [4]. CONCLUSIONS Cutaneous leukocytoclastic vasculitis can be caused by levamisole, which is used as an adulterant in cocaine [5].

The use of compression bandages and hosiery after interventional and Surgical procedures for varicose veins is based on experience but not on randomized controlled trials [6]. Our study highlights the multitude of causes of leukocytoclastic Vasculitis [7]. Precise history-taking related to contact with rats and detection of skin Eruptions suggestive of leukocytoclastic vasculitis on the extremities, especially on the Feet, can be clues to Streptobacillus moniliformis infection [8]. To establish the correlation of deposition of Immune complexes at the blood vessel walls with underlying causes and prognosis of LCV, we performed a retrospective study from January 2007 to December 2014 [9]. For the statistical analysis, we included only patients with positive DIF exclusively in vessel walls (235/282 patients) [10].

We planned to find a correlation between the DIF profiles of LCV patients and the epidemiology data, underlying causes and prognosis [11]. Immunoglobulin A (IgA) deposition at the blood vessel wall was related to age and absence of autoimmune/inflammatory diseases [12]. Immunoglobulin M (IgM) deposition at the blood vessel wall was related to females, autoimmune/inflammatory disorders, C3 and C4 consumption and antinuclear Antibody and anti-SSA/anti-SSB positivity [13]. The treatment of cryosections with rh-chymase decreased the IF staining of C3c, but not that of immunoglobulins [14]. In conclusion, mast Cells can be one source for C3 in the early and late phases of Vasculitis pathogenesis [15].

All 6 cases met the classification criteria for the diagnosis of HSP, had relapsing symptoms despite Corticosteroid use, were successfully treated with Azathioprine and were tapered off of Corticosteroids [16]. All children aged up to 18 years that have been diagnosed with a Vasculitis disorder from 2002 [17]. All patients had elevated Inflammatory markers (C-reactive protein and erythrocyte sedimentation rate) [18]. Serological methods are recommended for diagnosis because pneumonia or respiratory symptoms are often minimal or even absent in extrapulmonary manifestations due to M [19]. Concomitant use of immunomodulators, such as Corticosteroids or immunoglobulins with Antibiotics effective against M [20].

LCV is characterized as a small-vessel Vasculitis of the cutaneous area [21]. Antinuclear antibodies, rheumatoid factor, Immune complexes, and cryoglobulinemia were negative, as were B and C hepatitis virus serological tests [22]. We report a rare case of Isoniazid induced cutaneous leucocytoclastic Vasculitis [23]. The Skin Biopsy report was consistent with cutaneous leukocytoclastic vasculitis [24]. Many different clinical and serological signs have been suggested as possible predictive factors for malignancy in dermatomyositis: age, increased erythrocyte sedimentation rate (ESR), presence of cutaneous leukocytoclastic Vasculitis, cutaneous rash and skin lesions as cutaneous necrosis and periungueal erythemas, neoplastic markers or dysphagia [25].

There is no established standard for the treatment of leukocytoclastic vasculitis associated with gastroenterologic diseases [26]. Histopathology was consistent with leukocytoclastic vasculitis [27]. iga vasculitis or cutaneous leukocytoclastic vasculitis), hemorrhagic Papules and Necrotic Plaques which occur in Acral areas after cooling indicate cryoglobulinemic vasculitis, hemorrhagic Papules and Macules which develop in patients who start to feel worse and develop Fever should arouse suspicion of septic vasulitis, while the simultaneous presence of ulcerating Nodules and hemorrhagic Papules without predilection for the lower Legs will suggest ANCA-associated Vasculitis [28]. They can produce various skin adverse effects but are only rarely associated with cutaneous Vasculitis [29]. We report a case of acute cutaneous leucocytoclastic vasculitis that developed over two weeks after liver resection due to Metastatic rectal adenocarcinoma [30].

There are no other reports about erlotinib-induced leukocytoclastic vasculitis (LV) in the erlotinib-bevacizumab regimen for Bone Metastasis, from a relapsed hepatocellular carcinoma (HCC) in liver-transplanted patients [31]. The histopathology of the Purpuric skin Lesion was consistent with leukocytoclastic vasculitis [32]. Streptomycin, ethambutol and ofloxacin were administered as second-line anti-tuberculosis therapy during his hospitalization [33]. We report the case of an 18-year-old Female patient who developed erythema elevatum diutinum and whose diagnosis was based on the morphologic characteristics, the Distribution pattern of the cutaneous lesions and the histopathological findings of leukocytoclastic vasculitis [34]. A Skin Biopsy showed leukocytoclastic vasculitis with conspicuous Eosinophilic Infiltration of the tissue [35].

In rare cases, Multiple myeloma may be associated to skin involvement secondary to amyloidosis, cryoglobulinemia, and poems syndrome [36]. We report the case of an uncommon presentation of an IgA lambda Multiple myeloma in a 58 year-old woman preceded by Vascular purpura with cutaneous leukocytoclastic vasculitis (LV) and intense deposit of IgA and kappa light chains in the Dermal vessels [37]. Purpura resolved after specific treatment of Multiple myeloma and diagnosis of paraneoplastic purpura was asserted [38]. We propose a brief review of the literature about skin involvement during Multiple myeloma [39]. One patient previously hospitalized with documented exfoliative erythroderma during allopurinol treatment, developed biopsy-confirmed cutaneous leukocytoclastic Vasculitis [40].

References: 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 ,

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