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.

PTU-induced autoimmune syndromes can be classified into drug-induced lupus or Drug-induced Vasculitis [1]. PTU-induced Vasculitis is more common than PTU-induced lupus, and has a higher risk of morbidity and mortality [2]. Usually it is limited to the skin in a form of cutaneous leukocytoclastic vasculitis, but may also affect organs including Kidneys and Lungs [3]. And 1 week after starting this therapy, the patient presented with Palpable purpura on his ankles [4]. Skin Biopsy revealed neutrophilic infiltrates in and around Dermal vessels with destruction of vessel walls leading to Scattered Neutrophils, lymphocytes and histiocytes between collagen bundles, suggestive of leukocytoclastic vasculitis [5].

However, the clinical feature was acute hemorrhagic Edema of infancy, a Benign leukocytoclastic vasculitis that occurs in Children between 4 and 24 months of age and is characterized by Fever, large Purpuric Palpable target-like skin lesions affecting the Face, lobes of the Ears, limbs and frequently associated with Edema [6]. Differential diagnosis includes erythema multiforme, hemorrhagic urticaria, drug- induced Vasculitis, Kawasaki disease, infected eczema, sepsis (either meningococcal or non-meningococcal) and Child abuse [7]. Sin embargo, las características clínicas fueron de Edema agudo hemorrágico de la infancia, una vasculitis leucocitoclástica benigna que se presenta en niños de entre 4 y 24 meses y que se caracteriza por fiebre, máculas y lesiones purpúricas [8]. Los diagnósticos diferenciales son eritema multiforme, urticaria, Vasculitis inducida por droga, enfermedad de Kawasaki, eccema infectado, meningococcemia y maltrato infantil, algunas de ellas, con riesgo de mortalidad [9]. T helper Cells and granzyme B seem to be involved in the inflammatory cutaneous process of CLV [10].

It can cause agranulocytosis and cutaneous Vasculitis that can possibly lead to cutaneous necrosis [11]. 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 [12]. Ultimately, a final diagnosis was made by Skin Biopsy, which revealed findings suggestive of leukocytoclastic vasculitis [13]. CONCLUSIONS Cutaneous leukocytoclastic vasculitis can be caused by levamisole, which is used as an adulterant in cocaine [14]. 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 [15].

Our study highlights the multitude of causes of leukocytoclastic Vasculitis [16]. 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 [17]. 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 [18]. For the statistical analysis, we included only patients with positive DIF exclusively in vessel walls (235/282 patients) [19]. We planned to find a correlation between the DIF profiles of LCV patients and the epidemiology data, underlying causes and prognosis [20].

Immunoglobulin A (IgA) deposition at the blood vessel wall was related to age and absence of autoimmune/inflammatory diseases [21]. 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 [22]. The treatment of cryosections with rh-chymase decreased the IF staining of C3c, but not that of immunoglobulins [23]. In conclusion, mast Cells can be one source for C3 in the early and late phases of Vasculitis pathogenesis [24]. 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 [25].

All children aged up to 18 years that have been diagnosed with a Vasculitis disorder from 2002 [26]. All patients had elevated Inflammatory markers (C-reactive protein and erythrocyte sedimentation rate) [27]. Serological methods are recommended for diagnosis because pneumonia or respiratory symptoms are often minimal or even absent in extrapulmonary manifestations due to M [28]. Concomitant use of immunomodulators, such as Corticosteroids or immunoglobulins with Antibiotics effective against M [29]. LCV is characterized as a small-vessel Vasculitis of the cutaneous area [30].

The disease demonstrates purple lesions on the skin due to the destruction of small cutaneous blood vessels [31]. Antinuclear antibodies, rheumatoid factor, Immune complexes, and cryoglobulinemia were negative, as were B and C hepatitis virus serological tests [32]. We report a rare case of Isoniazid induced cutaneous leucocytoclastic Vasculitis [33]. The Skin Biopsy report was consistent with cutaneous leukocytoclastic vasculitis [34]. 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 [35].

There is no established standard for the treatment of leukocytoclastic vasculitis associated with gastroenterologic diseases [36]. Histopathology was consistent with leukocytoclastic vasculitis [37]. 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 [38]. They can produce various skin adverse effects but are only rarely associated with cutaneous Vasculitis [39]. We report a case of acute cutaneous leucocytoclastic vasculitis that developed over two weeks after liver resection due to Metastatic rectal adenocarcinoma [40].

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 [41]. Subsequently, he developed multiple, erythematous-to-purplish, non-blanchable Macules and Papules with an annular arrangement on his Extremities [42]. The histopathology of the Purpuric skin Lesion was consistent with leukocytoclastic vasculitis [43]. Streptomycin, ethambutol and ofloxacin were administered as second-line anti-tuberculosis therapy during his hospitalization [44].

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 , 41 , 42 , 43 , 44 ,

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About Me

I have varied research interests ranging from eHealth, Health Information Exchange, Clinical Trials and Research, Contact Dermatitis, Bioinformatics, and Cosmetic Dermatology. I have work experience in Canada as an eHealth analyst, and in Dubai and India as a Specialist Dermatologist.


Bell Raj Eapen
Hamilton, ON