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The skin
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Leukocytoclastic vasculitis presents as grouped purpuric lesions that do not blanch with pressure. Dependent areas prone to venous stasis such as the lower legs are most commonly affected (Figure 19.27A). Leukocytoclastic vasculitis tends to be acute and self-limited although relapses are not uncommon.
Vasculitis mimics
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Debdeep Mitra, Ajay Chopra, Neerja Saraswat
Hepatitis C virus: The patient presents with a triad of arthritis, palpable purpura, and type II cryoglobulinemia. It leads to small vessel leukocytoclastic vasculitis of the skin. Lower extremities are predominantly affected and are cold on examination. However, medium and small vessels may also be involved.
Inflammatory dermatoses affecting the nail
Published in Eckart Haneke, Histopathology of the NailOnychopathology, 2017
Leukocytoclastic vasculitis is a reaction pattern involving mainly the superficial dermal postcapillary venules. An infiltrate around these vessels predominantly consisting of neutrophils, which penetrate the vessel walls, is seen. There is fibrinoid change of the vessel wall, endothelial cell swelling, and fragmentation of the neutrophil nuclei called karyorrhexis. Depending on the severity of vessel damage, extravasated erythrocytes may almost obscure the neutrophils. Severe vessel injury will also cause circumscribed necroses, occasionally with small ulcerations. Sometimes, there are so many neutrophils that the aspect of a pustular vasculitis develops. Severe edema may cause a blister-like appearance.
A severe case of Levamisole-induced vasculitis
Published in Clinical Toxicology, 2022
Austin Ambur, Timothy Nyckowski
A 28-year-old African American male presented to the emergency department with complaint of a rapidly progressive painful cutaneous eruption and progressive shortness of breath. On initial evaluation, he appeared lethargic, confused, and became progressively combative with the eventual development of seizures. He was then intubated and sedated followed by admission to the ICU for respiratory support and further evaluation. Cutaneous evaluation revealed tender retiform plaques with a necrotic center on his face, ears, and upper arms (Figures 1 and 2). Laboratory investigation revealed anemia (Hb: 8.9 g/dL), agranulocytosis (Absolute neutrophil count: 95/mm3), thrombocytopenia (platelets: 125 k/µL), elevated acute-phase reactants (ESR: 120 mm/hour; CRP 62.5 mg/L), and acute renal failure (BUN: 51 mg/dL; Cr 3.23 mg/dL). Urine toxicology was remarkable for cocaine and levamisole. Blood and urine cultures were negative for infection. Autoimmune workup and a skin biopsy were performed for suspicion of vasculopathy. There was positivity for P-ANCA, antiproteinase 3, ANA, and hypocomplementemia. H&E staining demonstrated leukocytoclastic vasculitis with small vessel vasculitis with intravascular thrombi in the superficial dermis. The clinicopathological features were most consistent with a diagnosis of levamisole-induced vasculopathy/vasculitis. Unfortunately, the patient rapidly decompensated from suspected neurological vasculitis. His condition was deemed neurologically irreversible and life supportive measures were discontinued after discussion with the family. A post-mortem exam was not obtained.
Retinal Vasculitis and Posterior Pole Preretinal Exudates in Exogenous Bacterial Endophthalmitis: Management and Visual Outcomes
Published in Ocular Immunology and Inflammation, 2022
Kuan-Jen Chen, Yen-Po Chen, Nan-Kai Wang, Ming-Hui Sun, Chi-Chin Sun, Wei-Chi Wu, Chi-Chun Lai
Endophthalmitis is a serious intraocular inflammatory disorder resulting from infection of the vitreous cavity, often resulting in severe vision loss. Retinal vasculitis is one of the early signs of exogenous endophthalmitis.1–3 Recently, postoperative hemorrhagic occlusive retinal vasculitis has been reported in patients receiving intracameral antibiotics, such as vancomycin.4–7 Although the precise cause remains unknown, this disease may represent a delayed immune reaction similar to vancomycin-induced leukocytoclastic vasculitis.6 Inferior or posterior pole preretinal exudates are often present in an eye with severe endophthalmitis. Preretinal exudates consist largely of tissue debris, inflammation by-products, and recruited leukocytes. Posterior pole preretinal exudates with retinal vasculitis have been reported in uveitis and infectious endophthalmitis.1–3 However, these signs are difficultly recognized preoperatively and typically observed intraoperatively.
Predictive role of laboratory markers and clinical features for recurrent Henoch-Schönlein Purpura in childhood: A study from Turkey
Published in Modern Rheumatology, 2020
Şule Gökçe, Zafer Kurugöl, Güldane Koturoğlu, Aslı Aslan
Henoch Schönlein Purpura (HSP), also known as immunoglobulin A (IgA) vasculitis, is the most common vasculitis that affects the small vessels of the skin, joints, gastrointestinal tract and kidneys in childhood. It was originally recognized in 1801 by Heberden and described as having an association with arthritis by Schonlein in 1837. The disease is characterized by the quadruple of palpable purpura, abdominal pain, arthritis, and nephritis. It is seen with an incidence of about 20 cases per 100,000 yearly [1]. HSP is a type III hypersensitivity reaction mediated small vessel vasculitis. Purpuric skin lesions are the most common findings in HSP. Biopsy of the skin lesions characteristically demonstrates leukocytoclastic vasculitis which could also be seen in other types of vasculitis. Possible trigger factors have been reported including respiratory system infections, drugs, vaccines, and other environmental exposures [2,3]. Although the etiology of HSP is not clearly known, there is evidence to support immunopathological mechanisms. Renal and skin biopsies have shown that widespread abnormalities in IgA and IgA immune complexes such as IgA Rheumatoid factor (RF), IgA Anti-Neutrophil Cytoplasmic Antibody (ANCA) [4].