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Leukocytoclastic vasculitis (LCV) is a very rare immune complex-mediated condition affecting the small vessels walls. We present the case of a 48-year-old woman with necrotizing bilateral breast LCV on treatment with glatiramer acetate for multiple sclerosis. Bilateral mastectomies and debridement of the anterior abdominal wall were required due to the rapidly evolving necrotizing process. Rapid assessment and a multidisciplinary approach are fundamental in treating this rare life-threatening condition.

Made available in DSpace on 2022-05-01T09:31:07Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-01-01 Cutaneous involvement is one of the most common extraintestinal manifestations of inflammatory bowel disease (IBD). More commonly, pyoderma gangrenosum and erythema nodosum are noted, but psoriasis, aphthous stomatitis, Sweet's syndrome, and vasculitis may also occur. Leukocytoclastic vasculitis (LCV) is a rare cutaneous manifestation, characterized by the appearance of palpable purpura, urticaria, and ulcer-necrotic lesions predominantly in the lower extremities that improve with immunosuppressive therapy. In this case, we report a patient with CD and LCV. We also searched the literature on the diagnosis and treatment of LCV in patients with CD. Female, 31, presented with diarrhea containing mucus and blood, abdominal pain, arthralgia, and enanthematous plaques and ulcers with a hematinic background in the lower extremities. The results of the colonoscopy were compatible with CD and skin biopsy showed signs of LCV. Systemic autoimmune disease and primary vasculitis were ruled out. The patient received treatment with a systemic corticosteroid and the skin lesions improved. Outpatient treatment with antitumor necrosis factor therapy was initiated to promote skin healing and IBD clinical remission. As LCV is a rare manifestation of IBD, it is necessary to distinguish this dermatopathy from other systemic vasculitis. The engagement of a multidisciplinary team is essential for the correct diagnosis and management. São Paulo State University (Unesp) Medical School Clinica Universidad de Los Andes São Paulo State University (Unesp) Medical School

Rarely, patients with systemic lupus erythematosus (SLE) develop bullous eruptions, a disease called bullous SLE in a narrow sense that has autoantibodies against type VII collagen. We describe an unusual case in which a patient with SLE developed extensive bullae on her lower extremities. Histologically, the bullous lesions were suggestive of leukocytoclastic vasculitis with deposition of C3 within blood vessel walls. Immunoblot analyses and enzyme-linked immunosorbent assays were negative for anti-type VII collagen antibodies. We initially considered bullous SLE, but eventually made a diagnosis of secondary vasculitis in SLE. The oral prednisolone dose was increased, and the vesiculobullous lesions resolved. The clinical presentations of cutaneous vasculitis in SLE include palpable purpura, petechiae, papulonodular lesions, and livedo reticularis. Bullous lesions seem to be uncommon. Physicians need to be aware that extensive bullae can occur as a result of secondary vasculitis in SLE, even if the patient does not exhibit high disease activity.

Leukocytoclastic vasculitis (LCV) refers to the histopathological changes observed in a common form of small vessel vasculitis that can affect skin and/or internal organs. LCV can be precipitated by several causes (including infections, drugs, and collagen vascular diseases) or can be idiopathic. We report a 50-year-old man who presented with fever, parotid enlargement and skin rash (discrete and confluent erythematous macules, papules, and plaques and a few purpuric lesions on the back of trunk and upper limbs), 3 weeks after being diagnosed with coronavirus disease 2019 (COVID-19). The patient showed four out of the five features required to satisfy the working case definition of multisystem inflammatory syndrome in adults (MIS-A). Histopathology of rash was consistent with LCV. Whether, COVID-19 was the cause for LCV in our patient remains unclear. The fever, parotid enlargement and rash showed complete resolution following treatment with systemic corticosteroids and enoxaparin.

Although clinicians often put vasculitis and microvascular occlusion in the same differential diagnosis, biopsy findings often are either vasculitis or occlusion. However, both vasculitis and occlusion are present in some cases of levamisole-associated vasculopathy and certain infections. Depth of dermal involvement and vessel size should be reported, because superficial and deep small vessel leukocytoclastic vasculitis and/or involvement of medium-sized vessels may be associated with systemic disease. Microvascular occlusion of vessels in the fat should prompt consideration of calciphylaxis. Clues to ultimate clinical diagnosis can be garnered from depth of involvement, size of vessels affected, and presence of both vasculitis and occlusion.

Leukocytoclastic vasculitis has been reported in the setting of COVID-19 infection and post-COVID-19 vaccination. We report a case of post-COVID-19 vaccination IgA vasculitis with IgA immune deposits in the skin and renal involvement; SARS-CoV spike protein immunohistochemical staining was negative. IgA vasculitis with skin and renal involvement is a potential reaction to COVID-19 vaccination. This article is protected by copyright. All rights reserved.

Vasculitis is a disease process that results from inflammation of blood vessel walls. The clinical presentation is variable and dependent upon the size and location of the vessels involved.1 Cutaneous vasculitis refers to a vasculitis that results in skin manifestations, often due to involvement of small- and medium-sized vessels. The incidence of cutaneous vasculitis ranges from 15.4 to 29.7 cases per 1 million people every year.2 Clinical presentations vary and can include petechiae, purpura, purpuric papules, hemorrhagic vesicles, and bullae.1 Biopsy is the gold standard for making a diagnosis of cutaneous vasculitis.2 The collection of histopathologic findings in cutaneous small-vessel vasculitis are referred to as leukocytoclastic vasculitis (LCV) and include a polymorphonuclear neutrophilic infiltrate, primarily in postcapillary venules, with fibrinoid deposits in and around the vessel wall and extravasation of red blood cells.3 Although LCV is often idiopathic, it may occur secondary to infection, drugs, malignancy, or autoimmune processes, such as antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV).4 The following case report describes a patient with a history of antisynthetase syndrome (ASS) who subsequently developed IgA vasculitis with copositive ANCA.

Leukocytoclastic vasculitis (LCV) is a histopathologic description of a common form of small vessel vasculitis (SVV), that can be found in various types of vasculitis affecting the skin and internal organs. The leading clinical presentation of LCV is palpable purpura and the diagnosis relies on histopathological examination, in which the inflammatory infiltrate is composed of neutrophils with fibrinoid necrosis and disintegration of nuclei into fragments (“leukocytoclasia”). Several medications can cause LCV, as well as infections, or malignancy. Among systemic diseases, the most frequently associated with LCV are ANCA-associated vasculitides, connective tissue diseases, cryoglobulinemic vasculitis, IgA vasculitis (formerly known as Henoch–Schonlein purpura) and hypocomplementemic urticarial vasculitis (HUV). When LCV is suspected, an extensive workout is usually necessary to determine whether the process is skin-limited, or expression of a systemic vasculitis or disease. A comprehensive history and detailed physical examination must be performed; platelet count, renal function and urinalysis, serological tests for hepatitis B and C viruses, autoantibodies (anti-nuclear antibodies and anti-neutrophil cytoplasmic antibodies), complement fractions and IgA staining in biopsy specimens are part of the usual workout of LCV. The treatment is mainly focused on symptom management, based on rest (avoiding standing or walking), low dose corticosteroids, colchicine or different unproven therapies, if skin-limited. When a medication is the cause, the prognosis is favorable and the discontinuation of the culprit drug is usually resolutive. Conversely, when a systemic vasculitis is the cause of LCV, higher doses of corticosteroids or immunosuppressive agents are required, according to the severity of organ involvement and the underlying associated disease.

Anti-tumor necrosis factor (TNF) α agents, widely used for the treatment of Crohn's disease (CD), can sometimes induce skin-associated adverse events, which mainly include psoriasis-like eruptions, eczema, and cutaneous infections. In contrast, purpura caused by vasculitis is rarely seen. We herein report a unique case of leukocytoclastic vasculitis induced by infliximab administered for CD in which intermittent purpura development was noted. Fluorescent immunostaining showed no immunoglobulin A deposition on the vessel walls. No purpura was initially seen after starting infliximab, but it appeared approximately 10 months later; however, administration did not have to be discontinued, and the condition was later resolved. The present findings provide important details regarding vasculitis induced by anti-tumor necrosis factor-α agent administration.

Cutaneous vasculitides include a widespread and heterogeneous cluster of diseases affecting the blood vessels that are clinically characterized by polymorphic skin lesions, including palpable purpura, urticarial and/or necrotic-ulcerative lesions. Often, they can be manifestations of a systemic disease. Selected cases occur in the mouth. A 75-year-old female presented to her physician for the sudden appearance of blisters in her mouth, with severe orodynia and no history of other diseases or medication intake. A skin biopsy of the oral mucosa yielded a diagnosis of leukocytoclastic vasculitis. The direct immunofluorescence and immunohistochemistry stains demonstrated deposits of IgD, IgG, IgA, IgM, kappa, lambda, C1q, C3c, albumin and fibrinogen at the upper dermal neurovascular plexus. IgD also demonstrated positive nucleolar staining of the keratinocytes. Our case involves a rare presentation of oral cutaneous vasculitis with immune deposits of several immunoglobulins, complement, albumin and fibrinogen. Our case adds importance to studies of the IgD role in antigenic complex immune responses, especially in the mouth.

Leukocytoclastic vasculitis (LCV) is a small-vessel vasculitis that presents with palpable purpura. The most common identified triggers of LCV are infection or exposure to a new medication. Herpes zoster (HZ) occurs as a result of the reactivation of the varicella-zoster virus (VZV). VZV is able to infect endothelial cells directly, producing a spectrum of vasculitides, including that of large and medium vessels. We report a case of a patient with synchronous HZ infection and segmental small-vessel vasculitis.

La dermatosis neutrofílica acral (síndrome de Sweet localizado) fue descrita inicialmente como una manifestación cutánea de predominio en el dorso de las manos, con características histopatológicas de una vasculitis leucocitoclástica. Posteriormente se describió la presencia de neutrófilos y los cambios paraclínicos de una dermatosis neutrofílica localizada. Esta entidad se asocia a la presencia de infecciones, enfermedades autoinmunitarias, fármacos y neoplasias. Reportamos el caso de una mujer de 69 años con antecedente de carcinoma papilar de tiroides con nódulos dolorosos en palmas compatibles con síndrome de Sweet localizado.

Scabies is an itchy cutaneous parasitosis caused by Sarcoptes scabiei. Leukocytoclastic vasculitis (LCV) is a common vasculitis in adults and is often idiopathic but may develop due to infection, autoimmune diseases, malignancy, or drugs. Few cases of scabies-related LCV have been reported in the literature. We present a case of LCV, which we thought to be related to scabies, in light of the literature review. A 62-year-old male patient presented with complaints of cough, sputum, fever, and itchy rash on his legs for one and a half months. Treatment targeting pneumonia was initiated. He was diagnosed as scabies with pruritic maculopapular and purpuric eruption. We learned that itchy skin lesions were present in the spouse, as well. Topical permethrin treatment was initiated on both the patient and the spouse. Skin biopsy of the vasculitic lesions was reported as leukocytoclastic vasculitis pathologically. Mass malignancy, autoimmune diseases, infectious causes were excluded. Vasculitic lesions regressed with topical treatment. Improvement of the vasculitic lesions with topical permethrin treatment, exclusion of other causes, and presence of similar complaints in the patients’ spouse have led us to the diagnosis of scabies and LCV secondary to scabies. LCV due to scabies, which is a rarely seen condition especially in itchy lesions, is a challenging diagnosis. A detailed anamnesis would facilitate diagnosing such cases.

This article is a continuation of the literature review on skin vasculitis. In the first part, information was presented on the current nomenclature and prevalence of vasculitis, pathomorphological changes in the skin, as well as diagnostic algorithms for examining patients with this pathology are reflected. The second part of the article contains a detailed description of the elements of the skin rash with systemic and organ-specific vasculitis, presents the clinical manifestations observed with damage to other organs and systems, the development of possible complications. The data on modern treatment tactics are summarized, modern approaches using pathogenetic and symptomatic therapy of patients with various vasculitis are reflected.

We report a case of IgA vasculitis that developed during the treatment of tuberculosis. Patients with tuberculosis who are on antituberculosis treatment can be administered steroids for severe disease or complications.

Background Leukocytoclastic vasculitis (LCV) is an immune-complex mediated vasculitis characterized by neutrophilic inflammation and nuclear debris in post capillary venules. LCV is a rare dermatologic manifestation of Crohn’s disease (CD) and may occur with the onset of the disease or any time after the diagnosis including the period of exacerbation. Case presentation We present a 70 year old woman with history of psoriasis and treatment refractory CD requiring monoclonal antibody therapy with ustekinumab. One month prior to the current admission, she developed abdominal pain, worsening diarrhea and was diagnosed with CD exacerbation for which she was given ustekinumab. While her abdominal symptoms mildly improved with ustekinumab, she developed new bilateral lower extremity rash initially treated with levofloxacin for presumed cellulitis. The rash consisted of mild erythematous, non-scaling patches with scattered non-palpable petechiae on the lower extremities with subsequent involvement of abdomen, lower back and buttocks. Abdominal exam showed diffuse tenderness without mass, guarding or rebound while reminder of physical exam was unremarkable. Following the failure of antimicrobial therapy, she was diagnosed with LCV by skin biopsy. Complete work up was negative for infectious, malignant and inflammatory etiologies of LCV. Patient improved with increased dose of budesonide and subsequently continued to tolerate ustekinumab without recurrence of LCV. Discussion and conclusion LCV is a rare form of vasculitis and one of the rarest dermatologic manifestations of CD, appearing at any stage of the disease. LCV has been associated with autoimmune diseases, infections, specific drugs (levofloxacin, ustekinumab), and malignancy. Clinical presentation of LCV is variable and frequently mistaken for cellulitis. LCV should be considered in differential diagnosis of bilateral lower extremity rash in patients with CD after infectious, malignant and auto-immune/inflammatory etiologies are excluded. Unlike erythema nodosum (EN) and pyoderma gangrenosum (PG), LCV requires biopsy for diagnosis. Most patients respond well to steroids without scarring.

Henoch-Schönlein purpura (HSP) is a self-limiting vasculitic disease, commonly seen in children. It is characterized by palpable purpura, arthritis, hematuria and abdominal pain. Hematochezia is an uncommon symptom. The patient being reported is an adult male who presented with vomiting, abdominal pain and hematochezia, followed by appearance of palpable purpura and arthritis. He was diagnosed to have HSP. Hematochezia as one of the initial presentations of HSP in adults is an uncommon scenario.

Immunoglobulin A (IgA)-mediated leukocytoclastic vasculitis is a cutaneous small-vessel vasculitis characterized by skin findings of palpable purpura. It may occur secondary to infections, neoplasms, drugs, and systemic conditions, although it is most commonly idiopathic. A known, but rare, trigger for IgA vasculitis is alcohol consumption. We present a case of a man with IgA vasculitis associated with alcohol use and review the literature on alcohol-associated vasculitis. Although rarely reported, alcohol-associated IgA vasculitis is an important entity to consider for appropriate diagnosis and management of such patients.

The article presents as an introduction a mini-review devoted to the problem of cutaneous leukocytoclastic vasculitis. Despite the wide prevalence of this local vasculitis, cases of its combination with systemic lesions are rare. Isolated cases of combination of leukocytoclastic vasculitis with kidney damage are described. We present a clinical case of patient N. with leukocytoclastic vasculitis in combination with chronic glomerulonephritis. Both lesions were confirmed morphologically. We assume that vasculitis is systemic and kidney damage is caused by it. The stages of management of the patient, the response of the disease to the therapy are presented.

Background Skin involvement in granulomatosis with polyangiitis (GPA) is common and can appear as an initial presentation of the disease or more commonly through its course. Case presentation We report a case of a 24-year-old male patient, previously diagnosed as having GPA, admitted with fever, hemoptysis, generalized hemorrhagic blisters associated with arthralgia, fatigue, myalgia, nasal crusting, and vertigo. Three weeks prior to admission, he developed erythematous papules on both elbows, and purpuric papules on both lower limbs. Histopathological examination revealed: interstitial granulomatous dermatitis (elbows) and foci of dermal hemorrhage, foci of interstitial histiocytes and zones of altered necrobiotic collagen (lower limbs) consistent with cutaneous lesions of GPA. Two weeks later, his rash progressed to widespread purpura associated with hemorrhagic blisters. Another biopsy revealed leukocytoclastic vasculitis with fibrinoid necrosis of the vessel walls associated with perivascular infiltrate of neutrophils, nuclear dust and extravasated erythrocytes without an associated granulomatous inflammation or necrobiosis. The constellation of the results of the three biopsies together with clinical correlation pointed to a flare of GPA. Conclusion Skin involvement in GPA is quite common, and it can manifest in different forms in the same patient. Our patient developed three different skin pathologies within a short period of time.

Cutaneous vasculitis is a heterogeneous group of diseases caused by inflammation of the blood vessel wall of the skin. The variety of cutaneous vasculitis, their clinical similarity, lack of clear diagnostic criteria and common terminology cause an extremely complex process of diagnosis of this group of diseases. A dermatologist is often the first specialist to diagnose vasculitis. Currently there is no single "monodisciplinary" classification of v ascular damage, there is no generally accepted terminology and classification of cutaneous vasculitis. In domestic dermatovenerology, vasculitis is classified according to the morphological elements of the skin rash, and not by etiology and pathogenesis. This makes it difficult for different specialists to understand the diagnosis and maintain continuity in the management of patients. The article presents the nomenclature of vasculitis of the 2012 revised international Chapel Hill consensus conference nomenclature of vasculitides, supplemented by organ-specific cutaneous vasculitis, describes the pathomorphological and clinical manifestations of this group of dermatoses, summarizes information about modern treatment tactics.

A 27-year-old Peruvian woman living with human immunodeficiency virus (HIV) in clinical stage B3 and not on antiretroviral therapy presented with a ten-day history of fever, chills, night sweats and a two-day history of skin lesions. On physical examination, several erythematous-purplish lesions were found on the face and legs. Meningococcal infection was suspected and ceftriaxone was started. Blood culture grew nontyphoidal Salmonella enterica. A biopsy of the skin lesions showed leukocytoclastic vasculitis (LCV); therefore, corticosteroids were added. After two weeks of antibiotic and corticosteroid treatment, the lesions had resolved, but they recurred two days after treatment with prednisone was stopped. Corticosteroids and combination antiretroviral therapy were started simultaneously and the lesions resolved without recurrence. HIV infection has been associated with higher rates of skin lesions in salmonellosis. LCV has been described both in the setting of HIV infection and salmonellosis. However, our review of the literature found no previous cases of LCV in concurrent HIV and salmonellosis. Revisión por pares Revisión por pares

IgA vasculitis, also called Henoch-Schonlein purpura (HSP), is a form of cutaneous small-vessel vasculitis characterized by palpable purpura favoring the lower extremities, arthritis, nephritis, and IgA deposition within postcapillary venules of the skin and mesangium. In children, respiratory infections are well known to precede HSP. In adults, infectious endocarditis is a rare but potentially fatal trigger for HSP. We report the subtle presentations of subacute endocarditis in 2 adults with cutaneous IgA vasculitis.

Leukocytoclastic vasculitis (LCV) is a small-vessel vasculitis that most commonly affects the postcapillary venules in the skin. It classically presents with purpuric macules that progress to palpable purpura on the bilateral shins 7–10 days after an inciting medication or infection, or in the setting of connective tissue disease, malignancy, or inflammatory bowel disease. Up to 50% of cases have no identifiable cause. Lesions on the buttocks, abdomen, upper extremities, and face are uncommon, as are bullae and ulcers. We present a rare case of bullous LCV manifesting as grouped vesicles on the face and body mimicking varicella-zoster infection.

Chronic exposure to minocycline, a commonly used anti-acne medication, results in a variety of autoimmune syndromes. Minocycline-induced vasculitis often associated with the presence of antinuclear antibody (ANA) and antineutrophil cytoplasmic antibody (ANCA) has been reported in Western literature, mainly in adults. Herein, we report a rare case of a 15-year-old male child on minocycline treatment for 1 year, who presented with fever, skin rash, and polyarthralgia for 4 months. His erythrocyte sedimentation rate (ESR) level was elevated, ANA and myeloperoxidase ANCA were positive, and skin biopsy revealed leukocytoclastic vasculitis. Upon discontinuation of minocycline and prescribing a short course of oral steroids, all his symptoms resolved and ESR normalized within 2 weeks. The child remained asymptomatic with normal acute-phase reactants at 2-month follow-up. This outcome suggested that minocycline was the main cause of ANCA-associated vasculitis.

Leukocytoclastic vasculitis (LV) is an inflammation of the small vessels in the dermis characterised by the deposition of immunocomplexes in the involved vessel walls. It commonly manifests as palpable purpura, limited to the skin and predominantly of the lower limb. We report a rare case of necrotising LV (NLV) affecting bilateral breast, manifesting clinical features of necrotising fasciitis (NF), and emphasizes the potential diagnostic challenges that markedly influence the treatment and survival of patients. A 48-year-old female presented with an acute onset left breast skin necrosis and discolouration that rapidly progressed to the contralateral breast with surrounding erythema and oedema of the chest wall yet spared the intermammary cleft. Some non-blanching purpuric rash were also noted on upper abdomen and left lower limb. COVID-19 test was negative. CT scan showed extensive bilateral breast fat stranding and oedema. Patient became clinically septic with a moderately raised CRP and mild acute kidney injury. Radical mastectomies and chest wall excision were performed with intra-operative findings of cloudy fluid and easily peeled away subcutaneous tissue from fascia. Urgent gram stain and culture showed no organisms. Tissue biopsies subsequently showed the diagnosis of NLV. Chest wall defect was then reconstructed with split skin grafts, NLV treated with corticosteroids and patient made an uneventful recovery. This case highlights the incidence of a rare and aggressive manifestation of NLV on the breast that mimics NF, emphasizing the clinical differentiation that may lead to catastrophic results and significant cosmetic defect, if a differential diagnosis cannot be determined at the time.

Ulcerative colitis is an inflammatory bowel disease that in rare cases may develop extraintestinal manifestations. This case report aims to add to the limited clinical data on leukocytoclastic vasculitis and possible ANCA-associated vasculitis as rare cutaneous and rheumatologic extraintestinal manifestations of IBD, particularly in elderly patients. Our case involves a 79-year-old male with a history of mild-moderate ulcerative colitis on oral mesalamine 2.4 g daily and pyoderma gangrenosum who presented with recurrent bilateral polyarthralgia, joint swelling, diffuse lower extremity purpura, acute kidney injury, and scrotal rash. Autoimmune titers were significant for positive ANA and PR3-ANCA. Biopsy of purpuric lesions demonstrated findings suggestive of leukocytoclastic vasculitis. The patient was promptly treated with pulse-dose methylprednisolone for 3 days with rapid improvement of symptoms.

Leukocytoclastic vasculitis is a small vessel vasculitis that is usually confined to the skin with rare extracutaneous manifestation. While this condition can be idiopathic, it has been linked with systemic autoimmune conditions, malignancies, infections, and drugs. In this paper, we present a case of a patient who presented with leukocytoclastic vasculitis many years after her diagnosis of rheumatoid arthritis. It is important that physicians investigate leukocytoclastic vasculitis, as the condition, while often idiopathic, can be a presentation of something more sinister such as malignancy or systemic autoimmune condition.

Apixaban is a rare cause of leukocytoclastic vasculitis (LCV). To our knowledge, there is only one other reported case due to apixaban in the literature. We present a case of apixaban-induced leukocytoclastic vasculitis in a 95-year-old male. He had been started on apixaban 12 days prior to presentation and developed worsening palpable purpura of his lower extremities. Possible etiologies of this new rash were excluded, with biopsy showing extensive purpura with superficial perivascular neutrophilic infiltrate and leukocytoclasis. Apixaban was discontinued, and the patient was started on a slow prednisone taper with subsequent resolution of his rash.

Urticarial vasculitis (UV) is a form of cutaneous vasculitis which lasts for >24 h. Clinically, the patients present with erythema and wheals. The level of complement decides the type of UV. This is a case of a middle-aged lady, who developed vesiculobullous lesion over her leg after trekking. She was diagnosed to have normocomplementemic UV. Bullous presentation of UV is a rare scenario.

ÖZ Amaç: Lökositoklastik vaskülit, primer deri tutulumu ile seyreden, esas olarak post kapiller venülleri etkileyen bir küçük damar vaskülit formudur. Etiyolojide ilaçlar, enfeksiyonlar, maligniteler, sistemik inflamatuvar hastalıklar gibi çeşitli nedenler yer almaktadır. Ancak olguların bir kısmında neden saptanamamakta ve bu olgular idiyopatik olarak değerlendirilmektedir. Klinik olarak özellikle alt ekstremitelerde sınırlı palpe edilebilen purpuralar ile karakterize olup, nadiren yaygın tutulum da gözlenebilmektedir. Bu çalışmada, kliniğimizde lökositoklastik vaskülit tanısı almış hastalarda etiyolojik faktörler, demografik ve klinik özelliklerin belirlenmesi amaçlanmıştır. Gereç ve Yöntemler: Çalışmaya Ocak 2018 - Nisan 2019 arasında Romatoloji Bilim Dalında 2012 Uluslararası Chapel Hill Toplantısına göre lökositoklastik vaskülit tanısı konulan 40 hasta dahil edildi. Çalışmaya 18 yaş üstü hastalar dahil edildi. Hastaların epidemiyolojik, klinik, laboratuar bulguları ve tedavi bilgileri retrospektif olarak dosya kayıtları incelenerek elde edildi.Bulgular: Kırk hastanın (25 kadın, 15 erkek) yaş ortalaması 48.02±19.9 olduğu tespit edildi. Kutanöz lezyonlar en sık alt ekstremite yerleşimli, palpe edilebilen purpurik papül-plaklar şeklindeydi ve lezyonlara en sık eşlik eden semptomun kaşıntı olduğu saptandı. Hastaların %37.5 ’inde herhangi bir etyolojik neden saptanmamasına karşın, kalan hastaların %25’inde enfeksiyon ve/veya ilaç kullanımı öyküsü mevcuttu. Hastaların % 37.5’ine malignite ve romatizmal hastalık eşlik ediyordu. Sistemik kortikosteroidler en sık tercih edilen tedavi seçeneğiydi. Sonuç: Lökositoklastik vaskülit çoğunlukla ilaçlar ve enfeksiyon tarafından tetiklenen, malignite ve romatolojik hastalıkların da eşlik edebileceği iyi seyirli, kendi kendini sınırlayan bir hastalıktır. Altta yatan etiyolojinin belirlenmesi tedavide önemli bir basamak olmakla birlikte sistemik kortikosteroidler de etkin bir tedavi seçeneğidir.

Se trata de una enfermedad cutánea inflamatoria, benigna e infrecuente que corresponde a una vasculitis leucocitoclástica de vasos pequeños. Típicamente compromete el rostro, de etiología desconocida, aunque se ha planteado daño actínico, entre otras posibles causas. Se manifiesta como pápulas, placas o nódulos de color marrón rojizo a violáceo, bien definidas, infiltradas, de superficie brillante, que muestran acentuación folicular y telangiectasias. Esta entidad tiene un curso indolente y benigno, los pacientes suelen buscar tratamiento por estética y por su curso crónico. No existen guías de manejo ni buena calidad de evidencia con respecto al tratamiento, por lo que la estrategia de manejo debe individualizarse.

Major identifiable causes of leukocytoclastic vasculitis include certain infections and medications. Amongst antithyroid drugs, methimazole (MMI) is rarely implicated as a culprit drug. We report the first case, in Thailand, of MMI-induced leukocytoclastic vasculitis in a 41-year-old Thai female who had received MMI for relapsed Graves’ disease. MMI was discontinued and cholestyramine at a dose of 4 g four times daily was given instead. Her rashes on both legs resolved dramatically at 1-week follow-up. However, thyroid function test revealed unimproved thyrotoxicosis. She subsequently underwent radioiodine ablation as a definitive treatment. There were neither recurrent skin lesions nor other systemic involvements during the 3-month follow-up period. Notably, the most crucial step in the management of drug-induced leukocytoclastic vasculitis is the discontinuation of the offending drug in order to avoid further progression of the disease. The administration of immunosuppressive agents may not be necessary in patients with mild severity and non-vital organ involvement.

BACKGROUND: Erythema elevatum diutinum (EED) belongs to the spectrum of cutaneous leukocytoclastic vasculitides. EED is a very rare dermatosis presenting with reddish to browning papules and plaques. EED may be associated with infections, hematologic and autoimmune disorders. CASE REPORTS: We present two patients with EED, a 50-year-old woman and a 42-year-old man. While the woman shows an association with colitis ulcerosa, the man had an anti-thrombin deficiency. Treatment was started with oral corticosteroid and dapsone, respectively. In both cases, there was a partial and temporary response. CONCLUSIONS: EED is a rare vasculitis with an unusual clinical presentation and a chronic course. Response to treatment is unsatisfactory and in the long-term run sometimes frustrating.

The article is dedicated to the problem of differential diagnosis of hemorrhagic vasculitis on the level of primary medicine. Current classification of systemic vasculitides, namely International Chapel Hill Consensus Conference of 2012 is present. Clinical features of the often form of vasculitis – Henoch-Schönlein purpura and the less common form of vasculitis of the small vessels – leukocytoclastic vasculitis (hypersensitivity vasculitis) are analyzed. Material is given basing on scientific literature data and own clinical observations of skin vasculitis.

Frequently used in the management of hypertension and heart failure, hydralazine is associated with the development of adverse rheumatologic side effects. The authors highlight a unique case of drug-induced lupus and drug-induced anti-neutrophil cytoplasmic antibody (ANCA) vasculitis from hydralazine use in a 50-year-old man with sarcoidosis and hypertension.

Although it is unquestionable that monoclonal gammopathy causes occlusive nonvasculitic vasculopathy,1 it is not clear yet, if it can cause immunoglobulin-mediated leukocytoclastic vasculitis (LcV) and how vigorously both conditions should be treated in monoclonal gammopathy of unclear significance (MGUS). In the recent nomenclature of cutaneous vasculitides (addendum to the CHCC2012),2 vasculitis in MGUS is mentioned as a possible, so-far unproven entity. Previous case reports did not sufficiently or explicitly distinguish it from occlusive vasculopathy. Adding to this dilemma is a lack of consensus with oncologists if or when chemotherapies are justified in MGUS with a paraprotein-associated disease. We provide evidence by means of 2 cases of MGUS that monoclonal gammopathy can cause primary immunoglobulin-mediated LcV and that its oncologic treatment abolishes it.

Thalidomide has become the gold standard for the treatment of erythema nodosum leprosum (ENL) within a few decades of its serendipitous discovery for this condition. It has also demonstrated efficacy in dermatoses such as recalcitrant oral aphthae, prurigo nodularis, and pyoderma gangrenosum. Despite a good safety profile, thalidomide is known to cause side effects such as sedation, constipation, peripheral neuropathy, and thromboembolism. Although rare and anecdotal, adverse cutaneous drug reactions (ACDRs) have been reported. Both thalidomide and its newer analogs have been implicated for maculopapular, urticaria-angioedema, Steven–Johnson-like, toxic epidermal necrolysis, and acneiform eruptions. Only a few cases of leukocytoclastic vasculitis (LCV) occurring in patients of multiple myeloma on this drug have been described till date. However, this unusual presentation of ACDR due to thalidomide in leprosy has not been hitherto documented. Herein, we describe a patient of lepromatous leprosy with ENL who developed thalidomide-induced LCV and discuss myriad aspects such as immunopathogenesis with emphasis on the possible role of various cytokines such as interleukin (IL)-2, IL-6, IL-12, and tumor necrosis factor-alpha.

Erythema elevatum diutinum (EED) is a rare chronic form of leukocytoclastic vasculitis that belongs to the group of neutrophilic dermatoses. The exact pathogenesis of the disease is still unclear. It has been associated with a number of systemic diseases including infections, autoimmune diseases, and both benign and malignant hematologic disorders. We report the case of a 50-year-old woman with complaints of symmetrical lesions on the extensor aspects of bilateral upper and lower limbs and pressure areas for 6 months. This case was difficult to manage because the patient was also hypersensitive to dapsone which is the drug of choice in EED.

Leukocytoclastic vasculitis is a disorder characterized by neutrophilic inflammation that is predominantly limited to the superficial cutaneous postcapillary venules. This condition may be idiopathic or may have a defined cause. Rivaroxaban and dabigatran have been widely used as warfarin alternatives, because of their efficacy and safety. In this case report, we describe a case of leukocytoclastic vasculitis induced by both rivaroxaban- and dabigatran-, which developed during the management of pulmonary thromboembolism. Keywords: Leukocytoclastic vasculitis, Rivaroxaban, Dabigatran