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Leukocytoclastic Vasculitis (leukocytoclastic + vasculitis)

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Medical Sciences	100%

Selected Abstracts

Leukocytoclastic vasculitis in urticaria induced by sun exposure

PHOTODERMATOLOGY, PHOTOIMMUNOLOGY & PHOTOMEDICINE, Issue 1 2007
Giuseppe Stinco
Background: Solar urticaria manifests itself immediately after solar or artificial light exposure and disappears a little later. Histopathologic findings of solar urticaria are essentially identical to those of classic urticaria. Case report: We report a 41-year-old man who developed urticarial lesions some hours after sunlight exposure, which resolved after approximately 1 week. Histologic examination of the lesions evidenced a leukocytoclastic vasculitis. Conclusion: In a literature review we found one case of solar urticaria with histologic aspects of leukocytoclastic vasculitis. [source]

P43 Acute urticaria to infliximab

CONTACT DERMATITIS, Issue 3 2004
Ana Giménez-Arnau
Infliximab is a chimeric antitumor necrosis factor-alpha monoclonal antibody used to treat Crohn's disease and rheumatoid arthritis. Acute infusion reactions, headache, fever, chills, urticaria and chest pain were seen in 17% of patients with infliximab compared with 7% of those receiving placebo. Other adverse cutaneous reactions are fungal dermatitis, eczema, seborrhoea, hordeolum, bullous eruption, furunculosis, periorbital oedema, hyperkeratosis, rosacea, verruca, skin pigmentation, alopecia, leukocytoclastic vasculitis, lichenoid drug eruption, erythema multiforme, perniosis-like eruption, granuloma annulare and acute folliculitis. Any pathogenic mechanism has been suggested. Patch test with infliximab can induce flare-up of lesions, nausea and malaise and suggest a percutaneous absortion. A sixty years-old man with atopy background and rheumatoid arthritis treated with Remicare®, infliximab who developed a severe acute urticaria with angioedema is presented. The lesions appearance after previous endovenous administrations and the worsening spreading wheals days after the injection clinically suggested an hypersensitivity mechanism. The protocolized study drug hypersensitivity performed showed only the Prick Test positivity with infliximab at 30/60 minutes. Patch test with infliximab was negative and any adverse event was reported. Actually the patient is treated with etanercept and this drug is well tolerated. This result suggested a type I hypersensitivity mediated reaction. Urticaria could be induced as immunologic reaction of the host against the murine part of infliximab, just as it hapens with other antichimeric antibodies. [source]

Different pathways leading to cutaneous leukocytoclastic vasculitis in mice

EXPERIMENTAL DERMATOLOGY, Issue 6 2001
C. Sunderkötter
Abstract: To investigate the pathomechanisms of leukocytoclastic vasculitis (LcV) we compared mouse models of LcV with non-vasculitic irritant contact dermatitis (ICD). Criteria for LcV as met by the immune complex-mediated Arthus reaction (Art-r) were also fulfilled by the localized Shwartzman reaction (Shw-r) and by cutaneous Loxoscelism (Lox) (injection of venom from Loxosceles reclusa containing sphingomyelinase D). After depletion of PMN (by ,-irradiation) vessel damage could not be elicited in these models, distinguishing them from models of direct endothelial insult (necrotizing ICD). Depletion of complement could only delay, but not inhibit the Art-r, and did not change ICD, Lox or the Shw-r. The Shw-r exclusively revealed a sustained local expression of vascular adhesion molecules for 24 h in the preparatory phase (LPS s.c.), not observed in the Art-r, in Lox or ICD. Subsequent challenge with LPS i.p. was associated with upregulation of Mac-1 and ICAM-1 on PMN, but not of VLA-4 or LFA-1 (FACS analysis). Cytokines which were able to replace LPS in priming for LcV in the Shw-r (TNF-, and IL-1,) also induced sustained expression of adhesion molecules, whereas IL-12 and IFN-, did neither. Neutralizing IL-12 or IFN-, also inhibited neither LcV nor sustained expression of adhesion molecules, whereas anti-TNF-, inhibited both. Anti-TNF-, had no marked inhibitory effects in the Art-r, in Lox or ICD. Combined (but not separate) neutralization of both E-selectin and VCAM-1 by antibodies suppressed LcV independent from reducing influx of PMN, proving that their sustained expression is decisive for the Shw-r and interferes with normal diapedesis. Since Loxosceles venom is known to dysregulate diapedesis and degranulation of PMN in vitro, since adherent immune complexes activate PMN at the vessel wall, and since adhesion molecules are dysregulated in the Shw-r, we suggest that LcV develops when activation of PMN coincides with vascular alterations which interfere with normal diapedesis. [source]

Nodular vasculitis in systemic lupus erythematosus

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 2008
Annet Westers-Attema MD
A 42-year-old man presented with fever, photosensitivity, headaches, myalgia, hyperhidrosis, muscle weakness, alopecia, nasal crustae, weight loss, painful nails, arthritis, oral ulcers, erythema, discoid cutaneous lesions, and painful subcutaneous nodes. We made a diagnosis of systemic lupus erythematosus (SLE), type II cryoglobulinemia, and nodular vasculitis. In the skin, different types of vasculitis may be observed. Typically, histology shows leukocytoclastic vasculitis of superficial vessels both in SLE and mixed cryoglobulinemia, which clinically results in palpable purpura. In our patient, however, histopathological examination of the subcutaneous nodes not only revealed leukocytoclastic vasculitis of the superficial vasculature but also showed even more extensive involvement of dermal and subdermal small and medium sized vessels, giving rise to a nodular vasculitis. [source]

Response to letter to the editor regarding: Role of direct immunofluorescence test in cutaneous leukocytoclastic vasculitis

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 11 2005
Maria A. Barnadas
No abstract is available for this article. [source]

Pigmented purpuric dermatosis and hepatitis profile: a report on 10 patients

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 6 2005
M. Wagdy Dessoukey MD
Background, Pigmented purpuric dermatosis comprises a group of vascular disorders of unknown etiology. Histologically, it is characterized by lymphocytic capillaritis in the papillary dermis. Although leukocytoclastic vasculitis confined to the skin is frequently reported with hepatitis C, lymphocytic vasculitis is rarely reported. Methods, Ten patients with pigmented purpuric dermatosis were studied clinically and histopathologically. Hepatitis profile was carried out in all of the patients to evaluate the possible relation. Results, Of the 10 patients, five tested positive for hepatitis C and two for hepatitis B antibodies. Conclusion, Hepatitis C and B virus may play a role in the pathogenesis of pigmented purpuric dermatosis. Further case,control studies are necessary to confirm this conclusion. [source]

Acute generalized exanthematous pustulosis mimicking toxic epidermal necrolysis

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 7 2001
Arnon D. Cohen MD
A 91-year-old patient presented with a nonfebrile, pruritic, widespread eruption that appeared 10 days after starting therapy with cefuroxime tablets, 1000 mg/day, due to stasis dermatitis with secondary infection. The patient was also treated with paracetamol tablets, 500,1000 mg/day, 10 days before the onset of the eruption. Previous diseases included congestive heart disease, hyperglycemia, and ectropion. There was no personal or family history of psoriasis. Additional medications, taken for more than 2 years at the time of the eruption, included indomethacin, captopril, hydrochlorothiazide, isosorbide-5-mononitrate tablets, and a combination drug Laxative®. Examination revealed widespread erythema involving 95% of the total body surface area, with numerous 1,2 mm nonfollicular pustules (Fig. 1). There was no predilection to the body folds. Within 24 h of hospitalization, during intravenous therapy with cefuroxime, the patient's condition worsened and bullae containing clear fluid appeared. Nikolsky's sign was positive on erythematous skin, and eventually skin detachment involved 41% of the total body surface area (Fig. 2). There were no target or target-like lesions and there was no involvement of the mucous membranes. Figure 1. Numerous, 1,2 mm, nonfollicular pustules, with confluence (viewed in the lower left part of the photograph), on erythematous skin Figure 2. Widespread skin detachment An early biopsy from a pustule revealed subcorneal and intraepidermal spongiform pustules, papillary edema, perivascular mononuclear infiltrate with a few eosinophils in the dermis, and leukocytoclastic vasculitis. A later biopsy showed similar findings with no evidence of full-thickness epidermal necrosis or necrotic keratinocytes. Direct immune fluorescence (DIF) taken from erythematous skin was negative. Laboratory studies showed the following results: sedimentation rate, 80 mm/h; white blood cell count, 26,200/mm3 with 87% polymorphonuclears and 1.8% eosinophils; hemoglobin, 13.0 g/dL; albumin, 2.8 g/dL (normal, 3.5,5.5 g/dL); other blood chemistry tests were normal. Immunologic studies for rheumatoid factor, antinuclear antibodies, antismooth muscle antibodies, antiparietal cell antibodies, antimitochondrial antibodies, C3, and C4 were normal or negative. Serology for venereal disease research laboratory (VDRL) test, Epstein,Barr virus, cytomegalovirus, hepatitis B virus, hepatitis C virus, human immunodeficiency virus, and antistreptolysin titer was negative. Chest X-ray was normal. Blood cultures were negative. Swab cultures taken from the pustules revealed Staphylococcus aureus as well as coagulase-negative Staphylococcus. All systemic drugs, including intravenous cefuroxime, were withdrawn with close monitoring for signs of heart failure or infection. Topical therapy consisted of application of wet dressings. Within 10 days, the eruption resolved with re-epithelialization of the erosions and the appearance of widespread post-pustular desquamation (Fig. 3) Figure 3. Post-pustular desquamation on the trunk [source]

Linezolid-induced purpuric medication reaction

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 7 2009
Flora S. Kim
A 64-year-old Caucasian male was seen in consultation for a petechial eruption that began 9 days after he started linezolid therapy for a retroperitoneal abscess. Skin findings included confluent non-blanching petechiae and purpura covering his entire body, without any active bleeding. A punch biopsy from the left lateral arm was performed and showed a perivascular inflammatory infiltrate composed of lymphocytes, histiocytes and rare eosinophils, and extravasated erythrocytes. Changes of leukocytoclastic vasculitis were not noted. Linezolid was promptly discontinued. To our knowledge, this is the first report of a biopsy-proven purpuric medication reaction secondary to linezolid therapy. [source]

Cutaneous manifestations of Wegener's granulomatosis: a clinicopathologic study of 17 patients and correlation to antineutrophil cytoplasmic antibody status

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 10 2007
Nneka I. Comfere
Background:, Wegener's granulomatosis (WG), a systemic vasculitis, can be associated with cutaneous signs and symptoms before, during or after the diagnosis of systemic disease. Methods:, We reviewed clinical and histologic features of cutaneous lesions from 17 patients with WG. The temporal relationship between development of cutaneous symptoms and onset of systemic disease was determined, and antineutrophil cytoplasmic antibody (ANCA) status of the patients was also established. Results:, In six patients, systemic and cutaneous disease developed concurrently. In eight patients, cutaneous disease developed after patients received the diagnosis of systemic disease. In three patients, cutaneous disease preceded systemic disease. Cytoplasmic ANCA or proteinase-3-ANCA [c-ANCA/proteinase 3 (PR3)-ANCA] serologic test results were negative for one patient when cutaneous disease developed, and one patient had c-ANCA/PR3-ANCA seroconversion a year before systemic disease developed. Histopathologic features of cutaneous WG were not limited to leukocytoclastic vasculitis; they also included acneiform perifollicular and dermal granulomatous inflammation and palisaded neutrophilic and granulomatous inflammation. Conclusions:, Patients with WG can present initially with cutaneous symptoms. Histopathologic patterns vary, but leukocytoclastic vasculitis is most commonly noted. Patients with WG and skin lesions are likely to have positive c-ANCA/PR3-ANCA serologic test results. [source]

Lichen planus and leukocytoclastic vasculitis induced by interferon alpha-2b in a subject with HCV-related chronic active hepatitis

JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 2 2003
JM De Sousa Pinto
ABSTRACT Lichen planus (LP) has been reported in association with chronic active hepatitis, primary biliary cirrhosis and other chronic liver diseases. The occurrence of LP in persons with hepatitis C virus (HCV) was reported by Robert et al., and the possible relationship between LP and hepatitis virus has also been supported by cases of LP following hepatitis B vaccination. Exacerbation or appearance of LP during the treatment of chronic hepatitis C, lymphoproliferative diseases and melanoma with alpha-interferon (IFN-,) and improvement of these diseases after discontinuation of this drug indicate that IFN-, may possibly induce LP. We present a case of cutaneo-mucous LP in a woman with chronic active hepatitis treated with IFN-, and in whom local leukocytoclastic vasculitis was induced by the intradermal injection of a very low dose of IFN-,. [source]

Kikuchi Fujimoto lymphadenitis: Case report and literature review

AMERICAN JOURNAL OF HEMATOLOGY, Issue 1 2003
Giuseppe Famularo
Abstract We describe a young woman with two severe episodes of Kikuchi Fujimoto disease occurring 16 years apart. Both episodes were proven by biopsy, and on the second occasion the patient remained dependent on high-dose prednisone for more than 6 months in order to control inflammation and achieve a reduction in cervical lymph node size. The second lymph node biopsy showed leukocytoclastic vasculitis in addition to the typical features of Kikuchi Fujimoto disease, but, even though the clinical interpretation of this finding was unclear, we documented no clinical or laboratory evidence of the development of other serious systemic disease over 20 years of follow-up. Kikuchi Fujimoto disease is considered a disorder with a self-limited course and a favorable outcome. However, on the basis of our experience with this patient and data from peer-reviewed literature, we suggest that this generally accepted postulate should be revised. Am. J. Hematol. 74:60,63, 2003. © 2003 Wiley-Liss, Inc. [source]

Leukocytoclastic vasculitis in urticaria induced by sun exposure

Purpuric drug eruption with leukocytoclastic vasculitis due to gefitinib

THE JOURNAL OF DERMATOLOGY, Issue 6 2010
Hiroshi UCHIMIYA
No abstract is available for this article. [source]

New algorithm (KAWAKAMI algorithm) to diagnose primary cutaneous vasculitis

THE JOURNAL OF DERMATOLOGY, Issue 2 2010
Tamihiro KAWAKAMI
Abstract Palpable purpura tends to indicate involvement of small vessel vasculitis in the upper dermis. Livedo racemosa, nodular lesion and skin ulceration are indicative of involvement of small to medium-sized vessel vasculitis in the lower dermis to subcutaneous fat. We set out to establish a new algorithm (KAWAKAMI algorithm) for primary cutaneous vasculitis based on the Chapel Hill Consensus Conference classification and our research results, and apply to the diagnosis. The first step is to measure serum antineutrophil cytoplasmic antibodies (ANCA) levels. If myeloperoxidase-ANCA is positive, Churg,Strauss syndrome or microscopic polyangiitis can be suspected, and if the patient is positive for proteinase 3-ANCA, Wegener's granulomatosis is most likely. Next, if cryoglobulin is positive, cryoglobulinemic vasculitis should be suspected. Third, if direct immunofluorescence of the skin biopsy specimen reveals immunoglobulin A deposition within the affected vessels, Henoch,Schönlein purpura is indicated. Finally, the presence of anti-phosphatidylserine,prothrombin complex antibodies and/or lupus anticoagulant and histopathological necrotizing vasculitis in the upper to middle dermis (leukocytoclastic vasculitis) indicates cutaneous leukocytoclastic angiitis, whereas if necrotizing vasculitis exists in the lower dermis and/or is associated with the subcutaneous fat, cutaneous polyarteritis nodosa is indicated. The KAWAKAMI algorithm may allow us to refine our earlier diagnostic strategies and allow for efficacious treatment of primary cutaneous vasculitis. In cutaneous polyarteritis nodosa, warfarin or clopidogrel therapies should be administrated, and in cases that have associated active inflammatory lesions, corticosteroids or mizoribine (mycophenolate mofetil) therapy should be added. We further propose prophylactic treatment of renal complications in patients with Henoch,Schönlein purpura. [source]

NOD2-Associated pediatric granulomatous arthritis, an expanding phenotype: Study of an international registry and a national cohort in spain

ARTHRITIS & RHEUMATISM, Issue 6 2009
Carlos D. Rosé
Objective To study the phenotype characteristics of the largest to date cohort of patients with pediatric granulomatous arthritis (PGA) and documented mutations in the NOD2 gene. Methods We analyzed merged data from 2 prospective cohorts of PGA patients, the International PGA Registry and a Spanish cohort. A systematic review of the medical records of interest was performed to identify phenotype characteristics. Results Forty-five patients with PGA (23 sporadic cases and 22 from familial pedigrees) and documented NOD2 mutations were identified and formed the basis of the study. Of these 45 patients, 18 had the R334W-encoding mutation, 18 had R334Q, 4 had E383K, 3 had R587C, 1 had C495Y, and 1 had W490L. The majority of patients manifested the typical triad of dermatitis, uveitis, and arthritis. In contrast, in 13 patients, the following "atypical" manifestations were noted: fever, sialadenitis, lymphadenopathy, erythema nodosum, leukocytoclastic vasculitis, transient neuropathy, granulomatous glomerular and interstitial nephritis, interstitial lung disease, arterial hypertension, hypertrophic cardiomyopathy, pericarditis, pulmonary embolism, hepatic granulomatous infiltration, splenic involvement, and chronic renal failure. In addition, 4 individuals who were asymptomatic carriers of a disease-causing mutation were documented. Conclusion NOD2 -associated PGA can be a multisystem disorder with significant visceral involvement. Treating physicians should be aware of the systemic nature of this condition, since some of these manifestations may entail long-term morbidity. [source]