Purpuric Plaques Research Articles

Retiform purpuric plaques: A classic sign of levamisole-induced vasculitis

Retiform purpuric plaques: A classic sign of levamisole-induced vasculitis

Nonhealing purpuric plaque with central ulceration: An underlying vascular insufficiency?

Nonhealing purpuric plaque with central ulceration: An underlying vascular insufficiency?

Generalized non-evanescent wheals with targetoid purpuric plaques

Metabolic syndrome (MetS) is a cluster of metabolic conditions that include abdominal obesity, reduction in cholesterol concentrations linked to high density lipoproteins (HLDc), elevated triglycerides, increased blood pressure and hyperglycaemia. Given that this is a multicausal disease, the aim of this study is to identify the psychological, emotional and lifestyle variables that can have an influence on the different MetS components.A cross-sectional study with 103 patients with diagnostic criteria for MetS (47 male and 56 female). Anthropometric, clinical and analytical measurements were collected to assess the variables associated with MetS. The main psychological and emotional variables were also assessed.Different multiple linear regression tests were performed to identify which variables were predictive of MetS. The dependent variables were body mass index (BMI), abdominal circumference, HDLc, and quality of life, and the predictive variables were psychological stress, anger and adherence to a Mediterranean diet. The results showed that psychological stress was a predictor of quality of life (β = −0.55, p ≤ 0). Similarly, anger was a predictor of BMI (β = 0.23, p = .047) and abdominal circumference (β = 0.27, p = .021). As expected, adherence to a Mediterranean diet was a predictor of HDLc (β = 0.2, p = .045) and of quality of life (β = −0.18, p = .031).The results confirm a link between adherence to certain dietary habits and lifestyle, however they go one step further and show the importance of psychological and emotional factors like psychological stress and anger in some MetS components.El síndrome metabólico (SM) es un conjunto de condiciones metabólicas que incluyen obesidad abdominal, reducción de las concentraciones de colesterol unido a las high density lipoproteins (c-HDL, «lipoproteínas de alta densidad»), triglicéridos elevados, aumento de la presión arterial e hiperglucemia. Dado que se trata de una enfermedad multicausal, el objetivo de este estudio es identificar las variables psicológicas, emocionales y de estilo de vida que pueden ejercer una influencia sobre los diferentes componentes del SM.Estudio transversal con 103 pacientes diagnosticados de SM (47 varones y 56 mujeres). Se recogieron medidas antropométricas, clínicas y analíticas para valorar las variables asociadas al SM. También se evaluaron las principales variables psicológicas y emocionales.Se realizaron diferentes pruebas de regresión lineal múltiple para identificar qué variables eran predictoras del SM. Las variables dependientes fueron el índice de masa corporal (IMC), la circunferencia abdominal, el c-HDL y la calidad de vida, y las variables predictoras fueron el estrés psicológico, la ira y la adherencia a la dieta mediterránea. Los resultados mostraron que el estrés psicológico era un predictor de la calidad de vida (β = −0,55, p ≤ 0). De igual modo, la ira fue un predictor del IMC (β = 0,23, p = 0,047) y de la circunferencia abdominal (β = 0,27, p = 0,021). Según lo previsto, la adherencia a la dieta mediterránea fue un predictor del c-HDL (β = 0,2, p = 0,045) y de la calidad de vida (β = −0,18, p = 0,031).Los resultados confirman un vínculo entre la adherencia a ciertos hábitos alimentarios y el estilo de vida; sin embargo, se sitúan un paso por delante y resaltan la importancia de los factores psicológicos y emocionales como el estrés y la ira en algunos componentes del SM.

Acute Hemorrhagic Edema of Infancy

We report a case of acute hemorrhagic edema of infancy (AHEI) occurred in an 11-month-old male infant after upper respiratory tract infection. The onset was dramatic with petechiae, ecchymosis, and annular, nummular, or targetoid purpuric plaques on the extremities, face, and ears. Acute hemorrhagic edema of infancy is a benign form of leukocytoclastic vasculitis that typically affects children between 4 and 24 months of age. The etiology remains still unknown. The potential triggers of AHEI include preceding bacterial or viral infections, immunizations, and drugs. Although the clinical picture is fearful, in the majority of cases, it involves only cutaneous small vessels. Recognizing this as a distinct clinical entity allows to establish an appropriate prognosis for this rare benign disease in children.This report could be a helpful reminder, especially for emergency physicians, to discriminate AHEI from other more severe diseases, such as meningococcal sepsis.

Diffuse dermal angiomatosis of the breast with adjacent fat necrosis: a case report and review of the literature

Diffuse dermal angiomatosis (DDA) is a type of reactive skin angioproliferation. Clinically, this rare disorder presents as red-violet purpuric papules and/or plaques (some with a greater tendency towards necrosis and ulceration), which can be localized in any body area, but is most often seen in the upper and lower extremities. Localization in the breast commonly presents with severe intractable breast pain and characteristic reticular violaceous erythematous plaques with central ulcerations. Histological examination is fundamental for the diagnosis and is characterized by varied patterns of lobular or diffuse hyperplasia of endothelial cells at the extravascular level. The condition is associated with various underlying conditions, many of which result in local tissue ischemia. In this report, we present a patient with DDA with an underlying mass lesion of the breast, which proved to be an adjacent fat necrosis. Various treatments have proven beneficial, including revascularization, oral corticosteroids, smoking cessation, and isotretinoin. In this case, our patient benefited from secondary excision of the affected area.

Cutaneous Manifestations of Small-Vessel Leukocytoclastic Vasculitides in Childhood.

In childhood, cutaneous small-vessel vasculitides include Henoch-Schönlein syndrome, a systemic vasculitis, and Finkelstein-Seidlmayer syndrome, a skin-limited vasculitis. Both Henoch-Schönlein and Finkelstein-Seidlmayer syndromes are seen more frequently in white or Asian compared with black children and occur especially in winter and spring with a male-to-female ratio of approximately 2:1. In everyday clinical practice, both conditions are diagnosed on clinical grounds without histological confirmation. The characteristic cutaneous hallmarks of Henoch-Schönlein syndrome include a purpuric rash in all and a subcutaneous edema in approximately every second case, which are often preceded by non-specific red or pink macular elements that mimic a non-itching urticarial rash. Recent data point out that Henoch-Schönlein children often present further cutaneous findings such as Köbnerization, Rumpel-Leede capillary fragility phenomenon, and blistering eruptions. Children with Finkelstein-Seidlmayer syndrome are usually ≤24months of age and not ill-appearing. They present with (a) large, round, red to purpuric plaques (often with a targetoid appearance) predominantly over the cheeks, ears, and extremities and (b) often tender non-pitting edema of the distal extremities, ears, and face (without pruritus). Both in Henoch-Schönlein syndrome and Finkelstein-Seidlmayer syndrome, there is often scrotal involvement. The cutaneous findings remit without sequelae within 2months in Henoch-Schönlein and 3weeks in Finkelstein-Seidlmayer syndrome.

Purpuric macules and plaques in a patient with myasthenia gravis

Purpuric macules and plaques in a patient with myasthenia gravis

Multifocal primary cutaneous nodular amyloidosis

Nodular cutaneous amyloidosis (NCA), the least common form of primary cutaneous amyloidosis, is characterized clinically by waxy, purpuric plaques and nodules and histologically by amyloid deposits in the dermis and subcutaneous tissue. We present a patient who developed multiple, non-contiguous NCA lesions over a three year period without evidence of systemic disease. We reviewed the literature and found few other cases of this unusual presentation.

Large Edematous Purpuric Plaques after Lipolysis Acupuncture.

Large Edematous Purpuric Plaques after Lipolysis Acupuncture.

Exercise-Induced Vasculitis: A Review with Illustrated Cases.

Although exercise-induced vasculitis (EIV) is usually misdiagnosed, it is not uncommon. Occurring mostly after prolonged exercise, especially in hot weather, EIV is an isolated cutaneous vasculitis with stereotypical presentation. This article reviews the clinical characteristics, treatments, and outcomes of EIV based on the published literature. We report 99 patients who developed EIV after walking, dancing, swimming, or hiking especially during hot weather, including the records of 16 patients with EIV treated at our hospital from 2007 to 2015. Erythematous or purpuric plaques arise on the lower legs, without the involvement of compression socks or stockings. Symptoms include itch, pain, and a burning sensation. EIV is an isolated cutaneous vasculitis. Lesions resolve spontaneously after 10 days. When triggering conditions persist, relapses are frequent (77.5 %). Histopathology demonstrates leukocytoclastic vasculitis in 95 % of cases with C3 or immunoglobulin M deposits in 88 and 46 % of cases, respectively. Blood investigations are negative. EIV appears to be a consequence of venous stasis induced by an acute failure of the muscle pump of the calf and thermoregulation decompensation. Both appear after prolonged and unusual exercise in hot weather. Treatment is not codified; topical corticosteroids may reduce symptoms and wearing light clothes might limit lesion occurrence.

Recurrent Cutaneous Eosinophilic Vasculitis: A Rare Entity.

Recurrent cutaneous necrotizing eosinophilic vasculitis is a rare entity described by Chen et al. It has a benign course without any systemic involvement. However, often long-term treatment with systemic steroids is required. The exact etiopathogenesis remains unknown. We report a female patient, who presented with recurrent pruritic purpuric papules and plaques affecting different body parts of long duration. Disease was well controlled with low dose systemic steroids, but invariably recurred on its withdrawal. Histology revealed the features of eosinophilic vasculitis. Subsequent detailed evaluation ruled out systemic involvement, underlying diseases, and any precipitating factors. Hence, a diagnosis of recurrent cutaneous eosinophilic vasculitis was made. Patient showed excellent response to prednisolone, and on tapering the drug, it was found that she needed a maintenance dose of 5 mg/day. We did not come across any previous reports of recurrent cutaneous eosinophilic vasculitis from India.

Striking but benign: acute haemorrhagic oedema of infancy

A previously healthy 6-month-old boy presented in September, 2014, with indurated and tender oedema of the left hand, associated with a rapidly spreading purpuric rash on the dorsum. He also had swelling of one side of his face, but examination was otherwise normal. Beginning 4 days previously he had had a 3-day upper respiratory tract infection, with no associated fever; his parents denied trauma or previous drug use. Blood tests including full blood count, coagulation studies, and circulating immune complexes were normal, apart from moderate thrombocytosis (platelets 518 × 109/L; normal range 168–392 × 109/L) and normochromic normocytic anaemia (haemoglobin 99 g/L; 105–135 g/L). Urinalysis was normal. We diagnosed acute haemorrhagic oedema of infancy, a leukoclastic small-vessel vasculitis that was initially thought to be a benign variant of Henoch-Schonlein purpura, but is now considered a distinct entity. Acute haemorrhagic oedema of infancy typically aff ects children between 4 and 24 months of age, whereas Henoch-Schonlein purpura is more common in children aged 3 to 6 years. Unlike Henoch-Schonlein purpura, systemic involvement is rare in acute haemorrhagic oedema of infancy; symptoms are usually restricted to the skin. Cutaneous lesions are typically large nummular red or purpuric plaques or cockade-like lesions involving the face, ears, and limbs, but sparing the trunk and mucosa. Non-pitting oedema is more frequently noted on the arms and legs but can involve the face. In Henoch-Schonlein purpura the legs and buttocks are more commonly aff ected. Patients with acute haemorrhagic oedema of infancy usually look clinically well. Lesions usually resolve within 1–3 weeks without treatment. Long-term sequelae have not been reported. In our patient, the purpuric rash resolved within 4 weeks and at follow-up 6 months later he had had no further symptoms. After excluding infectious, immune, or infl ammatory causes of purpuric rashes, physicians should consider this rare, striking but benign diagnosis when faced with a well-appearing infant with purpuric plaques and non-pitting oedema.

Generalized benign cutaneous reaction to cytarabine

Cytarabine-induced toxicity manifests as various cutaneous morphologies. A generalized papular purpuric eruption has not been well described. We aimed to characterize a distinct cytarabine-related eruption. We reviewed all cases of cytarabine-related toxicity with papular purpuric eruptions or violaceous erythema at the University of California, San Francisco between 2006 and 2011. Sixteen cases were identified. The eruption began as erythematous papules that evolved into coalescing purpuric papules and plaques. It had affinity for intertriginous areas, neck, ears, and scalp. Pruritus was common, but no systemic complications were documented. Thirteen patients (81.3%) developed the eruption after completion of chemotherapy. Differential diagnosis often included viral exanthem (62.5%), drug eruption (50%), and vasculitis (37.5%). Histopathology was nonspecific but commonly demonstrated sparse lymphocytic infiltrates, spongiosis, and/or red cell extravasation. Importantly, the eruption was neither predicted by past cytarabine exposure nor predictive of future recurrence. This is a review of cases from a single institution. Observation was limited to acute hospitalization, however, charts were reviewed for subsequent reactions on rechallenge. The eruption described herein represents a specific skin-limited reaction to cytarabine. Awareness of its characteristic morphology, distribution, and timeline will aid in clinical diagnosis. Reassurance concerning its benign nature will prevent unnecessary intervention or cessation of chemotherapy.

A Rare Case of Zosteriform Cutaneous Metastases from a Nasopharyngeal Carcinoma.

From a clinical point of view, the most common presentations of cutaneous metastatic disease are papules and nodules. However, a wide morphological spectrum of lesions has been described, including erythematous patches or plaques, inflammatory erysipelas-like lesions, diffuse sclerodermiform lesions with induration of the skin, telangiectatic papulovesicles, purpuric plaques mimicking vasculitis, and alopecia areata like scalp lesions. The so-called zosteriform pattern has been described to be in few cases and to the best of our knowledge has never been described associated with a metastasis of a nasopharyngeal carcinoma. This case highlights the relevance of including cutaneous metastases in the differential diagnosis of patients with nonhealing herpes zoster-like lesions, especially in those with underlying neoplasm recently diagnosed.

Cryoglobulinemic Vasculitis Occurring With Initiation of Interferon and Sofosbuvir for Treatment of Hepatitis C

Introduction: A 58-year-old Hispanic woman presented with a 2-day history of a pruritic rash that had started on her hands before spreading to her abdomen, chest, upper extremities, and lower extremities. Her history was significant for chronic hepatitis C (HCV), genotype 1, but no prior history of vasculitis. She had been started on ribavirin, peginterferon alfa 2-a, and sofosbuvir 6 weeks prior to admission, with an undetectable HCV RNA PCR after 4 weeks. However, treatment had been stopped 2 weeks prior to admission due to neutropenia (ANC 400 cells/mL). Her temperature on admission was 101.7 °F. On physical exam, she had edematous pink plaques on the dorsal hands, elbows, and proximal bilateral lower extremities. There were purpuric papules and plaques on the bilateral midlower thighs, shins, ankles, and feet. White blood cell count was 2,4000 cells/μL with normal differential, hemoglobin 11.9 mg/dL, platelets 119000 cells/μL, and creatinine 0.7 mg/dL. Urinalysis did not show proteinuria. Liver function and iron studies were unremarkable. ANA, ANCA, CRP, ESR, HIV, anticardiolipin antibodies, beta-2-glycoprotein, and lupus anticoagulant were normal. Cryoglobulins were positive, with low complement levels, mildly elevated rheumatoid factor, and undetectable HCV viral load. Punch biopsy showed leukocytoclastic vasculitis. She was started on a steroid taper, and at 2-week follow-up, her rash had resolved completely. Here, we present a case of a patient with cryoglobulinemic vasculitis on co-therapy with interferon (IFN) and sofosbuvir. Cryoglobulins may be seen in 40-56% of patients with HCV infection, with vasculitis only seen in <5% of patients with cryoglobulinemia. In these cases, vasculitis usually improves with treatment of HCV. However, there have been reports of cryoglobulinemic vasculitis initially appearing after initiation of treatment with interferon, with unknown rates of occurrence in the setting of co-therapy with sofosbuvir. Treatment in these cases usually consists of corticosteroids with or without immunosuppression using cyclophosphamide. In our patient’s case, administration of prednisone led to complete resolution of vasculitis, with no residual purpura, neuropathy, or renal insufficiency. Viral load remained undetectable at all times. This shows the importance of close monitoring of patients while on treatment with interferon and sofosbuvir, regardless of the viral load.

Association between HLA‐B*13:01 and DIHS/DRESS due to dapson in a Japanese patients of pityriasis lichenoides et varioliformis acuta (PLEVA)

Observation A 38-year old Japanese woman visited our dermatological department on June 24, 2013, with a three-day history of erythematous lesions on the trunk and extremities. She had been treated orally with 50 mg of diaminodiphenyl sulfone (dapson) daily for pityriasis lichenoides et varioliformis acuta (PLEVA) for 38 days. Physical examination on admission revealed fever (38.4°C), bilateral cervical lymphadenopathy, facial edema with erythema, and round erythematous and purpuric plaques on the trunk and extremities. Erythematous targetoid lesions were also found. Blood examination revealed an increased white blood cell count (13.4 ~ 109/l: normal 3.5-9 ~ 109/l), and mild liver dysfunction (alanine aminotransferase; 40 IU/l : normal 5-25 IU/l). A skin biopsy obtained from the patient’s abdomen revealed acanthosis, hydropic and vacuolar degeneration of epidermal basal cells and upper dermal infiltration consisting of lymphocytes and neutrophils. No extensive epidermal necrosis was found. A lymphocyte transformation test (LTT) for dapson was positive (stimulation index (SI) = 5.3, cut-off for LTT, SI = 1.8). These findings fulfilled the criteria for drug-induced hypersensitivity syndrome (DIHS)/drug reaction with eosinophilia and systemic symptoms (DRESS), and dapson therapy was discontinued. The patient was started on a course of systemic prednisolone (1.0 mg/kg daily). The dose was tapered over the next 70 days in line with the improvement of clinical symptoms. Both human herpesvirus-6 and cytomegalovirus reactivation had not been seen during the course. Human leukocyte antigen (HLA)-B*13:01 and HLA-C*03:04 were identified in this patient.

SkIndia Quiz 15: Hyperpigmented and purpuric plaques on trunk.

SkIndia Quiz 15: Hyperpigmented and purpuric plaques on trunk.

Purpuric plaque on the neck of a patient with breast carcinoma.

Purpuric plaque on the neck of a patient with breast carcinoma.

Bir olgu nedeni ile akut infantil hemorajik ödem

Acute infantile hemorrhagic edema (AIHE) is a leukocytoclastic vasculitis that is confined to the skin without visceral involvement. Edema and purpuric lesions characterize the disease. It is considered as an uncommon form of cutaneous vasculitis occurring in children younger than 2 years of age. By many authors, it is considered to be a variant of Henoch Schonlein Purpura because of similarities in causality and histopathology. In spite of its clinical violent onset, the course is often benign and spontaneous recovery is observed within several weeks. Although the etiology is unknown, AIHE often follows infections, drug treatment or vaccination. Here, a tenmonth-old girl presenting with purpuric plaques on the right buccal area and edema on the face and eye and clinically diagnosed as AIHE is presented.

Purple ear and retiform purpura

A 40-year-old female was presented to the hospital with bluish discoloration of ears, joint pain and skin rash. The past medical history was significant for hepatitis C infection. She was enrolled in a methadone program for heroin addiction, and she reported that she had been using crack cocaine for 10 years. Physical examination revealed purplish discoloration of both right (Fig. 1a) and left ears involving the external pinnae and helixes. The tip of the nose had a prominent necrotic purpura, and the right cheek showed a tender purpuric plaque (Fig. 1b). There were multiple large painful confluent retiform purpura over the lower extremities (Fig. 1c). Multiple joint tenderness without joint effusion was noted. Significant laboratory findings included leucopenia with a WBC count of 2 300 cells/mm (normal, 4 400–11 000 cells/mm) with a normal complete metabolic panel. Hepatitis C polymerase chain reaction (PCR) assay showed undetectable viral load and serum cryoglobulin level was normal. The antinuclear antibody (ANA), anti-Smith antibody and perinuclear antineutrophil cytoplasmic antibody (p-ANCA) were positive. Results of further work-up for infectious, hematologic and rheumatologic disorders were negative. Urine toxicology screening was positive for cocaine. The clinical picture was highly suggestive of levamisole-contaminated cocaineinduced cutaneous vasculitis. A punch biopsy of cutaneous purpura was performed, and showed small-vessel vasculitis with perivascular neutrophilic infiltrates (arrows) with dermal hemorrhages (asterisks), which were compatible with features of leukocytoclastic vasculitis (Fig. 1d, e). The patient was treated with systemic corticosteroids, and the leucopenia resolved and the cutaneous purpura improved significantly (Fig. 1f). Our patient presented with the clinical, biochemical and histologic features consistent with levamisole toxicity. According to the United States Centers for Disease Control and Prevention (CDC), 70 % of cocaine supply in the United States is adulterated with levamisole, which is being cut into the cocaine before it is smuggled into the United States [1]. Levamisole is an immunomodulatory agent, and has been used for the treatment of pediatric nephrotic syndrome, rheumatoid arthritis and colon cancer [1, 2]. However, it was withdrawn from the United States due to the risk of agranulocytosis. It is currently used in the United States as an anti-helminthic medication in the veterinary field [2, 3]. The reasons for addition of levamisole to cocaine are thought to be increasing the total weight of the cocaine due to its physical similarity to cocaine, and prolonging the cocaine-induced euphoria by potentiating the nicotinic acetylcholinergic effects [1–3]. Although levamisole is a more expensive additive agent, the major attractive incentive for using levamisole as a cocaine Z. Min (&) Department of Medicine, Division of Infectious Diseases, Allegheny General Hospital, 420 East North Avenue, East Wing, Suite 407, Pittsburgh, PA 15212, USA e-mail: zmin@wpahs.org