Perivascular Cellular Infiltration Research Articles

Comparative Histological Study of The Role of Platelet-Rich Plasma And Fetal Bovine Serum Supplemented Stem Cell in Treatment of Sciatic Nerve Crush Injury in Albino Rat

Background Injuries to peripheral nerves are one of the most serious obstacles that remain without solution for now. Although there are obvious advances in microsurgery, severe types of nervous system injuries are very difficult to cure without complications. Aim To evaluate and compare the effect of platelet-rich plasma-supplemented bone marrow mesenchymal stem cells (PRP-supplemented MSCs) and fetal bovine serum-supplemented bone marrow mesenchymal stem cells (FBS-supplemented MSCs) in treatment of surgically-induced sciatic nerve crush injury. Materials and methods Seventy five adult male albino rats were equally divided into five groups 15 each. Sciatic nerve specimens were obtained and examined by light microscope. Results Compared with control group, the sciatic nerve specimens of the injury group showed loosely packed nerve fibers with perivascular cellular infiltration surrounded by discontinuous perineurium. On the other hand, both FBS-supplemented MSCs group and PRP-supplemented MSCs group showed improvement in these changes. But the improvement was markedly observed in PRP-supplemented MSCs group more than FBS-supplemented MSCs. Conclusion PRP-supplemented MSCs can reduce the pathological changes induced by crush injury to the sciatic nerve of adult male albino rats more than FBS-supplemented MSCs.

Histological study on the toxic effect of titanium dioxide nanoparticles on the prostate gland of adult albino rats and the protective role of coenzyme Q10

Background Titanium dioxide nanoparticles have numerous clinical and commercial applications. Coenzyme Q10 has antioxidant and free radical-scavenging capabilities in addition to functions like vitamins. Aim To identify changes in the ventral prostatic lobe of adult albino rats exposed to titanium dioxide nanoparticles and to evaluate the possible protective role of coenzyme Q 10. Materials and methods Forty adult male albino rats were used in this study. Group I was the control, Group II received coenzyme Q10 at a dose of 20 mg/kg, Group III received titanium dioxide nanoparticles at a dose of 600 mg/kg, and Group IV received both coenzyme Q10 and nanoparticles. Prostate glands sections were stained with hematoxylin and eosin. A morphometric study and statistical analysis were performed on the epithelial height. Results Sections of group III showed some histological abnormalities in the form of widely spaced prostatic acini, an increase in the amount of connective tissue stroma, with numerous dilated blood vessels and perivascular cellular infiltration. The mean height of the prostatic epithelium in group III was significantly higher than in the control group. Prostatic epithelial height was found to be significantly lower in group IV as compared to group III. Conclusion Titanium dioxide nanoparticles induce changes in the prostatic ventral lobe which can be ameliorated by coenzyme Q10 supplementation.

Nephrotoxicity induced by different diameters of sphere gold nanoparticles with special emphasis on the nephroprotective role of quercetin.

Although, gold nanoparticles (GNPs) are attracting more and more attention due to their ease of synthesis, modification, and great potential value in biomedical applications, exhibited harmful effects on human health and other living species. Quercetin (Qur) clarifies diverse pharmacological effects, especially anti-inflammatory, antiapoptotic, and antioxidant ones. This study aimed to evaluate the probable nephrotoxicity induced by different diameters of sphere GNPs, as well as the nephroprotective role of Qur. A total of 54 healthy mature male albino rats were grouped and treated with or without sphere GNPs; 10, 20, and 50 nm and Qur (200 mg/kg b.wt.). The effects of GNPs and Qur were estimated through the collection of blood and kidney samples from euthanized rats and performed biochemical, histopathological, and immunohistochemical investigations. In comparison between different diameters of GNPs, the 10 nm GNPs revealed more significant elevations in all renal function parameters: creatinine, urea, blood urea nitrogen, and uric acid followed by 20 nm then 50 nm. Pre-cotreatment with Qur decreased all renal functional values. Histopathologically, 10 nm revealed the most potent renal pathological changes represented in the renal cortex with cloudy swelling of renal tubules, hypercellularity of some glomeruli, severe congestion of renal blood vessels, focal inter tubular edema, and vascular endotheliosis (degeneration of endothelium). In addition, the renal medulla revealed perivascular inflammatory cellular infiltration, perivascular fibrosis, intra tubular glycogen deposition, and casts deposition of mainly cellular casts. On the other hand, the Qur treatment ameliorated most of these pathological changes. The size of GNPs is pivotal in their pathological effect on renal tissues where the small-sized GNPs; 10 nm have more potent cytotoxic, inflammatory, and apoptotic effects rather than the larger ones. Otherwise, Qur clarified a significant mitigating role against the nephrotoxicity of the GNPs.

M113 BLEPHAROCHALASIS: A HEREDITARY ANGIOEDEMA-MASQUERADER. RECURRENT ANGIOEDEMA IN A 12 YEAR-OLD AFRICAN AMERICAN MALE

Blepharochalasis is a rare disorder involving periocular edema classically of the upper eyelid, but has also been described in the entire periocular tissue. The resultant edema may be mistaken for allergy or hereditary angioedema. Etiology is unclear, possibly inflammatory, with some cases involving IgA deposition in the dermis, as well as perivascular inflammatory cellular infiltrates. Age of presentation ranges from just prior to puberty through the 20’s. Episodes of periocular edema tend to occur for 3-4 months for the first multiple years, then tend to space out, with acute attacks followed by quiescent phases.

Ultrastructural aberrations, histological disruption and upregulation of the VEGF, CD34 and ASMA immunoexpression in the myocardium of anemic albino rats

Iron deficiency anemia (IDA) is a global health problem affecting various body systems and tissues including the cardiovascular system. Several literatures described the associated physiological and clinical changes in the cardiovascular system and heart. However, the associated structural changes were poorly investigated. Therefore, the main aim of the present work was to elucidate whether IDA induces structural changes and alterations in the VEGF, CD34 and ASMA immunoexpression in the myocardium of albino rats. Thirty adult male albino rats were divided into two groups (fifteen rats each); control and anemic. Hematological data for all animals were assessed weekly and statistically analyzed. Three weeks later, animals were sacrificed, and heart specimens were obtained and processed for light and electron microscopy. All hematological parameters showed a statistically significant decrease in the anemic group. Structurally, the anemic group showed markedly degenerated, disrupted and disorganized cardiomyocytes in addition to markedly congested blood vessels, fibroblasts, collagen fibers deposition and perivascular cellular infiltration were noted. Also, positive immunostaining for VEGF, CD34 and ASMA was observed. Ultra-structurally, the myocardium of the anemic group showed disrupted and degenerated myofibrils with degenerated nuclei, perinuclear edema, widened interstitial spaces and marked collagen deposition. Mitochondria markedly increased with abnormal shapes. IDA induced myocardial injury that may propagate to regeneration through activated CD34 progenitor cells and increased VEGF or to degeneration and fibrosis through collagen fibers deposition and enhanced ASMA. So, early diagnosis and treatment of IDA is mandatory to avoid the associated myocardial structural changes.

The Pathogenesis of Chronic Spontaneous Urticaria: The Role of Infiltrating Cells

Chronic spontaneous urticaria is characterized by a perivascular non-necrotizing cellular infiltrate around small venules of the skin. It consists primarily of CD4(+) lymphocytes, a prominence of the T helper (Th)2 subtype but also Th1 cells, with Th17 cell-derived cytokines elevated in plasma. There are also neutrophils, eosinophils, basophils, and monocytes. Chemokines derived from mast cells and activated endothelial cells drive the process. Although the role of the cellular infiltrate has not previously been addressed, each constituent can contribute to the overall pathogenesis. It is of interest that CSU responds to corticosteroid, yet, short-term steroids do not affect autoimmunity or degranulation of mast cells, and act on margination of cells along the endothelium and chemotaxis to enter the surrounding dermis. In this review, we address each cell's contribution to the overall inflammatory response, as it is currently understood, with a view toward development of therapeutic options that impede the function of critical cells and/or their secretory products.

Haploinsufficiency of immune checkpoint receptor CTLA4 induces a distinct neuroinflammatory disorder.

BACKGROUNDCytotoxic T lymphocyte antigen 4 (CTLA4) is essential for immune homeostasis. Genetic mutations causing haploinsufficiency (CTLA4h) lead to a phenotypically heterogenous, immune-mediated disease that can include neuroinflammation. The neurological manifestations of CTLA4h are poorly characterized.METHODSWe performed an observational natural history study of 50 patients with CTLA4h who were followed at the NIH. We analyzed clinical, radiological, immunological, and histopathological data.RESULTSEvidence for neuroinflammation was observed in 32% (n = 16 of 50) of patients in this cohort by magnetic resonance imaging (MRI) and/or by cerebrospinal fluid analysis. Clinical symptoms were commonly absent or mild in severity, with headaches as the leading complaint (n = 13 of 16). The most striking findings were relapsing, large, contrast-enhancing focal lesions in the brain and spinal cord observed on MRI. We detected inflammation in the cerebrospinal fluid and leptomeninges before the parenchyma. Brain biopsies of inflammatory lesions from 10 patients showed perivascular and intraparenchymal mixed cellular infiltrates with little accompanying demyelination or neuronal injury.CONCLUSIONSNeuroinflammation due to CTLA4h is mediated primarily by an infiltrative process with a distinct and striking dissociation between clinical symptoms and radiological findings in the majority of patients.FUNDINGNIAID, NIH, Division of Intramural Research, NINDS, NIH, Division of Intramural Research, and the National Multiple Sclerosis Society-American Brain Foundation.TRIAL REGISTRATIONClinicalTrials.gov NCT00001355.

The Biochemical and Histological Effect of Cadmium Chloride on the Pancreas of Adult Albino Rats and the Possible Protective Effect of Nigella Sativa Seeds

Aim: The current study evaluates the important role of Nigella Sativa against cadmium (Cd) induced toxic changes in pancreasof rats.Materials and Methods: Eighteen adult Wistar albino rats were divided into three equal groups. Control group, cadmiumtreated group that received 5 mg CdCl2/kg BW/day dissolved in water orally for three months, and cadmium with Nigellasativa (NS) group received a mixture of 1g/kg/day of aqueous suspension of Nigella sativa seeds powder and 5 mgCdCl2/kg BW/day dissolved in water for three consecutive months. Hormonal assay of insulin was done. Pancreatic tissueswere prepared for both Hematoxylin and Eosin and toluidine blue. Electron microscopic study of pancreatic tissues was alsodone.Results: The present study showed that the administration of CdCl2 induced evident decrease in insulin serum level. Thebiochemical results were confirmed by histological investigations where degenerative changes of pancreatic acini with lossof normal lobular architecture, distorted pancreatic acini, degenerated and widely separated cells in the islets of Langerhans,blood vessels congestion and aggregation of perivascular cellular infiltrates were detected in pancreatic tissues stained withH&E. Toluidine blue-stained sections showed few deeply stained apical zymogen granules in some acini, whereas other acinishowed absence of these granules.Administration of NS with CdCl2 showed a significant improvement in the measured serum insulin level and histologicalpictures.Conclusion: CdCl2 induced several toxic changes in the exocrine and endocrine parts of pancreas of rats. NS could protect thepancreas against these alterations.

563 Incisional biopsy-induced spontaneous regression with halo phenomenon in a congenital melanocytic nevus

Congenital melanocytic nevus (CMN) is a hamartoma derived from neural crest appearing at birth. CMN has a dynamic course and may show various changes even spontaneous regression. CMN may grow in size during childhood and show pigmentary regression with increasing age and develop a hypopigmentation halo and regress spontaneously after halo formation, or undergo malignant transformation resulting in melanoma. A 9-year-old boy presented with solitary brownish to blackish patch on the right forearm which had appeared since birth. We performed incisional biopsy from the brownish patch and nests of nevus cells were observed in the entire dermis. The infiltration of melanocytes in adnexal-centric fashion was also shown. From these findings, the patient was diagnosed as CMN. Staging operations were additionally performed 5 times more to remove the lesion. After the first incisional biopsy, the brownish patch showed spontaneous regression with a halo phenomenon, especially around the suture sites. From the histologic findings, the regressed skin lesion showed perivascular cellular infiltration composed of lymphohistiocytes and decreased nevus cells. After the sixth incisional biopsy, the patch was completely removed, remaining halo around the suture sites. Spontaneous regression with a halo is a rare phenomenon in CMN. The mechanism is suggested to be a destruction of melanocytes by immune responses of CD 8+ T cells or IgM autoantibodies. There are some triggering factors that induce the process of halo phenomenon including UV radiation or local trauma. Also, inflammatory reactions associated with surgery may evoke the proliferation of CD8+ T cells targeting melanocyte. Herein, we report an interesting case in which surgical procedures act as a triggering factor to CMN regression with a halo phenomenon.

Chronic or atrophie masticatory myositis in the dog. A report of two spontaneous cases

Two young adult dogs (case 1: German wirehaired pointer male, case 2: mongrel female) were admitted to our Clinic because of a progressive, bilateral and symmetrical atrophy of the masticatory muscles, that was most obvious in the temporal muscles. No signs of mandibular dysfunction were detected in both animals. The clinical diagnosis of chronic or atrophic myositis was confirmed by the histopathology of temporal muscle biopsies, which revealed the typical of the disease lesions, such as myofiber degeneration, regeneration and atrophy, interstitial or perivascular cellular infiltrates, chiefly of lymphocytes and plasma cells plus perimysial fibrosis. Temporal muscle electromyography, done only in case 1, showed abnormal spontaneous activity indicating myositis. The use of prednisolone at immunosuppressive doses, with or without azathioprine, not only stopped the progression of the disease but resulted in a partial restoration of the masticatory muscle mass.

MORPHOLOGY OF NASAL POLYPS IN PATIENTS WITH ALTERED IMMUNOLOGICAL REACTIVITY

Morphological-functional characteristics of nasal polyps were studied in 88 patients with rhinosinusitis polyps. The tissue of a polyp had typical picture, multi-rows ciliated epithelium with a large number of goblet celts. Different stages of polyp maturation were observed: from edematous to perivascular and diffuse cellular infiltrates consisting of eosinophils, lymphocytes and mast cells. Their presence proves allergic nature of rhinosinusitis, which as any pathology process by stress is accompanied. At the early stage, chronic stress downregulate pro-inflammatory cytokines, while upregulating the anti-inflammatory cytokines. All the steps induced continued increased pro-inflammatory cytokines and finally inflammation, which induce various diseases. The final stage of polyp maturation was characterized by fibrous induration of its stroma with cirrhosis signs.

Toxoplasma gondii tachyzoite-extract acts as a potent immunomodulator against allergic sensitization and airway inflammation

Epidemiological and experimental studies have shown an inverse relationship between infections with certain parasites and a reduced incidence of allergic diseases. We and others have shown that infection with Toxoplasma gondii prevents the development of allergy in mice. To establish whether this beneficial effect could be recapitulated by soluble products of this parasite, we tested an extract derived from T. gondii tachyzoites. Immunization of BALB/c mice with tachyzoites lysate antigen (TLA) elicited mixed Th1/Th2 responses. When TLA was applied together with the sensitizing ovalbumin (OVA), the development of allergic airway inflammation was reduced, with decreased airway hyperresponsiveness associated with reduced peribronchial and perivascular cellular infiltration, reduced production of OVA-specific Th2 cytokines in lungs and spleens and reduced levels of serum OVA-specific IgG1 as well as IgE-dependent basophil degranulation. Of note, TLA retained its immunomodulatory properties, inducing high levels of IL-6, TNFα, IL-10 and IL-12p70 in bone marrow-derived dendritic cells after heat-inactivation or proteinase K-treatment for disruption of proteins, but not after sodium metaperiodate-treatment that degrades carbohydrate structures, suggesting that carbohydrates may play a role in immunomodulatory properties of TLA. Here we show that extracts derived from parasites may replicate the benefits of parasitic infection, offering new therapies for immune-mediated disorders.

Cutaneous Extranodal Natural Killer/T-Cell Lymphomas Histopathologically Mimicking Benign Inflammatory Disease.

Few studies have evaluated the histopathological features of cutaneous extranodal NK/T-cell lymphoma (ENKTL). The authors' study aims to describe cases of cutaneous ENKTL that histopathologically mimic benign inflammatory dermatosis. The authors searched the database of Asan Medical Center to identify cases of cutaneous ENKTL that were confirmed by skin biopsy between January 1998 and December 2014. The authors included cases that were initially diagnosed as benign inflammatory disorders on the histopathological examination, but finally diagnosed as cutaneous ENKTL on further evaluation. This study included 10 cases of cutaneous ENKTL. Six cases demonstrated nonspecific perivascular cellular infiltration, 2 cases demonstrated lupus erythematosus-like histological features, 1 case demonstrated psoriasiform lichenoid reaction, and 1 case demonstrated vasculitis-like features on histopathological examination. All cases were positive for CD56 and Epstein-Barr virus in situ hybridization. Perivascular infiltrations throughout the superficial and deep dermis with vasculopathy and panniculitic infiltration were common histopathological findings. The clinical features included 7 cases of erythematous to purpuric patches, 2 cases of facial swelling, and 1 case of cellulitis-like swelling. In conclusion, cutaneous ENKTL can histopathologically mimic benign inflammatory dermatosis. Cutaneous ENKTL should be suspected when histopathology shows perivascular dermal infiltration with vasculopathy and panniculitic cellular infiltration.

(176) - Probe-based Confocal Laser Endo-microscopy (pCLE) Can Identity Perivascular Cellular Infiltration in Patients with Acute Cellular Rejection

(176) - Probe-based Confocal Laser Endo-microscopy (pCLE) Can Identity Perivascular Cellular Infiltration in Patients with Acute Cellular Rejection

Fascin-expressing Dendritic Cells Dominate in Polymyositis and Dermatomyositis

Dendritic cells (DC) have been reported among inflammatory infiltrating cells in muscle tissue in idiopathic inflammatory myopathies (IIM), but to our knowledge no studies concerning the expression of langerin (CD207) or fascin (markers of immature and mature DC, respectively) in IIM have been published. Immunohistochemical analyses of langerin and fascin expression were performed on specimens from normal muscles, as well as those affected by polymyositis (PM) and dermatomyositis (DM). The results were analyzed by Mann-Whitney U test. In PM and DM, fascin-positive cells were numerous in the majority of the studied samples in perimysial, endomysial, and perivascular cellular infiltrates. Sporadic langerin-positive cells were detected. Fascin-positive DC predominance in inflammatory infiltrates in myositic muscles confirms the prevalence of mature forms and indicates that there are conditions stimulating DC maturation in both PM and DM. The induction of immunological tolerance by inhibiting DC maturation may be a promising direction for studies of myositis treatment.

Tamoxifen‐induced eccrine squamous syringometaplasia

A 74-year-old woman had carcinoma of her right breast for which surgery was performed. Four weeks following the start of tamoxifen therapy, she developed papules and plaques over her face, trunk and limbs. A skin biopsy showed perivascular and periadnexal mixed inflammatory cellular infiltrate with fibroplasia. Notably, the dermis also showed squamous epithelial islands, which in foci were noted to be closely associated with eccrine epithelium. This was confirmed with double peroxidase - alkaline phosphatase immunohistochemistry - the eccrine lumina highlighted with carcinoembryonic antigen (polyclonal) and the squamous metaplasia positive for cytokeratin 5/6. Eccrine squamous syringometaplasia was diagnosed. With close clinicopathological correlation, the cutaneous eruption was attributed to tamoxifen. Following discontinuation of the drug, the eruption resolved. Eccrine squamous syringometaplasia has been reported to occur in association with diverse conditions, including skin ulcers, burns and as a cutaneous adverse drug reaction, most commonly to chemotherapeutic drugs. This is believed to be the first report involving tamoxifen.

Cutaneous Leukocytoclastic Vasculitis Associated With A Fast Food Diet

Leukocytoclastic vasculitis (LCV) is the inflammation and necrosis of the wall of small blood vessels exhibited by endothelial swelling, perivascular polymorphonuclear cellular infiltrate, neutrophil fragmentation and nuclear debris and is typically localized to the skin. Many medications, diseases and infections have been implicated in the development of leukocytoclastic vasculitis. A review of available literature reveals case reports of leukocytoclastic vasculitis induced by medications such as infliximab, rituximab, etanercept, cocaine and numerous others and infections such as HIV and Streptococcal pneumonia as well as malignancies and chronic inflammatory conditions such as ulcerative colitis and collagen vascular diseases. Leukocytoclastic vasculitis induced by food has also been reported. Here, we report an interesting case of cutaneous leukocytoclastic vasculitis that developed in a patient after months of consuming a fast food diet for breakfast, lunch and dinner, which would improve only after abstaining from such a diet. The proper diagnosis and management of leukocytoclastic vasculitis remains a challenge for many clinicians and this report serves to give a brief overview of this condition, its causes, epidemiology, diagnosis and management.

Increased autoimmune disease activity in MRL-lpr mice following influenza infection. (135.21)

Abstract Influenza virus infection induces IFNα and TNFγ, which have been linked to increased severity of select autoimmune diseases. Influenza also stimulates TRL3 and TLR7, which are associated with increased kidney damage in mouse models of lupus. Therefore it seems likely that influenza infection of individuals with systemic lupus erythematosus, or lupus, would accelerate autoimmune disease progression. We used the MRL-lpr mouse model of spontaneous lupus-like disease to examine the impact of influenza infection on end stage organ damage. Influenza infection of MRL-lpr mice resulted in significant peri-vascular cellular infiltrates in the kidneys, composed primarily of CD4+ T cells. The infected mice also had accelerated proteinuria and lymphadenopathy of the cervical and mediastinal lymph nodes. Infection also resulted in a transient but significant increase in the concentration of anti-cardiolipin antibodies, but no changes in other autoimmune specificities. Experiments are underway to determine if this end-stage organ damage is dependent upon virus replication or if exposure to viral proteins, such as following vaccination, would result in increased kidney damage. This model will provide a unique system to dissect the immune-pathogen interaction in an autoimmune disease setting. These data will also provide valuable information on how infection impacts autoimmune disease development and progression.

A Mouse Model of Picornavirus-induced Airway Infection and Inflammation

RATIONALE: Rhinoviruses, which are members of the picornavirus family, are important causes of asthma exacerbations and early life wheezing illnesses that are associated with increased asthma risk. Given the absence of natural rhinovirus infections in rodents, we used attenuated mengovirus, a picornavirus whose wild-type form causes systemic infections in its natural murine hosts, to induce respiratory infections in mice, which we hypothesized would serve as a useful model for neutrophilic inflammatory processes in human rhinovirus infections. METHODS: BALB/c mice received intranasal inoculations with active or UV-inactivated attenuated mengovirus or vehicle. On various days postinoculation, inflammatory cells and mediators were assessed in the bronchoalveolar lavage (BAL) fluid and lung tissue, and pulmonary function was measured. RESULTS: Mice inoculated with attenuated mengovirus, compared with those inoculated with vehicle or UV-inactivated virus, shed infectious virus for 5 days, had peribronchiolar, perivascular, and alveolar cellular infiltrates, had significantly elevated (p < 0.05) levels of BAL neutrophils, neutrophil chemoattractant CXCR2 ligands (CXCL1, CXCL2, CXCL5), other chemokines/cytokines upregulated during rhinovirus infections (CXCL10, CCL2, and interferon-α, -β, and -λ), and exhibited significant increases (p < 0.05) in BAL fluid myeloperoxidase levels and wet-dry lung weight ratios, indicating neutrophil activation and airway injury, respectively. In these healthy mice, there were no virus-related changes in pulmonary function, consistent with experimental rhinovirus inoculations in healthy humans. CONCLUSIONS: Attenuated mengovirus caused respiratory infections in mice with several days of viral shedding accompanied by lower airway neutrophilic inflammation. These features suggest that this model will be useful for defining mechanisms of rhinovirus-induced airway inflammation in humans.

Eruptive pseudo‐angiomatosis lesions are associated with intravascular neutrophils and do not harbour Epstein–Barr virus

Eruptive pseudo-angiomatosis (EPA) is a rare, relatively newly described cutaneous disorder characterized by the sudden onset of several bright red, angioma-like papules surrounded by blanched halo. Its aetiology is unknown; however, viral infection or mosquito bites have been speculated as possible causes. This study aims to determine the clinical and histopathological features of EPA, and whether it is associated with Epstein-Barr virus (EBV) infection. We conducted a retrospective chart review of 25 EPA cases from 2006 to 2008. In order to determine latent EBV infection, EBV-encoded small RNA (EBER) in situ hybridization was performed in 18 subjects. To determine EPA's distinguishing histological characteristics, we compared the cases with 22 control cases of perivascular lymphocytic infiltration for haematoxylin and eosin, CD3, CD4, CD8, CD31 and c-kit staining patterns. The patient sample's female-to-male ratio was 2.1 : 1, and the patients' age ranged from 5 to 79 years (average 46 years). The lesions appeared during the months of July to September in all but 3 patients. Skin biopsies demonstrated capillary ectasia with perivascular mononuclear cellular infiltrates in the upper dermis. Most patients were otherwise healthy, and routine laboratory results were all normal except in one patient who had diabetes. The skin lesions faded without any treatment in 1-2 weeks. Results of EBER in situ hybridization were all negative. The only histological distinguishing feature of EPA was the presence of intravascular neutrophils, which was found to be present in 19 of the 20 EPA cases (95%), in contrast to only 3 of the 22 control subjects (14%) (P < 0.0001). The sudden onset of lesions during the summer months among our patients supports the 'paraviral eruption' concept of this probably underdiagnosed condition. The significant presence of intravascular neutrophils may be a diagnostic clue of EPA in South Korea.