Prominent Eosinophilic Infiltration Research Articles

Noneosinophilic asthma in children: relation with airway remodelling

Noneosinophilic asthma is increasingly recognised as an important clinical-pathological phenotype in adults. However, this entity has scarcely been investigated in children. In particular, it is unknown whether airway remodelling would develop in children with non-eosinophilic asthma to the same degree as in children with eosinophilic disease. We analysed bronchial biopsies from 80 children undergoing bronchoscopy for appropriate clinical indications: 21 with noneosinophilic asthma, 34 with eosinophilic asthma and 25 control children. Features of airway remodelling - basement membrane thickening, epithelial loss and angiogenesis - and immune activation - inflammatory infiltrate, interleukin (IL)-4, IL-5, transforming growth factor (TGF)-β, TGF-β receptor type II - were quantified by histology and immunohistochemistry. The main components of airway remodelling were present in children with noneosinophilic asthma just as in those with eosinophilic disease. Indeed, compared with control children, both noneosinophilic and eosinophilic asthmatic children had thickened basement membrane, increased epithelial loss and higher number of vessels. Moreover, in both groups of asthmatics, expression of IL-4 and IL-5 was increased, while that of TGF-β receptor type II was reduced, compared with controls. This study demonstrates that structural changes typical of asthma develop in asthmatic children even in the absence of a prominent eosinophilic infiltrate, indicating that other mechanisms, besides eosinophilic inflammation, may promote airway remodelling early in life.

Churg-Strauss syndrome with coexistence of eosinophilic vasculitis, granulomatous phlebitis and granulomatous dermatitis in bullous pemphigoid-like blisters

The main histopathological features in the cutaneous lesions of Churg-Strauss syndrome (CSS) are dermal leukocytoclastic vasculitis with a variable eosinophilic infiltrate and non-vasculitic tissue eosinophilia with granuloma formation. This wide histopathological spectrum may account for the various skin manifestations of CSS. However, the unique histopathological combination of dermal eosinophilic vasculitis and subcutaneous granulomatous phlebitis accompanied by bulla formation has not been previously described. We report an unusual CSS case showing dermal necrotizing eosinophilic vasculitis and granulomatous phlebitis in purpuric lesions coupled with subepidermal blistering. The blisters showed dermal granulomatous dermatitis and eosinophilia without evidence of vasculitis. Dermal necrotizing eosinophilic vasculitis was characterized by fibrinoid alteration of the vessel wall, a prominent perivascular eosinophilic infiltrate, a few infiltrating histiocytes along the affected vessel wall, and the absence of neutrophilic infiltration. The underlying subcutaneous granulomatous phlebitis was characterized by an angiocentric histiocytic infiltrate surrounded by marked eosinophilic infiltrate. Deposition of cytotoxic proteins and radicals derived from eosinophils in the vessel walls and papillary dermis followed by a secondary granulomatous response may account for the unique clinical and histopathological features in this case.

The Characteristics and Diagnostic Methods of Food Protein Induced Proctocolitis

Food protein induced proctocolitis (FPIPC) is a non-IgE mediated food allergy. FPIPC occurs exclusively among breast-fed infants within the first months of life. FPIPC is often diagnosed clinically in normal-conditioned infants with rectal bleeding. But FPIPC among infancy with rectal bleeding is less general than conceived. The endoscopic findings reveal an edematous and erythematous mucosa with superficial erosions or ulcerations, bleeding and lymphoid nodular hyperplasia. The prominent eosinophilic infiltrates in the rectosigmoid mucosa are important for the histopathologic diagnosis of FPIPC. However, in explaining eosinophilic infiltration within the lamina propria of the mucosa, it is necessary to differentiate whether it is a part of normal findings or occurs due to inflammatory reactions. Oral food challenge and elimination test is performed to identify the same clinical reaction as the symptom of FPIPC by the administration of a specific type of food to infants. The most common causal food is cow’s milk. Thus oral food challenge and elimination test can be the effective way of confirming FPIPC, reducing the possibility of misdiagnosis. The purpose of this report is to identify the characteristics of FPIPC, to introduce its diagnostic methods, and to suggest the future direction of research. (Korean J Pediatr Gastroenterol Nutr 2011; 14(Suppl 1): S47∼S54)

Myeloid Neoplasm with PDGFRB Translocation, t(1;5)(q21;q33): A Congenital Presentation of An Imatinib Responsive Congenital JMML with Eosinophilia

AbstractAbstract 4092Eosinophilia is seen in several myeloproliferative disorders (MPD), including the newly WHO recognized category of MPDs associated with translocations involving alpha and beta chains of PDGFR (platelet derived growth factor receptor). A subset of these MPDs, which consistently involve the PDGFRB (platelet derived growth factor receptor beta) gene rearrangement at 5q31–33, demonstrate a t(1;5) (q23;q33). Only a few cases of MPD with this translocation have been described, with the youngest patient being 5 months old at presentation. Imatinib mesylate was recently shown to be efficacious in MPDs with PDGFR rearrangements.Here we describe the first case of a congenital presentation of a myeloproliferative neoplasm with t(1;5) (q21;q33) resulting in PDGFRB rearrangement. The patient, born at 34 weeks gestation, was noted at birth to have hepatomegaly and multiple nodular purpuric cutaneous lesions over his entire body. An extensive work up for congenital infections was negative. A biopsy of the skin lesion shortly after birth demonstrated myeloid proliferation with prominent eosinophilic infiltrate. He continued to demonstrate hepatosplenomegaly and nodular skin lesions at 3 months of age, at which time his white blood cell count (WBC) was 91K/uL with 20% eosinophils, hemoglobin 7g/dl, platelets 35K/uL. Chromosome analysis of peripheral blood revealed a t(1;5) (q21;q33) in 64% of the cells and FISH analysis showed evidence of 5q33 rearrangement involving the PDGFRB locus.The patient was initially treated with a 10 day course of hydroxyurea which resulted in a decrease in the total WBC count, but showed no improvement of the rash or hepatosplenomegaly. After the diagnosis was confirmed, he was started on Imatinib at a dose of 100 mg QD (370 mg/m2). His WBC decreased from 69K/uL to 21K/uL within 4 days and normalized within a month of initiating Imatinib. The dose of Imatinib was decreased to 50 mg QD (185mg/m2) after the first week of therapy. His counts remained normal and a repeat chromosomal analysis of peripheral blood after 10 months of therapy showed no evidence of the prior t(1;5) (q21;q33) abnormality. His dose, therefore, remains at 50 mg QD, which, taking into account his interval growth corresponds to 113 mg/m2. The child is currently 16 months old with normal peripheral blood counts. He is clinically well, growing and developing normally and is tolerating Imatinib without any significant side effects.Summary: Here we describe the first case of a congenital presentation of a myeloid neoplasm with a t(1;5) (q21;q33) translocation and eosinophilia. The child presented at birth with an extensive “blueberry muffin” pattern of cutaneous lesions, hepatomegaly, leukocytosis with eosinophilia, thrombocytopenia and anemia and demonstrated a complete and rapid response to Imatinib monotherapy. There are currently no guidelines on dosing Imatinib in newborns. Three remaining clinical challenges regarding this patient include choosing the best method for monitoring the leukemic clone, choosing the proper dose of Imatinib for this growing child and determining the potential role of bone marrow transplant in an otherwise well infant. Disclosures:No relevant conflicts of interest to declare.

Gastrointestinal: Gastric anisakiasis presenting as a submucosal tumour diagnosed by endoscopic submucosal dissection

We report a case of gastric anisakiasis presenting as a submucosal tumour that was completely resected by endoscopic submucosal dissection. A 55-year-old woman without an obvious history of raw-fish consumption or severe abdominal pain was referred to our hospital for a comprehensive examination of a gastric submucosal tumour detected by barium gastrography. Gastroscopy revealed a 2 cm diameter submucosal tumour at the greater curvature of the gastric mid-body (Figure 1A). Endoscopic ultrasound (EUS) revealed a heterogeneous hypoechoic mass with a hyperechoic core (Figure 1B). The lesion occupied the submucosa and muscularis propria. The possibility of a malignant tumour could not be excluded, because the tumour was newly identified and showed a heterogeneous pattern on the EUS images. ESD was performed after obtaining the patient's informed consent 3 months after the initial gastroscopy. Submucosal dissection during ESD was difficult because of severe fibrosis. The submucosal tumour was completely resected but complicated by a tiny perforation, which was managed by application of endoclips. Pathological examination of the lesion revealed a granulomatous lesion with prominent eosinophilic infiltration and a lumen-like structure consistent with the characteristics of gastric anisakiasis (Figure 2A,2B). Contributed by

CASE REPORT: Multicentric mast cell tumors in a horse

A 6-year-old female Rocky Mountain horse was presented for evaluation of draining tracts and distal limb subcutaneous edema on the left front and left hind limbs that had been present for 2 weeks. Direct smears of fluid collected by fine-needle aspiration of subcutaneous fluid from both limbs were highly cellular with a predominance of eosinophils accompanied by numerous, moderately atypical, variably granulated mast cells. The cytologic diagnosis was mast cell tumor (MCT) with prominent eosinophilic infiltration with a differential diagnosis of eosinophilic granuloma. Histologic evaluation of surgical biopsies of lesions from both limbs was performed on sections stained with H&E, toluidine blue, and Luna stains. The histologic diagnosis was MCT, and staining with toluidine blue and Luna stains confirmed the presence of mast cells and eosinophils, respectively. In addition, the mast cells strongly expressed CD117. This is the first reported case of cutaneous mast cell neoplasia in a horse in which primary presenting complaints were draining tracts and distal limb subcutaneous edema involving multiple limbs. This case illustrates the utility of staining for CD117 expression in combination with traditional stains, such as toluidine blue and Luna, in differentiating MCTs from other eosinophilic lesions in horses.

Redefining the role of lymphocytes in gastroesophageal reflux disease and eosinophilic esophagitis

Eosinophilic esophagitis (EoE) and reflux esophagitis (RE) overlap clinically and histologically. RE is characterized by epithelial infiltration with small numbers of neutrophils and eosinophils, EoE by a prominent eosinophilic infiltrate. Lymphocytic esophagitis (LE), a new entity characterized by peripapillary lymphocytosis, questions the role lymphocytes play in esophageal inflammation. We test the hypothesis that lymphocyte infiltration in RE differs from EoE. One blinded pathologist read esophageal biopsies from 39 RE and 39 EoE patients. Both groups demonstrated significant numbers of lymphocytes (RE 22.7 +/- 2.2/HPF, EoE 19.8 +/- 1.8/HPF). Eosinophils/HPF in RE and EoE were 2.8 +/- 0.7 and 74.9 +/- 8.2, respectively (P < 0.001). Neutrophils were uncommon in RE (0.26 +/- 0.16/HPF) and EoE (0.09 +/- 0.04; P = 0.07). Eight of the 39 RE specimens had >or=50 lymphocytes in >or=1 HPF. Two were consistent with LE. There was an inverse correlation between numbers of eosinophils and lymphocytes in EoE (R = -0.47; P = 0.002), and no correlation between them in RE (R = 0.18; P = 0.36). The patients with EoE who used antireflux medications had fewer lymphocytes (16.3 +/- 1.3 vs 22.2 +/- 2.3/HPF; P = 0.030) and eosinophils (55.6 +/- 5.2 vs 76.0 +/- 8.7/HPF; P = 0.042) than those who did not. The pathological role of lymphocytes in RE and EoE may be underestimated. Our observation that 5% of the RE specimens meet histopathological criteria for LE potentially blurs the line between these entities. The observation that eosinophil counts are lower in EoE when antireflux meds are used supports the notion that reflux plays a role in the clinical expression of EoE.

Impaired olfactory function in mice with allergic rhinitis

Objective It has been reported that olfactory function is impaired in patients with allergic rhinitis. However, the mechanism of olfactory dysfunction in allergic rhinitis remains poorly understood. Because of difficulties in obtaining and analyzing human olfactory mucosa due to both technical and ethical issues, an animal model needs to be established to clarify the mechanism of olfactory dysfunction in allergic rhinitis. The purpose of this study was to study olfactory function and changes in olfactory mucosa using allergic rhinitis mice. Methods A model of allergic rhinitis mice with olfactory dysfunction was developed by sensitizing with ovalbumin (OVA), and intranasally challenging with the same allergen. Olfactory function of mice with or without allergic rhinitis was assessed by odor detection ability test with cycloheximide and local field potential (LFP) with 1-octanal. We also evaluated histological changes in the olfactory mucosa of allergic rhinitis mice by both light and electron microscopy. Results Both of odor detection ability test and LFP showed that olfactory function was impaired in mice with allergic rhinitis, but not in mice without allergic rhinitis. Histopathological findings showed prominent infiltration of eosinophils, plasma cells, neutrophils, mast cells, and macrophages in lamina propria of olfactory mucosa of mice with allergic rhinitis, although infiltration of these cells was not seen in control mice. Allergic rhinitis also increased the number and size of glands in olfactory mucosa, suggesting an elevated amount of mucin in olfactory mucosa. Conclusion This study showed for the first time that mice with allergic rhinitis have impaired olfactory function, increased size and number of olfactory glands, and infiltration of eosinophils, neutrophils, mast cells, plasma cells, and macrophages in the olfactory mucosa. This suggests that allergic reactions are seen in olfactory mucosa of mice with allergic rhinitis, and that greater olfactory gland activity is associated with olfactory dysfunction. Also, this mouse model could provide an expedient system for analyzing mechanisms of olfactory dysfunction.

Herpetiform pemphigus without anti‐desmoglein 1/3 autoantibodies

We report a patient with herpetiform pemphigus who was negative for autoantibodies to desmoglein (Dsg)1 or 3. He had erythemas with vesicles lining the margins on the trunk and extremities. Histopathology revealed intraepidermal blister with prominent eosinophil infiltration. Direct and indirect immunofluorescence demonstrated the presence of depositing and circulating immunoglobulin (Ig)G autoantibodies, but no IgA antibodies, to keratinocyte cell surface. Nonetheless, neither anti-Dsg1 nor Dsg3 antibodies were detected by enzyme-linked immunosorbent assay. Immunoblotting using human epidermal extracts also showed no reactivity with known intraepidermal or epidermal-dermal junctional substances. Immunoelectronmicroscopy revealed the reactivity on the portion of keratinocyte cell surface but not on the desmosomes. This case suggests that non-desmoglein antigen on keratinocyte cell surface can be targeted in some patients with this unusual variant of pemphigus.

Clinical Characteristics of 17 Cases of Eosinophilic Gastroenteritis

Eosinophilic gastroenteritis (EG) is a rare disease characterized by prominent eosinophilic infiltration that may involve a variable depth of one or more gastrointestinal organs. We analyzed the largest number of patients with EG among the studies carried out at a single center in Korea. We retrospectively analyzed the clinical, laboratory, endoscopic, and radiologic features, management, and clinical outcome in 17 patients who were diagnosed as EG from January 1994 to February 2008. Median age was 36 (2-67 years). Two of the 17 patients had a history of allergy. The most common symptoms were abdominal pain and diarrhea. Fifteen patients (88.2%) had hypereosinophilia. The ESR was moderately raised in 6 out of 14 patients. Eleven patients (64.7%) had predominant involvement of the mucosa, 1 (5.9%) of muscularis, and 5 (29.4%) of subserosa. EGD revealed non-specific findings such as erythema and edema. Abdominal Computed tomography revealed gastrointestinal wall thickenings of the involved organ, and all of 5 cases of the subserosal type had ascites. Thirteen patients (76.5%) were improved by corticosteroid treatment. Among five patients who had been followed for more than one year (12-84 months), two experienced relapse after discontinuing corticosteroids. EG should be considered in the differential diagnosis of unexplained gastrointestinal symptoms even in the absence of peripheral eosinophilia and in non-specific endoscopic findings.

Eosinophilic Airway Inflammation in a Cynomolgus Monkey

The present article describes an occurrence of eosinophilic airway inflammation of a 4-year-old female cynomolgus monkey in a vehicle control group of a routine toxicology study. Histologically, the airway lesion was characterized by prominent eosinophilic infiltrates, accompanied by mast cells, lymphocytes, and plasmacytes. The eosinophilic infiltrates were distributed throughout the airway: from trachea through respiratory bronchioles in the lung. The morphological feature of the lesion was indicative of an allergic airway disorder that can occur in humans with asthma. The present case is remarkable in that there is a paucity of reports on naturally occurring allergic airway disorders in nonhuman primates.

Recent Development of Drug Delivery Systems for the Treatment of Asthma and Related Disorders

It is well established that airway inflammatory processes are pivotal as the pathological features of asthma. Prominent infiltration of eosinophils and Th2 lymphocytes is a hallmark of the allergic inflammation, and inhaled corticosteroids markedly suppress such inflammatory changes, resulting in clinical beneficial effects. Aerosol delivery of anti-asthma drugs such as corticosteroids is ideal from the standpoint of maximizing local effects in the lung as well as minimizing systemic side effects compared with oral therapy. The 1987 Montreal protocol banned chlorofluorocarbon (CFC) propellant in pressurized metered-dose inhalers (pMDIs), which has been replaced with hydrofluoroalkane (HFA) propellant. The aerodynamic diameters of HFA are much smaller than those of CFC, suggesting a greater distribution in peripheral airways. New types of dry powder inhalers (DPIs) and nebulizers, that do not use propellants, also have been introduced. Performance of each drug delivery device depends on a variety of factors including the device type, particle size and distribution, the product formulation and patient-related factors. Therefore, drug delivery can differ even when the same drug is delivered via an HFA pMDI, a CFC pMDI, a DPI or a nebulizer. New and advanced devices can be helpful to maximize the advantages of these modes of drug delivery, and patents of novel invention of inhalation devices are described.

Herpes Simplex and Eosinophilic Oesophagitis: The Chicken or the Egg?

Herpes Simplex and Eosinophilic Oesophagitis: The Chicken or the Egg?

Establishment of Experimental Eosinophilic Vasculitis by IgE-Mediated Cutaneous Reverse Passive Arthus Reaction

Prominent eosinophil infiltration is a characteristic of some forms of vasculitis, such as Churg-Strauss syndrome, also known as allergic granulomatous vasculitis. In the current study, we established a mouse model of cutaneous eosinophilic vasculitis by the cutaneous reverse passive Arthus reaction using IgE injection instead of IgG. Wild-type C57BL/6 mice were injected with IgE anti-trinitrophenyl antibodies, followed immediately by intravenous administration of trinitrophenyl bovine serum albumin. IgE-mediated immune complex challenge induced substantial hemorrhage with marked infiltration of eosinophils in which neutrophils, mast cells, and macrophages were also mixed. This finding contrasted remarkably with the neutrophil-dominant infiltration pattern in IgG-mediated immune complex challenge. In the lesion, the expression level of monocyte chemotactic protein-3 was increased, and anti-monocyte chemotactic protein-3 treatment resulted in a significant but incomplete blockade of eosinophil recruitment. Furthermore, mice lacking E-selectin, P-selectin, L-selectin, or intercellular adhesion molecule-1, as well as wild-type mice that received anti-vascular cell adhesion molecule-1-blocking antibodies were assessed for the IgE-mediated Arthus reaction. After 24 hours, the loss of P-selectin resulted in a significant reduction in eosinophil accumulation compared with both wild-type mice and other mouse mutants. Collectively, the Fc class of immunoglobulins, which forms these immune complexes, critically determines the disease manifestation of vasculitis. The IgE-mediated cutaneous reverse passive Arthus reaction may serve as an experimental model for cutaneous eosinophilic infiltration in vasculitis as well as in other diseases.

Inflammatory myofibroblastic tumor as adverse outcome of eosinophilic esophagitis

An emergency esophagogastroduodenoscopy performed in a dyspeptic 19-year-old girl with hematemesis, abdominal pain, and anemia ([Fig. 1]) revealed a polypoid esophageal mass with distal erosion. A subsequent CT scan confirmed the bulky lesion (14 × 4 × 3.5 cm) extending from the carina to the cardia level. Both extraesophageal extension and nodal and extranodal metastases were excluded. The extent and location of the mass ruled out any endoscopic resection and a total esophagectomy with gastric pull-up was performed. Both histology and immunophenotyping (positive for vimentin, MNF116, and smooth muscle actin; negative for S100 and CD117) were consistent with the “classical variant” of inflammatory myofibroblastic tumor (IMT). A prominent eosinophilic infiltrate ([Fig. 2 a – c]) was also present, spreading from the lesional to the extralesional area, where the squamous epithelium featured rich eosinophic infiltrate, fully consistent with eosinophilic esophagitis ([Fig. 2 d]).

Lymphoepithelioma-like carcinoma of the prostate

In this report, we summarized the clinicopathologic features of 5 cases of lymphoepithelioma-like carcinoma of the prostate, a rare variant of prostate cancer characterized by a malignant epithelial component densely infiltrated by lymphoid cells. In all 5 patients, there were obstructive symptoms and elevated prostate-specific antigen; one patient had also hematuria. Their ages ranged from 69 to 82 years (mean age, 76 years). The initial diagnosis of lymphoepithelioma-like carcinoma of the prostate was made on transurethral resection in 3 cases and radical prostatectomy in 2 others. In one case the diagnosis of lymphoepithelioma-like carcinoma admixed with conventional acinar adenocarcinoma was an unexpected finding at time of transurethral resection for benign prostatic hyperplasia. Three patients had clinical stage T3 tumors and another had stage T4 disease; stage T1b was present in the remaining case. Microscopically, all tumors contained lymphoepithelioma-like carcinoma, which comprised 10% to 90% of the entire tumor. All cases were associated with adenocarcinoma, either as the sole pattern in 5 cases or with an additional ductal component in 3 cases. One case had additional features of adenosquamous carcinoma. The lymphoepithelioma-like carcinoma component was characterized by indistinct cytoplasmic borders and a syncytial growth pattern. The stroma was densely infiltrated by lymphoid cells admixed with some plasma cells and neutrophils; one case had a prominent infiltration of eosinophils. Immunohistochemical staining demonstrated that lymphoepithelioma-like carcinoma was positive for prostate-specific antigen, prostate acid phosphatase, alpha-methylacyl coenzyme A racemase, and epithelial membrane antigen; several cytokeratins (AE1/AE3, 7, 8, and 20 [rare cells]) were also immunoreactive. The mean Ki-67 labeling index was 53% (range, 40%-70%), and the p53 expression in all cases was low (10%-20%). The lymphoid component was mainly composed of T with a minor subset of B cells, admixed with some dendritic cells and histiocytes as seen by S100 and CD68 immunoreactivity. Latent membrane protein 1 immunostaining and in situ hybridization for Epstein-Barr virus were negative in all 5 lymphoepithelioma-like carcinoma cases. DNA ploidy of lymphoepithelioma-like carcinoma tumors gave DNA histograms with aneuploid peaks. DNA ploidy of the concurrent adenocarcinoma gave DNA aneuploid peaks except in one DNA diploid case. Four patients died of disease from 8 to 26 months; one patient was lost to follow-up. In summary, lymphoepithelioma-like carcinoma of the prostate arise in aggressive prostate cancers at advanced clinical stage. Morphologic recognition and distinction from other prostatic lesions and tumors with prominent lymphoid stroma is critical for its clinical management.

Acute interstitial nephritis with prominent eosinophil infiltration

Acute interstitial nephritis (AIN) is common, but prominent eosinophil infiltration in patients with acute interstitial nephritis is rare. The possible etiologies, predisposing factors and treatment of such patients are the subjects of this study. one patient was reported from our medical center; nine more patients with similar findings were reviewed from the literature. Suspected offending drugs, clinical presentations, predisposing factors and patient outcomes after therapy were recorded. A case of clam extract-associated acute interstitial nephritis with prominent eosinophil infiltration was reported. Ten cases including ours were analyzed. A variety of drugs was thought to be causative. In all, 7 of the 10 patients had a preexisting nephrotic syndrome, and eosinophilia was found in 6. Bone marrow biopsy was not performed in most cases and only available for 2 patients including ours. 9 patients treated with steroids had good responses but 1 patient died despite treatment. Acute interstitial nephritis with prominent eosinophil infiltration can be caused by a great diversity of drugs, which can include clam extract tablets. A preexisting nephrotic syndrome seemed to be a predisposing factor for this condition. This disease rarely led to fatality and most patients responded well to steroid therapy.

A case of hypereosinophilic syndrome presenting withintractable gastric ulcers

We report a rare case of hypereosinophilic syndrome (HES) presenting with intractable gastric ulcers. A 71-year-old man was admitted with epigastric pain. Initial endoscopic findings revealed multiple, active gastric ulcers in the gastric antrum. He underwent Helicobacter pylori (H pylori) eradication therapy followed by proton pump inhibitor (PPI) therapy. However, follow-up endoscopy at 4, 6, 10 and 14 mo revealed persistent multiple gastric ulcers without significant improvement. The proportion of his eosinophil count increased to 43% (total count: 7903/mm(3)). Abdominal-pelvic and chest computed tomography scans showed multiple small nodules in the liver and both lungs. The endoscopic biopsy specimen taken from the gastric antrum revealed prominent eosinophilic infiltration, and the liver biopsy specimen also showed eosinophilic infiltration in the portal tract and sinusoid. A bone marrow biopsy disclosed eosinophilic hyperplasia as well as increased cellularity of 70%. The patient was finally diagnosed with HES involving the stomach, liver, lung, and bone marrow. When gastric ulcers do not improve despite H pylori eradication and prolonged PPI therapy, infiltrative gastric disorders such as HES should be considered.

Significant Eosinophilic Infiltrate of the Breast

Background: Prominent tissue eosinophilic infiltrate is encountered in a number of inflammatory states, particularly in allergic diseases, parasitic infection, collagen diseases and hematological malignancies. We searched for significant or prominent eosinophilic infiltrates of the breast in benign and malignant diseases. Methods: All breast cases reported in our institution during the period of 1999-2008 were reviewed for significant or prominent eosinophilic infiltrate.Results: Eight cases were identified. Four cases diagnosed as granulomatous mastitis, one eosinophilic mastitis, two ductal carcinomas and one gynecomastia.Conclusion: Significant eosinophilic infiltrate was identified mainly in cases of mastitis and rarely in breast carcinomas. Although eosinophils can degranulate and release toxic inhibiting factors into tumors, they are uncommonly encountered in breast carcinomas.

Persistent urticaria characterized by recurrent lasting urticarial erythema with histological features of prominent perivascular eosinophilic infiltration

We report a 29-year-old woman with a 15-year history of recurrent pruritic urticarial erythemas. The individual lesions lasted for > 24 h, and antihistaminic agents were not effective. Histological examination of a skin biopsy revealed interstitial oedema of the dermis and perivascular infiltration of numerous eosinophils without vasculitis. No internal organ involvement or peripheral blood eosinophilia was present. A diagnosis of persistent urticaria was made and the patient was successfully treated with oral corticosteroid therapy. Persistent urticaria has been described as an unusual reaction that lasts longer than typical urticaria. It is effectively treated with corticosteroids, but not with antihistaminic agents. In order to choose the most effective treatment, persistent urticaria should be recognized as a different clinical condition from typical urticaria.