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Peripheral Eosinophilia (peripheral + eosinophilia)
Selected AbstractsSevere strongyloidiasis in corticosteroid-treated patientsCLINICAL MICROBIOLOGY AND INFECTION, Issue 10 2006L. Fardet Abstract Severe strongyloidiasis, caused by Strongyloides stercoralis, is a preventable life-threatening disease that can occur in any corticosteroid-treated patient who has travelled to a country with infested soil, even if the contact occurred up to 30 years previously. This diagnosis should be considered in corticosteroid-treated patients who experience either unusual gastrointestinal or pulmonary symptoms, or who suffer from unexplained sepsis caused by Gram-negative bacilli. Peripheral eosinophilia is not observed systematically and, even if present, is moderate in most cases. Ivermectine is the best prophylactic and therapeutic option, and thiabendazole should no longer be used. However, guidelines for the prevention and management of S. stercoralis infection in such patients have not yet been established. [source] Elemental signals regulating eosinophil accumulation in the lungIMMUNOLOGICAL REVIEWS, Issue 1 2001Paul S. Foster Summary: In this review we identify the elemental signals that regulate eosinophil accumulation in the allergic lung. We show that there are two interwoven mechanisms for the accumulation of eosinophils in pulmonary tissues and that these mechanisms are linked to the development of airways hyperreactivity (AHR). Interleukin-(IL)-5 plays a critical role in the expansion of eosinophil pools in both the bone marrow and blood in response to allergen provocation of the airways. Secondly, IL-4 and IL-13 operate within the allergic lung to control the transmigration of eosinophils across the vascular bed into pulmonary tissues. This process exclusively promotes tissue accumulation of eosinophils. IL-13 and IL-4 probably act by activating eosinophil-specific adhesion pathways and by regulating the production of IL-5 and eotaxin in the lung compartment. IL-5 and eotaxin co-operate locally in pulmonary tissues to selectively and synergistically promote eosinophilia. Thus, IL-5 acts systemically to induce eosinophilia and within tissues to promote local chemotactic signals. Regulation of IL-5 and eotaxin levels within the lung by IL-4 and IL-13 allows Th2 cells to elegantly co-ordinate tissue and peripheral eosinophilia. Whilst the inhibition of either the IL-4/IL-13 or IL-5/ eotaxin pathways resulted in the abolition of tissue eosinophils and AHR, only depletion of IL-5 and eotaxin concurrently results in marked attenuation of pulmonary inflammation. These data highlight the importance of targeting both IL-5 and CCR3 signalling systems for the resolution of inflammation and AHR associated with asthma. S.M. is a Postdoctoral Fellow funded by a grant from the Human Frontiers Foundation to P.S.F. and M.E.R. J.M. is supported by the German Research Association (grant MA 2241/1-1) and S.P.H by a NH&MRC CJ Martin Postdoctoral Fellowship. [source] Utility of eosinophilia as a diagnostic clue in lower abdominal pain in northern Australia: a retrospective case,control studyINTERNAL MEDICINE JOURNAL, Issue 4 2008P. J. Clark Abstract Acute eosinophilic enteritis is a difficult diagnosis to make. Insufficient consideration of eosinophilia may commit patients to surgical treatment when medical therapy may be appropriate. The aim of the study was to determine whether the eosinophil count was considered in the diagnostic evaluation of patients presenting with acute abdominal pain who subsequently underwent appendectomy and whether eosinophilia was related to subsequent histology. The method used in the study was retrospective case,control. None of three patients with increased eosinophil counts had histologically proven appendicitis (Fisher's exact test 0.025); worm segments were seen in two patients. None of 39 patients who had histologically proven appendicitis had increased eosinophil counts. Eosinophilia may be underutilized and helminth infection may not be considered in the differential diagnosis of abdominal pain. A normal eosinophil count in the setting of clinically suspected appendicitis may make the diagnosis of eosinophilic enteritis less likely, but does not exclude it. Patients with abdominal pain and peripheral eosinophilia appear less likely to have acute appendicitis on subsequent histology; however, further study is required to validate these findings. The decision to operate remains one of clinical judgement. [source] Genetic resistance to Teladorsagia circumcincta: IgA and parameters at slaughter in Churra sheepPARASITE IMMUNOLOGY, Issue 6 2005M. MARTÍNEZ-VALLADARES SUMMARY Previous experiments have shown that genetic resistance to infection by Teladorsagia circumcincta in sheep can be measured by the level of IgA in gastric mucus, jointly with other parameters. The aim of this study has been to observe the influence of IgA on adult worms. The experiment was carried out with Churra sheep experimentally infected with T. circumcincta. At slaughter, gastric content, gastric mucus, blood samples and faeces were recovered to determine the number of eggs in utero, length of adult females, worm burden, number of L4, titre of serum pepsinogen, peripheral eosinophilia and eggs per gram (epg). IgA activity in gastric mucus, serum, nasal secretions and saliva were tested against somatic antigen from fourth-stage larvae (L4), somatic antigen from the adult stage and excretory,secretory (E/S) antigen from the adult stage. The results showed a significant correlation between serum IgA and gastric mucus (P < 0·01) as well as in nasal secretions (P < 0·01). We found negative correlations between IgA activity in gastric mucus with the eggs in utero and with adult female length. Furthermore there were also strong relationships between the peripheral eosinophilia with serum (P < 0·01) and gastric mucus IgA activity (P < 0·01). Moreover serum pepsinogen and the number of L4 at slaughter were related (P < 0·01). [source] Lower levels of plasmacytoid dendritic cells in peripheral blood are associated with a diagnosis of asthma 6 yr after severe respiratory syncytial virus bronchiolitisPEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 5 2009Eli Silver Plasmacytoid dendritic cells (pDC) play a crucial role in antiviral immunity and promoting Th1 polarization, possibly protecting against development of allergic disease. Examination of the relationship between peripheral blood plasmacytoid DC levels and manifestations of asthma and atopy early in life. We have isolated peripheral blood mononuclear cells (PBMC) from 73 children (mean age ± SD: 6.6 ± 0.5 yr old) participating in the RSV Bronchiolitis in Early Life (RBEL) study. Flow cytometry was performed on PBMC detecting DC surface-markers: Blood Dendritic Cell Antigens (BDCA) 1, 3, and 2 which identify myeloid type 1, type 2, and plasmacytoid cells, respectively. Total serum IgE, peripheral eosinophil count, and allergy skin tests were documented. About 45% (n = 33) of study participants had physician-diagnosed asthma by 6 yr of age. These children had significantly lower quantities (mean ± SD) of plasmacytoid DC than their non-asthmatic counterparts (1020 ± 921 vs. 1952 ± 1170 cells per 106 PBMC, p = 0.003). We found significantly lower numbers of myeloid dendritic cells in children with asthma (3836 ± 2472 cells per 106 PBMC) compared with those without asthma (4768 ± 2224 cells per 106 PBMC, p = 0.02); however, this divergence was not significant after adjusting for covariates of age, gender, race, skin test reactivity, smoke exposure, and daycare attendance. We did not identify any direct association between DC levels and markers of atopy: skin test reactivity, peripheral eosinophilia, and IgE level. Children who are diagnosed with asthma after severe RSV bronchiolitis appear to have a relative deficiency of plasmacytoid DC in peripheral blood. [source] Incontinentia Pigmenti in Boys: A Series and Review of the LiteraturePEDIATRIC DERMATOLOGY, Issue 6 2006Daniela Ardelean M.D. Occurrences of this disease in boys have been reported, however, its clinical phenotype has not been well characterized. The purpose of this study was to report on additional instances of incontinentia pigmenti in boys and to review the clinical, laboratory, and molecular characteristics of all published such patients. A retrospective chart review and Medline search using the keywords incontinentia pigmenti, males, and NEMO gene was undertaken. Six new boys with incontinentia pigmenti were found in our database and 36 more were previously reported in the literature. The vesiculo-bullous stage was the most frequent clinical presentation at diagnosis (80%). Fifteen percent of patients had an initial unilateral presentation. Recurrences of this stage were noted in 16%. Stages 2 and 3 of the disease were present in only 72.5% and 75% of patients, respectively. Only 15% of the boys had a documented stage 4. Extracutaneous manifestations were also documented (30%, central nervous system manifestations, 35%, eye involvement, 30%, alopecia, 40%, teeth anomalies). Thirty two percent of boys had peripheral eosinophilia. Only five had evidence of NEMO gene mutation. The male phenotype has clinical features similar to those of the female phenotype. Unilateral presentation is a distinct occurrence in boys, especially in early stages. Anomalies are the most common extracutaneous findings, followed by eye, hair, and central nervous system abnormalities. [source] Hypereosinophilic syndrome presenting as cutaneous necrotizing eosinophilic vasculitis and Raynaud's phenomenon complicated by digital gangreneBRITISH JOURNAL OF DERMATOLOGY, Issue 3 2000K-A. Jang Cutaneous necrotizing eosinophilic vasculitis is a recently identified type of vasculitis that is characterized by an eosinophil-predominant necrotizing vasculitis affecting small dermal vessels. Clinically, it presents with pruritic erythematous and purpuric papules and plaques, peripheral eosinophilia and a good response to systemic steroid therapy. This vasculitis can be idiopathic or associated with connective tissue diseases. Although the pathogenic roles of eosinophil-derived granule proteins and interleukins have been documented in diseases associated with eosinophilia, a role of CD40 (a glycoprotein of the tumour necrosis factor receptor superfamily) has rarely been described. We describe two patients with idiopathic hypereosinophilic syndrome (HES) presenting with multiple erythematous patches and plaques on the lower extremities and Raynaud's phenomenon. They satisfied the criteria for the diagnosis of HES by clinical and laboratory investigations. Histopathology of the cutaneous lesions revealed prominent eosinophilic infiltration with local fibrinoid change in vessel walls in the dermis and subcutis. Immunohistochemical detection of CD3, CD4, CD8 and CD40 was performed. Infiltrating eosinophils were strongly stained by anti-CD40 monoclonal antibody. One patient improved with prednisolone, pentoxifylline and nifedipine, without recurrence. The other patient initially improved with steroids, but after self-withdrawal of steroid developed digital ischaemia that evolved to severe necrosis and required amputation. Cutaneous necrotizing eosinophilic vasculitis, Raynaud's phenomenon and digital gangrene may develop as cutaneous manifestations of HES. CD40 may play a part in the pathogenesis of eosinophilic vasculitis in HES. [source] DRESS syndrome caused by efalizumabCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 1 2008J. M. L. White Summary We report a case of drug reaction with eosinophilia and systemic symptoms (DRESS) to efalizumab. A 52-year-old man developed a widespread papulovesicular rash after 4 weeks of treatment with efalizumab (1.0 mg/kg/week) for treatment-resistant severe psoriasis. Histology revealed a subepidermal blister with eosinophil-rich inflammatory cell infiltrate. Subsequently, the patient developed high peripheral eosinophilia, abnormal liver function, malaise and fever, all requiring inpatient admission. Efalizumab was discontinued immediately, but the rash persisted for 4 months and was only controlled by oral prednisolone at a dose of 30 mg/day. To our knowledge, this is the first reported case of DRESS caused by efalizumab. [source] | ||||||||||||||||||||||