SEARCH · PubMed Health

Results for “EOSINOPHILIA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources

PubMedDate not supplied

Delayed nasal mucociliary clearance in patients with nonallergic rhinitis and nasal eosinophilia.

This study investigated nasal mucociliary clearance as related to nasal eosinophilia in nonallergic rhinitis patients using the technique of nasal saccharin challenge. Fifty-six consecutive patients with nonallergic rhinitis were evaluated with nasal cytology and saccharin challenge. A saccharin challenge time of greater than 25 minutes was considered abnormal. Twelve of 56 patients (21.4%) had nasal eosinophilia. Fifteen of 56 patients (26.8%) had prolonged nasal circulation times greater than 25 minutes, indicating delayed mucociliary clearance. Although 7 of 12 patients (58.3%) with nasal eosinophilia had delayed mucociliary clearance, only 8 of 44 patients (18.2%) without eosinophilia had circulation times longer than 25 minutes. The correlation of nasal eosinophilia with prolongation of the nasal circulation time is statistically significant (chi square 5.84, P = .0156). We postulate that damage to the nasal mucociliary system may be an etiologic factor for a subset of patients with nonallergic rhinitis and that this damage may be mediated by eosinophils.

Adult↗

PubMed1992

Pathologic manifestations of the eosinophilia myalgia syndrome: analysis of 11 cases.

We describe the histopathologic changes of skin, muscle, vessels, and fascia in 11 patients with eosinophilia myalgia syndrome, a newly described entity that has been linked to the ingestion of L-tryptophan. This syndrome is defined clinically by severe incapacitating myalgias and a peripheral eosinophilia. Arthralgias, edema of the extremities, morbilliform rashes, skin induration, weakness, fatigue, and respiratory weakness may be present as well. The earliest apparent histologic changes were observed at the septa between subcutaneous fat lobules and in the deep dermis or fascia. The septa and fascia were infiltrated with a sparse mixture of lymphocytes and histiocytes. In the deep fascia, in addition to inflammatory cells, there were distinctive, reactive mesenchymal cells that showed features of both histiocytes and fibrocytes. Minimal tissue eosinophilia was seen despite the extent of blood eosinophilia. Dermal thickening and homogenization of collagen bundles occurred with replacement of fat and adnexa (changes indistinguishable from scleroderma or morphea). Vessel walls in the dermis and fascia showed thickening and endothelial swelling, but no overt vasculitis was noted. Skeletal muscle biopsies showed a perimysial, epimysial, and/or fascial inflammatory infiltrate of lymphocytes and distinctive reactive mesenchymal cells with some eosinophils. Minimal myofiber atrophy, regeneration, or necrosis was seen despite the clinical history of severe myalgias in almost all patients. This syndrome should help gain insight into the mechanisms of fibrosis in environmental-induced, scleroderma-like syndromes and in idiopathic, scleroderma-like disorders as well.

Adult↗

PubMed1996

Plasma histamine in patients with tropical disorders and acute asthma who exhibit eosinophilia.

The mean venous plasma histamine of 14 patients with eosinophilia was 18.7 nmol/L (range 0-86.4) and significantly higher than that of 4.0 nmol/L for 29 normal subjects [range 0-10.8 (P < 0.01)]. The eosinophilia of schistosomiasis (two patients), strongyloidiasis (one patient), and asthma (four patients) was accompanied by raised plasma histamine concentrations. Normal levels occurred in onchocerciasis (four patients) and in two of three patients with non-specific eosinophilia. Plasma histamine concentrations in the tropical disorders are not thought to have been reported previously. The initial arterial and venous plasma histamine concentrations of 14 acute asthmatics, were significantly positively correlated with the respective arterial (P < 0.01) and venous (P < 0.05) eosinophil counts. The results in acute asthma support the hypothesis that increased plasma histamine may have a role in promoting eosinophil release from the bone-marrow. Eosinophilia is not dependent upon a raised plasma histamine in some disorders, but may be in others, such as schistosomiasis.

Acute Disease↗

PubMed1992

[Mianserin agranulocytosis followed by oxitriptan eosinophilia].

A patient suffering from endogenous depression was treated with mianserin and developed agranulocytosis. After recovering from this, and with the depression in remission, the patient was given L-tryptophan. When this medication was removed from the market, due to the newly described eosinophilia-myalgia syndrome, a change was made to oxitriptan, which then caused a serious asymptomatic eosinophilia. No similar cases have yet been reported. Following withdrawal of oxitriptan, the eosinophilia disappeared. Evidence for any other cause of the condition was not found. Causes and physiopathology of drug-induced agranulocytosis and eosinophilia and the circumstances of such complications following use of mianserin and oxitriptan are discussed.

5-Hydroxytryptophan↗

PubMed1992

Central nervous system involvement in the eosinophilia-myalgia syndrome.

A patient with eosinophilia-myalgia syndrome developed progressive central nervosa system involvement that did not improve despite discontinuation of L-tryptophan therapy. Neurologic impairment was manifested initially by spastic monoparesis, which was improved by treatment with methyl-prednisolone and hydroxyurea. Recurrence of weakness was accompanied by gait ataxia, dysphagia, and complaints of a gradual decline in memory and concentration. Neuropsychological testing identified a broad pattern of cognitive deficits suggestive of a subcortical dementia, and magnetic resonance imaging demonstrated multiple high-signal lesions in the white matter. Cognitive deficits appear to be underrecognized in patients with the eosinophilia-myalgia syndrome. The response of our patient's initial symptoms to corticosteroid therapy suggests a possible role for autoimmune mechanisms in the pathogenesis of central nervous system involvement in the eosinophilia-myalgia syndrome. Neuropsychological evaluation should be performed in patients with cognitive complaints to delineate the full spectrum of central nervous system impairment associated with the eosinophilia-myalgia syndrome.

Central Nervous System Diseases↗

PubMed1999

IL-9 induces chemokine expression in lung epithelial cells and baseline airway eosinophilia in transgenic mice.

Recent data have identified IL-9 as a key cytokine in determining susceptibility to asthma. These data are supported by the finding that allergen-exposed IL-9-transgenic mice exhibit many features that are characteristic of human asthma (airway eosinophilia, elevated serum IgE and bronchial hyperresponsiveness) as compared to the background strain. A striking feature of these animals is a robust peribronchial and perivascular eosinophilia after allergen challenge, suggesting that IL-9 is a potent factor in regulating this process. In an attempt to gain insights into the molecular mechanism governing IL-9 modulation of lung eosinophilia, we investigated the ability of this cytokine to induce the expression of CC-type chemokines in the lung because of their effect on stimulating eosinophil chemotaxis. Here we show that IL-9-transgenic mice in contrast to their congenic controls exhibit baseline lung eosinophilia that is associated with the up-regulation of CC-chemokine expression in the airway. This effect appears to be through a direct action of IL-9 because the addition of recombinant IL-9 to primary epithelial cultures and cell lines induced the expression of these chemokines in vitro. These data support a mechanism for IL-9 in regulating the expression of eosinophil chemotactic factors in lung epithelial cells.

Allergens↗

PubMed1981

Carcinomas of the cervix with intense stromal eosinophilia.

Stromal inflammatory reactions dominated by eosinophilic leukocytes have been reported in a small number of invasive cervical carcinomas. The clinicopathologic features of six patients whose cervical carcinomas were accompanied by an intense infiltrate of eosinophils were analyzed. Several patients also manifested an eosinophilia of peripheral blood and regional lymph nodes. The cervical carcinoma cells were regarded as the most likely cause of the tissue and blood eosinophilia since other etiologic factors were not identified. Eosinotactic and eosinopoietic substances probably either were produced directly by the carcinoma cells or resulted from immunologic interactions of inflammatory lymphoid cells and mast cells with antigens of the tumors. While stromal eosinophilia alone may not be of prognostic significance, eosinophilia of the peripheral blood may be an adverse sign in some patients with cervical carcinoma.

Adult↗

PubMed1989

Paraneoplastic eosinophilia. Report of a case with in vitro studies of hemopoiesis.

Eosinophilia is an unusual paraneoplastic manifestation. The authors describe for the first time the association of eosinophilia and metastatic medullary carcinoma of the thyroid. The eosinophil count normalized during remission after chemotherapy but increased at time of relapse. The patient's serum enhanced eosinophilic differentiation of human multipotential hemopoietic precursors but was inhibitory to in vitro growth of murine myelopoietic precursors. The number of multipotential colonies which could be cultured in vitro was lower in the patient's peripheral blood than in normal controls. The authors conclude that a tumor-related circulating factor caused eosinophilia by inducing eosinophilic differentiation and inhibiting myeloid differentiation. Such a mechanism of paraneoplastic eosinophilia has not been previously described.

Cells, Cultured↗

PubMed1993

Interleukin-5 mRNA in three T-cell lymphomas with eosinophilia.

The objective of this controlled pilot study was to determine if mRNA coding for interleukin-5 (IL-5), a cytokine that promotes eosinophil differentiation, growth, and migration, could be detected in three T-cell lymphomas that were infiltrated extensively by eosinophils. To detect mRNA coding for IL-5, we performed an RNA polymerase chain reaction on mRNA extracted from three T-cell lymphomas with eosinophilia and from 29 positive and negative validation controls. Using this procedure, we detected a 293-base pair, IL-5-specific amplification product in the three cases of T-cell lymphoma with eosinophilia and in 11 of 12 positive validation controls, including 10 cases of Hodgkin's disease with eosinophilia. IL-5 mRNA was not detectable in the 17 negative validation controls. This preliminary study suggests that IL-5 mRNA is detectable by polymerase chain reaction in three cases of T-cell lymphoma with eosinophilia.

Actins↗

PubMed1993

Aspergillus fumigatus antigen induced eosinophilia in mice is abrogated by anti-IL-5 antibody.

A murine model of allergic bronchopulmonary aspergillosis (ABPA), developed by exposure to Aspergillus fumigatus antigens, demonstrated eosinophilia of peripheral blood (PB), bone marrow (BM), and lung. The eosinophilia was abrogated by monoclonal anti-interleukin-5 (IL-5) antibody (TRFK-5) and not by an isotype control antibody (GL 113). Eosinophils in PB were enumerated from stained smears and their relative increase or decrease in cells from BM and lung was determined by an eosinophil peroxidase (EPO) assay (measured in optical density). Intraperitoneal injection of TRFK-5 in mice exposed to A. fumigatus antigen produced a significant reduction in eosinophils (PB 6.6 +/- 1.14% vs. 3.8 +/- 0.8%, P < .01) and EPO production in BM (0.935 +/- 0.03 vs. 0.615 +/- 0.02, P < .001). A similar reduction in EPO production in the lung (0.691 +/- 0.12 vs. 0.495 +/- 0.05, not significant) was also reflected in the histopathology for the different groups of mice. These findings confirming the role of IL-5 in eosinophilia, although not surprising, are significant in elucidating the immunopathogenesis of ABPA in the murine model. We conclude that in this model, eosinophilia may be due largely to the Th2 cytokine -IL-5 induced by A. fumigatus antigens.

Animals↗

PubMed2002

Kinetics of airway hyperresponsiveness and airway eosinophilia in BALB/c mice and their modulation by different dexamethasone treatment regimens.

The mechanisms of airway hyperresponsiveness (AHR) are still poorly understood. In this study we have established a model of persistent AHR and eosinophilia and evaluated the prophylactic vs. therapeutic effects of dexamethasone on these parameters. Mice were immunised with ovalbumin (OVA) on day 0 and challenged intranasally on days 10, 11, 12 and 13 with OVA or phosphate buffer saline (PBS). Airway responsiveness to methacholine, measured 24-h post multiple intranasal OVA challenges, was significantly increased compared to time matched PBS-controls (P<0.05). AHR could be detected for up to 14 days after the last OVA challenge although the magnitude of the AHR had diminished by day 14 compared to day 1. OVA challenge of mice induced a significant airway eosinophilia at 24h (P<0.05); this persisted for 2 weeks after the challenge. Prophylactic treatment with dexamethasone (1mg x kg (-1)) reduced the OVA induced AHR, eosinophilia and mucus cell hyperplasia/metaplasia measured 24h post challenge. Therapeutic treatment, with dexamethasone (2 mg x kg(-1)), significantly inhibited established airway eosinophilia, measured at 72 h post OVA challenge, only when treatment was initiated at 24h but not 48 h after challenge. In contrast, AHR measured at 72 h post OVA challenge was significantly reduced when treatment was started at either 24 or 48 h post challenge. Our data shows that the immunization and challenge procedures employed resulted in a persistent type of AHR. Prophylactic intervention with steroids almost completely inhibited its development; however therapeutic intervention only partially resolved AHR.

Animals↗

PubMed1983

Evidence for the control of eosinophilia by the major histocompatibility complex in mice.

The genetic control of eosinophilia has been studied in congenic strains of mice. Eosinophilia was induced with cyclophosphamide followed by keyhole limpet hemocyanin in complete Freund's adjuvant. After this treatment, BALB/c mice developed a high eosinophil response, whereas CBA, C57BL and A/J mice developed a low one. The major histocompatibility complex (MHC) was found to exert a control on eosinophilia, as B10.D2 mice developed a higher eosinophil response than B10, B10.A, or B10.BR. BALB/c-H-2k mice had a lower response than BALB/c, and A.TL mice had a higher response than A/J or A.TH. If a single gene within the MHC is responsible for these effects, the most likely position for it is in the vicinity of the Tla locus. Splenectomy reduced eosinophilia in BALB/c and A.TL mice, but not in A/J mice, indicating that the spleen is a significant site of eosinophil production in high responder strains.

Animals↗

PubMed1993

Induction of lung eosinophilia and neutrophilia in guinea pigs following injection of sephadex beads.

We have developed a method of induction of airway eosinophilia and neutrophilia in guinea pigs by intravenous injection of various types of Sephadex beads. In the first series of experiments, we have shown that G-50 Sephadex beads (Superfine, 24 mg/kg in conscious animals) induced a large accumulation of inflammatory cells in alveolar walls. The bronchoalveolar lavage (BAL) fluid from animals treated with this dose of Sephadex beads contained about 85 x 10(6) cells as compared to 20 x 10(6) cells in control animals. The eosinophils corresponded to 41% of the BAL cell population as assessed with Wright-Giemsa staining. However, in the BAL fluid from these bead-treated animals, a significant increase of monocytes, lymphocytes, and neutrophils was also observed. We have also tested the potency of G-75, G-100, and G-200 Sephadex beads (Superfine) to induce eosinophilia in guinea pig. Nonlethal intravenous doses of G-75 (14.27 mg/kg), G-100 (8.0 mg/kg), and G-200 (10.71 mg/kg) Sephadex beads were selected and induced variable levels of airway eosinophilia and neutrophilia in conscious guinea pigs. The percentage of eosinophil recovered in the BAL fluid corresponded to 35, 61, and 44% of total cells for G-75, G-100, and G-200, respectively. The neutrophils corresponded to 24, 2, and 12% of the total BAL cells for G-75, G-100, and G-200, respectively. Since the size of the beads did not seem to correlate with the intensity of airway eosinophilia and neutrophilia, the effect of lower doses of the G-50 Sephadex beads (9.86-0.43 mg/kg) on the inflammatory cell infiltration was also tested. Results showed that there was a correlation between the neutrophil number and the number of beads (r = 0.996), whereas the number of eosinophils was less directly correlated to the bead number (r = 0.812). The alveolar eosinophils were purified from BAL fluid by centrifugation on a continuous Percoll gradient (65%) to separate eosinophils from neutrophils. Normodense eosinophils (density 1.087-1.100 g/ml) obtained from Sephadex-treated animals were found at the bottom of the continuous Percoll gradient (25 x 10(6); 98% purity). These highly purified eosinophils released thromboxane A2 (TxA2) following stimulation with 2 microM ionophore A23187. The method of accumulation and purification of guinea pig alveolar eosinophils is simple, rapid, and provides a large number of pure normodense cells for further biological studies.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1997

Eosinophilia in patients infected with the human immunodeficiency virus.

The prevalence and significance of peripheral blood eosinophilia in patients infected with the human immunodeficiency virus (HIV) were evaluated. Fifteen of 119 consecutive patients had absolute eosinophil counts of > 450/mm3. During a mean follow-up period of 419 days eosinophilia could be identified as secondary to a parasitic infection in only one patient. Correlation with disease stage showed a higher rate of advanced disease in patients with absolute eosinophilia. In a multivariate regression analysis, only low CD4+ cell counts, not the CDC disease stage or the use of antiretroviral therapy or primary prophylaxis, contributed significantly to the prevalence of eosinophilia. It is concluded that expensive laboratory investigations in asymptomatic patients with advanced-stage HIV disease are neither necessary nor cost effective.

Adult↗

PubMed1996

Inhibition of PAF-, LPS-, and cytokine-induced granulocyte accumulation in guinea pig lung by dexamethasone: evidence that inhibition of IL-5 release is responsible for the selective inhibition of eosinophilia by glucocorticoids in guinea-pigs.

The potency of dexamethasone has been determined as an inhibitor of intratracheally administered platelet activating factor- (PAF), or interleukin (IL)-5-induced eosinophilia, and of lipopolysaccharide-(LPS), tumour necrosis factor alpha-(TNF alpha) or cytokine-induced neutrophil chemoattractant- (CINC) induced neutrophilia in guinea-pig lungs. Dexamethasone was a potent inhibitor of PAF- induced eosinophil accumulation, but higher doses of dexamethasone were required to inhibit IL-5-induced eosinophilia. LPS-induced neutrophilia was less sensitive to the inhibitory effects of dexamethasone, than PAF-induced eosinophilia. Both LPS- and TNF alpha-induced neutrophilia were inhibited by the same doses of dexamethasone. In contrast, higher doses of dexamethasone were required to inhibit CINC-induced neutrophilia. Since data in the literature show that PAF-induced eosinophilia in guinea-pig lungs is dependent on the generation of IL-5, it is concluded that inhibition of this response, by dexamethasone, is due to inhibition of release of IL-5. Similarly, although data in the literature show that LPS-induced neutrophilia is dependent on the generation of TNF alpha, it is concluded that inhibition of this response, by glucocorticoids, is due to an action on an event which occurs after the release of TNF alpha, possibly through inhibition of chemokine release.

Analysis of Variance↗

PubMed2001

Acute myocarditis with transient eosinophilia and serum hyper-IgE-emia in a patient with atopic dermatitis.

A 14-year-old girl with acute myocarditis, transient eosinophilia, and hyper-IgE-emia associated with atopic dermatitis is described. The patient was admitted because of severe heart failure and shock, and severe atopic dermatitis was seen. Blood examinations showed moderate eosinophilia (1917/mm3) and hyper-IgE-emia (830IU/ml). The response to treatment with dopamine was excellent, and the congestive heart failure was gradually ameliorated, followed by improvement in her atopic dermatitis. In addition, rapid improvement in eosinophilia and hyper-IgE-emia was observed. Histopathological examination of the right ventricular myocardium obtained by endomyocardial biopsy showed mild interstitial fibrosis and mild infiltrations of inflammatory cells, indicating myocarditis. We speculated that the transient eosinophilia and hyper-IgE-emia in the present case indicated that an allergen induced strong allergic reactions, including type 1 allergy, and caused both acute myocarditis and deterioration of the atopic dermatitis; specifically noteworthy is that the patient's disease rapidly improved without corticosteroid treatment.

Adolescent↗

PubMed1997

[Idiopathic eosinophilia].

Peripheral and tissue eosinophilia are associated with a wide variety of inflammatory syndromes. These include both multisystem and limited diseases with vasculitis or non-vasculitic tissue damage and variable expression of end-stage-fibrosis. The idiopathic hypereosinophilic syndrome (IHS) represents a multisystem disorder defined by sustained eosinophilia of an undetectable cause with significant organ system dysfunction. Although not specified as such in the criteria for the diagnosis of IHS, there are idiopathic eosinophilic syndromes that are clinically distinct from IHS by virtue of the fact that the eosinophilic inflammation is limited to specific tissues (such as the skin) with an overall good prognosis. The pathogenic role of the eosinophilic granulocyte in these conditions is attested by evidence of eosinophil activation and degranulation at sites of tissue injury. The recruitment and localization of eosinophils to specific sites of tissue inflammation involves cytokines with haematopoietic growth factor activity, adhesion molecules expressed both by the vascular endothelium and eosinophils, and chemoattractants that stimulate eosinophil migration. Recently, overexpression of IL-5 in transgenic mice was shown to lead to both peripheral blood eosinophilia and tissue eosinophilia. With the advances in our understanding of cytokine-dependent regulatory mechanisms that control the peripheral eosinophil number as well as the recruitment and survivability of eosinophils at sites of inflammation, more targeted ways of manipulating the eosinophil reaction can be expected in the future.

Animals↗

PubMed1975

Pulmonary eosinophilia after substitution of aerosol for oral corticosteroid therapy.

Three patients with chronic asthma developed pulmonary eosinophilia while oral prednisolone was being withdrawn after the introduction of treatment with beclomethasone dipropionate aerosol. These observations suggest that the development of pulmonary eosinophilia in patients with chronic asthma can be prevented by the systemic administration of corticosteroids, but not by a corticosteroid aerosol given by inhalation. It is considered that radiological examination of the chest should be carried out at frequent intervals during and for a few months after the substitution of corticosteroid aerosol therapy for oral corticosteroid therapy in order to ensure that those patients who are liable to develop pulmonary eosinophilia will be identified at an early stage. These precautions are even more essential when there is a previous history of pulmonary eosinophilia.

Administration, Oral↗