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Results for “EOSINOPHILIA”

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PubMed1992

Eosinophilia associated with chronic pancreatitis: an analysis of 122 patients with definite chronic pancreatitis.

Among 122 patients with chronic pancreatitis, marked eosinophilia (greater than 500 eosinophils/mm3 in the peripheral blood) was observed in 21 cases (17.2%). All of the affected patients were males, and there was no significant difference in the incidence of eosinophilia between patients with alcoholic and nonalcoholic pancreatitis. In the patients with eosinophilia, endocrine pancreatic function was maintained comparatively well, despite marked exocrine pancreatic dysfunction. The eosinophilia of chronic pancreatitis frequently developed in association with severe damage to neighboring organs (pleural effusion, pericarditis, and ascites), as well as in association with pancreatic pseudocyst. Our findings suggest that there is a close correlation between marked eosinophilia and severe tissue injury during acute exacerbations of chronic pancreatitis.

Adult↗

PubMed2003

[Episodic angioedema associated with eosinophilia in relapsing erythema and swelling of the right thigh].

On March 16, 2000, a 37-year-old male was admitted to another hospital for fever, erythema of the limbs, and swelling of the right lower leg. The leukocyte count was 19,800/microliter, and the ratio of eosinophils was 61%, suggesting marked eosinophilia. Thoracic computed tomography (CT) revealed pneumonia in the left lung. However, the patient was negative for autoantibodies or parasitic antibodies. Administration of prednisolone at 80 mg/day resulted in a marked improvement of the symptoms and the eosinophilia. For diagnosis, detailed examination, and treatment, the patient was referred and admitted to our department on March 28. The dose of prednisolone was gradually decreased. On April 15, the agent was discontinued. Eosinophilia was not observed, however erythema of the limbs and swelling of the right lower leg recurred. Skin biopsy revealed in mild edema of the corium and eosinophilic infiltration, suggesting episodic angioedema associated with eosinophilia (EAE). In 1984, Greich et al. reported 4 patients with repeated angioedema, hives, and marked eosinophilia, and proposed the term EAE. Since then, more than 50 patients have been reported in Japan. Only 4 of these patients were males. We report on the present male patient together with the pathological findings.

Adult↗

PubMed2004

[Eosinophilia caused by solid malignancy].

A 48-year-old woman with exanthema, pruritus and eosinophilia was found upon further examination to have a small-cell bronchus carcinoma; after chemotherapy and radiotherapy there was an almost complete response and the skin symptoms disappeared. A 70-year-old man who was recently treated due to primary malignant fibrous histiocytoma associated with eosinophilia became cachectic and anaemic. He was found to have a metastased leiomyosarcoma and died shortly afterwards. Worldwide the most common cause of eosinophilia is a parasitic infection, whereas in Western Europe the most common causes are allergic reactions and medicine use. Paraneoplastic symptoms are present in 7-10% of adults with cancer. However, the frequency of eosinophilia as a paraneoplastic phenomenon is unknown. It is important to recognise this phenomenon of paraneoplastic eosinophilia for the timely diagnosis and treatment of the underlying disease.

Aged↗

PubMed1992

[Abnormalities of coagulation, fibrinolysis and kallikrein-kinin system in 2 cases with remarkable eosinophilia].

We evaluated an initial activation of hemostasis (coagulation, fibrinolysis and kallikrein-kinin system) in two remarkable eosinophilia cases. The first case was a 29-year-old male who complained of a high fever, general exanthema and numbness of the limbs. He had peripheral blood eosinophilia (61.075/microliters) unknown etiology, and hypereosinophilic syndrome (HES) was diagnosed. The second case was a 60-year-old female who complained of numbness in her lower limbs. She also presented eosinophilia (10,379/microliters), and had clinical features of allergic granulomatous angitis (AGA). The administration of prednisolone led to clinical remission in both cases, including rapid improvement of eosinophilia, normalization of hypercoagulability and correction of platelet dysfunction. In hemostatic parameters, the titer of the soluble fibrin monomer complex (SFMC) became negative, and each value of FDP D-dimer, fpB beta 15-42, thrombin-antithrombin III complex (TAT) decreased, whereas the value of prekallikrein increased. A decrease in platelet aggregation with ADP, collagen and epinephrine was normalized by prednisolone administration. Hemostatic data in both cases indicate a possible relationship between the initial activation of hemostasis and the eosinophils, as well as the possibility of general and/or organic inflammations and intravascular thrombi formations in eosinophilia such as HES and AGA.

Adult↗

PubMed1992

Elevated serum levels of interleukin-5 in patients with the syndrome of episodic angioedema and eosinophilia.

The syndrome of episodic angioedema and eosinophilia is characterized by cyclic edema, marked peripheral blood eosinophilia, and eosinophil degranulation in the dermis. Using a sensitive immunoenzymetric method, we measured serum interleukin (IL)-5 levels in four patients with this syndrome. We also determined the percentage of activated T cells in the peripheral blood of a new patient before and during an attack. In the patient presented, IL-5 levels peaked several days before maximal eosinophilia and then declined. This patient's lymphocytes showed an increased percentage, 28% (normal 2% to 3%), of activated T cells staining for both CD3 and HLA-DR 10 days before maximal eosinophilia, but no increase at the time of peak eosinophilia. In serum from three previously reported cases, elevated serum IL-5 levels were found during attacks. After glucocorticoid administration, IL-5 levels became undetectable in three of the four patients. Production of IL-5 is likely an important determinant of the pathophysiology of this syndrome.

Adult↗

PubMed1990

Role of IL-5 in IL-2-induced eosinophilia. In vivo and in vitro expression of IL-5 mRNA by IL-2.

We recently demonstrated in vivo that IL-5 was an important mediator of eosinophilia in mice with parasite infections. In this study, we examined whether or not IL-5 was actually responsible for the eosinophilia induced by injection of human rIL-2. Mice administered hIL-2 developed eosinophilia during the course of the series of injections. This eosinophilia could be suppressed by a single injection of mAb against murine IL-5. The number of eosinophilic precursors increased more in the spleen cells of the IL-2-treated mice in comparison to the control mice, although in bone marrow precursors showed little change. Similarly, the number of granulocytic precursors increased markedly in the spleen cells of IL-2-treated mice. In vitro polymerase chain reaction amplification of cDNA subfragments corresponding to IL-5 mRNA (reverse transcription-polymerase chain reaction), followed by Southern blot analysis, revealed enhancement of IL-5 mRNA expression in spleen cells 3 days after starting the human IL-2 injections. We also observed enhanced murine IL-5 mRNA expression in spleen cells stimulated with IL-2 in vitro. The level of murine IL-5 mRNA expression by IL-2-stimulated spleen cells from normal mice increased at 24 h, reached a plateau after 48 h, and decreased again within 72 h of starting culture. These results indicate that the eosinophilia induced by IL-2 in vivo is presumably mediated by IL-5 released from IL-2-stimulated lymphocytes.

Animals↗

PubMedDate not supplied

[Limitations of normal eosinophilia or possible influence of nonsteroidal anti-inflammatory agents].

Statistical analysis of eosinophilia of 331 patients at the onset of hospitalisation define a logarithmic standard population of 327 patients whose eosinophilia rates stand between 0 and 810/mm3, among them 24 lies between 500 and 810, and 4 whose eosinophilia rise over 1,000/mm3. These 4 patients had transient hypereosinophilia whose etiology was defined only in 2 cases. The 24 patients with eosinophilia between 500 and 810/mm3 were significantly more frequently men, with rheumatoid disease (specially sciatica) and users of non steroidal antiinflammatory drugs (NSAID) than the general population. It suggest that NSAID may rise eosinophilia rates inside normal limits.

Adult↗

PubMed1989

[Cerebrospinal fluid eosinophilia preceding central nervous system leukemia].

Cerebrospinal fluid eosinophilia are an uncommon finding that is most often the result of a helminthic infection of the central nervous system. Information from the recorded literature suggests the differential diagnosis of this clinical observation is relatively limited. This is a report of a girl with acute lymphoblastic leukemia who developed central nervous system relapse of leukemia following 3 years of remission. She showed marked eosinophilia in the cerebrospinal fluid 6 weeks preceding central nervous system leukemia. No cause for the eosinophilia was identified. The gradual accumulation of case reports of eosinophilia in the cerebrospinal fluid with or without blood eosinophilia in patient with leukemia suggests that this finding is of some importance.

Brain Neoplasms↗

PubMed1983

Prevalence of eosinophilia during gold therapy for rheumatoid arthritis.

The prevalence of eosinophilia in 82 rheumatoid arthritis patients receiving gold sodium thiomalate (GSTM) and 30 patients receiving auranofin (AF) was determined in a retrospective study. Eosinophilia occurred in 21% taking GSTM and in 13% on AF. The simultaneous occurrence of toxicity and eosinophilia occurred in 14% receiving GSTM and in 10% receiving AF. In contrast, eosinophilia only occurred in 24% of those with suspected toxicity receiving GSTM and in 30% of those with suspected toxicity receiving AF. The value of eosinophilia as a marker of toxicity is discussed.

Adult↗

PubMed1984

Eosinophilia in rheumatoid patients treated with D-penicillamine.

The prevalence of eosinophilia in 66 patients with rheumatoid arthritis receiving D-penicillamine was determined in a retrospective study. Eosinophilia occurred in 24%. The simultaneous occurrence of toxicity and eosinophilia occurred in 3%. In contrast, eosinophilia only occurred in 10% of those with suspected toxicity. The value of eosinophilia as a marker of toxicity is discussed.

Adult↗

PubMed1982

Reduction of carrageenan- bradykinin- and histamine-induced acute inflammation by experimental eosinophilia in rats.

An examination was made of the effects of eosinophilia on acute inflammation. Sprague Dawley rats were infected with Trichinella spiralis larvae which resulted in a blood eosinophilia. Groups of rats with the induced eosinophilia, and untreated rats without the eosinophilia, were treated with carrageenan, bradykinin or histamine in the hind paw to induce local inflammation. Paw oedema induced by carrageenan as a measure of the inflammation was much reduced in those rats with an eosinophilia, and slightly but significantly reduced in the site treated with histamine or bradykinin. Though other anti-inflammatory factors may have participated, it is believed that the reduction in inflammation was due to the eosinophils. Pretreatment of the rat paws with an eosinophil chemotactic factor tetrapeptide (ECF-A) caused no chemotaxis and therefore no effect on histamine-induced oedema.

Animals↗

PubMed1995

[Peripheral blood eosinophilia in patients with bronchial asthma before and after bronchial provocation].

The study was set up in order to check the usefulness of peripheral blood eosinophilia in asthma diagnosis and asthma therapy monitoring. Twenty mild asthmatics entered the study--ten atopic and ten nonatopic. Eosinophilia was estimated twice: on the day of admission and twenty four hours after bronchial provocation. Bronchial hyperreactivity was measured on both occasions. We showed, that there was no difference in eosinophilia between atopic and nonatopic subjects before provocation but the difference was significant 24 hrs after provocation. In both groups of asthmatics eosinophilia correlated with bronchial hyperreactivity before and after provocation. We concluded, that eosinophilia is an easy and valuable parameter in monitoring the degree of allergic inflammation in asthmatics.

Adult↗

PubMed1993

Interleukin-5 is necessary for eosinophilia induced by cyclophosphamide in immunized mice.

Interleukin-5 (IL-5) has an important role in the induction of eosinophilia, which is associated with parasitic infestations and with allergic conditions, and which can be induced in a number of experimental systems. One of these model systems involves the administration of cyclophosphamide (CY) to immunized animals. In order to assess the role of IL-5 in this model, eosinophilia was induced in vivo and cell suspensions of spleens or lymph nodes were stimulated in vitro. IL-5 protein secretion was detected by bioassay using an IL-5-dependent cell line (T88-m), and mRNA was assessed by reverse transcription and polymerase chain reaction (RT-PCR). The production of IL-5 protein and mRNA were greatly enhanced in the cells from mice given CY with ovalbumin (OVA), compared with mice given either agent alone. IL-5 protein and mRNA were increased both in spleen and in lymph node cells, and in response either to OVA or to polyclonal stimuli. Further evidence for the importance of IL-5 in this model of eosinophilia was provided by experiments with monoclonal antibodies (mAb) in vivo. A single injection of an IL-5-specific mAb at the time of immunization completely abolished the eosinophilia. By contrast, a monoclonal antibody to IL-4 had no effect. These experiments indicate that IL-5 is required for the eosinophilia induced by CY in immunized mice.

Animals↗

PubMed1993

[Pulmonary eosinophilia].

Pulmonary eosinophilia is a disease entity which is characterized by an increase of eosinophils in the bronchoalveolar lavage fluid or in tissue. While there are several disease states encountered in pulmonary eosinophilia, some have a definite cause and diagnosis, while others are of unknown etiology. The diagnosis of idiopathic eosinophilic pneumonia is given when other pulmonary eosinophilia with known cause and diagnosis are excluded. Simple pulmonary eosinophilia and chronic eosinophilic pneumonia are well established disease entities, but recent papers have clarified a new concept of acute eosinophilic pneumonia. In this article, the clinical features of three idiopathic eosinophilic pneumonias simple pulmonary eosinophilia as a self-limiting lung infiltrates, chronic eosinophilic pneumonia as a disease with longstanding symptoms requiring steroids administration and a tendency to relapse, and acute eosinophilic pneumonia as an acute respiratory distress which responds dramatically to steroids administration and without relapse after discontinuation of therapy are discussed.

Adult↗

PubMed1995

[Eosinophil colony stimulating factor (Eo-CSF) activity and soluble interleukin-2 receptor (sIL-2R) in patients with reactive eosinophilia].

To explore the pathophysiology of patients with reactive eosinophilia from unknown cause, we measured the eosinophil colony stimulating factor (Eo-CSF) activity in the interleukin-2 (IL-2) stimulated lymphocyte conditioned medium (CM) prepared from 22 patients with reactive eosinophilia. Eo-CSF activity, the levels of interleukin-5 (IL-5) and granulocyte-macrophage colony stimulating factor (GM-CSF) were increased in the CM from patients with high IgE levels. Hydrocortisone decreased the level of Elo-CSF in the CM. Elevated serum levels of soluble IL-2 receptor (sIL-2R) were presented in 13 out of 15 patients with eosinophilia. The sIL-2R levels in patients with marked eosinophilia (>3000/mu l) were higher than those in patients with mild eosinophilia (< or = 3000/mu l). High sIL-2R levels were noted in T cell CM from 3 out of 15 patients and in eosinophil CM from 1 out of 4 patients. These data suggested that lymphocyte from eosinophilic patients with elevated IgE produce Eo-CSF, IL-5 and GM-CSF by IL-2 stimulation. Eo-CSF production is inhibited by hydrocortisone. SIL-2R is released from lymphocyte and in some case may be released from eosinophils.

Adolescent↗

PubMed2001

Eosinophilia and musculoskeletal disease.

Eosinophilia is occasionally a feature of rheumatic disease. The differential diagnosis of eosinophilia includes parasitic infection, systemic vasculitides, eosinophilic arthritis, and myopathies, together with the idiopathic hypereosinophilic syndrome and malignancy. Careful evaluation of the patient should enable an accurate diagnosis to be made. Parasitic infection is the commonest cause of eosinophilia worldwide and can cause systemic disease, as illustrated by the report of Sarcocystis myositis in a group of military personnel in Malaysia. A persistent arthropathy associated with eosinophilia, but not with parasitic infection, has been reported from the far East. Drugs may also cause eosinophilia, and there has recently been much discussion of the relation between Churg-Strauss syndrome and the leukotriene antagonist zafirlukast. The present view is that reduction of steroid dose allows unmasking of previously undiagnosed Churg-Strauss syndrome. The idiopathic hypereosinophilic syndrome may represent a lymphoproliferative process; evidence for this comes from the demonstration that many patients have a clonally expanded population of aberrant T cells.

Journal Article↗

PubMed2004

Effect of Mycobacterium tuberculosis chaperonins on bronchial eosinophilia and hyper-responsiveness in a murine model of allergic inflammation.

BACKGROUND: Epidemiological evidence suggests that infection with Mycobacterium tuberculosis protects children against asthma. Several laboratories have shown that, in mouse models of allergic inflammation, administration of the whole live tuberculosis vaccine, Mycobacterium bovis bacillus Calmette-Guerin (BCG), prevents ovalbumin (OVA)-induced pulmonary eosinophilia. OBJECTIVE: The aim of this study was to characterize specific M. tuberculosis molecules that are known to modulate immune responses to see if they affected pulmonary eosinophilia and bronchial hyper-responsiveness. METHODS: C57Bl/6 mice were sensitized to OVA on days 0 and 7 and subsequently challenged with OVA on day 14 over a 3-day period. Pulmonary eosinophilia and bronchial hyper-responsiveness were measured 24 h following the last antigen challenge. In some groups, mice were pre-treated with M. tuberculosis or M. tuberculosis chaperonins (Cpns)60.1, 60.2 and 10, and the effect of this treatment on the allergic inflammatory response to aerosolized OVA was established. RESULTS: We show that M. tuberculosis Cpns inhibit allergen-induced pulmonary eosinophilia in the mouse. Of the three Cpns produced by M. tuberculosis, Cpn60.1, Cpn10 and Cpn60.2, the first two are effective in preventing eosinophilia when administered by the intra-tracheal route. Furthermore, the increase in airways sensitivity to inhaled methacholine following OVA challenge of immunized mice was suppressed following treatment with Cpn60.1. The allergic inflammatory response was also characterized by an increase in Th2 cytokines IL-4 and IL-5 in bronchoalveolar lavage fluid, which was also suppressed following treatment with Cpn60.1. CONCLUSION: These data show that bacterial Cpns can suppress eosinophil recruitment and bronchial hyper-responsiveness in a murine model of allergic inflammation.

Animals↗

PubMed1999

The relationship of skin test positivity, high serum total IgE levels, and peripheral blood eosinophilia to symptomatic and asymptomatic airway hyperresponsiveness.

The relationships of skin test positivity, high serum total IgE levels (> 100 kU/L), and peripheral blood eosinophilia (>/= 275 cells/microliter) to symptomatic (either chronic cough, chronic phlegm, bronchitis episodes, dyspnea, wheeze, or asthma) and asymptomatic bronchial hyperresponsiveness (BHR) were studied cross-sectionally in 620 adult subjects who participated in the Vlagtwedde-Vlaardingen Study of 1989 and 1990. Eosinophilia (OR = 2.06, 95% CI = 1.28 to 3.31) and skin test positivity (OR = 1.66, 95% CI = 1.02 to 2.71) were both significantly associated with BHR independent of age, sex, smoking, and urban area of residence. High serum total IgE levels were not associated with BHR (OR = 1.29, 95% CI = 0.81 to 2.03). Separate analyses for symptomatic and asymptomatic subjects showed that the higher risk of BHR with skin test positivity applied only to symptomatic subjects (OR = 5.78, 95% CI = 1.63 to 20.51), independent of eosinophilia and high serum total IgE levels. The higher risk of BHR with eosinophilia was not different between symptomatic and asymptomatic subjects, and independent of skin test positivity and high serum total IgE levels. The results of this study show that, in the general adult population, eosinophilia is associated with BHR both in symptomatic and asymptomatic persons, whereas skin test positivity is associated with BHR only in symptomatic subjects.

Adult↗