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PubMed1992

Frequency of eosinophilia in adult T-cell leukemia/lymphoma.

Cases of adult T-cell leukemia/lymphoma (ATLL) display several peculiar clinical features, including skin rash, hypercalcemia, and an increase in the absolute neutrophil count. The patients rarely have pronounced eosinophilia. In this study, the eosinophilia observed in lymphoproliferative disorders of 62 patients with ATLL, 27 with T-cell lymphoma (TL), and 19 with B-cell lymphoma (BL) was investigated. The incidence of eosinophilia (greater than or equal to 570/microliters) was higher in patients with ATLL than in patients with TL or BL. Thirteen patients with ATLL (21.0%), 3 with TL (11.1%), and 2 with BL (10.5%) had eosinophilia. Of these patients, three with ATLL and one with TL who had a pathologic diagnosis of immunoblastic lymphadenopathy (IBL) showed pronounced eosinophilia up to 10,934/microliters. Because the number of eosinophils in the peripheral blood of these patients correlated both with the number of ATLL cells and the degree of lymphadenopathy and because this fluctuated with chemotherapy, it seems likely that the secretion of some lymphokines by the lymphoma cells is responsible for the eosinophilia.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2007

Non-small-cell lung cancer associated with excessive eosinophilia and secretion of interleukin-5 as a paraneoplastic syndrome.

Eosinophilia associated with solid tumors is an infrequent occurrence. The pathogenesis of tumor-associated eosinophilia is not well understood. Interleukin-5 (IL-5) is a cytokine that has been implicated in the development of eosinophilia in mice and humans. However, there is little data associating IL-5 production with eosinophilia in the presence of tumor. We report, in a patient with locally advanced NSCLC, the presence of excessive eosinophilia and elevated serum IL-5 levels at diagnosis. Immunohistochemical staining of the primary tumor showed large amounts of intracellular IL-5. Both eosinophil count and IL-5 levels normalized after surgical removal of the tumor. Tumor-associated eosinophilia observed in this case is mediated by IL-5. The production of IL-5 is related to the presence of the tumor.

Aged↗

PubMed1995

Rapid and selective induction of blood eosinophilia in guinea pigs by recombinant human interleukin 5.

Interleukin 5 (IL-5) has been implicated as a causal mediator in the development of pulmonary eosinophilia and airway hyperreactivity in human asthma. Supportive evidence for a pathogenic role of IL-5 in this disease has been provided by guinea pig models in which antigen-induced lung eosinophilia and bronchial hyperresponsiveness have been specifically attenuated with a neutralizing antibody to IL-5. In the present report, we describe a rapid mechanism-based model of IL-5-induced eosinophilia in the guinea pig. Our results show that intravenous injection of human IL-5 induced a 5-10-fold increase in the percentage and number of eosinophils in blood within 1 hour. In contrast, neutrophils and mononuclear cells were not recruited during this time. The increase in eosinophils was blocked by pretreatment of animals with an anti-IL5 monoclonal antibody (TRFK5) in doses similar to those which inhibit eosinophilia in guinea pig asthma models. Furthermore, dexamethasone, a potent inhibitor of eosinophilia in guinea pig asthma, profoundly suppressed the eosinophilia induced by human IL-5. This rapid model will be useful for elucidating the eosinophil activating properties of IL-5 in vivo and may potentially facilitate the development of IL-5 receptor antagonists for the specific blockade of the eosinophilic inflammation observed in human asthma.

Analysis of Variance↗

PubMed1996

Kinetics of eosinophilia and eosinophil activation in the development of non-allergic bronchial hyperresponsiveness in guinea pigs injected with Sephadex beads.

Eosinophils are believed to play a crucial role in the pathogenesis of airway hyperresponsiveness (AHR). In the present study, the involvement of blood and pulmonary eosinophilia as well as the eosinophil activation in the onset of non-allergic AHR caused by the injection of G-50 Sephadex beads in guinea pigs was investigated. Reactivity of the isolated lower bronchus to histamine was measured ex vivo in a bioassay system. The increase of reactivity of the isolated lower bronchus of Sephadex-injected animals to histamine was observed as early as 3 h after the Sephadex injection and was maximal between 6-24 h. Sephadex-induced blood eosinophilia was characterized by two successive increases of blood eosinophil counts peaking at 3 and 12 h respectively. The recruitment of inflammatory cells into the lungs as measured in bronchoalveolar lavage fluid (BALF) have shown that the neutrophils were initially increased at 3 h whereas the number of eosinophils increased only 6 h after the bead injection; both cell populations were maximal 24 h later. Eosinophil peroxidase (EPO) activity was used as a marker for the apparent number of eosinophils in airways and the degree of activation of eosinophils recovered in BALF. Results have shown that EPO activity in the lower bronchus of Sephadex-injected animals increased at 6 h, decreased at 12 h and was maximal 24 h later. The EPO activity recovered in BALF was maximal between 6 to 24 h after the bead injection in guinea pigs. Correlation between the number of eosinophils and the EPO activity in BALF suggests that BALF eosinophils have been activated and have degranulated in airways. Correlation studies also indicated that both Sephadex induced blood eosinophilia and eosinophil activation were associated to the development of AHR. In contrast, the increase of EPO activity in the lower bronchus and BALF eosinophilia were not correlated to the development of AHR in our model. In conclusion, our results suggest that Sephadex induced non-allergic AHR in guinea pigs could be related, at least in part, to blood eosinophilia and eosinophil activation. Whether blood, airway and BALF eosinophilia as well as eosinophil activation are relevant factors to determine the potential role of eosinophils in the pathogenesis of AHR is discussed.

Animals↗

PubMed1984

Diagnostic utility of pleural fluid eosinophilia.

It has been stated that pleural fluid eosinophilia (defined as greater than 10 percent eosinophils in the pleural white cell differential count) is not helpful in the diagnosis of exudative effusions. By review of the recent literature, it was found that pleural fluid eosinophilia was associated most often with idiopathic effusions or with air previously introduced into the pleural space. Also, a high proportion of "idiopathic" and benign asbestos effusions were characterized by pleural fluid eosinophilia, a previously unrecognized phenomenon. The diagnostic utility of finding eosinophils in the pleural space was assessed from its impact on prior probabilities of disease. Estimates of pretest likelihoods of malignant versus nonmalignant pleural effusions and the prevalence of eosinophilia in effusions of known cause were obtained from extensive literature review. These were modified by using Bayes' rule to estimate the revised probability of disease in the presence of an eosinophilic effusion. The presence of pleural fluid eosinophilia considerably reduced the probability of malignancy or tuberculosis and increased the likelihood of an underlying benign disorder. Pleural fluid eosinophilia is a useful finding that can aid in the diagnosis of an exudative pleural effusion.

Eosinophilia↗

PubMed1992

Graft eosinophilia in lung transplantation.

Graft eosinophilia was observed in lung biopsies from nine patients who received lung allografts. Five cases were associated with moderate to severe acute cellular rejection and responded well to steroid therapy. In this group the eosinophilia occurred early after transplantation and was associated with an elevated white blood cell count and occasional peripheral blood (one of five cases) and bronchoalveolar lavage (one of five cases) eosinophilia. A second group of four patients had graft eosinophilia due to infectious agents. In these cases patients frequently had underlying bronchiolitis obliterans (two of four cases) and developed tissue eosinophilia late after transplantation. Bronchoalveolar lavage cell profiles often demonstrated dramatic eosinophilia. Histologically, the biopsy specimens displayed an acute eosinophilic pneumonia, which was attributed to Aspergillus sp (two cases), coxsackie A2 virus (one case), and Pseudomonas maltophilia (one case). Two patients in this group died from infection. While eosinophils are a frequent cellular component of acute rejection reactions, they also may be the dominant cellular component in graft infection.

Adolescent↗

PubMed1996

Pulmonary eosinophilia.

The pulmonary eosinophilias are a diverse group of disorders characterised by pulmonary infiltrates, rich in eosinophils usually associated with a peripheral blood eosinophilia. Known causes of pulmonary eosinophilia include fungi--in particular Aspergillus fumigatus, parasites, toxins and drugs. Pulmonary eosinophilias of unknown cause include Löffler's syndrome, acute and chronic eosinophilic pneumonia, the hypereosinophilic syndrome, bronchocentric granulomatosis and pulmonary eosinophilia associated with vasculitis. The chest radiographic appearances of pulmonary eosinophilia are often characteristic and HRCT in selected cases can give important additional information.

Aspergillosis, Allergic Bronchopulmonary↗

PubMed2004

Rebound eosinophilia after treatment of hypereosinophilic syndrome and eosinophilic gastroenteritis with monoclonal anti-IL-5 antibody SCH55700.

BACKGROUND: Hypereosinophilic syndrome and eosinophilic gastroenteritis with peripheral eosinophilia are characterized by sustained eosinophilia and eosinophil-mediated tissue damage. Although treatment with the humanized monoclonal anti-IL-5 antibody SCH55700 resulted in improvement of eosinophilia and clinical symptoms in 6 of 8 of patients with hypereosinophilic syndrome or eosinophilic gastroenteritis with peripheral eosinophilia for as long as 12 weeks, eosinophil counts subsequently rose above baseline levels, accompanied by an exacerbation of symptoms. OBJECTIVE: To identify the mechanism underlying this rebound eosinophilia. METHODS: Purified eosinophils from patients or normal donors were cultured with IL-5, patient serum, and/or anticytokine antibodies, and eosinophil survival was assessed by flow cytometry. Serum and intracellular cytokine levels were measured by multiplex sandwich ELISA and flow cytometry, respectively. RESULTS: Before treatment with SCH55700, in vitro eosinophil survival in media and in response to recombinant IL-5 was similar in patients and normal donors. At 1 month posttreatment, the eosinophil survival curves were unchanged in 4 of 5 patients in media and in all 5 patients in response to recombinant IL-5. Normal eosinophil survival was prolonged in cultures containing posttreatment but not pretreatment sera (pretreatment vs posttreatment, 10.74% vs 73.02% live cells; P = .01). This posttreatment serum effect on eosinophil survival was reversed by the addition of the monoclonal anti-IL-5 antibody TRFK5. Although increased levels of serum IL-5 were observed at 1 month compared with 2 to 3 days posttreatment in 5 of 6 patients ( P = .04), intracellular cytokine analysis did not reveal increased production of IL-5 by peripheral blood mononuclear cells. CONCLUSIONS: The rebound eosinophilia after SCH55700 treatment is a result of a serum factor that enhances eosinophil survival. Reversal of this effect by the addition of antibody to IL-5 suggests that this factor may be IL-5 itself.

Adult↗

PubMed1979

Eosinophilia in premature infants: relationship to weight gain.

Serial eosinophil counts were determined in 38 hospitalized, appropriately grown premature infants whose gestational ages ranged from 27 to 35 weeks. Absolute eosinophilia (greater than 700/mm3) was documented in 76% (29/38). Eosinophilia was mild (700 to 999/mm3) in 9, moderate (1,000 to 2,999/mm3) in 17, and marked (greater than or equal to 3,000/mm3) in 3 patients. The average time of onset was day 19. Peak eosinophilia was usually seen within one week of onset and lasted an average of 16 days. A consistent relationship (r = 0.86) was found between the day of peak eosinophilia (mean = day 27) and the day on which birthweight was regained (mean = day 22). No association was apparent between the occurrence or degree of eosinophilia and gestational age, birth stress, presence of umbilical catheter, parenteral alimentation solution, and time of beginning or type or oral feeds. The data suggest that eosinophilia is strongly associated with the establishment of an anabolic state.

Body Weight↗

PubMed2003

Eosinophilia and uterine leiomyosarcoma.

BACKGROUND: Tumor-associated blood eosinophilia and tumor-associated tissue eosinophilia have been described in association with a spectrum of neoplasms. A case of uterine leiomyosarcoma exhibiting both blood and tissue eosinophilia is presented. CASE: A 67-year-old postmenopausal woman was evaluated for a 6-month history of postmenopausal bleeding. An office-based endometrial biopsy yielded atypical mesenchymal tissue with marked eosinophilic infiltrate suspicious for a uterine sarcoma, and the patient was referred to the gynecologic oncology service in a tertiary care hospital. There was evidence of leukocytosis and eosinophilia in preoperative laboratory assessment. The patient underwent an exploratory laparotomy, a total abdominal hysterectomy, bilateral salpingo-oophorectomy, and pelvic lymph node dissection. Histopathology confirmed a low-grade uterine leiomyosarcoma confined to the uterus. There was extensive infiltration of the tumor with eosinophils. The systemic leukocytosis and the absolute eosinophilia responded to surgical removal of the tumor, with normalization of values in the immediate postoperative period. CONCLUSION: A differential diagnosis of malignancy should be entertained during an evaluation of systemic eosinophilia.

Aged↗

PubMed1995

Peripheral blood eosinophilia in infants at 3 months of age is associated with subsequent development of atopic disease in early childhood.

BACKGROUND: We tested the hypothesis that eosinophilia in peripheral blood and nasal mucosa of infants is an early sign of allergic disease. METHODS: The appearance of eosinophilic leukocytes in peripheral blood and nasal mucosa was studied prospectively in 67 infants up to 18 months of age, with or without a family history of atopy. RESULTS: Eosinophilia was associated with simultaneous presence or subsequent development of atopic disease at 3, 9, and 18 months of age, but not significantly so at 6 months. At 3 months children in whom atopic disease developed later during the observation period had significantly higher numbers of blood eosinophils than children without atopy (p < 0.01). Thus pronounced eosinophilia (> 7 x 10(8) cells/L) at that age was associated with moderate or severe allergic disease during the 18-month observation period. These children continued to have eosinophilia throughout the follow-up period. Blood eosinophilia at 3 months of age also correlated significantly to cord blood IgE levels and to skin prick test reactivity later during the follow-up period. Nasal eosinophilia was a common finding and therefore had little diagnostic or predictive value. CONCLUSIONS: Elevated eosinophil counts in peripheral blood of apparently healthy infants at 3 months of age is associated with a subsequent diagnosis of atopic disease.

Dermatitis, Atopic↗

PubMed1998

Eosinophilia in the returning traveler.

Eosinophilia is one of the most common laboratory abnormalities seen in the returning traveler. Although elevations in peripheral eosinophil levels can occur in a wide variety of disease processes, worldwide, helminth parasites are the major group of infectious agents responsible for eosinophilia. While often directed at helminth infections in their early stages of clinical evolution, the approach to the evaluation of the returning traveler with eosinophilia must consider the many causes of eosinophilia including those not casually related to travel. This article reviews the major parasitic causes of eosinophilia and provides a systematic approach to the evaluation of eosinophilia following travel.

Eosinophilia↗

PubMed1999

Idiopathic maxillary pain: prevalence of maxillary sinus hyperreactivity in relation to allergy, chronic mucosal inflammation, and eosinophilia.

OBJECTIVE: In patients with chronic orofacial pain, an underlying sinus hyperreactivity may contribute to the clinical symptoms of a diagnosis of atypical odontalgia, trigeminal neuralgia, or temporomandibular disorders. The purpose of this study was to assess the prevalence of histamine-related maxillary sinus hyperreactivity in patients manifesting signs and symptoms of idiopathic maxillary pain and to correlate the respective findings with the presence or absence of chronic maxillary sinusitis-related diagnoses such as allergy, chronic mucosal inflammation, and eosinophilia. STUDY DESIGN: Fifty patients who had been assigned a diagnosis of idiopathic maxillary pain underwent skin allergy tests, maxillary sinus histamine provocation tests, and maxillary sinus mucosa biopsy. Histamine challenge to a selected area was performed during transoral sinuscopy of the maxillary sinus; a positive test result was defined as the development of a significant local mucosa response such as reddening and swelling. RESULTS: Comparison of the data showed most patients (38%) to have an absence of chronic maxillary sinusitis-related diagnoses, whereas the most common multiple diagnosis was found to be chronic mucosal inflammation in combination with eosinophilia (22%). Regarding the prevalence rates of positive histamine provocation test outcomes, a significant difference was found between the diagnostic subgroup "absence of chronic maxillary sinusitis-related diagnoses" (36.9%) and the diagnostic subgroups "chronic mucosal inflammation" (20%; P< .05), "chronic mucosal inflammation in combination with eosinophilia" (18.2%; P< .05), and "chronic mucosal inflammation in combination with eosinophilia and allergy" (14.3%; P < .01). An analysis of the distribution of chronic maxillary sinusitis-related diagnoses revealed absence of chronic mucosal inflammation-related diagnoses to be significantly more frequently associated with positive histamine provocation test outcomes than with negative histamine provocation test outcomes (41.2% vs 19.7%; P< .01), whereas chronic maxillary sinusitis (41.0% vs 29.4%), eosinophilia (26.2% vs 17.6%), and allergy (13.1% vs 11.8%) were found to be more prevalent in patients with negative histamine provocation test outcomes. CONCLUSIONS: The findings of this study suggest patients with idiopathic maxillary pain to be associated with a low rate of sinus hyperreactivity, whereas a positive test outcome with histamine provocation may not be linked to the presence of chronic maxillary sinusitis-related diagnoses such as allergy, chronic mucosal inflammation, and eosinophilia. Further investigations using a larger sample size of patients with idiopathic maxillary pain and nonidiopathic maxillary pain are necessary to demonstrate the presence or absence of an idiopathic maxillary pain-specific prevalence of maxillary sinus hyperreactivity.

Adult↗

PubMed2000

House dust mite-specific IgE antibodies in induced sputum are associated with sputum eosinophilia in mite-sensitive asthmatics.

BACKGROUND: Although allergen-specific IgE antibodies have been considered to play an important role in the pathogenesis of atopic asthma, the role of IgE antibodies in the development of airway inflammation is not well defined. OBJECTIVE: To evaluate the association between allergen-specific IgE antibodies and inflammation of the asthmatic airway. METHODS: We measured house dust mite (HDM; Dermatophagoides farinae)-specific IgE antibodies in both serum and induced sputum from 16 HDM-sensitive asthmatic patients, and evaluated their association with sputum eosinophilia and eosinophil cationic protein (ECP) levels in induced sputum. RESULTS: Levels of HDM-specific IgE antibodies in induced sputum were significantly higher in asthmatic patients than in controls (P < .01). In asthmatic patients, levels of HDM-specific IgE antibodies were significantly higher in induced sputum samples with eosinophilia (sputum eosinophil count > or = 5% of 200 counted non-squamous cells) than in those without eosinophilia (P < .05). There were no significant differences in serum levels of HDM-specific IgE antibodies between asthmatic patients with sputum eosinophilia and asthmatic patients without sputum eosinophilia. In asthmatic patients, sputum ECP levels were significantly correlated with levels of HDM-specific IgE antibodies (r = 0.60, P = .01) in induced sputum but not with those in serum. CONCLUSION: We conclude that allergen-specific IgE antibodies in induced sputum from atopic asthmatics are associated with sputum eosinophilia. This result suggests that IgE-dependent mechanisms are involved in eosinophilic inflammation of the airway in atopic asthmatics.

Allergens↗

PubMed1999

Glucocorticosteroid treatment for cerebrospinal fluid eosinophilia in a patient with ventriculoperitonial shunt.

BACKGROUND: Cerebrospinal fluid (CSF) eosinophilia commonly occurs in patients with ventriculoperitoneal (VP) shunts and is associated with shunt complications such as obstruction or infection. Glucocorticosteroids (GCS) are effective in reducing eosinophilia and eosinophils in skin, nasal mucosa, and airway epithelium. Effects of GCS on CSF eosinophils has not been reported. OBJECTIVE: To demonstrate glucocorticosteroid effects on the CSF eosinophil levels and to propose that GCS may be used as a therapeutic agent for CSF eosinophilia. RESULT: A case report of a patient with congenital hydrocephalus and a VP shunt developed CSF eosinophilia associated with latex allergy and shunt malfunction. Daily treatment with 2 mg/kg of methylprednisolone was associated with reduced peripheral eosinophilia and slightly reduced CSF eosinophil counts. Pulse methylprednisolone, 15 mg/kg, was associated with complete reduction of CSF eosinophils and prolonged VP shunt survival. CONCLUSION: Systemic glucocorticosteroids effectively reduce CSF eosinophils. Glucocorticosteroids may be beneficial for treatment of CSF eosinophilia associated with VP shunt malfunction.

Anti-Inflammatory Agents↗

PubMed2000

Inhibition of pulmonary eosinophilia and airway hyperresponsiveness in allergic mice by rolipram: involvement of endogenously released corticosterone and catecholamines.

This study investigates the role of adrenal-derived catecholamines and corticosterone on the inhibition by rolipram, a phosphodiesterase (PDE)-4 inhibitor, of pulmonary eosinophilia and airway hyperresponsiveness (AHR) in allergic mice. The following experimental groups were studied in mice sensitized and challenged with ovalbumin (OVA): normal, adrenalectomized, propranolol (beta-adrenoceptor antagonist) and metyrapone (corticosterone synthesis inhibitor) treated. These interventions were studied both in the absence and in the presence of rolipram. Eosinophil numbers in the bronchoalveolar lavage (BAL) and AHR to methacholine were measured 24 h after OVA challenge. Treatment of sensitized mice with rolipram (0.3 - 10 mg kg(-1), p.o.), inhibited pulmonary eosinophilia and the AHR to methacholine in OVA-challenged mice. Adrenalectomy increased the number of eosinophils in the BAL of OVA-challenged mice but had no effect on AHR to methacholine. Adrenalectomy attenuated both the rolipram-induced inhibition of BAL eosinophilia and AHR to methacholine in OVA challenged mice. Propranolol (10 mg kg(-1), p.o.) had no effect on the inhibition of eosinophilia by rolipram but attenuated the inhibition of AHR to methacholine in OVA challenged mice. On the other hand, metyrapone (10 mg kg(-1), p.o.) attenuated the inhibition of eosinophilia by rolipram but had no effect on the inhibition of AHR to methacholine in OVA challenged mice. Metyrapone-treatment alone increased the number of eosinophils in the BAL of OVA-challenged mice. These results identify an important role for adrenal-derived catecholamines and corticosterone on the inhibition of pulmonary eosinophilia and AHR by rolipram in allergic mice.

Animals↗

PubMed2005

Evaluation of eosinophilia in hospitalized preterm infants.

OBJECTIVE: To characterize changes in eosinophil counts over time, and to draw comparisons across four gestational age groups with respect to the incidence of, and clinical conditions associated with eosinophilia over the first months of life in a single neonatal intensive care unit (NICU). STUDY DESIGN: Weekly complete blood counts (CBCs) were collected from all NICU patients. Eosinophilia was classified as mild, moderate, or severe. Changes in eosinophil counts were examined over time, the incidence of eosinophilia was determined by gestational age group, and clinical correlations sought. RESULTS: Eosinophil data from 1652 CBCs were analyzed from 332 infants. Eosinophilia occurred in 148 infants (45%) during their hospitalization. The prevalence, severity, and timing of eosinophilia varied by gestational age, infection, and red blood cell transfusions. CONCLUSIONS: The incidence and severity of eosinophilia increased with immaturity, and was temporally associated with infection, necrotizing enterocolitis, and packed red blood cell transfusion.

Eosinophilia↗

PubMed2006

Acute peritoneal eosinophilia in a child with prune-belly syndrome following peritoneal dialysis catheter placement.

Peritoneal eosinophilia, although uncommon, was reported after placement of catheters for peritoneal dialysis. We describe a 7-year-old African-American boy with prune-belly syndrome who developed acute onset of peritoneal eosinophilia after placement of a peritoneal dialysis catheter. Peripheral-blood eosinophilia also was noted with the peritoneal eosinophilia, but was not correlative. Intraperitoneal and systemic corticosteroid therapy led to successful resolution of peritoneal eosinophilia. Radioallergosorbent tests indicated sensitization to latex. Unrecognized latex sensitization should be considered in any child with multiple urological surgeries who develops sudden onset of peritoneal eosinophilia.

Acute Disease↗