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Results for “EOSINOPHILIA”

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PubMed1990

Pulmonary eosinophilia and granulomatous pulmonary arteritis induced in rats by intravenous Sephadex.

Airway eosinophilia has been proposed as a major pathogenetic event in bronchial asthma and airway hyperresponsiveness. Intravenous injection of Sephadex G200 in rats induces pulmonary and blood eosinophilia and alters pulmonary responsiveness to 5-hydroxytryptamine. To characterize the early pulmonary inflammatory responses following Sephadex administration, and to determine the timing of the onset of pulmonary eosinophilia relative to blood eosinophilia, Sprague-Dawley rats were injected intravenously with Sephadex G200 beads. Lungs and other tissues were examined by light and transmission electron microscopy at 4, 12, 24, 48, 72, and 96 hours after injection. Blood eosinophil counts were determined at 0, 24, and 96 hours after injection. Sephadex beads were trapped initially in small caliber muscular pulmonary arteries associated with terminal bronchioles and in intra-acinar locations. There was marked infiltration of eosinophils and macrophages around the beads and into arterial walls and edematous periarterial and peribronchiolar connective tissue as early as 4 hours after injection. Periarterial-peribronchiolar eosinophil aggregates peaked in density at 24 and 48 hours. Macrophages and multinucleated cells dominated the inflammatory cell responses in arteries immediately surrounding partially degraded Sephadex beads from 24 to 96 hours. Bone marrow eosinophilopoiesis and blood eosinophilia were not detected until 96 hours. We conclude that Sephadex induces pulmonary eosinophilia prior to blood eosinophilia and suggest that Sephadex may induce pulmonary release of one or more eosinophil chemotactic substance(s). This model may prove useful in the study of factors that influence eosinophil migration into the lung in various disease states.

Animals↗

PubMedDate not supplied

Papillary thyroid carcinoma producing granulocyte-macrophage colony-stimulating factor is associated with neutrophilia and eosinophilia.

Thyroid tumors producing colony-stimulating factors associated with neutrophilia and/or eosinophilia are very rare and almost all of them concern anaplastic thyroid cancer. Only one case of papillary thyroid carcinoma associated with neutrophilia and one case of medullary thyroid carcinoma associated with eosinophilia have been reported. In this report a 72-year old male patient with metastatic papillary thyroid carcinoma associated with neutrophilia and eosinophilia is described. While investigating the cause of neutrophilia and eosinophilia, a blind bone marrow biopsy of the posterior iliac crest was performed, which showed infiltration by papillary thyroid carcinoma. High blood levels of granulocyte-macrophage colony-stimulating factor (GM-csF) were found using an enzyme-linked immunosorbent assay. As other causes of neutrophilia and eosinophilia were excluded, we assumed that these were paraneoplastic manifestations induced by GM-csF produced by the thyroid tumor. the disease progressed rapidly, despite appropriate treatment which included thyroidectomy and postoperative radioactive (131)I administration. the patient died 11 months after diagnosis because of extensive lung metastasis. Neutrophilia and eosinophilia were stable findings, while serum thyroglobulin levels remained elevated throughout the follow-up period. to our knowledge, this is the first report of a patient with metastatic papillary thyroid carcinoma in whom neutrophilia and eosinophilia associated with high circulating levels of GM-csF were detected.

Aged↗

PubMed2006

A third locus for Eosinophilia on chromosome 1 of the MES rats.

Matsumoto Eosinophilia Shinshu (MES) is a rat strain that spontaneously develops eosinophilia and eosinophil-related inflammatory lesions in many organs. In a previous study, we performed chromosomal mapping of the gene for eosinophilia in MES rats using backcross progeny and found that the major locus for eosinophilia was located on chromosome 19. In addition, another quantitative trait locus showing suggestive linkage for blood eosinophil count was found on chromosome 2. In this study, we examined additional marker loci in the backcross progeny and discovered that a third locus for eosinophilia was also located on chromosome 1. These data reinforce the notion that eosinophilia in MES rats is a rather complex genetic trait. However, these results will form the basis for identifying the candidate genes for eosinophilia.

Animals↗

PubMed1992

Eosinophilia and cellular cytokine responsiveness in hemodialysis patients.

Eosinophilia in hemodialysis (HD) patients has been associated with allergy to dialyzers and exaggerated activation of complement during HD. Its etiology, however, remains unknown. Complement activation can lead to cytokine production, and interleukin-2 (IL-2) administration has been shown to cause eosinophilia. Because abnormalities in cellular cytokine production in renal patients were previously demonstrated, the relationship between dialysis-associated eosinophilia and IL production in this HD population was studied. Twelve patients on chronic HD therapy with normal eosinophil counts (mean, 0.23 +/- 0.03 cells/nL) were compared with nine patients with eosinophilia (mean, 0.85 +/- 0.17 cells/nL). Measurements of cellular IL-1 and IL-2 production were performed before (pre) and after (post) HD with cuprammonium dialyzers. In patients with eosinophilia, stimulated cellular IL-1 production increased by 117 +/- 40% (P < 0.01) when post-HD measurements were compared with pre-HD values and IL-2 production increased by 127 +/- 65% (P < 0.05). In contrast, there was no difference in stimulated cellular cytokine production when values before and after HD were compared in patients without eosinophilia. Individual responses were reproducible during subsequent dialysis. It was concluded that cellular cytokine production in response to HD is not uniform. Eosinophilia is a clinically useful marker of exaggerated HD-associated cytokine production. Cytokine production depends on individual responsiveness and is probably related to atopy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1996

Nasal smear eosinophilia for the diagnosis of allergic rhinitis and eosinophilic non-allergic rhinitis.

OBJECTIVE: To evaluate nasal smear eosinophilia for the diagnosis of allergic rhinitis and eosinophilic non-allergic rhinitis in general practice. DESIGN: Nasal smear eosinophilia was assessed and compared with 'consensus diagnoses' made by three experts in a modified Delphi method. SETTING: Nineteen general practices in The Netherlands. SUBJECTS: 363 consecutive patients aged 12 years or over who visited their general practitioner because of chronic or recurrent nasal symptoms between 1 March 1990 and 1 March 1991. MAIN OUTCOME MEASURES: The predictive value of nasal smear eosinophilia for allergic rhinitis; the prevalence of eosinophilic non-allergic rhinitis. RESULTS: The positive predictive value of nasal smear eosinophilia (> or = 10% eosinophils) for allergic rhinitis was 30/37 = 81% (95% confidence interval (CI): 65-92%), the negative predictive value 172/312 = 55% (95% CI: 50-61%). Addition of the result of nasal smear eosinophilia to the information that was already obtained from the medical history resulted in a significant but very small improvement in the discrimination between patients with and without allergic rhinitis. The prevalence of eosinophilic non-allergic rhinitis was 7/349 = 2.0% (95% CI: 0.8-4.1%). CONCLUSION: Nasal smear eosinophilia contributes significantly to the diagnosis of allergic rhinitis; however, this contribution is very small and considered clinically irrelevant. Eosinophilic non-allergic rhinitis has a low prevalence; identifying this disorder is of minor importance. In conclusion, nasal smear eosinophilia is not recommended for use in general practice.

Adolescent↗

PubMed1991

Ventricular cerebrospinal fluid eosinophilia in children with ventriculoperitoneal shunts.

To determine the significance of cerebrospinal fluid (CSF) eosinophilia, the charts of 106 patients treated with shunt-related procedures during the calendar year 1985 were reviewed. Sixty-nine patients presented for a shunt revision; their charts were retrospectively reviewed from the time of shunt insertion until January, 1988. The remaining 37 patients had a ventriculoperitoneal shunt inserted during the study period and were subsequently followed to January, 1988. A total of 558 shunt-related procedures were performed on these patients during the study period, with a mean follow-up period of 6.9 years. The infection rate was 3.8%. Eosinophilia was diagnosed when eosinophils accounted for 8% or more of the total CSF white blood cell count. Ventricular CSF eosinophilia occurred in 36 patients sometime during their clinical course. These 36 patients required a mean of 8.5 shunt revisions, while the remaining patients required a mean of 2.5 revisions (p less than 0.001). Shunt infections were also more frequent in patients with eosinophilia (p less than 0.01). In no case was peripheral eosinophilia or a parasitic infection present. This study demonstrates that CSF eosinophilia is common in children with shunts. Children with this laboratory finding will experience more shunt failures. In addition, the new appearance of eosinophilia in the CSF of a patient with a shunt in place suggests the possibility of a shunt infection.

Brain Diseases↗

PubMed2002

[Analysis of eosinophilia and ECP levels in blood and nasal secretions of 119 nasal polyposis patients].

OBJECTIVE: The aim of this prospective study was to determine eosinophilia and ECP (Eosinophilic Cationic Protein) levels in blood and in nasal secretions of patients with nasal polyposis (NP). PATIENTS: 119 patients with NP were prospectively studied. The control group included 25 patients. METHODS: They included: questionnaire about asthma and intolerance to aspirin; nasal endosopic grading; nasal symptoms scoring; allergy testing; measurements of serum and nasal values of eosinophilia expressed as a percentage; measurements of serum and nasal values of ECP expressed in ng/ml; the Spearman correlation test, the T series and Khideux tests were used in the statistical analysis. RESULTS: In NP group, 66 were asthmatic (As) and 53 non asthmatics (NAs), 40 were atopic (ATo), and 79 were non atopic (NAto). Values of nasal eosinophilia and nasal ECP in NP patients were significantly higher (respectively 40.7+/-35.6% and 22.8+/-48.0 ng/ml) than the control group (respectively 3.0+/-14% and 2.1+/-3.6 ng/ml). Nasal and serum eosinophilia values in asthmatic patients (As) (respectively 47+/-36% and 7.6+/-6.3%) were significantly higher (p<0.05) than in non asthmatic patients (NAs) (respectively 32.6+/-33.8% and 4.6+/-3.1%). No difference was found in nasal and serum ECP values between asthmatic and non asthmatic patients. Nasal eosinophilia values were significantly correlated (p=0.02) with nasal scoring in NP patients. No correlation was found between nasal ECP and serum ECP values and clinical scoring. CONCLUSION: Nasal eosinophilia and nasal ECP values are significantly increased in NP. Nasal eosinophilia seems to be a relevant biological marker of clinical severity (association with asthma and a high clinical score) in NP patients. By contrast, nasal ECP cannot be consider as a marker of clinical severity.

Adult↗

PubMed2002

Diagnostic importance of serological methods and eosinophilia in tissue parasites.

This case-control study was carried out to investigate whether eosinophilia is a common finding in parasitic diseases and to determine the prevalence of the parasitic diseases in definitive groups. Toxocariasis and fasciolosis were investigated in patients with eosinophilia, patients with non-eosinophilia, and healthy controls. All cases were analyzed for antibodies against Toxocara canis and Fasciola hepatica by modified enzyme-linked immunosorbent assay (ELISA) employing, as antigen, excretory/secretory products of Toxocara and Fasciola (ES-ELISA). Seropositivity was determined in 39 (29.1%) and 12 (8.9%) toxocariasis and fasciolosis patients with eosinophilia respectively. The seropositivity was found in 26 (19.4%) and 5 (3.7%) toxocariasis and fasciolosis patients without eosinophilia respectively. The seropositivity was found in 13 (15.5%) and 1 (1.2%) toxocariasis and fasciolosis patients in the control group. The total seropositivity in both toxocariasis and fasciolosis in the eosinophilic group (8.5%) increased significantly compared to patients without eosinophilia (23.1%) and healthy controls (6.6%) (chi2:6.343, p < 0.05 and chi2:10.293, p < 0.01). Eosinophilia correlated with antibodies against Toxocara and E. hepatica. The results suggest that serological methods can be used for diagnosis of parasitic infections in tissue. Thus, the actual prevalence of tissue parasites can be revealed particularly in developing and emerging countries.

Case-Control Studies↗

PubMed1980

Induction of T cell-independent eosinophilia in mice with polymyxin B and schistosome infection.

This study examined the elevation of blood eosinophil counts in athymic and thymus-intact mice after repeated injections of polymyxin B with and without infection by Schistosoma mansoni. In athymic mice, a modest, comparable eosinophilia occurred after polymyxin B injection or parasite infection alone, or after a combination of both. In thymus-intact mice, polymyxin B injection caused a similar low grade eosinophilia, and schistosome infection produced a much higher level of eosinophilia. The combination resulted in the highest levels during the early weeks after infection; this hyperresponsive phenomenon was most apparent following 5 to 7 weekly polymyxin B injections, and the total eosinophil count approximated that derived by adding the eosinophil counts induced by polymyxin B injections or schistosome infection alone. In spite of the changes in blood eosinophil counts, tissue eosinophilia in the liver revealed no apparent differences. Furthermore, in schistosome-infected and polymyxin B-injected thymus-intact mice, hepatic granulomas reached a maximal size earlier than in mice that were only infected, and there was an over-all reduction in mast cell counts. The findings indicate that a T cell-independent eosinophilia occurs under a variety of circumstances. In athymic mice, it accounts for all peripheral eosinophilia, whereas in thymus-intact mice, it operates independently from the well known T cell-dependent eosinophilia of parasite infections.

Animals↗

PubMed1980

Eosinophilia in the hospitalized neonate.

The incidence of and clinical associations with eosinophilia in a cross-section of hospitalized newborns had not been studied previously. The medical records of 200 such infants less than 29 days of age were reviewed. Total eosinophil counts were calculated and associations with a variety of clinical factors were examined. Eosinophilia (adjusted for day of age) occurred at least once in 22% of the infants studied. No significant skew could be detected in the age of onset of eosinophilia. Statistical analysis revealed eosinophilia to be significantly associated (p less than .05) with length of hospitalization, number of days of antibiotic therapy and use of parenteral alimentation. A trend toward eosinophilia was noted in lower birth weight infants (0.05 less than p less than 0.10). Eosinophilia was not associated with sex, age, Apgar score at birth, Caesarian section delivery, transfusions, phototherapy, specific diagnoses or type of oral feeding. Multiple regression analysis showed a highly positive correlation (r = .81) of associated factors with hospitalized days as the dependent variable. Eosinophilia appears to be a non-specific finding in sick neonates and is related to the severity of illness and the number of diagnostic or therapeutic procedures performed.

Aging↗

PubMed1995

Lung eosinophilia is dependent on IL-5 and the adhesion molecules CD18 and VLA-4, in a guinea-pig model.

Blood and tissue-eosinophilia is a characteristic feature of a number of disease states. In experimental animals, the intravenous injection of parasitic larvae induces a profound eosinophilia that can be mimicked by the intravenous injection of Sephadex particles. In the present study, this procedure was used to investigate the mechanisms involved in the development of lung eosinophilia in a guinea-pig model. Intravenous administration of Sephadex particles to guinea-pigs resulted in a significant increase in the influx of eosinophils in the airways and in lung tissue eosinophil peroxidase (EPO) activity (at t = 24 hr). An anti-interleukin-5 (IL-5) monoclonal antibody (mAb) totally inhibited the eosinophilia in the airways and significantly reduced the lung tissue EPO activity. The concomitant accumulation of neutrophils and mononuclear cells, however, was not affected by this treatment. Monoclonal antibodies to VLA-4 and CD18 caused 58% and 62% suppression of eosinophilia in the bronchoalveolar lavage (BAL), respectively, whilst having no effect on lung tissue EPO activity. Co-administration of the two mAb resulted in total inhibition of eosinophil accumulation into BAL and significant suppression of lung tissue EPO activity (55% inhibition). This procedure also resulted in 72% inhibition of mononuclear cell influx and 68% inhibition of neutrophil influx in the BAL, the latter effect being entirely due to the actions of the anti-CD18 mAb. The results of this study indicate for the first time a requirement for IL-5 in the development of lung eosinophilia in this model. Further, it is clear that both the molecules VLA-4 and CD18 contribute to the development of this response and that maximal inhibition of lung eosinophilia is achieved only when the two adhesion pathways are simultaneously blocked.

Animals↗

PubMed1995

Mechanisms of eosinophilia in BALB/c-nu/+ and congenitally athymic BALB/c-nu/nu mice infected with Toxocara canis.

We studied the mechanism of eosinophilia in BALB/c-nu/+ (nu/+) and BALB/c-nu/nu (nu/nu) mice infected with Toxocara canis. Eosinophilia with two peaks on days 11 and 21 of infection was observed in infected nu/+ mice, and with a peak on day 11 in nu/nu mice. Interleukin-5 (IL-5) mRNA was expressed on day 5 of infection in the lung and spleen of nu/+ mice and in the lung of nu/nu mice, but not in the spleen of nu/nu mice. Large numbers of eosinophils and lymphocytes infiltrated the lung of both mice 1 week after infection. The number of larvae in the lung was the largest on day 5. Anti-IL-5 monoclonal antibody (mAb) treatment completely inhibited eosinophilia of both mice, with no change of larval distribution. Administration of anti-CD4 or anti-CD3 mAb markedly reduced the second peak of eosinophilia on day 21 of infection in nu/+ mice, and slightly reduced the first peak of eosinophilia on day 11 in both mice. Anti-CD8 mAb had no effect on the eosinophilia. These results suggest that eosinophilia in both mice is caused by IL-5, and that IL-5 is produced by cells other than CD4+ T cells, in addition to CD4+ T cells.

Animals↗

PubMed1994

Eosinophilia after allogeneic bone marrow transplantation using the busulfan and cyclophosphamide preparative regimen.

Eosinophilia may complicate allogeneic bone marrow transplantation (BMT) after treatment with preparative regimens that include total body irradiation (TBI). This complication is of uncertain significance and has not been reported after treatment protocols which do not contain TBI. We reviewed our experience using busulfan and cyclophosphamide (CY), instead of TBI, as the preparative regimen for allogeneic BMT to study the incidence and relationship to graft-versus-host disease (GVHD) of post-treatment eosinophilia. Fifty-five consecutive patients receiving busulfan 16 mg/kg and CY 120 mg/kg for the treatment of leukemia were reviewed. All patients received non-T cell-depleted, HLA-matched sibling or unrelated donor marrow 2 days after chemotherapy was complete. Cyclosporine (CYA) and methylprednisolone were given to prevent GVHD. Thirty-nine patients surviving 100 days post-transplant were evaluated; 11 (28%) patients developed eosinophilia (defined as an absolute eosinophil count of > 500 x 10(6)) after transplant. Only 2 patients were still taking methylprednisolone at the onset of eosinophilia. At the onset of eosinophilia 5 of these 11 patients (45%) and GVHD that worsened within 2 months. In the other 6 patients (55%), GVHD was not present initially but developed in all 6 patients at a median of 4 months after the onset of eosinophilia. We conclude that eosinophilia can complicate allogeneic BMT not preceded by TBI and that it often heralds the onset of worsening of, or de novo, GVHD.

Adolescent↗

PubMed1994

[Eosinophilia in primary biliary cirrhosis: regression under therapy with ursodeoxycholic acid].

Eosinophilia can be observed in up to 40% of patients with primary biliary cirrhosis (PBC). Eosinophilia is transient, tends to occur in the early stages of the disease and seems to be associated with episodes of florid bile duct destruction [42-45]. 14 Patients with PBC were examined before and during treatment with ursodeoxycholic acid (UDCA) (10 mg/kg/d) for episodes of eosinophilia and the number of eosinophilic granulocytes in differential white blood cell counts. Group A consisted of 5 patients with one or several episodes of eosinophilia before the start of UDCA. Group B included 9 patients without known episodes of eosinophilia. Observation time before and after start of treatment for group A was 3-96 (mean 25) months and 6-24 (mean 14) months, and for group B 3-108 (mean 34) months and 6-27 (mean 19) months respectively. During treatment with UDCA the mean counts of eosinophilic granulocytes decreased in both groups from 309 +/- 47/mm3 to 135 +/- 14/mm3 (p < 0.001). In group A there was a decrease from 529 +/- 89/mm3 to 157 +/- 17/mm3 (p < 0.001) and in group B from 151 +/- 15/mm3 to 128 +/- 15/mm3 B (n.s.). In group A 9/18 differential white blood cell counts showed eosinophilia before UDCA medication (3 x relative [> or = 6%], 6 x absolute [> or = 500/mm3]) and 0/24 after the onset of UDCA (p < 0.001). In group B 0/25 differential white blood cell counts showed eosinophilia before UDCA and 2/72 after start of the therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Tropical pulmonary eosinophilia in an Orissa village.

BACKGROUND: Tropical pulmonary eosinophilia is usually seen in areas endemic for filariasis. It affects only a small proportion of the population at risk and microfilaria are rarely demonstrated in the peripheral blood. The actual prevalence of the tropical pulmonary eosinophilia syndrome has not been previously studied in an area endemic for filariasis. METHODS: We screened the population of a village in the Puri district of Orissa, where filarial infection is endemic, to determine the prevalence of tropical pulmonary eosinophilia by clinical examination measuring the absolute eosinophil counts, performing a chest X-ray and examining the stools for the presence of the parasite. Sera from symptomatic cases who had an eosinophil count above 2000 per cmm were further tested for filarial specific IgG and total IgE and the results compared with control sera obtained from 15 age- and sex-matched normal individuals. RESULTS: We were able to screen 1754 (91%) out of 1918 villagers who were more than 5 years old and found 69 cases who had typical clinical features of tropical pulmonary eosinophilia. Only 6 (0.34%) of these had eosinophil counts above 3000 per cmm and were considered to have the disease. Only 2 of the 6 had associated filarial lesions, one had microfilaraemia and 3 had typical chest X-ray changes. The mean (+/- SD) titres for filaria specific IgG (0.355 +/- 0.315 v. 0.120 +/- 0.092) and total IgE (0.455 +/- 0.316 v. 0.114 +/- 0.075) were significantly higher in cases with tropical pulmonary eosinophilia than in control subjects. The level of eosinophilia was related neither to the patients' immune status nor to the severity of the radiological lesions. All cases recovered after therapy with diethylcarbamazine. CONCLUSION: Tropical pulmonary eosinophilia is not uncommon in this community in Orissa where filariasis is endemic. However, the syndrome is rarely associated with clinical filarial lesions.

Adolescent↗

PubMed2005

Modern diagnosis and treatment of primary eosinophilia.

The recent discovery of an eosinophilia-specific, imatinib-sensitive, karyotypically occult but fluorescence in situ hybridization-apparent molecular lesion in a subset of patients with blood eosinophilia has transformed the diagnostic as well as treatment approach to eosinophilic disorders. Primary (i.e. nonreactive) eosinophilia is considered either "clonal" or "idiopathic" based on the presence or absence, respectively, of either a molecular or bone marrow histological evidence for a myeloid neoplasm. Clonal eosinophilia might accompany a spectrum of clinicopathological entities, the minority of whom are molecularly characterized; Fip1-like-1-platelet-derived growth factor receptor alpha (FIP1L1-PDGFRA(+)) systemic mastocytosis, platelet-derived growth factor receptor beta (PDGFRB)-rearranged atypical myeloproliferative disorder, chronic myeloid leukemia, and the 8p11 syndrome that is associated with fibroblast growth factor receptor 1 (FGFR1) rearrangement. Hypereosinophilic syndrome (HES) is a subcategory of idiopathic eosinophilia and is characterized by an absolute eosinophil count of > or =1.5 x 10(9)/l for at least 6 months as well as eosinophil-mediated tissue damage. At present, a working diagnosis of primary eosinophilia mandates a bone marrow examination, karyotype analysis, and additional molecular studies in order to provide the patient with accurate prognostic information as well as select appropriate therapy. For example, the presence of either PDGFRA or PDGFRB mutations warrants the use of imatinib in clonal eosinophilia. In HES, prednisone, hydroxyurea, and interferon-alpha constitute first-line therapy, whereas imatinib, cladribine, and monoclonal antibodies to either interleukin-5 (mepolizumab) or CD52 (alemtuzumab) are considered investigational. Allogeneic transplantation offers a viable treatment option for drug-refractory cases.

Antineoplastic Agents↗

PubMed2001

Tissue eosinophilia in chronic sinusitis: quantification techniques.

OBJECTIVE: To ascertain the reliability of a proposed method for quantifying tissue eosinophilia in sinus mucosa. DESIGN: Prospective cohort study. INTERVENTIONS AND OUTCOME MEASURES: Pathology slides from patients undergoing endoscopic sinus surgery for chronic rhinosinusitis were independently assessed by 2 reviewers. Using a proposed systematic counting method, the degree of tissue eosinophilia was quantified. Disease severity was assessed by computed tomographic (CT) staging. Intrarater, interrater, and intrapatient reliability was determined using correlational reliability analysis. The degree of correlation between tissue eosinophilia and CT stage was determined. RESULTS: One hundred thirty-two slides from 65 patients were reviewed. The mean (SD) eosinophil density was 23.4 (37.2) eosinophils per high-power field. Only 12 patients (18%) had no eosinophils on histopathologic analysis. Strong intrarater (r> or =0.91 for each rater, P<.001) and interrater reliability (r> or =0.82 between raters, P<.001) was noted for the quantification method. A moderate degree of correlation was found between CT scan stage and degree of tissue eosinophilia (Spearman rho = 0.62, P<.001). CONCLUSIONS: The proposed method for quantifying tissue eosinophilia in sinus mucosa is reliable and valid. A relatively strong correlation exists between CT scan stage and tissue eosinophilia in chronic rhinosinusitis.

Chronic Disease↗

PubMed1988

Eosinophilia associated with adult T-cell leukemia/lymphoma.

Eosinophilia is associated with a number of disorders including malignancies. A patient is described who had eosinophilia associated with adult T-cell leukemia/lymphoma (ATL) induced by human T-lymphotropic virus type I (HTLV-I). Both tissue and peripheral blood eosinophilia and high titers of HTLV-I antibody were present. The eosinophilia was most likely caused by the malignant cells producing one or more lymphokines. The patient has achieved a durable complete remission from combination chemotherapy. Because durable remissions in ATL are rare with any known therapy and eosinophilia has not previously been associated with ATL, it is possible that the tumor in this patient was derived from a T-cell subset not usually transformed by HTLV-I. ATL is another malignancy now known to cause eosinophilia.

Adult↗