Significant Blood Eosinophilia Research Articles

Accuracy of a New Algorithm to Identify Asthma–COPD Overlap (ACO) Patients in a Cohort of Patients with Chronic Obstructive Airway Disease

ObjectivesWe aimed to characterize the clinical, functional and inflammatory features of patients diagnosed diagnosed with ACO according to a new algorithm and to compare them with those of other chronic obstructive airway disease (COAD) categories (asthma and COPD). MethodsACO was diagnosed in a cohort of COAD patients in those patients with COPD who were either diagnosed with current asthma or showed significant blood eosinophilia (≥300cells/μl) and/or a very positive bronchodilator response (>400ml and >15% in FEV1). ResultsEighty-seven (29.8%) out of 292 patients fulfilled the ACO diagnostic criteria (12.8% asthmatics who smoked <20 pack-years, 100% of asthmatics who smoked ≥20 pack-years, 47.7% of COPD with >200eosinophils/μl in blood and none with non-eosinophilic COPD). ACO, asthma and COPD patients showed no differences in symptoms or exacerbation rate. Mean pre-bronchodilator FEV1 in ACO and asthma were similar (1741 vs 1771ml), higher than in COPD (1431ml, p<0.05). DLCO was lower in ACO than in asthma (68.1 vs 84.1%) and similar to COPD (64.5%). Mean blood eosinophil count was similar in ACO and asthma (360 vs 305cells/μl) and higher than in COPD (170cells/μl). Periostin levels were similar in ACO to COPD (36.6 and 36.5IU/ml) and lower than in asthma (41.5IU/ml, p<0.05), whereas FeNO levels in ACO were intermediate. ConclusionThis algorithm classifies as ACO all smoking asthmatics with non-fully reversible airway obstruction and a considerable proportion of e-COPD patients, highlighting those who can benefit from inhaled corticosteroids.

Accuracy of a New Algorithm to Identify Asthma–COPD Overlap (ACO) Patients in a Cohort of Patients with Chronic Obstructive Airway Disease

ObjectivesWe aimed to characterize the clinical, functional and inflammatory features of patients diagnosed diagnosed with ACO according to a new algorithm and to compare them with those of other chronic obstructive airway disease (COAD) categories (asthma and COPD). MethodsACO was diagnosed in a cohort of COAD patients in those patients with COPD who were either diagnosed with current asthma or showed significant blood eosinophilia (≥300cells/μl) and/or a very positive bronchodilator response (>400ml and >15% in FEV1). ResultsEighty-seven (29.8%) out of 292 patients fulfilled the ACO diagnostic criteria (12.8% asthmatics who smoked <20 pack-years, 100% of asthmatics who smoked ≥20 pack-years, 47.7% of COPD with >200eosinophils/μl in blood and none with non-eosinophilic COPD). ACO, asthma and COPD patients showed no differences in symptoms or exacerbation rate. Mean pre-bronchodilator FEV1 in ACO and asthma were similar (1741 vs 1771ml), higher than in COPD (1431ml, p<0.05). DLCO was lower in ACO than in asthma (68.1 vs 84.1%) and similar to COPD (64.5%). Mean blood eosinophil count was similar in ACO and asthma (360 vs 305cells/μl) and higher than in COPD (170cells/μl). Periostin levels were similar in ACO to COPD (36.6 and 36.5IU/ml) and lower than in asthma (41.5IU/ml, p<0.05), whereas FeNO levels in ACO were intermediate. ConclusionThis algorithm classifies as ACO all smoking asthmatics with non-fully reversible airway obstruction and a considerable proportion of e-COPD patients, highlighting those who can benefit from inhaled corticosteroids.

Metastatic Uterine Leiomyosarcoma and Eosinophilia

Uterine sarcomas account for approximately 3% to 7% of all uterine malignancies. Distinguishing benign and malignant myomas based on physical examination and imaging alone is challenging. A postmenopausal woman with a history of leiomyomas presented to the Emergency Department with chest pain and a right upper lobe lung mass. Blood tests demonstrated profound eosinophilia (58,000/mm). Positron emission tomography-computed tomography scan to exclude distant disease as work-up for presumed lung cancer revealed increased tracer uptake in the lung mass and a pelvic mass. The patient died from complications of hypereosinophilia, and a postmortem diagnosis of metastatic uterine leiomyosarcoma was made. Significant blood eosinophilia is uncommon in leiomyomas and should raise suspicion of malignant etiology for a pelvic mass.

Dapsone Treatment for Eosinophilic Fasciitis

A previously healthy 38-year-old woman was seen regarding severe skin stiffness and thickening. Previous findings are summarized. The patient originally saw her primary care practitioner with a 3-month history of limb aches, ankle swelling, and malaise. She was taking no medication. Findings showed an increased serum C-reactive protein level (80 mg/L [to convert to nanomoles per liter, multiply by 9.524]), mild anemia (hemoglobin level, 11.3 g/dL [to convert to grams per liter, multiply by 10.0]), elevated plasma viscosity (1.74 mPa·s), eosinophilia (eosinophil count, 2.92 10/μL[toconvert tovalue 10/L,multiplyby10]), and low serum ferritin and folate levels. A gastroenterologic consultation to investigate suspected malabsorption excluded celiac disease, parasitic infection of the bowel, and a gastrointestinal or gynecological malignant neoplasm. Computed tomography of the abdomen showed only a thickened proximal jejunal loop. Because of persisting eosinophilia (eosinophil count, 4.77 10/μL and 6.97 10/μL on 2 further occasions), hypereosinophilic syndrome was considered. The jejunal abnormalities were presumed to represent eosinophilic enteritis, but this condition was excluded histologically. Because of increasing symmetrical arthralgias, the patient was seen in the rheumatology department. Generalized tightening and tautness of the skin, restricted joint movement (particularly the elbow and metacarpophalangeal [MCP] joints), and a positive prayer sign (inability to oppose the palms of the hands) were documented. A negative result for rheumatoid factor and normal autoimmune screening findings and complement levels made scleroderma spectrum disorders unlikely. A polyclonal increase in -globulins (mainly IgG) was found. In the dermatology department, the stiff induration and predominantly distal limb distribution of skin tethering, together with significant blood eosinophilia, were viewed as highly suggestive of eosinophilic fasciitis (EF). A deep incisional biopsy to the fascia, from the right forearm, supported this diagnosis. Septae between fat lobules were thickened by fibrosis, and a mononuclear infiltrate including numerous eosinophils was seen. Overlying skin appeared normal. Treatment with oral prednisolone was started, initially at 40 mg/d. After 2 weeks, some symptomatic improvement and a reduction of skin edema were apparent, so the prednisolone dose was reduced to 30 mg/d. At review some weeks later, however, there had been little, if any, further improvement.

Idiopathic chronic eosinophilic pneumonia

Idiopathic chronic eosinophilic pneumonia (ICEP) is characterized by subacute or chronic respiratory and general symptoms, alveolar and/or blood eosinophilia, and peripheral pulmonary infiltrates on chest imaging. Eosinophilia is present in most cases, usually in excess of 1000/mm3. In absence of significant blood eosinophilia, a diagnosis of ICEP is supported by the demonstration of bronchoalveolar lavage eosinophilia. ICEP is typically associated with eosinophil counts higher than lymphocyte counts in the bronchoalveolar lavage. ICEP is a rare disorder of unknown cause. Its exact prevalence remains unknown. ICEP may affect every age group but is rare in childhood. It is twice as frequent in women as in men. One third to one half of the ICEP patients have a history of asthma. The mainstay of treatment of ICEP is systemic corticosteroids. Response to oral corticosteroid therapy is dramatic and has led to the consideration of corticosteroid challenge as a diagnostic test for ICEP. Nevertheless, relapses or development of severe asthma are frequent when tapering or withdrawing treatment. Long-term oral corticosteroid therapy is necessary in up to half of the patients.

The role of Mac-1 (CD11b/CD18) in antigen-induced airway eosinophilia in mice.

Mac-1 (CD11b/CD18) is an important adhesion molecule involved in the migration of leukocytes, cell signaling, and subsequent secretory responses. Its precise role in eosinophil recruitment and activation in vivo is not entirely clear. We wished to directly examine the role of Mac-1 in eosinophil migration in a murine model of allergic pulmonary inflammation. Briefly, wild-type (C57Bl/6) and Mac-1-deficient/knockout (Mac-1 KO) mice were intraperitoneally sensitized with ovalbumin (OVA) and alum (AlOH) on Days 0 and 14, and intranasally challenged with OVA either once on Day 14 or five times on Days 14 and 25 through 28. Control animals were challenged with saline. Bronchial hyperresponsiveness was measured, bronchoalveolar lavage (BAL) fluid was collected, and lungs were harvested for histology 24 h after the last challenge. The data demonstrate that wild-type (WT) mice do not respond to one OVA challenge but do develop bronchial hyperreactivity and airway and tissue eosinophilia after five OVA challenges. Conversely, Mac-1 KO mice develop significant airway eosinophilia after one OVA challenge, and the degree of airway inflammation is comparable to that observed in allergic WT mice after five challenges. In Mac-1 KO mice, after five challenges, bronchial hyperreactivity and airway inflammation was significantly enhanced compared with their wild-type counterparts. Administration of an anti-Mac-1 antibody to WT mice, before each of five intranasal OVA challenges, significantly reduces the airway eosinophilia but has no effect on tissue eosinophilia or bronchial hyperresponsiveness. Intravenous injection of interleukin-5 induced a significant blood eosinophilia in both WT and Mac-1 KO mice. Intranasal eotaxin administration induced similar levels of eosinophil migration into the lung tissues and airways of both WT and Mac-1 KO mice. In conclusion, Mac-1-deficient mice develop enhanced eosinophilic inflammation in the lung in response to allergic antigen challenge.

Detection of IL-5 and IL-1 receptor antagonist in bronchoalveolar lavage fluid in acute eosinophilic pneumonia

BACKGROUND: Acute eosinophilic pneumonia is an idiopathic cause of respiratory failure, characterized by very high numbers of alveolar eosinophils without significant blood eosinophilia. OBJECTIVE: The purpose of this study was to determine which cytokines are associated with acute eosinophilic pneumonia. METHODS: Soluble IL-1 type II receptor and the cytokines IL-1β, IL-1ra, IL-3, IL-5, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor-α were measured in serum and in bronchoalveolar lavage fluid from two patients with acute eosinophilic pneumonia during both acute and convalescent phases. RESULTS: Compared with patients with adult respiratory distress syndrome, the patients with acute eosinophilic pneumonia had high bronchoalveolar lavage fluid levels of IL-5, IL-1ra, and soluble type II IL-1 receptor but not IL-1β, tumor necrosis factor-α>, IL-3, or granulocyte-macrophage colony-stimulating factor. Bronchoalveolar lavage fluid levels of IL-5 and IL-1ra fell after resolution of symptoms. In the serum of patients with acute eosinophilic pneumonia, IL-5 was not detectable, and IL-1ra was initially high but fell after corticosteroid treatment. CONCLUSION: Acute eosinophilic pneumonia is characterized by locally high levels of IL-5, IL-1ra, and soluble type II IL-1 receptor in the alveolar space. (J ALLERGY CLIN IMMUNOL 1996;97:1366-74.)

Kimura’s Disease and Membranous Nephropathy

An interesting association of Kimura's disease and membranous nephropathy is reported in a 71-year-old Chinese patient, 40 years after emigrating to the UK from Hong Kong. Significant blood eosinophilia and a very high serum IgE level were detected, the latter with a moderate level of specificity to Candida albicans. Light microscopy of renal biopsy was unremarkable despite a proteinuria of nephrotic proportions; diffuse subepithelial dense deposits compatible with membranous nephropathy were identified on electron microscopy. The atopic nature of Kimura's disease is confirmed and C. albicans is suggested as a possible causative agent.

Eosinophilia as a marker for chronic strongyloidiasis--use of a serum ELISA test to detect asymptomatic cases.

In a previously published survey of 602 former Far East prisoners of the 2nd World War (FEPOWs), 88 (15%) were found to have Strongyloides stercoralis infections. A further 25 (4.2%) had significant blood eosinophilia for no obvious parasitological or other medical cause. We have reinvestigated this latter group several years (range nine to 19 years) later, using a recently developed serum ELISA test as well as other standard parasitological procedures. Of the 11 who were still alive and traceable five (45%) were diagnosed as having strongyloidiasis. Eosinophilia in high risk groups such as former FEPOWs is very suggestive of Strongyloides infections. The serum ELISA test appears to be a useful, sensitive and specific screening test for this diagnostically difficult infection.

Eosinophilia VI, spontaneous synthesis of chemokinetics, chemotactic, complement receptor-inducing activities for eosinophils by bronchial t lymphocytes of asthmatic-bronchitic patients.

T lymphocytes were separated from the bronchial mucus of five patients with extrinsic asthma and chronic and mild bronchitis and who had numerous eosinophils in the bronchial mucus but no significant blood eosinophilia. The bronchial lymphocytes spontaneously, that is without treatment with antigens or mitogens, released into serum-free synthetic medium one or more substances in the molecular weight range of 30 000 to 60 000 daltons. These substances when tested on eosinophils of normal persons stimulated random movement (chemokinesis), attracted them (chemotaxis), enhanced their chemotactic response to activated complement, and increased the expression of C4 and C3b receptors. Chemokinetic and chemotactic activity for neutrophils was weak. No eosinophil-stimulating activity was found in cultures of bronchial lymphocytes treated with puromycin to inhibit synthesis. The blood lymphocytes did not spontaneously synthesize the substance(s). It is not known if the several eosinophil-stimulating activities are due to one or more substance(s), but the nature of the eosinophil responses, molecular weight and other features, indicate similarities with the 'eosinophil stimulation promoter-chemotactic' factor reported to be released from mouse or human lymphocytes treated with antigen. Eosinophil stimulation resulting in increased expression of specific receptors, and potential for non-specific adherence, by trapping or arresting randomly migrating cells, is believed to mediate accumulation of cells in an affected organ. Prolonged synthesis of such products as from activated lymphocytes in the lung, could account for much of the local eosinophilia.

Subcutaneous angioblastic lymphoid hyperplasia with eosinophilia (Kimura's disease).

Six patients with peculiar angioblastic lesions associated with lymphoid infiltrates and a tissue eosinophilia are described. In 2 of the cases the newly formed vessels are apparently of arterial origin. The lesions which are solitary or multiple present as tumor-like swellings in the subcutaneous tissue of the head and neck. In addition, one patient had multiple cutaneous lesions distributed over the trunk and extremities. A significant blood eosinophilia was present in 2 cases. The disease is benign, but in its active phase may be mistakenly diagnosed as angiosarcoma. The lesions apparently respond to therapy with adrenocorticosteroids and to irradiation. Spontaneous remissions also occur.