Studies in experimental eosinophilia. X. Dissociation of histamine-induced vascular eosinophilia and antigen-induced tissue eosinophilia.
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Eosinophilia in athymic nude (rnu/rnu) rats--thymus-independent eosinophilia?
We have investigated the ability of genetically athymic (nude) rats to develop an eosinophilia to stimuli which are known to cause an eosinophilia in normal rats. Nude rats developed eosinophilia following (a) the pulmonary embolization of bovine gammaglobulin (BCG)-coated latex particles, and (b) experimental infection with the nematode parasite Ascaris suum. Eosinophilia in nude rats was not dependent on the presence of specific homocytotropic antibodies, haemagglutinating antibodies or allergic bronchoconstriction. In the latex-BCG system, all normal litter-mates (rnu/+) demonstrated haemagglutinating antibodies and a percentage demonstrated IgE and IgG2a homocytotropic antibodies to BGG in conjunction with BGG-induced bronchoconstriction. Nude rats failed to display any of these phenomena yet developed lung eosinophilia with an identical time course to that seen in their normal litter-mates. Similar observations were made following infection with A. suum. IgE antibodies were only demonstrable in normal litter-mates, which also demonstrated significantly higher levels of haemagglutinating antibodies to the parasite compared to those seen in the nude rats. However, the time course and magnitude of eosinophilia following infection with Ascaris was similar in each group. In addition, nude rats developed a significantly higher peripheral blood eosinophilia compared with normal litter-mates following secondary infection with Ascaris. In view of the immunological studies demonstrating the thymus deficiency and T-cell deficiency of the nude rat, it can either be proposed that eosinophilia is not exclusively under T-cell control or that a sub-population of T cells capable of mediating an eosinophil response exists in these animals.
Animals↗
Eosinophilia-myalgia syndrome, toxic-oil syndrome, and diffuse fasciitis with eosinophilia.
Eosinophilia-myalgia syndrome reached epidemic proportions in 1989. Its precise etiology remains uncertain, yet virtually all cases were associated with the ingestion of L-tryptophan containing trace amounts of several chemicals. Clinical and pathologic features of eosinophilia-myalgia syndrome are similar to those of the toxic-oil syndrome, which occurred in Spain in 1981 in association with the ingestion of adulterated rapeseed oil. During the past year, the epidemiology of eosinophilia-myalgia syndrome has been better defined, with a second trace contaminant linked to this condition. Knowledge of the clinical and histopathologic features of eosinophilia-myalgia syndrome has also expanded. These and other important advances in the understanding of eosinophilia-myalgia syndrome, toxic-oil syndrome, and diffuse fasciitis with eosinophilia are presented.
Brassica↗
A histopathologic comparison of Shulman's syndrome (diffuse fasciitis with eosinophilia) and the fasciitis associated with the eosinophilia-myalgia syndrome.
A comparison of the histopathologic features of Shulman's syndrome (diffuse fasciitis with eosinophilia) and the fasciitis associated with the eosinophilia-myalgia syndrome is presented. The study population consisted of eight biopsy specimens of seven patients with Shulman's syndrome and 11 specimens from 10 patients with eosinophilia-myalgia syndrome. Both groups exhibited inflammatory changes in the subcutaneous fat, septa, and fascia; cutaneous changes were more prominent in cases of eosinophilia-myalgia syndrome. Eosinophils and plasma cells were not consistently present in either condition; mast cells and factor XIIIa-positive cells were consistently present in the inflammatory infiltrates. Although there was overlap in the histopathologic findings, Shulman's syndrome tends to involve the subcutis alone and the eosinophilia-myalgia syndrome tends to be a pancutaneous-subcutaneous process.
Eosinophilia↗
Eosinophilia-myalgia syndrome, toxic-oil syndrome, and diffuse fasciitis with eosinophilia.
The eosinophilia-myalgia syndrome, which is associated with the ingestion of L-tryptophan that contained products, occurred as an epidemic in the United States in 1989. Eosinophilia-myalgia syndrome is similar in many ways to the toxic-oil syndrome, which occurred in Spain in 1981, and to diffuse fasciitis with eosinophilia, which has been noted since 1974 to occur sporadically. Recent studies have clarified the epidemiology, histopathology, and clinical features of eosinophilia-myalgia syndrome. These studies are reviewed, and comparisons to the related syndromes, toxic-oil syndrome and diffuse fasciitis with eosinophilia, are made.
Brassica↗
Characteristics of an anti-eosinophil monoclonal antibody that recognizes granulocytes from patients with blood eosinophilia but not from subjects without eosinophilia.
To investigate cell surface antigens of activated human eosinophils using monoclonal antibodies, we established a murine anti-human eosinophil monoclonal antibody AE500 by immunizing with blood eosinophils from patients with idiopathic hypereosinophilic syndrome (HES) and characterized the reactivity to a variety of human leucocytes by a fluorescence-activated cell sorter. AE500 reacted with blood eosinophils and neutrophils in nine out of 11 patients with marked eosinophilia (greater than or equal to 2500/microliters) (seven with idiopathic eosinophilia including HES and two with asthma), but not with those in asthmatic patients with mild eosinophilia (n = 10) or in healthy subjects (n = 8). AE500 did not react with blood lymphocytes, monocytes or platelets. AE500 did not react with human myeloid or lymphoid cell lines, including eosinophilic leukemia cell lines EOL-1 and EOL-3. The reactivity of AE500 to blood eosinophils and neutrophils in patients with marked eosinophilia changed in relation to blood eosinophil counts and prednisolone therapy. In addition, the reactivity of AE500 to blood eosinophils was increased in three out of four AE500-positive eosinophils by the incubation of the cells with granulocyte-macrophage colony-stimulating factor (GM-CSF) at 37 degrees C for 30 min, but not with interleukin 3 or interleukin-5. These results suggest that the anti-eosinophil antibody AE500 detects a cell surface antigen expressed on blood granulocytes in a hypereosinophilic state. This anti-eosinophil antibody would be useful for analysing the mechanism of eosinophilia.
Antibodies, Monoclonal↗
Eosinophilia. V. Delayed hypersensitivity, blood and bone marrow eosinophilia, induced in normal guinea-pigs by adoptive transfer of lymphocytes from syngeneic donors.
Dinitrochlorobenzene (DNCB) induced delayed hypersensitivity but no eosinophilia in guinea-pigs from two colonies. Citraconic anhydride (CA) induced delayed hypersensitivity and eosinophilia of the blood and bone marrow, and sites of skin tests were also infiltrated by eosinophils. In adoptive transfer of lymphocytes separated from peritoneal exudate cells of strain XIII-sensitized donors, lymphocytes from DNCB-sensitized guinea-pigs transferred antigen-specific delayed hypersensitivity; lymphocytes from CA-sensitized guinea-pigs transferred delayed hypersensitivity, and induced eosinophilia of the blood and bone marrow of the recipients. Treatment of the lymphocytes before transfer with antilymphocyte (thymocyte) globulin or puromycin suppressed the manifestations in the recipients; normal globulin did not. Active sensitization with DNCB induced formation of small amounts, and with CA larger amounts of anaphylactic antibody. Sera from the actively sensitized animals elicited no significant eosinophilia of blood or bone marrow in one group of recipients. Passive anaphylaxis elicited a transient eosinophilia of the blood, but not of the bone marrow. It is postulated that T-helper cells interact with B-lymphocyte precursors, particularly IgE B cells, to stimulate eosinopoeisis. This results in a reserve of mature eosinophils that may be released in any subsequent anaphylactic event.
Anaphylaxis↗
The mediation of tissue eosinophilia in hypersensitivity reactions. V. Comparative study of tissue eosinophilia in the skin lesions of local and systemic passive cutaneous anaphylactic reactions.
Tissue eosinophilia in active cutaneous anaphylaxis reactions is biphasic: the early phase (6 hr) is induced by a low molecular (mol. wt. 300) factor (early ECF), and the delayed phase (24 hr) is mediated by synergy of two different factors (delayed ECF-a and -b). In this study, we report the mediation of tissue eosinophilia in passive cutaneous anaphylactic (PCA) reaction sites. Tissue eosinophilia in systemic PCA showed two phases with peaks at 6 hr and 24 hr, while that in local PCA was monophasic and peaked at 12 hr. A dialysable eosinophil chemotactic factor was isolated from the early stage (0-6 hr) of local PCA skin sites, and another chemotactic factor (mol. wt. 15,000), sharing a common antigenicity with guinea-pig serum C5, from 12-hr-old local PCA skin sites. On the other hand, a different chemotactic factor with a mol. wt. of about 70,000, sharing a common antigenicity with delayed ECF-b isolated from active cutaneous anaphylactic skin lesions, was isolated from 24-hr-old systemic PCA skin lesions. Although the dialysable factor was also isolated from systemic PCA skin sites, the factor from systemic PCA delayed skin sites may not contribute to delayed tissue eosinophilia, since the activity paralleled the intensity of basophil accumulation but not to that of eosinophils. It is thus suggested that tissue eosinophilia in systemic and local PCA reactions is mediated by different chemotactic factors.
Animals↗
Eosinophilia-myalgia syndrome, toxic-oil syndrome, and diffuse fasciitis with eosinophilia.
Eosinophilia-myalgia syndrome, a recently described illness, reached epidemic proportions in 1989 and was linked to the ingestion of L-tryptophan containing trace amounts of several contaminants. Eosinophilia-myalgia syndrome shares many clinical and pathologic similarities with toxic-oil syndrome, an epidemic linked to the ingestion of adulterated cooking oil that occurred in Spain in 1981, and to diffuse fasciitis with eosinophilia, a condition first described in 1974. Over the past year, much work has been done in understanding the etiology and pathogenesis of eosinophilia-myalgia syndrome and toxic-oil syndrome. Follow-up data detailing the long-term sequelae and mortality rates for these two conditions are becoming available. The results from these studies are reviewed in this paper.
Brassica↗
[Clinical analysis of 90 cases of eosinophilia and pulmonary infiltrates with peripheral eosinophilia].
90 patients diagnosed as eosinophilia and pulmonary infiltrates with peripheral eosinophilia in PUMC Hospital from 1957 to 1986 were reported. The cause of the eosinophilia was unknown in 42% of the patients. Among these patients, hypereosinophilic syndromes (HES) were suspected in 11 patients. The most common presenting symptoms of HES were fever, skin lesions gastrointestinal symptoms and hepatosplenomegaly, the mean peripheral blood eosinophil count was as high as 25.6 x 10(9) cells/L. Biopsies of bone marrow and involved organs revealed extensive eosinophilic infiltration and severe necrosis. In the past ten years, eosinophilia and pulmonary infiltrates caused by parasitic infections obviously decreased. The most common parasites were ascaris Lumbricoides, Ancylostoma duodenale and Clonorchis sinesis. The other main causes which induced pulmonary infiltrates were allergic bronchopulmonary mycosis (ABPM) and chronic eosinophilic pneumonia. The prevalence of ABPM increased recently; early diagnosis and effective therapy could prevent the irreversible damage resulting in airways obstruction and fibrosis.
Ancylostomiasis↗
Genetic control of eosinophilia in guinea pig strains inbred for high or low bronchial allergic reactivity. 2. A genetic study of spontaneous and immunization-induced eosinophilia.
In 4 inbred strains of guinea pig the tendency to develop peripheral high-eosinophilia was shown to be genetically controlled. The development of eosinophilia with age and following immunization was examined in high- and low-eosinophilic parental strains, in F1-hybrids and in backcross offspring. The results show that probably only one or a very few segregating genes control eosinophilia, and they also indicate that different genes are involved in the determination of spontaneous (age-related) and immunization-induced eosinophilia.
Animals↗
[L-tryptophan-induced eosinophilia-myalgia syndrome with features of diffuse fasciitis with eosinophilia].
Two female patients developed localized scleroderma on the trunk and the thighs after oral ingestion of L-tryptophan for some years. Both patients reported acute progressive myalgia and weakness of the proximal parts of the extremities. On laboratory evaluation, the leucocyte count was approximately 20,000/mm3, with 38% blood eosinophils in one patient and 53% in the other. The ESR was slightly elevated; electrophoresis and muscle enzymes were normal. Skin and muscle biopsies revealed characteristic features of diffuse fasciitis with eosinophilia. High-dose glucocorticoid therapy resulted in a rapid normalization of the ESR and blood eosinophilia, whereas the scleroderma showed little improvement. The diffuse edema observed in one patient receded within a few days. A correlation between oral ingestion of L-tryptophan and the eosinophilia-myalgia syndrome has been reported recently, and the present case reports must be discussed in the light of this observation. Both patients developed a tryptophan-induced scleroderma-like illness resembling diffuse fasciitis with eosinophilia (Shulman's syndrome).
Eosinophilia↗
Eosinophilia-myalgia syndrome. A clinical case series of 21 patients. New Mexico Eosinophilia-Myalgia Syndrome Study Group.
We reviewed 21 cases of eosinophilia-myalgia syndrome to describe the range of clinical findings in these patients. Most patients were women (20 [95%]) and middle-aged (mean, 46 years) and had taken the food supplement L-tryptophan (95%). All cases involved eosinophilia (eosinophil count, greater than or equal to 2.0 x 10(9)/L) and incapacitating myalgias. Fourteen (88%) of the 16 patients tested had mild liver function abnormalities. Aldolase levels were abnormal in all patients tested. Muscle biopsies were done in five patients; four showed eosinophilic perimyositis, and one had interstitial inflammation. No physical finding was pathognomonic or universal, but muscle tenderness, tachycardia, and rash were the most common signs found during physical examinations. Seven patients were treated with prednisone, and six showed improvement in muscle pain and a decrease in eosinophilia. The cause of this disorder is still unknown.
Biopsy↗
[Pulmonary infiltrations with eosinophilia (pulmonary eosinophilia)].
The pulmonary eosinophilias are characterised by radiographic lung shadows with either a peripheral blood eosinophilia of more than 450/microliter or histologic abnormalities consisting of both interstitial and intraalveolar accumulations of eosinophils and macrophages. We describe the clinical features, radiographic changes, results of bronchoscopy and follow-up studies of three women with chronic eosinophilic pneumonia of unknown aetiology. In all patients the illness resolved rapidly after treatment with corticosteroids, however one patient experienced a second episode after treatment withdrawal. We demonstrate the wide differential diagnosis of the syndrome of pulmonary eosinophilia.
Adult↗
Eosinophilia-myalgia syndrome, toxic-oil syndrome, and diffuse fasciitis with eosinophilia.
The similarity of eosinophilia-myalgia syndrome (EMS) and toxic-oil syndrome (TOS) to systemic sclerosis and diffuse fasciitis with eosinophilia (DFE) highlights the potential for environmental agents to induce autoimmune disease. Further, a candidate etiologic agent for EMS, 3-(phenylamino)alanine, is chemically similar to the aniline derivative identified in samples of oil implicated in TOS, 3-(N-phenylamino)-1,2-propanediol, suggesting pathogenic overlap. The late-stage manifestations of EMS and TOS are muscle cramping, arthralgia, severe fatigue, and cognitive impairment. This review focuses on the divergent and parallel findings in EMS, TOS, and DFE. The formation of the Environmentally Associated Connective Tissue Disease Study Group within the American College of Rheumatology will provide a forum for the development of registries to study suspected toxin-induced disorders.
Brassica↗
Montelukast reduces peripheral blood eosinophilia but not tissue eosinophilia or symptoms in a patient with eosinophilic gastroenteritis and esophageal stricture.
BACKGROUND: Eosinophilic gastroenteritis (EG) is an uncommon entity of which the pathogenesis is unclear. As no controlled treatment trials exist, treatment of EG remains largely empiric. Limited results have been achieved with oral cromolyn, ketotifen, and other antihistamines. Oral corticosteroids are effective, but long-term use is complicated by side effects including growth retardation, diabetes, and osteoporosis. OBJECTIVES: We sought to determine whether treatment with montelukast would improve symptoms and decrease both peripheral blood and tissue eosinophilia (TE) in a patients with steroid-dependent EG for 20 years complicated by esophageal stricture. METHODS: In an unblinded, n = 1 trial, we treated the patient for 5 months with montelukast (20 to 30 mg daily) while his baseline dose of prednisone (10 mg daily) was continued. Complete blood counts and symptoms were monitored weekly. Esophageal biopsies were obtained before and after 5 months of therapy with montelukast. After the posttreatment biopsy was obtained, montelukast was discontinued. Outcome measures included patient symptoms and peripheral and tissue eosinophil counts. RESULTS: During treatment with montelukast, the mean peripheral blood eosinophil count fell from 5,064 cells/microL (average 28 determinations over 20 years; range 1,408 to 12,500 cells/microL) to 1,195 cells/microL (average 14 determinations over 16 weeks; range 556 to 2,193 cells/microL), a 76% reduction. The corresponding TE as calculated from esophageal biopsies was 31 eosinophils/high power field before and 70 eosinophils/high power field after treatment. The patient noted no appreciable improvement in esophageal symptoms. CONCLUSIONS: Montelukast dramatically reduced peripheral blood eosinophilia, but did not affect TE or symptoms in this patient with severe, long-standing EG complicated by esophageal stricture.
Acetates↗
Studies in experimental eosinophilia. XI. Dependence of eosinophilia, apparently induced by histamine, on acidity.
A solution of histamine in saline elicited eosinophil response in both lymph nodes and the blood stream. The lymph node response was not inhibited by the antihistamine, mepyramine maleate, but was inhibited by puromycin. Both the lymph node and the systemic response were essentially abolished when the pH of the solution (5.0 and 4.7, respectively) was brought to neutrality by phosphate buffer. Serum could bring the pH of histamine to neutrality or higher, but the histamine-serum mixture retained in vivo activity, unless the histamine was buffered before addition to the serum. When normal guinea pig gamma-globulin was incubated with histamine, a nondialyzable factor was generated which had the same activity as histamine. Thirteen different amino acids induced lymph node eosinophilia and each was acid in saline solution; when one of them, trytophane, was brought to neutral pH, its activity was considerably reduced. During the period when the circulating level of eosinophils was rising, there was no detectable fall in the bone marrow stores of mature of immature eosinophils. Thus, the activity of histamine, vis-a-vis eosinophils, is nonspecific and is attributable to its acidity. The data suggest that histamine, in the acidic state, generates autoantigens, which, in turn, lead to antibody-mediated eosinophilia in lymph nodes.
Amino Acids↗
Tryptophan contaminants associated with eosinophilia-myalgia syndrome. The Eosinophilia-Myalgia Studies of Oregon, New York and New Mexico.
Eosinophilia-myalgia syndrome (EMS) has been linked to ingestion of tryptophan contaminated with 1,1'-ethylidene-bis[L-tryptophan] (EBT), but other contaminants have received little study. The authors identified 101 lots of L-tryptophan that had been consumed either by persons with EMS or by asymptomatic tryptophan users and quantified the amounts of EBT and five other contaminants in each lot. After stratification of case and noncase lots by time of manufacture to adjust for the strong sequential pattern over time among case and noncase lots, higher EBT levels were still associated with a lot's case status, but the association lacked statistical significance (p = 0.120, odds ratio = 1.56, 95% confidence interval 0.758-3.23). While these findings do not rule out the possibility that EBT is the etiologic agent in EMS, they raise the possibility that other chemical contaminants in manufactured tryptophan modify the effects of EBT or that the causal agent of EMS is an entirely distinct compound.
Drug Contamination↗