SEARCH · PubMed Health

Results for “EOSINOPHILIA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources

PubMed1994

Eosinophilia in newborn infants.

To evaluate the clinical significance of eosinophilia in newborn infants, 261 admissions to the neonatal unit over a 12-month period were studied retrospectively; 33 babies with eosinophilia (> 1.0 x 10(9)/l) were studied. Clinical and laboratory data for the first month of life were compared, where available, between gestational age-matched pairs with and without eosinophilia. Of the 33 babies with eosinophilia, 23 were > 26 weeks' gestation and all had age-matched controls; 10 were < or = 26 weeks' gestation but had no appropriate gestational age-matched controls. Babies > 26 weeks' gestation with eosinophilia had a significantly higher number of septic episodes than controls: 20 of 23 versus 4 of 23. All 10 babies < or = 26 weeks' gestation with eosinophilia developed sepsis. Infections with gram-negative organisms and necrotizing enterocolitis occurred only in babies who developed eosinophilia. In 5 babies no cause for the eosinophilia was found. In conclusion, eosinophilia in the newborn is usually explainable and is most often associated with infection.

Bacterial Infections↗

PubMed1993

Epidemiology of pulmonary eosinophilia in rural south India--a prospective study, 1981-86.

STUDY OBJECTIVE: The study aimed to determine the prevalence and incidence of pulmonary eosinophilia, with special reference to tropical pulmonary eosinophilia, in a rural community. DESIGN: This was a five year prospective study from 1981-86. SETTING: The study was conducted in four villages of Tamil Nadu in south India. SUBJECTS: The study population consisted of 24,950 subjects. MEASUREMENTS AND MAIN RESULTS: After being questioned about pulmonary symptoms, the selected subjects had peripheral blood examined for total leukocyte and eosinophil counts; stools for ova, cysts, and parasites; sputum for acid-fast bacilli, and chest radiography. Subjects with blood eosinophilia of > or = 2000/mm3 were classified as having pulmonary eosinophilia. One of the 200 asymptomatic control subjects had blood eosinophilia > 2000/mm3. Twenty two (7.7%) of a further 286 subjects selected at random were found to have microfilaraemia. Between 1981 and 1984 the annual incidences of pulmonary eosinophilia were estimated at 4.1, 3.1, and 2.7/1000 while the prevalence rates were 6.4, 9.3, and 11.9/1000 respectively. This rising prevalence over time occurring simultaneously with a falling incidence suggests that the final incidence rate (2.7/1000) was likely to be the most accurate of the three estimated. At resurvey in 1986, 314 cases were classified as pulmonary eosinophilia giving a prevalence rate of 12.6/1000. Altogether 214 of them also had intestinal worm infestations, including 58 in whom eosinopenic remission was recorded after deworming alone. Eosinopenic remission was documented in 135 of 182 cooperative patients who were considered to have tropical pulmonary eosinophilia and agreed to be treated with diethylcarbamazine. CONCLUSIONS: This study found that tropical pulmonary eosinophilia, either alone or with worm infestation, was a major cause or morbidity in this rural population.

Adolescent↗

PubMed2003

Peripheral blood eosinophilia associated with gastrointestinal administration of iodinated contrast media.

OBJECTIVE: This study was designed to assess whether gastrointestinal administration of iodinated contrast media results in peripheral blood eosinophilia. MATERIALS AND METHODS: We studied 110 patients in a retrospective review. Diatrizoate meglumine and diatrizoate sodium for abdominal CT were administered to 98 of these patients; 22 of the 98 had also been given the same contrast medium administered by enema. The remaining 12 patients were given diatrizoate sodium for gastrointestinal fluoroscopy. A control group of 65 patients underwent single-contrast barium upper gastrointestinal or enema examinations. WBC and eosinophil counts were determined approximately 24 hr before the examination and every 24 hr thereafter, through the ninth day. RESULTS: Eosinophilia was detected in 17 (15.5%) of 110 patients after gastrointestinal administration of iodinated contrast media. The prevalence of eosinophilia after administration of iodinated contrast media was statistically significantly different compared with that in the control group, in which none of the 65 patients had eosinophilia (p < 0.001). Eosinophilia was detected 48 hr after application of iodinated contrast agents and lasted through the sixth day, with a peak on the fifth day. The prevalence of eosinophilia was independent of route of application, dose, or type of iodinated contrast medium. Eosinophilia in all cases was clinically asymptomatic. CONCLUSION: Eosinophilia that is caused by gastrointestinal administration of iodinated contrast media is a transient, clinically silent phenomenon. It may lead to unnecessary workup for known conditions associated with eosinophilia.

Administration, Oral↗

PubMed2005

Pelvic irradiation-induced eosinophilia is correlated to prognosis of cervical cancer patients and transient elevation of serum interleukin 5 level.

PURPOSE: To determine the significance of eosinophilia and serum interleukin 5 (IL-5) levels induced by radiotherapy in patients with gynecological cancer. MATERIALS AND METHODS: First, we examined changes in the number of eosinophils before and during radiotherapy in 145 patients with cervical cancer who underwent external radiotherapy and brachytherapy. Eosinophilia was defined as > or =10% eosinophils or > or =500 eosinophils/mm3. Next, we determined serum IL-5 levels prospectively in 20 patients, comprising 18 cases of cervical cancer, one of uterine corpus cancer, and one of vaginal cancer. RESULTS: Eosinophilia was seen in 88 patients (61%). Patients with advanced disease stage IV showed 32% eosinophila, lower than those of stage I (63%), II (69%), and III (65%) disease patients (p=0.03). The 5-year cause-specific survival rate was 76% for patients with eosinophilia (+) and 53% for patients without eosinophilia (p=0.0003). Thus, eosinophilia correlates to stage classification and a good prognosis. Of the 20 patients studied prospectively, the six with elevated serum IL-5 level at one week (6/20=30%) all showed eosinophilia (100%), whereas only six of the other 14 patients had eosinophilia (43%, p=0.04). CONCLUSION: Radiotherapy induced transient elevation of serum IL-5 levels and is related with eosinophilia, which is correlated to prognosis.

Adult↗

PubMed1981

Cyclophosphamide pretreatment induces eosinophilia to nonparasite antigens.

Eosinophilia is usually regarded as a T cell-dependent hemopoietic response, although in most instances of immune responses by T cells there is no accompanying eosinophilia. BALB/c mice immunized with keyhole limpet hemocyanin (KLH) in complete Freund's adjuvant (CFA) were found not to develop eosinophilia, whereas pretreatment of such mice with 150 mg/kg cyclophosphamide (CY) induced marked eosinophilia in the blood (1000 to 3000/mm3) and bone marrow. CY as well as CY and KLH in CFA cause a leukocytosis and neutrophilia, but significant eosinophilia was seen only in mice receiving both CY and KLH-CFA. The eosinophilic response depended on the dose of CY and peaked 13 days after immunization, and was preceded by a bone marrow eosinophilia that peaked 8 days after immunization. No eosinophilia occurred in BALB/c nu/nu mice after CY and KLH-CFA but did occur in the nu/+ littermates. This model in mice of eosinophilia in response to CY followed by a nonparasite antigen should be useful in the analysis of T cell signals that might regulate eosinophilia.

Animals↗

PubMed1998

Host genetic determinants of vaccine-induced eosinophilia during respiratory syncytial virus infection.

In BALB/c mice, sensitization with the attachment protein (G) of respiratory syncytial virus (RSV) leads to CD4+ T cell-mediated lung eosinophilia during subsequent challenge with RSV. To determine the host genetic influences on this model of lung eosinophilia, we tested 15 different inbred mouse strains. Eosinophilia developed in all H-2d (BALB/c, DBA/2n, and B10.D2), but not in H-2k (CBA/Ca, CBA/J, C3H, BALB.K, or B10.BR) mouse strains. Among H-2b mice, 129 and BALB.B developed eosinophilia, whereas C57BL/6 and C57BL/10 did not. Testing first generation crosses between sensitive and resistant strains showed that eosinophilia developed in all H-2dxk (n = 5), irrespective of background genes, but not in H-2dxb (n = 2) mice. In vivo depletion of CD8+ T cells or IFN-gamma rendered C57BL/6, but not BALB.K mice, susceptible to eosinophilia. Analysis of B10 recombinant mice showed that the Dd allele (in B10.A(5R) mice) prevented CD8+ T cell accumulation in the lung, resulting in intense lung eosinophilia. However, the Db allele (in B10.A(2R) and B10.A(4R) mice) supported CD8+ T cell expansion and prevented eosinophilia. Intracellular cytokine staining showed that lung eosinophilia correlated with reduced IFN-gamma and increased IL-10 expression in lung T cells. These results are compatible with the unifying model that Th2 cells mediate the disease but can be inhibited by CD8+ T cells secreting IFN-gamma. Our findings have important implications for the development of protective, nonpathogenic vaccines for RSV disease.

Animals↗

PubMed1998

Circulating, but not local lung, IL-5 is required for the development of antigen-induced airways eosinophilia.

IL-5 is induced locally in the lung and systemically in the circulation during allergic airways eosinophilic inflammation both in humans and experimental animals. However, the precise role of local and systemic IL-5 in the development of allergic airways eosinophilia remains to be elucidated. In our current study, we demonstrate that compared with their IL-5(+/+) counterparts, IL-5(-/-) mice lacked an IL-5 response both in the lung and peripheral blood, yet they released similar amounts of IL-4, eotaxin, and MIP-1alpha in the lung after ovalbumin (OVA) sensitization and challenge. At cellular levels, these mice failed to develop peripheral blood and airways eosinophilia while the responses of lymphocytes, neutrophils, and macrophages remained similar to those in IL-5(+/+) mice. To dissect the relative role of local and systemic IL-5 in this model, we constructed a gene transfer vector expressing murine IL-5. Intramuscular IL-5 gene transfer to OVA-sensitized IL-5(-/-) mice led to raised levels of IL-5 compartmentalized to the circulation and completely reconstituted airways eosinophilia upon OVA challenge, which was associated with reconstitution of eosinophilia in the bone marrow and peripheral blood. Significant airways eosinophilia was observed for at least 7 d in these mice. In contrast, intranasal IL-5 gene transfer, when rendered to give rise to a significant but compartmentalized level of transgene protein IL-5 in the lung, was unable to reconstitute airways eosinophilia in OVA-sensitized IL-5(-/-) mice upon OVA-challenge, which was associated with a lack of eosinophilic responses in bone marrow and peripheral blood. Our findings thus provide unequivocal evidence that circulating but not local lung IL-5 is critically required for the development of allergic airways eosinophilia. These findings also provide the rationale for developing strategies to target circulating IL-5 and/or its receptors in bone marrow to effectively control asthmatic airways eosinophilia.

Adenoviridae↗

PubMed1981

[Pulmonary eosinophilia: current concepts, diagnostic and therapeutic advances].

Pulmonary eosinophilia is a parenchymatous disorder with tissue eosinophilia (with or without blood eosinophilia). It remains ill understood whether from the pathophysiological, diagnostic, aetiologic or therapeutic standpoint. This paper takes stock of the principal classifications used and the necessary stages in the diagnostic approach. First, current understanding of the function of the eosinophil is discussed. The method of searching for a precise aetiological diagnosis is reviewed under the general headings of "parasitic", "fungal" and "drug induced". Pulmonary eosinophilia wih vasculitis and idiopathic eosinophilia have then considered. The authors stress the importance of establishing a eosinophilia have then considered. The authors stress the importance of establishing a precise aetiology and searching for extra pulmonary lesions or evidence of vasculitis in the management of pulmonary lesions or evidence of vasculitis in the management of pulmonary eosinophilia. As regards treatment, particularly of prolonged pulmonary eosinophilia, corticosteroids are relied upon. For some this may be after a test trial of anti-parasitic therapy.

Aspergillosis, Allergic Bronchopulmonary↗

PubMed1981

Presence of eosinophilia in progressive systemic sclerosis and localized scleroderma.

Recent studies on eosinophilic fasciitis have lead to this investigation of eosinophilia in progressive systemic sclerosis and localized scleroderma. Eosinophilia (eosinophilic count greater than 300/cmm) was found in ten of 63 progressive systemic sclerosis patients (15.8%) and in two of nine localized scleroderma cases (22.2%). In patients with progressive systemic sclerosis eosinophilia was found occasionally in six cases; it was transitory, but frequent in three cases; it was constant and very high in one case. In patients with localized scleroderma eosinophilia was found occasionally in one case and frequent, but not constant, in the other one. The possible influence of drugs could be excluded in five cases: three progressive systemic sclerosis cases and two affected with localized scleroderma. Therefore, it is possible to confirm that eosinophilia is not a distinctive sign of eosinophilic fasciitis in patients suffering from scleroderma-like syndromes. While eosinophilia is related to inflammation in eosinophilic faciitis, eosinophilia and disease activity could not be correlated in our patients with PSS. Recently, it has been suggested that eosinophilia might be an unfavorable prognostic criterion in progressive systemic sclerosis. Our data does not allow confirmation of this assumption.

Adult↗

PubMed1999

Eosinophilia during fludarabine treatment of chronic lymphocytic leukemia.

Although eosinophilia has been reported as a side effect of purine analogues, there is no report on fludarabine-induced eosinophilia in chronic lymphocytic leukemia (CLL). During chemotherapy with fludarabine and cyclophosphamide, we observed two cases of significant eosinophilia. A 67-year-old patient with CLL developed bone marrow and peripheral blood eosinophilia up to 7.9x10(9)/l, the highest eosinophil count ever reported during treatment with a purine analogue. The eosinophilia persisted for 33 days. Another patient developed bone marrow eosinophilia without eosinophilia in the peripheral blood. These are the first documented cases of fludarabine-induced eosinophilia in CLL, and this side effect may conceivably be more common than previously recognized.

Aged↗

PubMed2005

A locus for eosinophilia in the MES rat is on Chromosome 19.

Matsumoto Eosinophilia Shinshu (MES) is a rat strain that spontaneously develops eosinophilia and eosinophil-related inflammatory lesions in many organs. We performed chromosomal mapping of the gene for eosinophilia by breeding backcross progeny. The onset of eosinophilia appeared to be delayed in the progeny compared with that in MES, with the prevalence of eosinophilia in the backcross progeny at 12 weeks of age being 22.5%. Genetic linkage analysis with marker loci indicated the major locus for eosinophilia was located at the end of the q arm region of Chromosome 19 (between D19Rat8 and telomere). The locus was denoted eosinophilia 1 (eos1). These data will form the basis for identification of the eos1 gene using a reverse genetic approach, which will hopefully lead to elucidation of the mechanisms involved in eosinophilia and eosinophilopoiesis.

Animals↗

PubMed2001

Tissue eosinophilia in acute and chronic atopic dermatitis: a morphometric approach using quantitative image analysis of immunostaining.

BACKGROUND: The frequency and amount of tissue eosinophilia in spontaneous lesions of acute and chronic atopic dermatitis (AD) are still a matter of controversy, and little is known about the distribution of eosinophilia in skin. OBJECTIVES: To give a quantitative description of tissue eosinophilia in spontaneous lesions of acute and chronic AD based on morphometric data. METHODS: Thirty-one lesional skin biopsies of AD were evaluated using our recently described method for the quantitative assessment of eosinophilic granule protein (EGP) deposition by image analysis of immunostaining using the antibodies EG1, EG2, MBP, EPO and neutrophil elastase (NE). The frequency, amount and distribution of protein deposition including extracellular EGP deposition as an indicator of complete activation and degranulation of eosinophils were determined. Eosinophil count was performed in addition. Histopathological parameters of acute dermatitis (spongiosis) and chronic dermatitis (epidermal hyperplasia) were scored to look for a correlation with tissue eosinophilia. RESULTS: Tissue eosinophilia was found in nearly all biopsies (30 of 31). The most protein was detected by EG2, followed by EG1, MBP and EPO, with very small amounts of NE. A superficial tissue distribution of eosinophilia was found, with < 10% of total EGP deposition below a depth of 1.39 mm from the epidermis. Eosinophils were involved in acute, spongiotic dermatitis, but more tissue eosinophilia including EGP deposition was detected in lesions with pronounced epidermal hyperplasia than in biopsies without. CONCLUSIONS: These data provide further evidence for the involvement of activated eosinophils in acute and chronic AD by a new quantitative in situ approach. Pronounced tissue eosinophilia, especially EGP deposition as the result of complete activation of eosinophils, is found in chronic AD and may be involved in the development or maintenance of chronicity.

Acute Disease↗

PubMed2003

Investigation of tropical eosinophilia; assessing a strategy based on geographical area.

OBJECTIVES: Patients with eosinophilia are an important clinical problem. This study aimed to assess the most efficient manner of investigating patients with peripheral eosinophilia (eosinophil count >0.5x10(9)ml(-1)) presenting from the tropics. METHODS: Patients attending the Hospital for Tropical Diseases, London, from October 1997 to March 2002 for investigation of eosinophilia were identified prospectively. Laboratory, clinical and demographic data were recorded from laboratory and clinical records. An investigation set was proposed prospectively and assessed for all geographical areas (stool microscopy, strongyloides culture and serology), all of Africa (additional schistosomal serology, terminal urine microscopy and filarial serology) and West Africa (additional day-bloods for microfilaria). RESULTS: Data was analysed for 261 patients. At least one helminthic cause for eosinophilia was found in 64% of patients (median eosinophilia 1.2x10(9)ml(-1)). Seventeen per cent of patients had more than one helminth species found. Median eosinophilia increased with number of diagnoses per patient. The proposed investigation sets were validated, with high yield for all proposed tests apart from filarial serology outside West Africa, and good sensitivity. CONCLUSIONS: Initial investigation of eosinophilia in patients presenting from the tropics may be guided by a simple investigation set depending on broad area of travel which has high sensitivity and yield. Patients frequently have more than one helminthic cause of eosinophilia.

Adolescent↗

PubMed1990

Acute lymphoblastic leukemia with eosinophilia.

Acute lymphoblastic leukemia with eosinophilia is a rare but distinctive clinical entity. The eosinophilia in these patients can present before, concomitantly, or after the diagnosis of leukemia. Patients with this syndrome often suffer from the cardiovascular complications of severe eosinophilia, suffering excess morbidity and mortality as a result of their eosinophilia. Treatment of the eosinophilia in this syndrome consists of administration of induction chemotherapy, followed by prednisone and hydroxyurea if required for persistent eosinophilia. Eosinophilia often resolves with remission of leukemia, only to return at the time of relapse in a high percentage of cases. Patients with this syndrome characteristically have cytogenetic abnormalities involving the long arms of chromosomes 5 and 14. These cytogenetic abnormalities are not commonly seen in acute lymphoblastic leukemia and suggest that this syndrome may have a distinct pathophysiology and etiology. The affected region on chromosome 5 contains genes that control hematopoiesis, including eosinophilopoiesis. Further investigations into these cytogenetic abnormalities may provide insight into the etiology of the leukemia and eosinophilia characteristic of this syndrome.

Chromosome Aberrations↗

PubMed1997

2-Chlorodeoxyadenosine (cladribine)-related eosinophilia in patients with lymphoproliferative diseases.

Eosinophilia and allergic skin reactions are uncommon events after 2-chlorodoxyadenosine (2-CdA, cladribine) administration. A multicentre retrospective analysis of eosinophilia in 360 patients treated with 2-CdA for lymphoid malignancies has been made. B-cell chronic lymphocytic leukaemia (B-CLL) was diagnosed in 153, hairy cell leukaemia (HCL) in 68, low-grade non-Hodgkin's lymphoma (LGNHL) in 119, high-grade NHL in 2 and Waldenstrom's macroglobulinaemia (WM) in 18 patients. 2-CdA was administered at a dose 0.12 mg/kg/d in 2-h intravenous infusion for 5 consecutive d. The courses were repeated monthly. Patients with HCL received 1 cycle of 2-CdA, with NHL 2-6 (mean 3.5) cycles and with B-CLL 3-6 (mean 5) cycles. Twenty patients (5.5%), including 5 with HCL, 6 with LGNHL, 7 with B-CLL and 2 with WM, developed peripheral blood eosinophilia. The mean values of absolute eosinophil count were 0.78x10(9)/l (0.58-1.06x10(9)/l), 0.71x10(9)/l (0.52-1.3x10(9)/l), 85 (0.56-1.82x10(9)/l) and 0.75 (0.74-0.76x10(9)/l), respectively. Eosinophilia occurred in 13 patients after 1 course, in 4 after 2 courses, and in 5 after > or =3 courses of the therapy. In 17 cases it resolved spontaneously. Allergic skin lesions with pruritus were noticed in 3 patients simultaneously with an increase in eosinophil count. All of them required antihistaminic drugs and/or corticosteroids. One patient with B-CLL experienced repeated episodes of eosinophilia. The highest incidence of 2-CdA-induced eosinophilia was noticed in patients with MW (11.1%) and HCL (7.4%) who received only 1 cycle of this drug and entered a complete remission. This side effect was less frequently observed in LGNHL and B-CLL, i.e. in 5.0% and 4.6% of cases, respectively. The mechanism of 2-CdA-induced eosinophilia is not clear. It has been postulated that massive tumour cell lysis may trigger a release of IL-5 and probably other cytokines. The allergic mechanism of 2-CdA-induced eosinophilia is also possible, especially in patients with simultaneous skin reactions.

2-Chloroadenosine↗

PubMed1995

Adverse effects of eosinophilia and smoking on the natural history of newly diagnosed chronic bronchitis.

BACKGROUND: Little is known about risk factors for the progression of disease in individuals with newly developed chronic bronchitis (CB). In addition to the effects of smoking, there was specific clinical and epidemiologic interest in the importance of traits such as eosinophilia and wheezing, more commonly associated with asthma, in the progression of this disease. METHODS: We evaluated adult individuals with and without diagnosed CB longitudinally in a representative community population in Tucson, Ariz. These subjects were followed up for 13 years since 1972. Because we were interested in CB specifically, those with diagnoses of emphysema and asthma were removed from the data set. Initial level of FEV1 (%FEV1) and slopes in FEV1 were corrected for covariates and other important variables. RESULTS: As expected, persistent and newly diagnosed CB was significantly more common in current and ex-smokers. Furthermore, initial lung function was lower, and decline in FEV1 was steeper in smokers with persistent and newly diagnosed CB. Newly diagnosed cases had steeper declines in FEV1 (-6.84 mL/yr below grand mean of -11.18 mL/yr) than normal subjects (+0.95 mL/yr). The incidence rate of newly diagnosed CB was significantly higher in those with eosinophilia (13.7%) than without eosinophilia (6.7%). Finally, new cases with eosinophilia had similar initial %FEV1 (95.4 +/- 1%) but much larger declines in function than new cases without eosinophilia: -24.5 versus -16.6 mL/yr. Adverse effects of wheeze were largely explained by smoking and eosinophilia. CONCLUSION: Eosinophilia is an important aspect of CB in addition to smoking, and it should be considered in its evaluation. The presence of eosinophilia in newly diagnosed CB, with or without wheeze, may warn the clinician of the possibility of a rapid decline in FEV1.

Adult↗

PubMed1997

Eosinophilia after commencement of clozapine treatment.

OBJECTIVE: While clozapine-associated agranulocytosis has received extensive attention, a number of recent publications have identified that the incidence of eosinophilia may also be of concern. This retrospective review identifies the incidence of eosinophilia within a group of people commencing clozapine at a large hospital in Australia. METHOD: The pathology reports of all people (n = 160) who commenced clozapine within a 3.5-year period were retrospectively reviewed for incidences of eosinophilia. RESULTS: The incidence of eosinophilia was identified as 13%, comprising 17 males and four females. All cases of eosinophilia developed within 4 weeks of commencing clozapine. One male reached a peak eosinophil level of 9 x 10(9)/L, which resolved after clozapine was withdrawn. In all other cases, the eosinophilia resolved without intervention. CONCLUSIONS: With a rate of eosinophilia at 13% in this population under review, and given that there have been reports of 25 cases of eosinophilic cardiomyopathy resulting in four deaths worldwide, clinicians should be alert to the incidence and sequelae of eosinophilia in people receiving clozapine treatment.

Adult↗

PubMed1992

The cause and pathogenesis of the eosinophilia-myalgia syndrome.

OBJECTIVE: To review recent advances in the understanding of the cause and pathogenesis of the eosinophilia-myalgia syndrome associated with ingestion of L-tryptophan. DATA SOURCES: Studies published from 1989 to 1991 were identified using a MEDLINE literature search. Additional references were selected from the bibliographies of identified articles. DATA SYNTHESIS: The eosinophilia-myalgia syndrome was epidemiologically associated with ingestion of L-tryptophan-containing preparations. Analysis of case-associated lots of L-tryptophan has revealed several chemical impurities. One of these, labeled "peak E," is an unusual dimeric form of L-tryptophan (1,1'-ethylidenebis[tryptophan]), and its presence is associated with the eosinophilia-myalgia syndrome (P = 0.022). Evidence of abnormal metabolism of tryptophan has been found in some patients with the syndrome. Eosinophil activation and the release of major basic protein and other eosinophil-derived toxic proteins into the extracellular space is a striking feature in the eosinophilia-myalgia syndrome and implicates eosinophils or their products in the pathogenesis. Mononuclear cell activation and infiltration of various affected tissues as well as fibrosis of the integument and of the connective tissue components of blood vessels, nerves, and muscles are additional frequent findings. CONCLUSIONS: Current evidence suggests that the epidemic of the eosinophilia-myalgia syndrome was caused by contaminated L-tryptophan preparations originating from a single manufacturer. Peak E or other, as yet unidentified, contaminants may trigger activation of eosinophils and inflammatory cells and increase biosynthesis of connective tissue components, resulting in the clinical and pathologic manifestations of the eosinophilia-myalgia syndrome. Further studies of the interaction of eosinophils, inflammatory cells, and fibroblasts may increase the understanding of the pathogenesis of the eosinophilia-myalgia syndrome. The insights gained from the epidemic may be applicable to more common idiopathic diseases associated with eosinophilia and fibrosis.

Drug Contamination↗