Extreme Eosinophilia Research Articles

Severe Eosinophilia in Children

The differential diagnosis of hypereosinophilia includes both primary (clonal and idiopathic) and secondary medical conditions. Here we raise the awareness of physicians to the unusual causes of hypereosinophilic states and describe the molecular assays used in the diagnosis of hypereosinophilia. Two unusual cases of hypereosinophilia in children that were initially misdiagnosed are reported. T-cell receptor gene rearrangement, skewed X inactivation, fluorescence in situ hybridization analysis, and chromosomal karyotyping were used to reach the final correct diagnosis. Both patients displayed significant eosinophilia and were initially misdiagnosed as having parasitic infection. Nonspecific T-cell clonal expansion was diagnosed in 1 patient based on the clonality of the T-cell receptor variable γ-chain and the skewed chromosome inactivation. The second patient was diagnosed with B-lineage acute lymphoblastic leukemia with a translocation (5;14) (q13;q32) that is well known to be associated with hypereosinophilia. The level of awareness to clonal expansion of WBC subsets which can cause hypereosinophilia should be high when evaluating a patient with extreme eosinophilia. Advanced molecular assays to detect clonal expansion should be used to exclude aberrant clonal processes in such patients.

Extreme Peripheral Eosinophilia in a Patient With a Skin Rash and Abnormal Chest Imaging

Extreme Peripheral Eosinophilia in a Patient With a Skin Rash and Abnormal Chest Imaging

Extreme eosinophilia in a setting of metastatic leiomyosarcoma: An unusual case report

Extreme eosinophilia in a setting of metastatic leiomyosarcoma: An unusual case report

Dissection of the posterior inferior cerebellar artery in the hypereosinophilic syndrome

Dissection of the posterior inferior cerebellar artery in the hypereosinophilic syndrome

A Case of Severe Eosinophilia in a Preterm Infant

Eosinophilia of prematurity is commonly seen in premature infants as a result of many causes, although a sustained or progressive form is uncommon. Different pathophysiological hypotheses include decreased circulating adrenal steroids and foreign antigen exposure. We present here a case of prolonged extreme eosinophilia in a preterm infant complicated by thrombocytopenia. The patient's eosinophil count reached 91.48 × 10(9)/L and remitted with nonspecific treatment. A comprehensive clinical, laboratory, and radiologic assessment is usually required in the context of a hypereosinophilic preterm infant to recognize the triggering etiology. Nonspecific treatment was the modality of choice because of unclear etiology in our case. Preterm infants with blood eosinophilia might not need immunomodulatory treatment despite extremely high absolute eosinophil counts.

Extreme eosinophilia caused by interleukin-5-producing disseminated colon cancer

Eosinophilia is caused by various pathological conditions, and can be divided into two entities based on the mechanism of eosinophil proliferation: i.e., clonal proliferation of eosinophils (chronic eosinophilic leukemia) and reactive proliferation of eosinophils. Clonal proliferation of eosinophils often accompanies chromosomal aberrations resulting in the generation of specific fusion genes, such as FIP1-like1 (FIP1L1)-PDGFRa [1]. Reactive proliferation of eosinophils is caused by various underlying diseases, including malignant diseases, allergy, autoimmune diseases, and infection, although the underlying diseases are sometimes unidentified in certain patients (idiopathic eosinophilia) [2]. With the exception of clonal eosinophilia, the pathophysiology of eosinophilia is not fully understood. However, overproduction of stimulatory cytokines involved in eosinophil proliferation, such as interleukin-5 (IL-5), granulocyte–macrophage colony-stimulating factor (GM-CSF), and IL-3, by pathological conditions is thought to play an important role in the development of this disease [3]. Among malignant diseases, hematological malignancies, such as Hodgkin’s and non-Hodgkin’s lymphoma, have been shown to be the major underlying diseases of eosinophilia [4, 5]. Although there have been several reports describing eosinophilia associated with solid tumors, such as lung cancer, colon cancer, and hemangioendothelioma, the incidence is quite low, and the level of increase in eosinophil count is mild [5–8]. Here, we report a case of extreme eosinophilia caused by colon cancer producing IL-5. A 72-year-old woman was admitted to our hospital because of malaise lasting for 2 months. She had no history of allergic or parasitic disease. Laboratory findings on admission showed anemia, leukocytosis (WBC: 232100/ll) with elevated eosinophil count (eosinophils: 141580/ll), and abnormal coagulopathy consistent with disseminated intravascular coagulation (DIC) (Table 1). Genetic studies showed no evidence of FIP1L1-PDGFRa or BCR-ABL fusions. Chromosomal analysis revealed normal karyotype. Serum CEA, CA19-9, CA125, CA15-3, IL-2R, and PIVKA-2 levels were significantly elevated (Table 1). Among these tumor markers, the level of sIL-2R was markedly elevated. It has been reported that the level of IL-2 is correlated with the activity of hypereosinophilic syndrome [9]. The elevation of IL-2R level may be induced by activated T cells; however, it is possible that IL-2R is secreted from activated eosinophils, because eosinophils from hypereosinophilic patients were shown to express IL-2Ra [10]. Bone marrow biopsy revealed no evidence of hematological malignancy. Whole-body CT showed multiple tumors in the colon, liver, lung, and pelvis with pleural effusion and ascites. Colonoscopy revealed an ileocecal tumor, but biopsy failed to yield a definitive diagnosis. As further H. Kato K. Kohata J. Yamamoto S. Ichikawa K. Ishizawa H. Harigae (&) Department of Hematology and Rheumatology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-cho, Aoba-ku, Sendai, Miyagi 980-8574, Japan e-mail: harigae@mail.tains.tohoku.ac.jp

Strongyloides stercoralis Hyperinfection in an Immunocompetent Patient with Extreme Eosinophilia

This report examines an unusual case of Srongyloides stercoralis hyperinfection in a 63-yr-old man. The patient had a history of vitamin B deficiency, on and off diarrhea, and clinical pellagra for a decade and a half. There was also evidence of extreme eosinophilia. The patient did not have any associated illness suggestive of immunosuppression. Treatment with ivermectin resulted in remarkable clinical improvement and reversion of eosinophil count to normal.

Chronic eosinophilic leukemia in a cat: cytochemical and immunophenotypical features

A 3-year-old, male, domestic shorthaired cat was presented with a 3-day history of anorexia and depression. The cat was moderately dehydrated, had pale, slightly icteric, mucous membranes, oral ulcerations, and mild hepatosplenomegaly. A feline leukemia virus (FeLV) antigen test was positive. CBC results obtained at initial presentation included severe normocytic, normochromic, nonregenerative anemia, severe thrombocytopenia, and marked leukocytosis (>100,000/microL) with 77% eosinophils. After 15 days of treatment with prednisone and doxycycline, the cat had persistent severe nonregenerative anemia (HCT 3.4%), thrombocytopenia (28,000/microL), and extreme eosinophilia (total eosinophils, 123.1 x 10(3)/microL; segmented 103.0 x 10(3)/microL; immature 20.1 X 10(3)/microL). Cytologic examination of aspirates from bone marrow, liver, lymph nodes, and spleen revealed a predominance of mature and immature eosinophils, many with dysplastic changes. The M:E ratio was 96.4. On histopathologic examination, multiple organs were infiltrated by eosinophilic granulocytes. Neoplastic cells in blood and bone marrow stained positive for alkaline phosphatase and were negative for myeloperoxidase, chloroacetate esterase, and alpha-naphthyl acetate esterase. On flow cytometric analysis of peripheral blood, the neoplastic cells were positive for CD11b and CD14. These findings were consistent with chronic eosinophilic leukemia. To our knowledge, this is the first report of chronic eosinophilic leukemia in a cat associated with naturally acquired FeLV infection, in which flow cytometry was used to characterize the neoplastic cells.

Hypereosinophilia with systemic thrombophlebitis

A 34-year-old Japanese woman developed subcutaneous induration in the left thigh, then showed extreme eosinophilia, and died of hemorrhagic infarction of the brain. Autopsy revealed endocarditis with eosinophil infiltration and systemic thrombophlebitis, including pulmonary veins and intrahepatic branches of the portal vein. Arterial structure was relatively preserved. She had no clinical history of asthma and had anti-ascarid IgE antibody at postmortem serological examination; thus, her disease does not fulfill the diagnostic criteria of Churg-Strauss syndrome and idiopathic hypereosinophilic syndrome (HES). Her organ involvement is, however, consistent with that of HES; thus, her pathophysiological conditions would resemble those of HES. Systemic thrombophlebitis without arterial lesion in patients with hypereosinophilia has never been reported, and this case would broaden the spectrum of vascular lesions in these patients.

Extreme eosinophilia with disseminated eosinophilic granulomatous disease in a horse.

Extreme eosinophilia with disseminated eosinophilic granulomatous disease is described in a 4-year-old Arabian mare. Clinical signs included weight loss, coughing, jugular distention, and ventral edema. Cutaneous lesions were not observed. Eosinophilic inflammation was observed in cytologic specimens from the respiratory tract, body cavities, and lymph nodes. At necropsy, a 20-cm diameter intrathoracic mass was observed. Smaller nodules were present in the lymph nodes, liver, spleen, adrenal glands, pancreas, and skeletal muscle. Histologically, these masses and nodules were characterized by infiltrates of eosinophils, macrophages, and multinucleated giant cells, reactive fibroplasia; and multifocal eosinophilic coagula. Microscopically, mild eosinophilic infiltrates were observed in sections of stomach, small intestine, colon, and pleura; however, gross lesions were not observed in these tissues at necropsy. The etiology of the extreme eosinophilia and disseminated eosinophilic granulomatous disease in this horse was not determined.

Hypereosinophilic Syndrome Resembling Chronic Inflammatory Bowel Disease with Primary Sclerosing Cholangitis

A patient who presented with chronic inflammation of the colon, and initially also the terminal ileum, accompanied by marked diarrhea, is described. Repeated high-dose steroid therapy was only temporarily successful, and symptoms recurred upon dose reduction. During the further course of the disease, a marked elevation of alkaline phosphatase and transaminases, as well as soft tissues swelling occurred. Clinically, the diagnosis of inflammatory bowel disease with primary sclerosing cholangitis was made. Irregularities in the walls of the common bile duct and the intrahepatic ducts seen at endoscopic retrograde cholangiopancreatography were consistent with the latter diagnosis. However, extreme eosinophilia of peripheral blood, bone marrow and bowel mucosa was present, and liver histology showed eosinophilic cholangiohepatitis. Under the diagnosis of hypereosinophilic syndrome with involvement of bowel, liver and biliary system, therapy with hydroxyurea was initiated. The patient's condition improved promptly. Eosinophil count and liver enzymes have remained normal under long-term medication with 1.0 g per day of this drug.

Idiopathic Hypereosinophilic Syndrome Terminating in Acute Lymphoblastic Leukemia

Idiopathic hypereosinophilic syndrome (IHES) is a heterogeneous group of disorders characterized by multisystem dysfunction and persistent, extreme eosinophilia of unknown cause. We describe a 9-1/2-year-old boy whose course included several unusual clinical features and terminated 2 years after diagnosis in acute lymphoblastic leukemia (ALL). Serial studies suggest that leukemia was not present earlier in his course. We speculate that this child may have had an evolving lymphoproliferative syndrome with a terminal blast crisis to which the eosinophilia was a nonmalignant leukemoid reaction.

Extreme eosinophilia during imipramine therapy.

Extreme eosinophilia during imipramine therapy.

VISCERAL LARVA MIGRANS

An analysis has been presented of the clinical features of visceral larva migrans based on the study of 20 cases seen during a 10-year period at the Ochsner Clinic. The disease is seen in small children who eat dirt and who thus ingest the ova of the canine roundworm, Toxocara canis. Larvae of the parasite invade the liver, causing hepatomegaly with extreme eosinophilia, and usually fever and anemia. Migration of the larvae to other organs may result in pneumonitis, encephalitis or myocarditis. Lesions may also be seen in skin, kidneys and possibly in bone. Proof of diagnosis requires biopsy of liver or other infected tissue. Treatment with diethylcarbamazine (Hetrazan) may be helpful, but even without treatment, once pica is stopped most patients recover. Serious sequelae are seen in the form of intraocular granulomata, sometimes causing blindness. These lesions, because they resemble retinoblastoma, have in the past led to unnecessary enucleation of the eye. Enucleation for suspected retinoblastoma, therefore, should not be performed without due consideration of the possibility of a benign granuloma caused by T. canis.

Eosinophilic leukemia: Report of a case, with review and classification

A patient with eosinophilic leukemia is described. Twenty acceptable cases of eosinophilic leukemia from the literature are reviewed. The diagnosis of eosinophilic leukemia cannot be definitely established unless there is an abnormal number of immature cells in the blood and tissues. When one is confronted with a patient who has an extreme eosinophilia consisting only of mature cells the diagnosis must be one of exclusion. The clinical, physical, laboratory and pathologic findings in eosinophilic leukemia are reviewed.

PULMONARY INFILTRATION WITH EOSINOPHILIA (LÖFFLER'S SYNDROME) DUE TO SMOKE INHALATION: REPORT OF A CASE AND COMMENT ON PATHOGENESIS

Case Reports1 September 1958PULMONARY INFILTRATION WITH EOSINOPHILIA (LÖFFLER'S SYNDROME) DUE TO SMOKE INHALATION: REPORT OF A CASE AND COMMENT ON PATHOGENESISWILLIAM TSCHUMY JR., M.D.WILLIAM TSCHUMY JR., M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-49-3-665 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptRecent reviews1, 2, 3 have emphasized the numerous and varied agents which may be responsible for the clinical syndrome of pulmonary infiltration with peripheral blood eosinophilia. It has become increasingly apparent that, in spite of the multiple causes, the basic pathogenesis probably represents a hypersensitivity reaction to various antigens to which the pulmonary tissues may be exposed. A review of the literature has failed to reveal a previously reported case following inhalation of smoke fumes. The present case demonstrates certain features suggesting a delayed allergic inflammatory reaction in the pulmonary interstitial tissues.CASE REPORTA 40 year old white fireman...Bibliography1. CroftonLivingstoneOswaldRoberts JWJLNCAT: Pulmonary eosinophilia, Thorax 7: 1, 1952. CrossrefMedlineGoogle Scholar2. Dias-RiveraRamos-MoralesCintron-Rivera RSFAA: Infiltrative eosinophilia, Arch. Int. Med. 94: 102, 1954. CrossrefGoogle Scholar3. ReederGoodrich WHBE: Pulmonary infiltration with eosinophilia (PIE syndrome), Ann. Int. Med. 36: 1217, 1952. LinkGoogle Scholar4. Engel D: Uber eine eigenartige, anaphylaktische Erkrankung der Lunge, Beitr. z. Klin. Tuberk. 87: 239, 1935. CrossrefGoogle Scholar5. Meyer HE: Zur Kenntnis fluchtiger mit Eosinophilie im Blut einhergehender Lungeninfiltrate, Med. Welt 11: 1808, 1937. Google Scholar6. WillettOppenheim FME: Pulmonary infiltrations with associated eosinophilia, Am. J. M. Sc. 212: 608, 1946. CrossrefMedlineGoogle Scholar7. HerbutKinsey PAR: Transitory pulmonary infiltrations (Loeffler's syndrome) in rabbits, Arch. Path. 41: 489, 1946. Google Scholar8. Harkavy J: Vascular allergy. III, J. Allergy 14: 507, 1943. CrossrefGoogle Scholar9. BaggenstossBayleyLindberg AHECDO: Loeffler's syndrome: report of a case with pathologic examination of the lung, Proc. Staff Meet., Mayo Clin. 21: 457, 1946. MedlineGoogle Scholar10. ChurgStrauss JL: Allergic granulomatosis, allergic angiitis, and periarteritis nodosa, Am. J. Path. 27: 277, 1951. MedlineGoogle Scholar11. ZuelzerApt WWL: Disseminated visceral lesions associated with extreme eosinophilia, Am. J. Dis. Child. 78: 153, 1949. CrossrefMedlineGoogle Scholar12. Bergstrand H: Morphological equivalents in polyarthritis rheumatica, periarteritis nodosa, transient eosinophilic infiltration of the lung and other allergic syndromes, J. Path. and Bact. 58: 399, 1946. CrossrefMedlineGoogle Scholar13. Braunstein H: Periarteritis nodosa limited to the pulmonary circulation, Am. J. Path. 31: 837, 1955. MedlineGoogle Scholar14. Löffler W: Zur Differential-Diagnose der Lungeninfiltrierungen: Ueber fluchtige Succedan-Infiltrate (mit Eosinophilie), Beitr. z. Klin. Tuberk. 79: 368, 1932. CrossrefGoogle Scholar15. MoritzHenriquesMcLean AEFCR: The effects of inhaled heat on the air passages and lungs, Am. J. Path. 21: 311, 1945. MedlineGoogle Scholar16. HendersonHaggard YHE: Noxious gases and the principles of respiration influencing their action, 2nd Ed., 1943, Reinhold Publishing Corp., New York. Google Scholar17. Hunter D: The diseases of occupations, 1955, Little, Brown and Co., Boston. Google Scholar18. DelaneySchmidtStroebel LTHWCF: Silo-filler's disease, Proc. Staff Meet., Mayo Clin. 31: 189, 1956. MedlineGoogle Scholar19. LowrySchuman TLM: "Silo-filler's disease"—a syndrome caused by nitrogen dioxide, J. A. M. A. 162: 153, 1956. CrossrefMedlineGoogle Scholar20. Grayson RR: Silage gas poisoning: nitrogen dioxide pneumonia, a new disease in agricultural workers, Ann. Int. Med. 45: 393, 1956. LinkGoogle Scholar21. Landsteiner K: The specificity of serological reactions, 1946, The Harvard University Press, Cambridge, Massachusetts. Google Scholar22. KassFinland EHM: Role of adrenal steroids in infection and immunity, New England J. Med. 244: 464, 1951. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Dallas, Texas*Received for publication March 1, 1957.From the Department of Internal Medicine, University of Texas Southwestern Medical School, Dallas, Texas.Requests for reprints should be addressed to William O. Tschumy, Jr., M.D., 1616 Medical Arts Building, Dallas 1, Texas. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byPulmonary Infiltrations with Eosinophilia as a Manifestation of CarcinomaThe Allergist and the Eosinophil 1 September 1958Volume 49, Issue 3Page: 665-672KeywordsAllergensAllergy and immunologyAntigensEosinophiliaFibrosisHypersensitivityInhalationPathogenesisProteinsVasculitis ePublished: 1 December 2008 Issue Published: 1 September 1958 PDF downloadLoading ...

Granuloma Faciale

In the February, 1947, issue of the Archives of Dermatology and Syphilology a resume, consisting of four articles, on the subject of eosinophilic granuloma of the skin, appeared. Dobes and Weidman discussed the case of granulomatous Hodgkin's disease of the skin with extreme eosinophilia. They thought that their thinking was too extreme to classify this as a case of eosinophilic granuloma but left the door open for it to qualify in the future, if such an entity as eosinophilic granuloma should be established. 1 Lewis and Cormia discussed the theoretic and practical considerations based on the study of a case of eosinophilic granuloma. 2 Lever discussed the eosinophilic granuloma of the skin in relation to erythema elevatum diutinum and eosinophilic granuloma of the bone. 3 Weidman discussed the eosinophilic granulomas of the skin. 4 In the October, 1948, Archives of Dermatology and Syphilology , Lever, Lane, Downing, and Spangler reported three

Extreme eosinophilia in childhood.

Extreme eosinophilia in childhood.

Extreme eosinophilia, increased blood heterophile-agglutination titer, and hyperglobulinemia.

PERSISTENT and marked eosinophilia of the blood is found in a variety of conditions, including parasitic infections, various skin diseases, allergic conditions, periarteritis nodosa, dermatomyositis, erythema multiforme, leukemia, Hodgkin's disease, rheumatoid arthritis, and convalescence after various infectious diseases; but there still remain isolated cases in which extreme eosinophilia occurs but which do not seem to fit any of the above categories. These have been classified as extreme eosinophilia and leucocytosis, 1 eosinophilia with splenomegaly, 2 chronic eosinophilia, 3 Loffler's syndrome, 4 eosinophilia leucemoides, 5 and familial eosinophilia. 6 However, it would appear that they may all be part of a clinical entity which was recently described by Zuelzer and Apt 7 under the title Disseminated Visceral Lesions Associated with Extreme Eosinophilia. The purpose of this paper is to present the case of a 27-month-old child in which there were many of the clinical and laboratory findings described by Zuelzer and

Extreme Eosinophilia and Leukocytosis in Connection with Bronchial Asthma

Extreme Eosinophilia and Leukocytosis in Connection with Bronchial Asthma