DOCSLIB.ORG

Hypereosinophilic Syndrome Presenting As an Unusual Triad of Eosinophilia, Severe Thrombocytopenia, and Diffuse Arterial Thromboses, with Good Response to Mepolizumab

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Hypereosinophilic Syndrome Presenting As an Unusual Triad of Eosinophilia, Severe Thrombocytopenia, and Diffuse Arterial Thromboses, with Good Response to Mepolizumab H & 0 C l i n i C a l C a s e s t u d i e s Hypereosinophilic Syndrome Presenting As an Unusual Triad of Eosinophilia, Severe Thrombocytopenia, and Diffuse Arterial Thromboses, With Good Response to Mepolizumab 1Department of Internal Medicine, University of Iowa 1 Roberto A. Leon-Ferre, MD Hospitals and Clinics, Iowa City, Iowa; 2Division of 2 Catherine R. Weiler, MD, PhD Allergic Diseases and Internal Medicine, Mayo Clinic, Thorvardur R. Halfdanarson, MD3 Rochester, Minnesota; 3Division of Hematology and Medical Oncology, Mayo Clinic Arizona, Scottsdale, Arizona Case Report Complement studies were normal. Fluorescence in situ hybridization (FISH) screening for FIP1L1-PDGFRA A previously healthy 47-year-old man presented with rearrangement was negative. A bone marrow biopsy 3 weeks of bilateral hand numbness, tingling, cyanosis, revealed a normocellular marrow, with marked eosino- and newly onset lower extremity edema and petechiae. philia (47%), adequate numbers of megakaryocytes, and On examination, both hands were dusky, cold, and exqui- no increase in blasts, mast cells, or reticulin fibrosis. Cyto- sitely tender. Bilateral radial pulses and left popliteal pulse genetic studies showed no abnormalities. Peripheral blood were not palpable. No lymphadenopathy, organomegaly, flow cytometry did not identify monoclonal cell popula- or masses were detected. Initial workup revealed severe tions, and no underlying T-cell clone was detected using a eosinophilia and thrombocytopenia (white blood cell T-cell receptor gene rearrangement polymerase chain reac- count, 20.3 × 103/μL; eosinophil count, 10.9 × 103/μL; tion (PCR) study. Serum protein electrophoresis, serum platelet count, 8 × 103/μL), and normal hemoglobin immunofixation electrophoresis, and urine immunofixa- of 15.2 g/dL. A peripheral blood smear (PBS) showed tion electrophoresis were all negative. Cryoglobulins were markedly increased eosinophils and decreased platelets. not detected. Hepatitis serologies were negative. Extensive No platelet clumps, schistocytes, or blasts were seen. A hypercoagulability workup was unrevealing. There was no magnetic resonance angiography (MRA) of the extremi- evidence of disseminated intravascular coagulation (DIC) ties revealed multiple arterial thromboses involving both or thrombotic thrombocytopenic purpura (TTP). Com- upper extremities and the left lower extremity. puted tomography (CT) of the chest, abdomen, and pelvis An investigation for underlying causes of eosinophilia did not show evidence of malignancy. An echocardiogram and thrombophilia was pursued. There was no recent was normal, with no evidence of intracardiac thrombus, travel history or use of suspicious medications. Parasitic patent foramen ovale, or cardiomyopathy. Given the lack infestation was ruled out with serial stool ova and parasites of a readily apparent cause for secondary eosinophilia and test (O&P), and serology was negative for strongyloides, the presence of thrombotic complications, the patient toxoplasma, toxocara, entamoeba, and trichinosis, among was diagnosed with life- and limb-threatening hypere- others. Serologic studies for connective tissue disease and osinophilic syndrome (HES), without evidence of cardiac, vasculitides were negative. Serum interleukin-5 (IL-5) renal, or pulmonary involvement. and tryptase were normal. Immunoglobulin E (IgE) was The patient was given 1 gram of intravenous slightly elevated at 178 IU/mL (reference, 0–100 IU/mL). (IV) methylprednisolone, which was followed by prednisone 1 mg/kg/day. Due to his extensive arte- Address correspondence to: rial thromboses, anticoagulation with IV heparin Roberto A. Leon-Ferre, MD, Department of Internal Medicine, University of Iowa was initiated, and he underwent multiple thrombec- Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA 52242; Phone: 319-356- 1616; Fax: 319-384-8955; E-mail: [email protected]. tomies. The anticoagulation was later transitioned Clinical Advances in Hematology & Oncology Volume 11, Issue 5 May 2013 317 LEON-FERRE ET AL to warfarin. The platelet count recovered within 2 The lack of a readily apparent cause of reactive eosino- weeks and the eosinophil count normalized within 3 philia should raise concern for clonal eosinophilic prolifera- weeks. Prednisone was slowly tapered over the follow- tions. Evaluation for these should include a careful review ing month. When the dose was down to 20 mg/day, of the PBS, measurement of serum tryptase (for evidence he developed chest pain and recurrent eosinophilia and of underlying myeloid malignancies), IL-5, bone marrow thrombocytopenia, requiring a dose increase in pred- biopsy, screening for FIP1L1-PDGFRA rearrangement nisone back to 1 mg/kg/day, with a prompt symptom (if positive, a working diagnosis of FIP1L1-PDGFRA– resolution and normalization of eosinophil and platelet associated neoplasm is made), cytogenetic studies (in counts. Two subsequent attempts in tapering the pred- search of clonal eosinophilia mutations), and peripheral nisone were unsuccessful and complicated by recurrent blood lymphocyte phenotyping and T-cell receptor gene eosinophilia, thrombocytopenia, and new extremity rearrangement studies (to exclude lymphocytic-variant arterial thromboses. Interferon-α (IFN-α) was started hypereosinophilia).1 Of note, FIP1L1-PDGFRA fusion is as a steroid-sparing agent at an initial dose of 3 million often karyotypically occult, which makes FISH screening units subcutaneously 3 times weekly (TIW), and was mandatory. If this workup is unrevealing, idiopathic HES later increased to 5 million units TIW due to persistent should be considered. digit ischemia and eosinophilia, but was subsequently The diagnosis of HES is established by fulfilling 3 discontinued due to lack of efficacy. A trial of imatinib criteria: 1) hypereosinophilia (blood eosinophilia with or (Gleevec, Novartis) 400 mg/day was pursued, without without tissue eosinophilia), 2) hypereosinophilia-related noticeable added benefit and worsening thrombocyto- organ damage, and 3) absence of an alternative explana- penia, prompting its discontinuation after 2 weeks. At tion for the observed organ damage.2 Eosinophil-related 7 months from diagnosis, IV mepolizumab 750 mg every organ damage refers to eosinophil infiltration associated 4 weeks was started. Adequate control of eosinophilia and with organ dysfunction that is seen with 1 or more of the thrombocytopenia was achieved; however, in spite of this following: fibrosis (lung, heart, gastrointestinal tract, skin, and the warfarin treatment, the patient developed recur- or others); thrombosis with or without thromboembolism; rent thrombosis, which resulted in index finger necrosis, cutaneous and mucosal erythema, edema/angioedema, infection, and subsequent amputation. Pathology of ulceration, or eczema; peripheral or central neuropathy the amputated finger revealed an organized blood clot with chronic or recurrent neurologic deficit; and other less with no evidence of vasculitis. His anticoagulation was common organ manifestations. In our patient, the major changed to low-molecular-weight heparin (LMWH), organ damage was a consequence of arterial thromboses. and with the third mepolizumab dose, hydroxyurea 500 Thrombocytopenia or thrombocytosis are noted in mg twice daily (BID) was started. Since then, predni- approximately 31% and 16% of HES cases, respectively.3 sone was slowly and successfully tapered, and ultimately Severe thrombocytopenia, as in our patient, is very infre- discontinued at 18 months from the time of diagnosis. quent, and appears to correlate with disease severity and At 44 months from diagnosis, the patient continues to treatment refractoriness.3 Approximately 25% of patients do well without steroids, and has not experienced recur- develop thromboembolic complications, most commonly rence of thrombosis, thrombocytopenia, or eosinophilia. venous (pulmonary, cutaneous, cerebral, hepatic, or portal He remains on monthly mepolizumab, now once-daily veins) or intracardiac.4,5 Arterial thrombosis, especially hydroxyurea, and lifelong anticoagulation with LMWH. with resultant digit necrosis, is exceedingly rare.4,6-9 Most arterial occlusions in reality reflect peripheral embolism discussion from intracardiac thrombi or the presence of vasculitis. Rare cases of DIC or TTP have also been reported.5 In our Persistent eosinophilia can be reactive (cytokine-driven in patient, the arterial thromboses were not associated with response to allergy, inflammation, or neoplasms), clonal vasculitis, and intracardiac thrombi were not identified by (in which the eosinophils themselves are considered echocardiogram. It is possible, however, that small intra- neoplastic), or idiopathic. Evaluation must include a cardiac thrombi may have been present and could not be complete history (including travel and medications) and visualized. A similar case of HES with thrombocytopenia physical exam. Serial stool cultures (especially for stron- and thrombosis was reported by Sherer and associates.10 gyloides, other ova, and parasite testing) and serologic However, their patient had venous thrombosis instead studies for specific parasites should be obtained. Evidence of arterial, and the thrombocytopenia was not as severe for underlying allergy, connective tissue disease, vasculitis, (69 × 103/μL). Their patient responded well to steroids, in organ-restricted eosinophilic disorders (pulmonary or gas- contrast to our patient, who had a much more protracted trointestinal eosinophilic disease), adrenal
Load more

Recommended publications
  • Hypersensitivity Reactions (Types I, II, III, IV)
    Hypersensitivity Reactions (Types I, II, III, IV) April 15, 2009 Inflammatory response - local, eliminates antigen without extensively damaging the host’s tissue. Hypersensitivity - immune & inflammatory responses that are harmful to the host (von Pirquet, 1906) - Type I Produce effector molecules Capable of ingesting foreign Particles Association with parasite infection Modified from Abbas, Lichtman & Pillai, Table 19-1 Type I hypersensitivity response IgE VH V L Cε1 CL Binds to mast cell Normal serum level = 0.0003 mg/ml Binds Fc region of IgE Link Intracellular signal trans. Initiation of degranulation Larche et al. Nat. Rev. Immunol 6:761-771, 2006 Abbas, Lichtman & Pillai,19-8 Factors in the development of allergic diseases • Geographical distribution • Environmental factors - climate, air pollution, socioeconomic status • Genetic risk factors • “Hygiene hypothesis” – Older siblings, day care – Exposure to certain foods, farm animals – Exposure to antibiotics during infancy • Cytokine milieu Adapted from Bach, JF. N Engl J Med 347:911, 2002. Upham & Holt. Curr Opin Allergy Clin Immunol 5:167, 2005 Also: Papadopoulos and Kalobatsou. Curr Op Allergy Clin Immunol 7:91-95, 2007 IgE-mediated diseases in humans • Systemic (anaphylactic shock) •Asthma – Classification by immunopathological phenotype can be used to determine management strategies • Hay fever (allergic rhinitis) • Allergic conjunctivitis • Skin reactions • Food allergies Diseases in Humans (I) • Systemic anaphylaxis - potentially fatal - due to food ingestion (eggs, shellfish,
    [Show full text]
  • Bronchopulmonary Aspergillosis
    Thorax: first published as 10.1136/thx.44.11.919 on 1 November 1989. Downloaded from Thorax 1989;44:919-924 Pulmonary eosinophilia with and without allergic bronchopulmonary aspergillosis B J CHAPMAN, S CAPEWELL, R GIBSON, A P GREENING, G K CROMPTON From the Respiratory Unit, Northern General Hospital, Edinburgh ABSTRACT Sixty five patients with pulmonary eosinophilia attending one respiratory unit were reviewed. All had fleeting radiographic abnormalities and peripheral blood eosinophil counts greater than 500 x 106/1. Eighteen had a single episode and 47 recurrent episodes during a median follow up period of 14 years. Thirty three patients had allergic bronchopulmonary aspergillosis on the basis of a positive skin test response to Aspergillusfumigatus, serum precipitins, or culture ofAfumigatus from sputum, or a combination of these. All but seven patients had asthma, six of the seven being in the group who did not have allergic bronchopulmonary aspergillosis. The patients with allergic bronchopulmonary aspergillosis were more often male and had a greater incidence ofasthma and an earlier age of onset of asthma than those without aspergillosis. The patients with aspergillosis had lower mean blood eosinophil counts and more episodes of pulmonary eosinophilia and more commonly had radiographic shadowing that suggested fibrosis or bronchiectasis (20 v 7). Pulmonary eosinophilia associated with allergic bronchopulmonary aspergillosis appears to be a distinct clinical syndrome resulting in greater permanent radiographic abnormality despite lower peripheral blood eosinophil counts. copyright. Introduction ated from secondary and tertiary referral centres, which makes it difficult to estimate the relative The term pulmonary eosinophilia describes a group of frequency of the various underlying conditions.
    [Show full text]
  • The Role of Eosinophils in Parasitic Helminth Infections: Insights from Genetically Modified Mice C.A
    Reviews The Role of Eosinophils in Parasitic Helminth Infections: Insights from Genetically Modified Mice C.A. Behm and K.S. Ovington Eosinophilia – an increase in the number of eosinophils in the it has been shown that IL-5, found at high levels in blood or tissues – has historically been recognized as a dis- helminth-infected hosts during the T-helper type 2 tinctive feature of helminth infections in mammals. Yet the (Th2) cytokine-biased immune response, appears to be precise functions of these cells are still poorly understood. important in mucosal immune responses and is re- Many scientists consider that their primary function is pro- sponsible for helminth-induced eosinophilia. IL-5 pre- tection against parasites, although there is little unequivocal sents quite a puzzle for immunologists. It has been in vivo evidence to prove this. Eosinophils are also respon- highly conserved during mammalian evolution – sible for considerable pathology in mammals because they are mouse IL-5, for example, has 71% amino acid identity inevitably present in large numbers in inflammatory lesions with human IL-5 – which suggests it has important associated with helminth infections or allergic conditions. In function(s) that have been selected during evolution. this review, Carolyn Behm and Karen Ovington outline some However, functions exclusive to IL-5 are not numer- of the cellular and biological properties of eosinophils and ous, and none appears to be essential for survival, at evaluate the evidence for their role(s) in parasitic infections. least for mice living in laboratory conditions. In mice, IL-5 controls or influences the development of two Eosinophils or ‘eosinophilic granulocytes’ normally major cell types: the elevated rate of development, mat- comprise only a small fraction (,1–5%) of circulating uration and survival of eosinophils during a Th2 cyto- leukocytes.
    [Show full text]
  • Eosinophilic Myocarditis Presenting with Hypoactive Delirium and Cardioembolic Stroke
    PRACTICE | CASES CPD Eosinophilic myocarditis presenting with hypoactive delirium and cardioembolic stroke Ka Hong Chan MD, Paul Gibson MD n Cite as: CMAJ 2019 October 21;191:E1159-63. doi: 10.1503/cmaj.190669 64-year-old woman with normal baseline functioning presented to hospital with an altered level of conscious- KEY POINTS ness. She had a history of hypertension (perindopril Hypereosinophilic syndrome is a rare condition manifested by 8 mg/d),A gout (allopurinol 200 mg/d) and anxiety (sertraline • hypereosinophilia with ensuing end-organ damage secondary 100 mg/d). She was brought to the hospital by her husband to tissue infiltration and inflammation by these cells; cardiac because of a 3-day history of being in a hypoactive state with uri- involvement from hypereosinophilic syndrome is known as nary and stool incontinence. Her husband reported no preceding eosinophilic myocarditis. infectious, allergic or constitutional symptoms. Family history • The pathophysiology of eosinophilic myocarditis is characterized and rheumatologic review of systems were noncontributory, and by 3 phases: acute necrosis (asymptomatic), thrombosis the patient had no recent history of rashes. There had been no (presents with secondary embolic phenomenon) and fibrosis (most common presentation; presents with cardiomyopathy). out-of-country travel in the preceding 2 years. Treatment of eosinophilic myocarditis relies on elucidating the On admission, the patient’s temperature was 36.3°C, she had a • underlying cause of eosinophilia, which can be broadly regular heart rate of 103 beats/min, her blood pressure was categorized as idiopathic, hypersensitivity, rheumatologic, 128/78 mm Hg and oxygen saturation was 95% on room air.
    [Show full text]
  • Original Article Anemia, Leukocytosis and Eosinophilia in a Resource-Poor
    Original Article Anemia, leukocytosis and eosinophilia in a resource-poor population with helmintho-ectoparasitic coinfection Daniel Pilger1, Jörg Heukelbach2, Alexander Diederichs1, Beate Schlosser1, Cinthya Pereira Leite Costa Araújo3, Anne Keysersa1, Oliver Liesenfeld1, Hermann Feldmeier1 1Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin, Institute of Microbiology and Hygiene, D-12203 Berlin, Germany 2Department of Community Health, School of Medicine, Federal University of Ceará, Fortaleza, CE 60430-140, Brazil 3Department of Hematology, Estate University of Health Science of Alagoas, Alagoas, CEP 57010-300, Brazil Abstract Introduction: Eosinophilia and anemia are very common hematological alterations in the tropics but population-based studies scrutinizing their value for diagnosing parasitic infections are rare. Methodology: A cross-sectional study was conducted in a rural district in northeast Brazil where parasitic infections are common. Stool and blood samples were collected and individuals were clinically examined for the presence of ectoparasites. Results: In total, 874 individuals were examined. Infection with intestinal helminths occurred in 70% (95% CI 67 – 75), infestation with ectoparasites in 45% (95% CI 42 - 49) and co-infection with both helminths and ectoparasites was found in 33% (95% CI 29% - 36%) of all inhabitants. Eosinophil counts ranged from 40/µl to 13.800/µl (median: 900/µl). Haemoglobin levels ranged from 4.8 g/dl to 16.8 g/dl (median: 12.5 g/dl), and anemia was present in 24% of the participants. Leukocytosis was found in 13%, eosinophilia in 74%, and hypereosinophilia in 44% of the participants. Eosinophilia was more pronounced in individuals co-infected with intestinal helminths and ectoparasites (p < 0.001) and correctly predicted parasitic infection in 87% (95% CI 84%-90.7%) of all cases.
    [Show full text]
  • I M M U N O L O G Y Core Notes
    II MM MM UU NN OO LL OO GG YY CCOORREE NNOOTTEESS MEDICAL IMMUNOLOGY 544 FALL 2011 Dr. George A. Gutman SCHOOL OF MEDICINE UNIVERSITY OF CALIFORNIA, IRVINE (Copyright) 2011 Regents of the University of California TABLE OF CONTENTS CHAPTER 1 INTRODUCTION...................................................................................... 3 CHAPTER 2 ANTIGEN/ANTIBODY INTERACTIONS ..............................................9 CHAPTER 3 ANTIBODY STRUCTURE I..................................................................17 CHAPTER 4 ANTIBODY STRUCTURE II.................................................................23 CHAPTER 5 COMPLEMENT...................................................................................... 33 CHAPTER 6 ANTIBODY GENETICS, ISOTYPES, ALLOTYPES, IDIOTYPES.....45 CHAPTER 7 CELLULAR BASIS OF ANTIBODY DIVERSITY: CLONAL SELECTION..................................................................53 CHAPTER 8 GENETIC BASIS OF ANTIBODY DIVERSITY...................................61 CHAPTER 9 IMMUNOGLOBULIN BIOSYNTHESIS ...............................................69 CHAPTER 10 BLOOD GROUPS: ABO AND Rh .........................................................77 CHAPTER 11 CELL-MEDIATED IMMUNITY AND MHC ........................................83 CHAPTER 12 CELL INTERACTIONS IN CELL MEDIATED IMMUNITY ..............91 CHAPTER 13 T-CELL/B-CELL COOPERATION IN HUMORAL IMMUNITY......105 CHAPTER 14 CELL SURFACE MARKERS OF T-CELLS, B-CELLS AND MACROPHAGES...............................................................111
    [Show full text]
  • Persistent Eosinophilia Is a Challenging Problem
    DOI: 10.26717/BJSTR.2017.01.000244 Nahla A M Hamed. Biomed J Sci & Tech Res ISSN: 2574-1241 Editorial Open Access Persistent Eosinophilia is a Challenging Problem Nahla AM Hamed* Professor of Hematology, Faculty of Medicine, Alexandria University, Egypt Received: July 25, 2017; Published: August 01, 2017 *Corresponding author: Nahla AM Hamed, Professor of Hematology, Faculty of Medicine, Alexandria University, Egypt Abstract 9 HE is defined as >1.5 x 10 /L eosinophils in the blood on 2 examinations (interval >1 mo) and/or tissue HE defined by: eosinophils percentage in BM section exceeding 20% of all nucleated cells; and/or extensive eosinophilic tissue infiltration by pathologist opinion; and/or presenceAbbreviations: of marked deposition of eosinophil granule proteins (in the absence or presence of major tissue eosinophils infiltration). AEC: absolute eosinophil count; HE: Hypereosinophilia; ABPA: Allergic Bronchopulmonary Aspergillosis; B-ALL: Acute B-cell lymphoblastic leukemia; GVHD: Graft-Versus-Host Disease; BM: Bone Marrow; PB: Peripheral Blood; IL5: Interleukin 5; AML: Acute Myeloid Leukemia; LV: Lymphocytic Variant; Th2:T-cells have a helper type 2; EPPER: Eosinophilic, polymorphic, and pruritic Eruption Associated with Radiotherapy; MPN: Myeloproliferative Neoplasm; HES: Hypereosinophilic Syndrome; PDGFRA: Platelet-Derived Growth Factor Receptor Alpha; PDGFRB: Platelet-Derived Growth Factor Receptor Beta; FGFR1: Fibroblast Growth Factor Receptor 1; CEL-NOS: Chronic Eosinophilic Leukemia-Not Otherwise Specified; MDS: Myelodysplastic Syndrome; IgH: Ig Heavy Chain; EBV: Epstein-Barr virus Introduction cystic structures (e.g. hydatid cyst, neurocysticercosis) are unlikely Eosinophilia3 is defined as an AEC >500/μL [1].3 The severity ), and severe to cause eosinophilia [7]. Disseminated coccidioidomycosis and of eosinophilia has3 been arbitrarily divided into mild9 (AEC: 500- aspergillosis (when presenting as ABPA) are well-known fungal 1,500/mm ), moderate (AEC: 1,500-5,000/mm causes of eosinophilia.
    [Show full text]
  • Anti-IL5 and Anti-Il5rα Therapy for Clinically Significant Bronchiectasis with Eosinophilic Endotype: a Case Series
    AGORA | RESEARCH LETTER Anti-IL5 and anti-IL5Rα therapy for clinically significant bronchiectasis with eosinophilic endotype: a case series To the Editor: Bronchiectasis is a chronic and often progressive disease, which frequently is associated with significant symptom burden, requiring intensive treatment. Regardless of the multiple potential underlying aetiologies, the vicious cycle of airway inflammation, structural airway damage, impaired mucus clearance and airway pathogen acquisition is the crucial pathogenic pathway for the progression of disease [1]. Although inflammation in bronchiectasis has been classically regarded as neutrophilic, it is increasingly recognised that eosinophils may play a role in the disease. Allergic bronchopulmonary aspergillosis (ABPA) is an example of a common cause of bronchiectasis that is primarily eosinophilic. Small studies suggest that a significant number of patients have airway eosinophilia even after exclusion of patients with underlying ABPA and asthma. TSIKRIKA et al. [2] found that among 40 patients with bronchiectasis excluding asthma and ABPA, 30% in total had sputum eosinophilia, defined as >3% cells. This supports the possibility that there may be an eosinophilic endotype of bronchiectasis, although published data on the prevalence and clinical significance of airway and systemic eosinophilia in bronchiectasis remain limited [2, 3]. Mepolizumab, a humanised monoclonal antibody, reduces eosinophil counts in blood and tissues by blocking interleukin (IL)-5, a key eosinophil cytokine, and preventing its binding to eosinophil surface receptors [4]. In patients with severe eosinophilic asthma, add-on mepolizumab treatment resulted in a decrease of exacerbation frequency, reduced symptom burden, improved of quality of life (QoL) and, moreover, had an oral corticosteroid (OCS)-sparing effect [4–8].
    [Show full text]
  • Peripheral Eosinophilia As an Indicator of Meningitic Angiostrongyliasis in Exposed Individuals
    942 Mem Inst Oswaldo Cruz, Rio de Janeiro, Vol. 105(7): 942-944, November 2010 Peripheral eosinophilia as an indicator of meningitic angiostrongyliasis in exposed individuals Kittisak Sawanyawisuth1,4/+, Kanlayanee Sawanyawisuth2, Vichai Senthong1, Panita Limpawattana1, Pewpan M Intapan3,4, Somsak Tiamkao1, Suthipun Jitpimolmard1, Verajit Chotmongkol1,4, Elizabeth Barrett-Connor5 1Department of Medicine 2Department of Biochemistry 3Department of Parasitology, Faculty of Medicine 4The Research and Diagnostic Centre for Emerging Infectious Disease, Khon Kaen University, 123 Mitraparp Friendship Rd., 40002 Khon Kaen, Thailand 5Department of Family and Preventive Medicine, School of Medicine, University of California, La Jolla, San Diego, CA, USA The diagnosis of meningitic angiostrongyliasis (MA) is based on clinical criteria. A lumbar puncture is used as a diagnostic tool, but it is an invasive procedure. The blood eosinophil levels are also assessed and used in the diag- nosis of this disease. We enrolled 47 patients with serologically proven MA and 131 controls with intestinal parasite infections. An absolute eosinophil count model was found to be the best marker for MA. An eosinophil count of more than 798 cells led to sensitivity, specificity, positive predictive and negative predictive values of 76.6%, 80.2%, 58.1% and 90.5%, respectively. These data support the use of testing for high blood eosinophil levels as a diagnostic tool for MA in individuals that are at risk for this disease. Key words: eosinophilia - diagnosis - meningitis - angiostrongyliasis - Angiostrongylus cantonensis Angiostrongylus cantonensis is the main pathogen evaluate the utility of blood eosinophils as a diagnostic that causes eosinophilic meningitis in humans (Chot- tool for meningitic angiostrongyliasis.
    [Show full text]
  • Clinical Relevance of Peripheral Blood Eosinophil Count in Allergic Bronchopulmonary Aspergillosis
    Journal of Infection and Public Health (2011) 4, 235—243 View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Clinical relevance of peripheral blood eosinophil count in allergic bronchopulmonary aspergillosis Ritesh Agarwal a,∗, Ajmal Khan a, Ashutosh N. Aggarwal a, Neelam Varma b, Mandeep Garg d, Biman Saikia c, Dheeraj Gupta a, Arunaloke Chakrabarti e a Department of Pulmonary Medicine, Postgraduate Institute of Medical Education and Research, Sector-12, Chandigarh 160012, India b Department of Hematology, Postgraduate Institute of Medical Education and Research, Chandigarh, India c Department of Immunopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India d Department of Radiodiagnosis and Imaging, Postgraduate Institute of Medical Education and Research, Chandigarh, India e Department of Medical Microbiology, Postgraduate Institute of Medical Education and Research, Chandigarh, India Received 21 February 2011; received in revised form 17 August 2011; accepted 21 August 2011 KEYWORDS Summary Allergic Background and aims: Currently, there is not a uniform consensus regarding the bronchopulmonary number of criteria or specific cut-off values for the variety of tests that are used to aspergillosis (ABPA); diagnose allergic bronchopulmonary aspergillosis (ABPA). Traditionally, an eosinophil ␮ Aspergillus fumigatus; count >1000 cells/ l is considered an important criterion in the diagnosis of ABPA. Eosinophils The goal of this study was to delineate the significance of the peripheral blood eosinophil count in the diagnosis of ABPA, and the relationship between eosinophil counts and lung function and immunological and radiological parameters. Methods: This study was a retrospective analysis of the data from ABPA patients who were managed in our chest clinic.
    [Show full text]
  • Eosinophilic Lung Diseases: Findings That a Radiologist Should Know
    Pictorial Essay Eosinophilic Lung Diseases: Findings that a Radiologist Should Know Juliana Couture1 Daniel Adri1 Juan Manuel Villegas1 Natalia Posadas1 Alberto Seehaus1 1 Imaging Diagnosis Department, Hospital Italiano de Buenos Aires, Ciudad Autónoma de Buenos Aires, Argentina Abstract Eosinophilic lung diseases include a broad spectrum of disorders. The final diagnosis of these diseases is made by patho- logical examination. However, medical history, physical examination and imaging studies allow better characterization of the condition. At present, high-resolution multislice computed tomography (MSCT) is the most sensitive and specific imaging method, since it allows an accurate assessment of diffuse pulmonary pathology, thus avoiding more invasive methods, providing detailed information and depicting lesions that have no specific clinical presentation by means of characteristic imaging patterns. Keywords Hypereosinophilic syndrome, Multislice computed tomography, Pulmonary eosinophilia Introduction depicts lesions that have no specific clinical presentation.7 The most characteristic MSCT findings of eosinophilic syn- Eosinophilic lung diseases are infectious and non-infectious dromes will be discussed below (Table 1). disorders associated with peripheral eosinophilia (a marker of pathology, exceeding 0.5 × 109/L)1,2 with tissue eosino- philia confirmed by pulmonary biopsy or an elevated eosino- Idiopathic eosinophilic lung diseases philic count (25%) in bronchoalveolar lavage (BAL) 3-5. These diseases may be classified as: idiopathic
    [Show full text]
  • A Case of Chronic Cavitary Pulmonary Aspergillosis Misdiagnose
    Misled by significant peripheral eosinophilia and travel history: a case of chronic cavitary pulmonary Aspergillosis misdiagnosed as a ruptured Echinococcus cyst Whitney Elg-Salsman,DO; Anna Brady, MD Oregon Health & Science University [ ] Introduction Imaging Discussion Chronic cavitary pulmonary CT: LLL Aspergillosis can have a diverse cavitary AspergillosisDevelopment of(CPA) a New Practice is Model clinical presentation from non- lesion and characterized by cavitary new LLL invasive Allergic Pulmonary lesion(s), elevated IgG titers to ground glass Aspergillosis (ABPA), semi- Aspergillus +/- elevated total IgE opacities and invasive chronic cavitary consolidation and Aspergillus IgE. This case accompanied Aspergillosis to invasive. illustrates the importance of by a small Her clinical presentation has keeping Aspergillus infection on pleural aspects of both ABPA (allergic effusion the differential with significant asthma and total elevated IgE) pleural eosinophilia and cavitary and chronic, semi-invasive lung lesion cavitary Aspergillosis. Take Home Points Case Description [ ] References A 53-year-old non-smoking 1.1. [ ] Differential for pleural fluid woman with well controlled eosinophilia includes: allergic asthma presented to the infection (TB, fungal, hospital with three days of dyspnea parasite), malignancy, without infectious symptoms. She GMS stain: showing Aspergillus fungal HE stain: Thick fibrotic wall with a Eosinophilic granulomatosis reported prior travel including wild hyphae with uniform septated hyphae, dense eosinophilic
    [Show full text]