Journal of Clinical and Diagnostic Research, ISSN - 0973 - 709X

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Dr. Mamta Gupta,
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Dr. Mamta Gupta
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Aug 2018

Dr. Rajendra Kumar Ghritlaharey

"I wish to thank Dr. Hemant Jain, Editor-in-Chief Journal of Clinical and Diagnostic Research (JCDR), for asking me to write up few words.
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Salient features of the JCDR: It is a biomedical, multidisciplinary (including all medical and dental specialities), e-journal, with wide scope and extensive author support. At the same time, a free text of manuscript is available in HTML and PDF format. There is fast growing authorship and readership with JCDR as this can be judged by the number of articles published in it i e; in Feb 2007 of its first issue, it contained 5 articles only, and now in its recent volume published in April 2011, it contained 67 manuscripts. This e-journal is fulfilling the commitments and objectives sincerely, (as stated by Editor-in-chief in his preface to first edition) i e; to encourage physicians through the internet, especially from the developing countries who witness a spectrum of disease and acquire a wealth of knowledge to publish their experiences to benefit the medical community in patients care. I also feel that many of us have work of substance, newer ideas, adequate clinical materials but poor in medical writing and hesitation to submit the work and need help. JCDR provides authors help in this regards.
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It is well said that "happy beginning is half done" and it fits perfectly with JCDR. It has grown considerably and I feel it has already grown up from its infancy to adolescence, achieving the status of standard online e-journal form Indian continent since its inception in Feb 2007. This had been made possible due to the efforts and the hard work put in it. The way the JCDR is improving with every new volume, with good quality original manuscripts, makes it a quality journal for readers. I must thank and congratulate Dr Hemant Jain, Editor-in-Chief JCDR and his team for their sincere efforts, dedication, and determination for making JCDR a fast growing journal.
Every one of us: authors, reviewers, editors, and publisher are responsible for enhancing the stature of the journal. I wish for a great success for JCDR."

Thanking you
With sincere regards
Dr. Rajendra Kumar Ghritlaharey, M.S., M. Ch., FAIS
Associate Professor,
Department of Paediatric Surgery, Gandhi Medical College & Associated
Kamla Nehru & Hamidia Hospitals Bhopal, Madhya Pradesh 462 001 (India)
On May 11,2011

Dr. Shankar P.R.

"On looking back through my Gmail archives after being requested by the journal to write a short editorial about my experiences of publishing with the Journal of Clinical and Diagnostic Research (JCDR), I came across an e-mail from Dr. Hemant Jain, Editor, in March 2007, which introduced the new electronic journal. The main features of the journal which were outlined in the e-mail were extensive author support, cash rewards, the peer review process, and other salient features of the journal.
Over a span of over four years, we (I and my colleagues) have published around 25 articles in the journal. In this editorial, I plan to briefly discuss my experiences of publishing with JCDR and the strengths of the journal and to finally address the areas for improvement.
My experiences of publishing with JCDR: Overall, my experiences of publishing withJCDR have been positive. The best point about the journal is that it responds to queries from the author. This may seem to be simple and not too much to ask for, but unfortunately, many journals in the subcontinent and from many developing countries do not respond or they respond with a long delay to the queries from the authors 1. The reasons could be many, including lack of optimal secretarial and other support. Another problem with many journals is the slowness of the review process. Editorial processing and peer review can take anywhere between a year to two years with some journals. Also, some journals do not keep the contributors informed about the progress of the review process. Due to the long review process, the articles can lose their relevance and topicality. A major benefit with JCDR is the timeliness and promptness of its response. In Dr Jain's e-mail which was sent to me in 2007, before the introduction of the Pre-publishing system, he had stated that he had received my submission and that he would get back to me within seven days and he did!
Most of the manuscripts are published within 3 to 4 months of their submission if they are found to be suitable after the review process. JCDR is published bimonthly and the accepted articles were usually published in the next issue. Recently, due to the increased volume of the submissions, the review process has become slower and it ?? Section can take from 4 to 6 months for the articles to be reviewed. The journal has an extensive author support system and it has recently introduced a paid expedited review process. The journal also mentions the average time for processing the manuscript under different submission systems - regular submission and expedited review.
Strengths of the journal: The journal has an online first facility in which the accepted manuscripts may be published on the website before being included in a regular issue of the journal. This cuts down the time between their acceptance and the publication. The journal is indexed in many databases, though not in PubMed. The editorial board should now take steps to index the journal in PubMed. The journal has a system of notifying readers through e-mail when a new issue is released. Also, the articles are available in both the HTML and the PDF formats. I especially like the new and colorful page format of the journal. Also, the access statistics of the articles are available. The prepublication and the manuscript tracking system are also helpful for the authors.
Areas for improvement: In certain cases, I felt that the peer review process of the manuscripts was not up to international standards and that it should be strengthened. Also, the number of manuscripts in an issue is high and it may be difficult for readers to go through all of them. The journal can consider tightening of the peer review process and increasing the quality standards for the acceptance of the manuscripts. I faced occasional problems with the online manuscript submission (Pre-publishing) system, which have to be addressed.
Overall, the publishing process with JCDR has been smooth, quick and relatively hassle free and I can recommend other authors to consider the journal as an outlet for their work."

Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
On April 2011

Dear team JCDR, I would like to thank you for the very professional and polite service provided by everyone at JCDR. While i have been in the field of writing and editing for sometime, this has been my first attempt in publishing a scientific paper.Thank you for hand-holding me through the process.

Dr. Anuradha
On Jan 2020

Important Notice

Case report
Year : 2011 | Month : June | Volume : 5 | Issue : 3 | Page : 625 - 627

Hyperesoinophilic syndrome with FIP1L1 PDGFRα mutation: A case study


Department of Pulmonary Medicine, Department of Medical Oncology Department of Medical Oncology

Correspondence Address :
Asmita A. Mehta, MD
Assistant Professor
Department of Pulmonary Medicine,
Amrita Institute Of Medical Sciences.
Kochi-682041, Kerala, India.
Tel No: +91- 9037450374 Fax: 0484-280 2177
E mail:


In India , a clinical and / or a laboratory diagnosis of hypereosinophilia is very common and is usually attributed to parasitic infestations (viz helminthiasis and filariasis) or atopy. The treatment usually includes deworming or antifilarial drugs in the filaria endemic regions. We report here, a case of hypereosinophilic syndrome ina middle-aged man, who presented with features which mimicked asthma with eosinophilia that did not respond to the routine treatment measures. He was found to have a FIP1L1-PDGFR-α mutation and he improved on treatment with the small molecule, tyrosine kinase inhibitor, Imatinib that is commonly used in patients with malignant diseases of haematological origin.


Eosinophilia, Asthma, Hypereosinophilic Syndrome, Imatinib

Eosinophilic diseases include various relatively uncommon conditions which are characterized by tissue-associated eosinophilic inflammation and, in some cases, peripheral blood eosinophilia, such as the eosinophilic gastrointestinal diseases (EGIDs), Churg-Strauss syndrome, and what is known as the hypereosinophilic syndrome (HES). No good method existed, to detect the molecular evidence of a myeloproliferative variant in the patients, until around 2003, with the discovery of an interstitial deletion on chromosome 4q12, that leads to the fusion of the FIP1-like 1 (FIP1L1) and the PDGFRα genes, with the fusion product encoding for a protein that has significant constitutive tyrosine kinase activity (6).The presence of this fusion protein was found to be responsible for pronounced eosinophilia in the affected patients. Patients who have this fusion mutation are now known to form most of the so-called myeolproliferative hypereosinophilic syndrome (M-HES) variants. Here, we are presenting one such case with the above mentioned mutation.

Case Report

A 48-year-old male, a daily wage labourer and a chronic smoker (twenty pack years), presented with the complaints of wheezing and cough of three months duration. He had stopped smoking since the onset of the symptoms (three to four months). He had no history of orthopnea, fever, weight loss, allergic rhinitis, sinusitis or epistaxis. He had already received treatment of inhaled corticosteroids for three months and a week’s course of oral steroids (prednisolone), without benefit. Thereafter, he had a three-week course of diethylcarbamazine (DEC) that again had no effect on his symptoms. He was referred to our center in March 2010, because of non-remitting wheezing and minimally productive cough, which was severe enough to prevent him from working. On clinical examination, he was found to have mild pallor, bilateral polyphonic wheezing, holosystolic murmur at the apex and mild splenomegaly. His lab investigation showed a haemoglobin level of 11.3 gm/dl, a total leukocyte count of 16500/mm3 and platlet counts 197000/mm3. His differential count showed 8% neutrophils, 9% lymphocytes, 82% eosinophils and 1% monocytes. His absolute eosinophil count was 13.43 x 109/ liter. His peripheral blood smear (Table/Fig 1) showed eosinophilia, with no immature cells. His immunoglobulin E(Ig E), anti-neutrophil cytoplasmic antibodies (ANCA) and his stool evaluation for parasites were negative. His chest radiograph (Table/Fig 2) showed prominent bronchovascular markings, with no parenchymal abnormality. He could not perform spirometry. An abdominal ultrasound confirmed splenomegaly. His 2-D echocardiography revealed severe mitral regurgitation, moderate tricuspid regurgitation and severe pulmonary artery hypertension. Oral dexamethasone (4mg twice daily) Was started, however, his blood eosinophilia persisted at 12680/mm3 . His bone marrow aspirate and trephine biopsy showed hyperproliferative marrow with eosinophilia. In view of the eosinophilia with significant cardiac involvement, a diagnosis of myeloproliferative hypereosinophilic syndrome was considered. Reverse transcriptase polymerase chain reaction(RT-PCR) analysis showed a hybrid transcript for FIP1L1-PDGFRα, which confirmed a diagnosis of FIP1L1-PDGFRα which was associated myeloproliferative hypereosinophilic syndrome (M-HES), with pulmonary and cardiac involvement. He was started on 100mg of Imatinib daily. His repeat blood count after one month of the Imatinib therapy, showed a normal eosinophil count. He is on regular follow-up and has improved symptomatically.


Elevated peripheral blood eosinophil counts are usually seen with helminthic and parasitic infections, atopy and drug hypersensitivity. (1),(2) Other less common causes of eosinophila are malignancy, connective tissue disorders, tissue-associated eosinophilic inflammation, eosinophilic gastrointestinal diseases (EGIDs), the Churg-Strauss syndrome and hypereosinophilic syndrome (HES). (3), (4) In 1975, Chusid and his colleagues defined three diagnostic criteria which have remained as the basis for the modern definition of HES (5): 1. Peripheral blood eosinophilia with the absolute eosinophil count being greater than 1500 cells/mL and it being sustained for more than 6 months. 2. No other evident cause for eosinophilia, including allergic diseases and parasitic infection. 3. Signs or symptoms of organ involvement by eosinophilic infiltration. In general, HES is seen more commonly in men than in women, with a reported male/female ratio of 9:1. Such cases have mostlybeen described in adults, with the age at diagnosis usually falling between 20 and 50 years(4),(6),(7) Nonspecific constitutional symptoms can be seen as a part of HES; the National Institutes of Health case series reported that fatigue is present in 26% of the patients and fever in 12% (8). Other presenting symptoms included cough (24%), breathlessness (16%), muscle pain (14%), angio-oedema (14%), rash (12%), and retinal lesions (10%) (7) A subset of the HES patients have an interstitial deletion in chromosome 4q12, which leads to the expression of a fusion gene, FIP1L1-PDGFRα (6),(7) Although the patients with this mutation are more adequately classified as chronic eosinophilic leukaemia (CEL) cases, given the clonal nature of the eosinophil expansion, the cells are morphologically indistinguishable from normal mature eosinophils and a large majority of the cases have a normal cytogenetic pattern. The patients therefore present clinically as typical HES cases, the only clue to the diagnosis being refractoriness to the standard modes of treatment(8)(9).

All patients who have HES, who do not respond to the initial standard therapy, should undergo an evaluation by RT-PCR or fluorescence in situ hybridization (FISH) for the presence of the FIP1L1-PDGFRα mutation, to help with the appropriate diagnosis and the guide therapy. The presence of this mutation mandates a therapy with imatinib, because these M-HES patients may be relatively refractory to corticosteroids, as was seen in our patient. (10) Imatinib selectively inhibits ABL, PDGFRα and KIT tyrosine kinases. FIP1L1-PDGFRα is particularly sensitive to Imatinib and a low initial dose is therefore appropriate. The early detection of FIP1L1-PDGFRα in patients with chronic unexplained hypereosinophilia is now considered to be critical for its optimal management, as its presence is associated with high morbidity and mortality rates. (11) There is an increased frequency of cardiac involvement in FIP1L1-PDGFRα positive HES patients(2). The pathophysiological reason for this increased tendency for endomyocardial fibrosis in the M-HES patients is unknown.(11) It may possibly be due to an eosinophil-mediated cardiac damage. The cardiac damage evolves through three stages: the acute necrotic stage, followed by the thrombotic stage, which then progresses to the fibrotic stage.(12) In the fibrotic stage, significant intramural fibrosis occurs, that leads to impaired cardiac function and output, and significant valvular damage. (2),(13). This leads to valvular dysfunction like mitral regurgitation, as was seen in our patient. Imatinib, a tyrosine kinase inhibitor, is an effective drug in PDGFRα associated HES. The Imatinib response rate in these patients is nearly 100%(14),(15). Generally, clinical improvement is seen within one month. Low dose imatinib (100 mg/d) is usually sufficient to control eosinophilia and its symptoms, as opposed to the higher doses of 400 – 800 mg which is used in chronic myeloid leukaemia. The side effects of low dose Imatinib therapy are generally mild and they rarely lead to the discontinuation of the therapy. Our patient was started on 100mg of Imatinib OD and he responded symptomatically in less than one month.


An early detection of FIP1L1-PDGFRα in patients with chronic unexplained hypereosiniphilia is critical for its optimal management and also to avoid organ damage, especially cardiac damage. The discovery of FIP1L1-PDGFRα has opened up avenues in understanding the molecular pathogenesis of HES and also the prospect of effective, molecularly targeted therapy like Imatinib.


Bain BJ. Hypereosinophilia. Curr Opin Hematol 2000; 7(1): 21–5.
Roufosse F, Cogan E, Goldman M. The hypereosinophilic syndrome revisited. Annu Rev Med 2003: 54:169-84
Klion AD, Bochner BS, Gleich GJ, et al. Approaches to the treatment of hypereosinophilc syndromes: a workshop summary report. J Allergy Clin Immunol 2006; 117:1292-302.
Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood 1994; 83: 2759–79.
Chusid MJ, Dale DC, West BC, et al. The hypereosinophilic syndrome: analysis of fourteen cases with review of the literature. Medicine (Baltimore) 1975; 54: 1–27.
Spry C. Eosinophils. A comprehensive review and guide to the scientific and medical literature. Oxford (UK): Oxford Medical Publications; 1988.
Fauci AS, Harley JB, Roberts WC, et al. NIH conference. The idiopathic hypereosinophilic syndrome. Clinical, pathophysiologic, and therapeutic considerations. Ann Intern Med 1982; 97:78–92.
Cools J, DeAngelo DJ, Gotlib J, et al. A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N Engl J Med 2003; 348: 1201–14.
Klion AD, Robyn J, Akin C, et al. Molecular remission and reversal of myelofibrosis in response to imatinib mesylate treatment in patients with the myeloproliferative variant of hypereosinophilic syndrome. Blood 2004; 103: 473– 478.
Roufosse F, Goldman M, Cogan E. Hypereosinophilic syndrome: lymphoproliferative and myeloproliferative variants. Semin Respir Semin Respir Crit Care Med 2006; 27: 158–70.
Klion AD, Noel P, Akin C, Law MA, Gilliland DG, Cools J et al. Elevated serum tryptase levels identify a subset of patients with a myeloproliferative variant of idiopathic hypereosinophilic syndrome associated with tissue fibrosis, poor prognosis, and imatinib responsiveness. Blood 2003; 101: 4660-6.
Parrillo JE. Heart disease and the eosinophil. N Engl J Med 1990; 323: 1560e1.
Brockington IF, Olsen EG. Eosinophilia and endomyocardial fibrosis. Postgrad Med J 1972; 48: 740-1.
Cools J, DeAngelo DJ, Gotlib J, et al. A tyrosine kinase created by fusion of the PDGFRα and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N Engl J Med 2003; 348: 1201–14.
Von Bubnoff N, Sandherr M, Schlimok G, et al. Myeloid blast crisis evolving during Imatinib treatment of a FIP1L1-PDGFRα positive chronic myeloproliferative disease with prominent eosinophilia. Leukemia 2005; 19: 286–287.

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