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Kazi, Nawal
- Hypereosinophilic Syndrome in Behcet’s Disease : Unearthing a Hidden Clonality
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Authors
Affiliations
1 Empire Centre Haematology and Oncology Specialty Clinic, Bandra West, Mumbai, IN
2 Dr Tahiliani’s Clinic, A-201/202, Gasper Enclave, Dr Ambedkar Road, Bandra West, Mumbai, IN
3 Empire Centre Haematology and Oncology Specialty Clinic, Hill Road, Bandra West, Mumbai, IN
1 Empire Centre Haematology and Oncology Specialty Clinic, Bandra West, Mumbai, IN
2 Dr Tahiliani’s Clinic, A-201/202, Gasper Enclave, Dr Ambedkar Road, Bandra West, Mumbai, IN
3 Empire Centre Haematology and Oncology Specialty Clinic, Hill Road, Bandra West, Mumbai, IN
Source
The Indian Practitioner, Vol 74, No 4 (2021), Pagination: 32-35Abstract
The association of hypereosinophilic syndrome (HES) and Behcet’s disease is not well understood. Commonly, patients are treated with standard medications for hypereosinophilia, with variable responses. However, persistent hypereosinophilia (absolute eosinophilic count >1500 cells/μL) not responding to standard treatment may be predictive of a primary clonal haematological disorder. According to the revised World Health Organization (WHO) classification, HES has six categories; one of which is myeloproliferative neoplasm (clonal eosinophilia) associated with FIP1-like-1-platelet-derived growth factor receptor-alpha (FIP1L1-PDGFRα). We report a case of a 38-year-old Indian male with Behcet’s disease with concomitant HES, who tested positive for clonal eosinophilia (FIP1L1-PDGFRα fusion) which is a rare imatinib-sensitive mutation. The patient was administered low-dose imatinib mesylate (100 mg daily), and showed an excellent response with complete resolution of HES. The causal relationship between Bechet’s disease and HES requires further investigation and research. Left untreated, HES has the potential to cause severe end-organ damage and this necessitates early detection and treatment which can significantly reduce patient morbidity and mortality.Keywords
Hypereosinophilia, FIP1L1-PDGFRα, Gene, Behcet’s Disease, Imatinib.
References
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- Fauci AS, Harley JB, Roberts WC, Ferrans VJ, Gralnick HR, Bjornson BH. NIH conference. The idiopathic hypereosinophilic syndrome. Clinical, pathophysiologic, and therapeutic considerations. Ann Intern Med. 1982 Jul;97(1):78-92.
- Ogbogu PU, Bochner BS, Butterfield JH, Gleich GJ, Huss Marp J, Kahn JE, Leiferman KM, Nutman TB, Pfab F, Ring J, Rothenberg ME, Roufosse F, Sajous MH, Sheikh J, Simon D, Simon HU, Stein ML, Wardlaw A, Weller PF, Klion AD. Hypereosinophilic syndrome: a multicenter, retrospective analysis of clinical characteristics and response to therapy. J Allergy Clin Immunol. 2009 Dec;124(6):1319-25.e3.
- Mashaleh MA, Burgan A, Khasawneh R, Khataybeh O, Kamal N, Heresh AA. Eosinophilic Leukemia Presenting with Behçet-Like Symptoms. Journal of the Royal Medicine Services. 2014;21(4):79-82.
- Valent P, Klion AD, Horny HP, Roufosse F, Gotlib J, Weller PF, Hellmann A, Metzgeroth G, Leiferman KM, Arock M, Butterfield JH, Sperr WR, Sotlar K, Vandenberghe P, Haferlach T, Simon HU, Reiter A, Gleich GJ. Contemporary consensus proposal on criteria and classification of eosinophilic disorders and related syndromes. J Allergy Clin Immunol. 2012 Sep;130(3):607-612.e9.
- Pardanani A, Ketterling RP, Li CY, Patnaik MM, Wolanskyj AP, Elliott MA, Camoriano JK, Butterfield JH, Dewald GW, Tefferi A. FIP1L1-PDGFRA in eosinophilic disorders: prevalence in routine clinical practice, long-term experience with imatinib therapy, and a critical review of the literature. Leuk Res. 2006 Aug;30(8):965-70.
- Challenges and Changing Trends in the Treatment of Haematological Cancers
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at a disease-free survival or clinical remission. Currently many protocols utilise a combination of drugs- one belonging to the older generations and one novel agent (chemoimmunotherapy), a combination of new agents (chemotherapy free protocols), or a combination of subcutaneous and oral medications in the treatment of various malignancies. Futuristically, our aim is to use therapy which avoids / reduces hospitalization with a finite duration of therapy, making treatment cost-effective and more compliant leading to better and deeper malignant cell destruction. However, with the ever evolving and mutating
cancer cell for its survival, novel drugs will become old tomorrow and our protocols, combinations and sequencing of drugs will change over time with the advent of new drugs. The singular end point in cancer treatment today is better efficacy, safety and user-friendly protocols (oral or subcutaneous routes) that will achieve a deep response - undetectable minimal residual disease (uMRD) that will ultimately lead to treatment discontinuation. This in turn will improve compliance, prevent unnecessary toxicity and hopefully provide a functional cure. We are nearly there but we still do not routinely use the word
cure…yet! Hopefully someday.
Authors
Affiliations
1 Haematologist, Lilavati Hospital and Research Centre; Empire Haematology Oncology Centre, Bandra west, Mumbai, IN
2 Fellow in Haematology, Lilavati Hospital and Research Centre, Bandra West, Mumbai, IN
3 Clinical Assistant, Empire Haematology Oncology Centre, Bandra west, Mumbai, IN
1 Haematologist, Lilavati Hospital and Research Centre; Empire Haematology Oncology Centre, Bandra west, Mumbai, IN
2 Fellow in Haematology, Lilavati Hospital and Research Centre, Bandra West, Mumbai, IN
3 Clinical Assistant, Empire Haematology Oncology Centre, Bandra west, Mumbai, IN
Source
The Indian Practitioner, Vol 74, No 12 (2021), Pagination: 23-31Abstract
Chemotherapy and radiotherapy were the only weapons against cancer in the past. Research has opened up many vistas for treatment— different classes of drugs, targeted therapy, monoclonal antibodies and immunotherapy to name a few—that have become available in routine practice for the treatment of cancer. This was possible due to research grants/funds and pharma interest to detect new antigens with pharmacogenomics that identified targetable drugs against the antigens on the malignant cells. Disease eradication was the end point in the past that was achieved with great difficulty. With novel agents targeting different antigens through new drug routes and newer drug combinations, including “chemotherapy free” treatment, we seem to be doing better with less toxicity in treatment naïve and relapsed patients, who can now get another shotat a disease-free survival or clinical remission. Currently many protocols utilise a combination of drugs- one belonging to the older generations and one novel agent (chemoimmunotherapy), a combination of new agents (chemotherapy free protocols), or a combination of subcutaneous and oral medications in the treatment of various malignancies. Futuristically, our aim is to use therapy which avoids / reduces hospitalization with a finite duration of therapy, making treatment cost-effective and more compliant leading to better and deeper malignant cell destruction. However, with the ever evolving and mutating
cancer cell for its survival, novel drugs will become old tomorrow and our protocols, combinations and sequencing of drugs will change over time with the advent of new drugs. The singular end point in cancer treatment today is better efficacy, safety and user-friendly protocols (oral or subcutaneous routes) that will achieve a deep response - undetectable minimal residual disease (uMRD) that will ultimately lead to treatment discontinuation. This in turn will improve compliance, prevent unnecessary toxicity and hopefully provide a functional cure. We are nearly there but we still do not routinely use the word
cure…yet! Hopefully someday.
Keywords
Malignancy, Chemotherapy, novel agents, chemoimmunotherapy, targeted therapy, monoclonal antibodies, uMRDReferences
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