Correlation of Serum IgE Levels and Clinical Manifestations in Patients Presenting with Cutaneous Adverse Drug Reactions in a Tertiary Care Centre, Eastern Zone of India
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Abstract
Objective: To examine the correlation between serum Immunoglobulin E (IgE) levels and the clinical spectrum and severity of Cutaneous Adverse Drug Reactions (CADRs) in patients attending a tertiary care center in Eastern India, evaluating IgE as a surrogate marker of immunopathological severity. Design: Cross-sectional, institution-based observational study conducted over twelve months, integrating clinical, pharmacovigilance, and immunoserological assessments. Subjects/Patients: Seventy-three patients with clinically diagnosed CADRs, aged 10-70 years (mean 38.25 ± 14.58 years), with slight female predominance (52.1%). Methods: Patients underwent detailed history, lesion morphology classification, and WHO-UMC (World Health Organization - Uppsala Monitoring Centre) causality assessment. Serum total IgE levels and absolute eosinophil counts were quantified. Statistical associations between IgE elevation and severity were analyzed using chi-square and t-tests. Patients were stratified into Severe Cutaneous Adverse Reactions (SCARs) and non-SCARs, with drug classes systematically mapped. Results: Fixed drug eruption (51.6%) was most frequent; SCARs comprised 12.3% (Stevens-Johnson Syndrome, TEN, DRESS). Antibiotics (40%) and NSAIDs (26.3%) were leading culprits. Mean IgE was 373.4 ± 341.7 IU/mL. Elevated IgE (>100 IU/mL) occurred in 81% of SCARs versus 36.5% of non-SCARs (p < 0.001). Eosinophilia was noted in 26%, especially in DRESS. Conclusion: Elevated IgE strongly correlates with CADR severity, positioning it as a pragmatic biomarker for SCAR triage and immunodermatologic risk stratification.
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Copyright (c) 2025 Debalina Kanjilal, MD, Suhena Sarkar, MD, Birupaksha Biswas, MD
This work is licensed under a Creative Commons Attribution 4.0 International License.
Creative Commons License All articles published in Annals of Medicine and Medical Sciences are licensed under a Creative Commons Attribution 4.0 International License.
Debalina Kanjilal, MD, Department of Dermatology, Medical College Kolkata, Kolkata, India.
Department of Dermatology, Medical College Kolkata, Kolkata, India.
Suhena Sarkar, MD, Associate Professor, Department of Pharmacology, Medical College Kolkata, India.
Associate Professor, Department of Pharmacology, Medical College Kolkata, India.
Birupaksha Biswas, MD, Department of Pathology, Burdwan Medical College, 3A Khalisakota, Kolkata-700032, India.
Department of Pathology, Burdwan Medical College, 3A Khalisakota, Kolkata-700032, India.
[1] Mustafa SS, Ostrov D, Yerly D. Severe Cutaneous Adverse Drug Reactions: Presentation, Risk Factors, and Management. Curr Allergy Asthma Rep. 2018;18(4):26. doi:10.1007/s11882-018-0778-6.
[2] Duong TA, Valeyrie-Allanore L, Wolkenstein P, Chosidow O. Severe cutaneous adverse reactions to drugs. Lancet. 2017;390(10106):1996-2011. doi:10.1016/S0140-6736(16)30378-6.
[3] Gibson A, Deshpande P, Campbell CN, et al. Updates on the immunopathology and genomics of severe cutaneous adverse drug reactions. J Allergy Clin Immunol. 2023;151(2):289-300.e4. doi:10.1016/j.jaci.2022.12.005.
[4] Knut Brockow. Detection of drug-specific immunoglobulin E (IgE) and acute mediator release for the diagnosis of immediate drug hypersensitivity reactions. J Immunol Methods. 2021;496:113101. doi:10.1016/j.jim.2021.113101.
[5] Cuevas-Gonzalez JC, Lievanos-Estrada Z, Vega-Memije ME, Hojyo-Tomoka MT, Dominguez-Soto L. Correlation of serum IgE levels and clinical manifestations in patients with actinic prurigo. An Bras Dermatol. 2016;91(1):23-26. doi:10.1590/abd1806-4841.20163941.
[6] Hadi MA, Neoh CF, Zin RM, Elrggal ME, Cheema E. Pharmacovigilance: Pharmacist’s perspective on spontaneous adverse drug reactions reporting. Integr Pharm Res Pract. 2017;6:91-8. doi:10.2147/IPRP.S125370.
[7] Thiessard F, Roux E, Miremont-Salamé G, et al. Trends in spontaneous adverse drug reaction reports to the French Pharmacovigilance System (1986-2001). Drug Saf. 2005;28(8):731-40. doi:10.2165/00002018-200528080-00006.
[8] Lobo MG, Pinheiro SM, Castro JG, et al. Adverse drug reaction monitoring: Support for pharmacovigilance at a tertiary care hospital in Northern Brazil. BMC Pharmacol Toxicol. 2013;14:5. doi:10.1186/2050-6511-14-5.
[9] Montastruc F, Sommet A, Bondon-Guitton E, et al. The importance of drug-drug interactions as a cause of adverse drug reactions: a pharmacovigilance study of serotoninergic reuptake inhibitors in France. Eur J Clin Pharmacol. 2012;68:767-75. doi:10.1007/s00228-011-1177-z.
[10] de Vries ST, Denig P, Ekhart C, et al. Sex differences in adverse drug reactions reported to the National Pharmacovigilance Centre in the Netherlands: An explorative observational study. Br J Clin Pharmacol. 2019;85(7):1507-1515. doi:10.1111/bcp.13902.
[11] Kalaiselvan V, Thota P, Singh GN. Pharmacovigilance Programme of India: Recent developments and future perspectives. Indian J Pharmacol. 2016;48(6):624-628. doi:10.4103/0253-7613.194851.
[12] Pichler WJ. Drug hypersensitivity: classification and clinical features. In: Pichler WJ, ed. Drug Hypersensitivity. Basel: Karger; 2007:168-189.
[13] Chen P, Lin JJ, Lu CS, et al. Carbamazepine-induced toxic effects and HLA-B*1502 screening in Taiwan. N Engl J Med. 2011;364(12):1126-1133. doi:10.1056/NEJMoa1009717.
[14] Galli SJ, Tsai M, Piliponsky AM. The development of allergic inflammation. Nature. 2008;454(7203):445-454. doi:10.1038/nature07204.
[15] Kano Y, Hirahara K, Sakuma K, Shiohara T. Several herpesviruses can reactivate in a severe drug eruption: a comprehensive analysis using real-time polymerase chain reaction. Br J Dermatol. 2006;155(2):344-351. doi:10.1111/j.1365-2133.2006.07276.x.
[16] Sakaeda T, Tamon A, Kadoyama K, Okuno Y. Data mining of the public version of the FDA adverse event reporting system. Int J Med Sci. 2013;10(7):796-803. doi:10.7150/ijms.6048.
[17] WHO-Uppsala Monitoring Centre. Annual Drug Safety Report: Emerging Signals from Asia-Pacific. UMC Report 2023.
[18] Chitturi S, Farrell GC. Herbal hepatotoxicity: an expanding but poorly defined problem. J Gastroenterol Hepatol. 2000;15(10):1093-1099. doi:10.1046/j.1440-1746.2000.02250.x.
[19] Descamps V, Valance A, Edlinger C, Fillet AM, Grossin M, Lebrun-Vignes B. Association of human herpesvirus 6 infection with drug reaction with eosinophilia and systemic symptoms. Arch Dermatol. 2001;137(3):301-304. doi:10.1001/archderm.137.3.301.
[20] Reiter H, Lobnig M, Peinhaupt M, et al. TSLP and IL-33 mediate immune-regulatory effects in human skin models of drug-induced inflammation. Exp Dermatol. 2022;31(1):79-86. doi:10.1111/exd.14386.
[21] Kalaiselvan V, Thota P, Singh GN. Pharmacovigilance Programme of India: Recent developments and future perspectives. Indian J Pharmacol. 2016;48(6):624-628. doi:10.4103/0253-7613.194851.
[22] Dhana A, Scott FI, Wang X, et al. Drug reaction with eosinophilia and systemic symptoms syndrome: A review for the internist in the age of precision medicine. Intern Med J. 2020;50(8):950-959. doi:10.1111/imj.14426.