Title:A Case Report of Cefixime, Paracetamol, and Nimesulide Induced Toxic
Epidermal Necrolysis in a Woman with Dengue Infection without any
Other Associated Comorbidities
Volume: 19
Issue: 2
Author(s): Renuka Munshi*Miteshkumar Maurya
Affiliation:
- Department of Clinical Pharmacology, Topiwala National Medical College & Bai Yamunabai Laxman Nair Charitable
Hospital, Mumbai, 400008, India
Keywords:
Adverse drug reaction, toxic epidermal necrolysis, dengue fever, cefixime, nimesulide, paracetamol (Acetaminophen).
Abstract:
Background: Toxic Epidermal Necrolysis (TEN) is a rare, acute, and life-threatening
mucocutaneous disease that occurs after the administration of certain drugs, resulting in extensive
keratinocyte cell death, skin involvement at the dermal-epidermal junction, and extensive bullous
skin eruptions and sloughing. Many published case reports have observed the presence of fever
with a viral infection, drug, and/or genetic association as a possible trigger for TEN but associated
with other comorbidities. Physicians still struggle to predict which individuals could be predisposed
to TEN. The case report that we present had a history of multiple drug intake and fever due
to dengue virus infection but was not associated with any other comorbidity.
Case Presentation: We present an unusual case of a 32-year-old woman of Western Indian origin
who had developed dengue infection and suffered toxic epidermal necrolysis following a five-day
course of a third-generation cephalosporin antibiotic, cefixime and a three-day course of 2 analgesic
drugs, paracetamol (acetaminophen), and nimesulide, with the adverse event occurring on the
fifth day of the dengue infection. The offending drugs were stopped, and patient survived with
supportive management and hydration.
Conclusion: The presence of comorbidities may not always be the triggering factor for TEN,
though it can affect patient outcomes. Rational drug use is always recommended for patient care.
Further research is required to understand the pathomechanism behind the viral-drug-gene interaction.
