Sulfasalazine-induced drug reaction with eosinophilia and systemic symptoms (DRESS) with concomitant acute chikungunya virus infection: possible role of new viral trigger

2021 ◽  
Vol 14 (10) ◽  
pp. e244063
Author(s):  
Abheek Sil ◽  
Moni Sankar Bhattacharjee ◽  
Atanu Chandra ◽  
Jayasri Das Pramanik
Keyword(s):  
Drug Reaction ◽  
Virus Infection ◽  
Renal Dysfunction ◽  
Skin Rash ◽  
Chikungunya Virus ◽  
Drug Effect ◽  
Signs And Symptoms ◽  
Viral Aetiology ◽  
Systemic Symptoms

Drug reaction with eosinophilia and systemic symptoms (DRESS) is designated as a potentially lethal adverse drug effect with characteristic signs and symptoms such as skin rash, fever, leucocytosis with eosinophilia or atypical lymphocytes, lymphadenopathy and liver or renal dysfunction. In addition to most commonly implicated drug category (aromatic anticonvulsants), lamotrigine, sulfonamides, dapsone and abacavir may also induce this syndrome. We describe here a case a sulfasalazine-induced DRESS with coexisting chikungunya fever. The shared presentation of fever with rash in both conditions made it a challenging diagnosis. Sulfasalazine hypersensitivity manifesting as DRESS has rarely been reported. Furthermore, we document chikungunya virus (CV) as a possible triggering agent for DRESS. To the best of our knowledge, CV as a viral aetiology in DRESS has not been reported previously in the literature.

scholarly journals Phenytoin Induced Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)

2015 ◽  
Vol 35 (1) ◽  
pp. 73-75 ◽  
Author(s):  
NK Natt ◽  
S Tarsem ◽  
Dr Anuba ◽  
S Simarjeet ◽  
M Sharma ◽  
...  
Keyword(s):  
Adverse Effect ◽  
Drug Reaction ◽  
Skin Rash ◽  
Drug Effect ◽  
Rapid Diagnosis ◽  
Age Group ◽  
Life Saving ◽  
Paediatric Age ◽  
Systemic Symptoms ◽  
High Index Of Suspicion

Drug reaction with eosinophilia and systemic symptoms (DRESS) is a rare and potentially fatal adverse effect characterized by a skin rash with visceral involvement and haematological abnormalities. This adverse drug effect is often misdiagnosed and under-reported especially in paediatric age group due to its rarity and high occurrence of skin rash in various other viral illnesses of children. We report a case of DRESS in a three months old male child. A high index of suspicion, rapid diagnosis and prompt withdrawal can be life-saving for the patient.J Nepal Paediatr Soc 2015;35(1):73-75

scholarly journals Human IFITM3 restricts Chikungunya virus and Mayaro virus infection and is susceptible to virus-mediated counteraction

2020 ◽  
Author(s):  
Sergej Franz ◽  
Thomas Zillinger ◽  
Fabian Pott ◽  
Christiane Schüler ◽  
Sandra Dapa ◽  
...  
Keyword(s):  
Virus Infection ◽  
Influenza A ◽  
Chikungunya Virus ◽  
Protein S ◽  
Human Cells ◽  
Structural Protein ◽  
Infected Cells ◽  
Mayaro Virus ◽  
The Impact

AbstractInterferon-induced transmembrane (IFITM) proteins restrict infection by enveloped viruses through interfering with membrane fusion and virion internalisation. The role of IFITM proteins during alphaviral infection of human cells and viral counteraction strategies remain largely unexplored. Here, we characterized the impact of IFITM proteins and variants on entry and spread of Chikungunya virus (CHIKV) and Mayaro virus (MAYV) in human cells, and provide first evidence for a CHIKV-mediated antagonism of IFITM proteins. IFITM1, 2 and 3 restricted infection at the level of alphavirus glycoprotein-mediated entry, both in the context of direct infection and during cell-to-cell transmission. Relocalization of normally endosomal IFITM3 to the plasma membrane resulted in the loss of its antiviral activity. rs12252-C, a naturally occurring variant of IFITM3 that has been proposed to associate with severe influenza in humans, restricted CHIKV, MAYV and influenza A virus infection as efficiently as wild-type IFITM3. Finally, all antivirally active IFITM variants displayed reduced cell surface levels in CHIKV-infected cells involving a posttranscriptional process mediated by one or several non-structural protein(s) of CHIKV.

Successful Phenobarbital Desensitization After DRESS Reaction in the Management of Refractory Status Epilepticus

2018 ◽  
Vol 32 (2) ◽  
pp. 228-230 ◽  
Author(s):  
Robert H. Witcher ◽  
Michelle M. Ramirez
Keyword(s):  
Drug Reaction ◽  
Status Epilepticus ◽  
Signs And Symptoms ◽  
Punch Biopsy ◽  
Refractory Status Epilepticus ◽  
Burst Suppression ◽  
Refractory Status ◽  
Life Threatening ◽  
Antiepileptic Medications ◽  
Systemic Symptoms

Purpose: Drug reaction with eosinophilia and systemic symptoms (DRESS) is associated with antiepileptic drug use and is a rare but life-threatening side effect. We present a case of phenobarbital-induced DRESS in a patient who subsequently required phenobarbital and was successfully desensitized. Summary: A 5-year-old male presented with medically refractory status epilepticus (SE). He had been trialed on several antiepileptic medications without achieving burst suppression. Burst suppression was achieved with a pentobarbital infusion, and thus, phenobarbital was initiated as the pentobarbital was weaned. After five days of phenobarbital, the patient developed signs and symptoms concerning for DRESS; a punch biopsy confirmed the drug reaction. Two months later, he again developed SE unresponsive to antiepileptic infusions. Burst suppression was achieved with pentobarbital, and it was decided to transition the patient to phenobarbital. Due to concerns of phenobarbital-induced DRESS, the patient underwent a phenobarbital desensitization consisting of 6 doses sequentially administered in 10-fold increasing concentrations before achieving therapeutic dosing. Three days later, the patient achieved therapeutic phenobarbital levels, was weaned off of pentobarbital, and remained seizure-free without recurrence of DRESS. Conclusions: Graded desensitization may be an option to minimize recurrence of DRESS in patients where avoidance of the offending agent is not possible.

Rate of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome with raltegravir and role of the HLA-B*53

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
M Lefebvre ◽  
A Walencik ◽  
C Allavena ◽  
E Billaud ◽  
A Kassi ◽  
...  
Keyword(s):  
Drug Reaction ◽  
Dress Syndrome ◽  
Systemic Symptoms

Drug Reaction with Eosinophilia and Systemic Symptoms or Herpes Virus Infection: Author's Reply

2016 ◽  
Vol 33 (6) ◽  
pp. 687-687
Author(s):  
Sarita Sasidharanpillai ◽  
Sasidharanpillai Sabitha ◽  
Najeeba Riyaz ◽  
Manikoth P. Binitha ◽  
Kunnummal Muhammed ◽  
...  
Keyword(s):  
Drug Reaction ◽  
Virus Infection ◽  
Herpes Virus ◽  
Herpes Virus Infection ◽  
Herpès Virus ◽  
Systemic Symptoms

Characterization of Chikungunya virus infection in human neuroblastoma SH-SY5Y cells: Role of apoptosis in neuronal cell death

2012 ◽  
Vol 163 (2) ◽  
pp. 563-572 ◽  
Author(s):  
R. Dhanwani ◽  
M. Khan ◽  
A.S.B. Bhaskar ◽  
Rajpriya Singh ◽  
I.K. Patro ◽  
...  
Keyword(s):  
Cell Death ◽  
Virus Infection ◽  
Chikungunya Virus ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Human Neuroblastoma

scholarly journals Drug Reaction with Eosinophilia and Systemic Symptoms: A Complex Interplay between Drug, T Cells, and Herpesviridae

2021 ◽  
Vol 22 (3) ◽  
pp. 1127
Author(s):  
Luckshman Ganeshanandan ◽  
Michaela Lucas
Keyword(s):  
Drug Reaction ◽  
Human Leukocyte ◽  
Molecular Techniques ◽  
Dress Syndrome ◽  
Complex Interplay ◽  
Drug Induced ◽  
Leukocyte Antigen ◽  
Systemic Symptoms ◽  
Delayed Hypersensitivity Reaction

Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, also known as drug induced hypersensitivity (DiHS) syndrome is a severe delayed hypersensitivity reaction with potentially fatal consequences. Whilst recognised as T cell-mediated, our understanding of the immunopathogenesis of this syndrome remains incomplete. Here, we discuss models of DRESS, including the role of human leukocyte antigen (HLA) and how observations derived from new molecular techniques adopted in key studies have informed our mechanism-based understanding of the central role of Herpesviridae reactivation and heterologous immunity in these disorders.

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