scholarly journals The Profiles of Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) Patients in Tertiary Hospital

2021 ◽  
Vol 33 (2) ◽  
pp. 116
Author(s):  
William Andrew Isaac ◽  
Damayanti Damayanti ◽  
Nurmawati Fatimah ◽  
Afif Nurul Hidayati
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
The United States ◽  
Tertiary Hospital ◽  
Stevens Johnson Syndrome ◽  
Drug Induced ◽  
Skin Reactions ◽  
Drug Eruptions ◽  
Johnson Syndrome ◽  
Epidemiological Profile ◽  
Common Manifestation

Background: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe eruptive skin reactions that can cause death. The incidence of SJS and TEN cases in the United States is 1.5–9.6 per 1,000,000 per year. Drugs are the primary etiology of SJS and TEN. Some drugs are at high risk and used frequently. The SJS and TEN mortality rates were relatively high, with SJS 4.8%, SJS / TEN overlap 19.8%, and TEN 14.8%. In Indonesia, there are lack of studies on the SJS and TEN. This study is needed to determine the epidemiological profile of SJS and TEN. Purpose: This study aimed to describe SJS and TEN patients' profiles. Methods: Drug-induced SJS and TEN cases from January 2016 to December 2019 were evaluated from the medical records patients' profile, incidence, suspected drugs, risk factors, and comorbidities of SJS and TEN were described. Result: There were 28 SJS and TEN patients, comprising of 24 SJS patients (85.7%), 3 TEN patients (10.7%), and 1 SJS overlapping TEN patients (3.5%). The most common suspected drugs were paracetamol (22.2%), carbamazepine (20.4%), cefadroxil (8.8%), and ciprofloxacin (8.8%). Women (53.5%) experienced more severe drug eruptions than men (46.4%). The largest age group was 25–44 years (35.7%). Most comorbidities were epilepsy (21%), diabetes (15.7%), hypertension (15.7%), and stroke (15.7%). Conclusion: The most common manifestation was SJS with paracetamol as the most common suspected drug, followed by carbamazepine.

scholarly journals Stevens - Johnson Syndrome and Toxic Epidermal Necrolysis; Extensive Review of Reports of Drug-Induced Etiologies, and Possible Therapeutic Modalities

2018 ◽  
Vol 6 (4) ◽  
pp. 730-738 ◽  
Author(s):  
Adegbenro Omotuyi John Fakoya ◽  
Princess Omenyi ◽  
Precious Anthony ◽  
Favour Anthony ◽  
Precious Etti ◽  
...  
Keyword(s):  
Adverse Drug Reaction ◽  
Toxic Epidermal Necrolysis ◽  
Stevens Johnson Syndrome ◽  
Hypersensitivity Reactions ◽  
Extensive Review ◽  
Drug Induced ◽  
Therapeutic Modalities ◽  
Johnson Syndrome ◽  
Mucous Membranes ◽  
Degrees Of Severity

Stevens - Johnson Syndrome and Toxic Epidermal Necrolysis are adverse hypersensitivity reactions that affect the skin and mucous membranes. They are characterised by erythematous macules and hemorrhagic erosions of the mucous membranes. Epidermal detachments of varying degrees of severity also occur in these conditions. Various aetiologies are associated with these conditions, with adverse drug reaction being the most common. Though the worldwide incidence of these conditions is recorded as low, diverse types of medication are being observed to lead to these conditions. This review compiles information on the details of Stevens-Johnson syndrome and Toxic Epidermal Necrolysis, the pathophysiology, therapeutic management, and largely considers the drug-induced etiologies associated with these conditions.

scholarly journals Fatal case of toxic epidermal necrolysis induced by ciproflfl oxacin in a child

2021 ◽  
Vol 12 (Supp 1) ◽  
pp. 26-29
Author(s):  
Thomas Schiestel
Keyword(s):  
Case Report ◽  
Toxic Epidermal Necrolysis ◽  
Adverse Reactions ◽  
Pediatric Population ◽  
Fatal Case ◽  
Stevens Johnson Syndrome ◽  
Delayed Treatment ◽  
Drug Eruptions ◽  
Johnson Syndrome ◽  
Life Threatening

Bullous drug eruptions such as Toxic Epidermal Necrolysis (TEN) and Stevens-Johnson syndrome (SJS) are rare but known adverse reactions of fluoroquinolones. Although uncommon, TEN can be life-threatening for the patient, especially in the context of delayed treatment and in fragile patients such as the pediatric population. In the present case, TEN occurred in a 13-year-old girl with no medical history following initiation of ciprofloxacin treatment for an inguinal cyst. We hope that the case report will make interrogate the practices concerning the use of antibiotics, in particular fluoroquinolones in the context of an use not prescribed by the Marketing Authorization of the drug in children.

scholarly journals Causative drugs and HLA-B polymorphism in drug-induced Stevens-Johnson syndrome - toxic epidermal necrolysis: A study in five hospitals in Jakarta

2019 ◽  
Author(s):  
Anesia Tania ◽  
Evita Halim Effendi ◽  
Inge Ade Krisanti ◽  
Yulia Ariani
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Drug Eruption ◽  
Stevens Johnson Syndrome ◽  
Allele Polymorphism ◽  
Exclusion Criteria ◽  
Drug Induced ◽  
Causative Drug ◽  
Johnson Syndrome ◽  
Luminex Technology ◽  
Referral Hospitals

Stevens-Johnson syndrome and toxic epidermal necrolysis is a very rare but lifethreatening form of cutaneous drug eruption. In recent years, several countries in Asia had succeded in preventing carbamazepine induced SJS/TEN by screening for HLA-B*15:02 before prescribing carbamazepine. This study aimed to acquire data regarding causative drugs and HLA-B allele polymorphism in SJS/TEN patient in Jakarta. We acquired data from 5 referral hospitals from March 2015 to March 2017. Subject fulfilling the inclusion and exclusion criteria was interviewed and blood sample was taken for DNA extraction. The DNA was examined with PCR SSOP and Luminex technology for high resolution HLA-B typing. We studied 22 subjects. The median age was 45,4 years old (14-74). The most common causative drug in this study is carbamazepine. HLA-B*15:02 and HLAB* 18:01 were the most common allele in all subjects. HLA-B*15:02 was found in five (72%) out of seven subjects whose condition was caused by carbamazepine. The most common causative drug of SJS/TEN in five hospitals in Jakarta is carbamazepine, with five (72%) out seven subjects had HLA-B*15:02 allele.

scholarly journals Drug-induced liver injury associated with stevens-Johnson syndrome/toxic epidermal necrolysis: Patient characteristics, causes, and outcome in 36 cases

Hepatology ◽  
2015 ◽  
Vol 63 (3) ◽  
pp. 993-999 ◽  
Author(s):  
Harshad Devarbhavi ◽  
Sujata Raj ◽  
Venu H. Aradya ◽  
Vijaykumar T. Rangegowda ◽  
Girish P. Veeranna ◽  
...  
Keyword(s):  
Liver Injury ◽  
Toxic Epidermal Necrolysis ◽  
Patient Characteristics ◽  
Stevens Johnson Syndrome ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Johnson Syndrome

Drug-Induced Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis Call for Optimum Patient Stratification and Theranostics via Pharmacogenomics

2018 ◽  
Vol 19 (1) ◽  
pp. 329-353 ◽  
Author(s):  
Chonlaphat Sukasem ◽  
Theodora Katsila ◽  
Therdpong Tempark ◽  
George P. Patrinos ◽  
Wasun Chantratita
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Clinical Care ◽  
Genomic Medicine ◽  
Stevens Johnson Syndrome ◽  
Future Research ◽  
Great Promise ◽  
Patient Stratification ◽  
Clinical Implementation ◽  
Drug Induced ◽  
Johnson Syndrome

The Global Genomic Medicine Collaborative, a multinational coalition of genomic and policy experts working to implement genomics in clinical care, considers pharmacogenomics to be among the first areas in genomic medicine that can provide guidance in routine clinical practice, by linking genetic variation and drug response. Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe life-threatening reactions to medications with a high incidence worldwide. Genomic screening prior to drug administration is a key opportunity and potential paradigm for using genomic medicine to reduce morbidity and mortality and ultimately eliminate one of the most devastating adverse drug reactions. This review focuses on the current understanding of the surveillance, pathogenesis, and treatment of SJS/TEN, including the role of genomics and pharmacogenomics in the etiology, treatment, and eradication of preventable causes of drug-induced SJS/TEN. Gaps, unmet needs, and priorities for future research have been identified for the optimal management of drug-induced SJS/TEN in various ethnic populations. Pharmacogenomics holds great promise for optimal patient stratification and theranostics, yet its clinical implementation needs to be cost-effective and sustainable.

Suspected Lamotrigine-Induced Toxic Epidermal Necrolysis

1997 ◽  
Vol 31 (6) ◽  
pp. 720-723 ◽  
Author(s):  
Julie J Chaffin ◽  
Steven M Davis
Keyword(s):  
Valproic Acid ◽  
Toxic Epidermal Necrolysis ◽  
Case Reports ◽  
Stevens Johnson Syndrome ◽  
Complex Partial Seizures ◽  
Skin Reactions ◽  
Johnson Syndrome ◽  
Patient Reported ◽  
History Of ◽  
Relationship Of

OBJECTIVE: To describe a patient who developed toxic epidermal necrolysis (TEN) possibly secondary to lamotrigine use. CASE SUMMARY: A 74-year-old white man with a history of probable complex partial seizures was admitted to the neurology service for a prolonged postictal state. His antiepileptic regimen was changed while he was in the hospital to include lamotrigine. After 19 days of hospitalization and 14 days of lamotrigine therapy, the patient became febrile. The next day he developed a rash which progressed within 4 days to TEN, diagnosed by skin biopsy. All suspected drugs were discontinued, including lamotrigine. The patient was treated with hydrotherapy in the burn unit. His symptoms improved and he was discharged from the hospital 26 days after the rash developed. DISCUSSION: During lamotrigine's premarketing clinical trials, the manufacturer reported several cases of Stevens-Johnson syndrome and TEN. There are several published case reports of lamotrigine-induced severe skin reactions. All of these reports included patients being treated with both valproic acid and lamotrigine. Our patient was exposed to phenytoin, carbamazepine, clindamycin, and lamotrigine, but not valproic acid. The patient reported prior use of phenytoin with no skin rash. Carbamazepine was the antiepileptic drug the patient was maintained on prior to his hospital admission, and the symptoms of TEN resolved while he was still receiving carbamazepine. The patient received only two doses of clindamycin, which makes this agent an unlikely cause of TEN. CONCLUSIONS: Because of the temporal relationship of the onset of the patient's rash and several drugs that are known to cause severe rashes, it is not certain which drug was the definite culprit. However, based on the evidence from the literature, lamotrigine appears to be the causative agent.

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