Összefoglaló. Két fiatal nőbetegnél a valproátról lamotriginre történő gyógyszerátállítás során a 3-4. héten influenzaszerű prodromalis tüneteket követően toxikus epidermalis necrolysis (TEN), más néven Lyell-szindróma alakult ki. Mindkét beteg 5 napja kezdődött bőr- és nyálkahártyatünetekkel, kiterjedt hámleválást okozó hámnekrózissal került felvételre a Debreceni Egyetem Bőrgyógyászati Klinikájának Égési Intenzív Osztályára. Multidiszciplináris szupportív terápia mellett nagy dózisú szteroid- és immunglobulin-terápiát alkalmaztunk. A 37 éves nőbetegnél 3 hét után a kórkép fatális kimenetellel végződött. A 19 éves nőbeteg tünetei 4 hét intenzív terápia után szövődményekkel gyógyultak. A TEN ritka, gyógyszer által okozott, életet veszélyeztető, késői hiperszenzitivitási reakció. Patogenezisében a gyógyszermolekula, a humán leukocytaantigén (HLA) I. osztályú molekula és a T-sejt-receptor kóros interakciója szerepel. Kezelésében a legfontosabb a kiváltó gyógyszer elhagyása, valamint az azonnal kezdett komplett szupportív terápia alkalmazása. A specifikus kezelést illetően nincsenek egységes szakmai irányelvek. A veszélyes gyógyszerek titrált bevezetése csökkentheti a kialakuló hiperszenzitivitás súlyosságát, ezenfelül a beteg szoros követése és az adverz tünetek korai felismerése javíthatja a TEN kimenetelét. Orv Hetil. 2020; 161(46): 1959-1965. Summary. After switching from valproate to lamotrigine, on the 3rd-4th weeks, two young female patients developed flu-like prodromal symptoms, followed by the development of toxic epidermal necrolysis (TEN), also known as Lyell syndrome. Both patients were admitted to the Burn Intensive Care Unit of the Department of Dermatology, University of Debrecen with skin and mucosa symptoms; extensive epithelial death and detachment started 5 days earlier. In addition to multidisciplinary supportive treatment, high-dose corticosteroid and immunoglobulin therapy were administered. In the case of the 37-year-old female patient, the disease resulted in a fatal outcome. The 19-year-old patient healed with some sequelae. TEN is a rare, life-threatening delayed-type hypersensitivity reaction caused by drugs. Its pathogenesis involves an interaction between small-molecule drug, human leukocyte antigen class I molecule and T-cell receptor. The most important treatment is immediate withdrawal of potentially causative drugs and prompt application of supportive therapy. There is no standard guidance on specific treatment. Slow dose escalation of dangerous drugs can be beneficial in avoiding severe reactions, furthermore, close patient follow-up and early detection of the possible adverse reactions contribute to a more favourable outcome of TEN. Orv Hetil. 2020; 161(46): 1959-1965.
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http://dx.doi.org/10.1556/650.2020.31888 | DOI Listing |
Front Med (Lausanne)
December 2024
Department of Oncology, Ganzhou People's Hospital, Ganzhou, China.
Background: Immune checkpoint inhibitors (ICIs) have been widely applicated for the treatment of patients with advanced esophageal cancer. Skin-related adverse reactions are frequent with ICIs, with toxic epidermal necrolysis (TEN) being a severe and potentially life-threatening cutaneous reaction.
Case Presentation: We present a case of a 70-year-old male with locally advanced esophageal cancer who developed severe toxic epidermal necrolysis (TEN) after 18 days of tislelizumab combined with chemotherapy.
Sci Rep
January 2025
Department of Ophthalmology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji, Kawaramachi, Kamigyoku, Kyoto, 602-0841, Japan.
Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe mucocutaneous disorders characterized by extensive tissue necrosis; they are often accompanied by severe ocular complications (SOC). The regulatory role of microRNAs (miRNAs) in modulating immune responses in SJS/TEN is not fully understood, particularly in relation to chronic SOC. We explored the expression profiles of specific miRNAs and their potential impact on the regulation of key innate immune genes in patients with SJS/TEN with SOC.
View Article and Find Full Text PDFInvest New Drugs
January 2025
College of Pharmacy, Changsha Medical University, No. 1501 Leifeng Avenue, Xiangjiang New District, Changsha, Hunan, 410219, China.
The understanding of pembrolizumab-induced Stevens-Johnson syndrome (SJS) /toxic epidermal necrolysis (TEN) primarily derives from case reports, leaving specific clinical features largely unknown. This study aims to investigate the clinical characteristics associated with pembrolizumab-induced SJS/TEN and to encourage the judicious use of pembrolizumab. Retrieve reports on pembrolizumab induced SJS/TEN before September 30, 2024 for retrospective analysis.
View Article and Find Full Text PDFDermatol Reports
November 2024
Pathology Department, Taibah University, Saudi Arabia.
Toxic epidermal necrolysis (TEN) is a life-threatening acute mucocutaneous syndrome. It is characterized by keratinocyte necrosis and apoptosis, which affect more than 30% of the body's surface. TEN is most commonly due to an altered immunological response to specific drugs, infections, and malignancies, or it can be idiopathic.
View Article and Find Full Text PDFNat Commun
December 2024
Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou Branch, Taoyuan, Taiwan.
Immune checkpoint inhibitors (ICI) represent new anticancer agents and have been used worldwide. However, ICI can potentially induce life-threatening severe cutaneous adverse reaction (SCAR), such as Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN), hindering continuous ICI therapy. We examine 6 cohorts including 25 ICI-induced SJS/TEN patients and conduct single-cell RNA sequencing (scRNA-seq) analysis, which shows overexpression of macrophage-derived CXCL10 that recruits CXCR3 cytotoxic T lymphocytes (CTL) in blister cells from ICI-SJS/TEN skin lesions.
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