COVID-19 vaccine-induced Stevens-Johnson syndrome.
Ontology highlight
ABSTRACT:
SUBMITTER: Dash S
PROVIDER: S-EPMC8239684 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description: Not available
| S-EPMC8733279 | biostudies-literature
Project description:Purpose:To report an unusual presentation of commercial cannabidiol (CBD) oil-induced Stevens-Johnson Syndrome/toxic epidermal necrolysis (SJS-TEN). Methods:A 56-year-old woman presented with acute onset of a diffuse, blistering, maculopapular rash with over 30% total body surface area (BSA) involvement two days after taking CBD oil sublingually for chronic pain. Biopsy confirmed SJS-TEN. Ophthalmology was consulted and mild eye involvement was found. She was started on topical cyclosporine, prednisone, moxifloxacin, and erythromycin ointment to prevent progression, which was successful. She was otherwise treated with supportive therapy in the intensive care burn unit and ultimately passed away from septic shock. Conclusion:In this case, we described an unusual drug-induced SJS from a commercial, non-FDA-regulated cannabis product. The use of a commercial CBD product should be cautioned due to potential for series of drug reactions to the cannabis product and the risk for reaction to other unregulated other pharmacological components.
| S-EPMC7053463 | biostudies-literature
Project description:The ocular surface microbiome is an essential factor that maintains ocular surface homeostasis. Since the ocular surface is continuously exposed to the external environment, its microbiome, tears, and local immunity are vital for maintaining normal conditions. Additionally, this microbiome helps prevent pathogen colonization, which commonly leads to opportunistic infection. The abnormal ocular surface microbiome has previously been reported in several conditions, including dry eyes, allergy, blepharitis, graft-versus-host disease (GVHD), and Stevens-Johnson syndrome (SJS). Several approaches were applied to identify the ocular microbiome, including conventional culture techniques and molecular sequencing techniques. By using 16s rRNA sequencing, alterations in the type, proportion, and composition of bacterial communities, described by alpha (α)-and beta (β)-diversity, were observed in SJS patients compared to the healthy group. Conventional culture techniques indicated a higher number of positive bacterial cultures in the SJS group, with a predominance of gram-positive cocci and gram-positive bacilli. Besides, there are increased variations and multiple detections of bacterial genera. Taken together, SJS causes structural changes in the ocular surface and significantly affects its microbiome. Further studies into the area of temporal relationship, metagenomics, proteomics, and metabolomics analysis of the microbiome will lead to a better understanding of this disease. Finally, the treatment using prebiotics and probiotics to re-establish the normal ocular ecosystem and bring back a healthy ocular surface await confirmation.
| S-EPMC8138458 | biostudies-literature
Project description:Stevens-Johnson syndrome (SJS) is an immune mediated hypersensitivity reaction. Significant involvement of oral, nasal, eye, vaginal, urethral, GI and lower respiratory tract mucous membrane may develop. It is usually a reaction due to a medication or due to an infection. In 95 % of case reports, drugs were found to be an important cause for the development of SJS. In this case report, a 32 year old female reported chief complaint of itch skin eruptions all over the body along with erosive lesions on tongue, lips, buccal mucosa and genital mucosa. The reaction occurred after administration of augmentin (containing amoxycillin and clavulanic acid). She was treated with antimicrobials, antiallergics and conservative management. The patient improved and was discharged from the hospital. Causality assessment using Naranjo Adverse Drug Reaction Probability Scale revealed that amoxycillin and clavulanic acid combination was a possible cause for the adverse reaction with a score of 4.
| S-EPMC5547378 | biostudies-other
Project description:OBJECTIVE:Quantitative Structure-Activity Relationship (QSAR) models can predict adverse drug reactions (ADRs), and thus provide early warnings of potential hazards. Timely identification of potential safety concerns could protect patients and aid early diagnosis of ADRs among the exposed. Our objective was to determine whether global spontaneous reporting patterns might allow chemical substructures associated with Stevens-Johnson Syndrome (SJS) to be identified and utilized for ADR prediction by QSAR models. MATERIALS AND METHODS:Using a reference set of 364 drugs having positive or negative reporting correlations with SJS in the VigiBase global repository of individual case safety reports (Uppsala Monitoring Center, Uppsala, Sweden), chemical descriptors were computed from drug molecular structures. Random Forest and Support Vector Machines methods were used to develop QSAR models, which were validated by external 5-fold cross validation. Models were employed for virtual screening of DrugBank to predict SJS actives and inactives, which were corroborated using knowledge bases like VigiBase, ChemoText, and MicroMedex (Truven Health Analytics Inc, Ann Arbor, Michigan). RESULTS:We developed QSAR models that could accurately predict if drugs were associated with SJS (area under the curve of 75%-81%). Our 10 most active and inactive predictions were substantiated by SJS reports (or lack thereof) in the literature. DISCUSSION:Interpretation of QSAR models in terms of significant chemical descriptors suggested novel SJS structural alerts. CONCLUSIONS:We have demonstrated that QSAR models can accurately identify SJS active and inactive drugs. Requiring chemical structures only, QSAR models provide effective computational means to flag potentially harmful drugs for subsequent targeted surveillance and pharmacoepidemiologic investigations.
| S-EPMC4997030 | biostudies-literature
Project description:Stevens-Johnson syndrome (SJS) is a disorder that causes severe damage to the skin and mucous membranes with bullous and erosive properties. Drug-induced liver injury (DILI) is closely related to non-steroidal anti-inflammatory drugs (such as ibuprofen). Liver injury caused by ibuprofen is often related to overdose, and liver injury caused by normal dose is rare, and there are individual differences in different situations. In this case, a child developed SJS and acute liver injury after treatment with ibuprofen suspension. We described the characteristics of related adverse reactions induced by ibuprofen, and analyzed the relationship between SJS caused by the drug and related drug genes. Glucocorticoids and antihistamines were used to treat dermatitis, reduced glutathione (GSH) to protect the liver and plasma exchange detoxification. Finally, the patient's dermatitis healed and the liver injury was significantly improved. Many studies have suggested that DILI may be related to human leukocyte antigen (HLA) genotyping. The detection of drug-related genes revealed that the SJS and liver damage caused by ibuprofen might have been related to the positive HLA-B*5801. This article suggests that attention should be paid to checking liver function indicators after taking ibuprofen, and genetic screening can be used to reduce the risk of gene-related adverse reactions when necessary.
| S-EPMC8261580 | biostudies-literature
Project description:Lamotrigine (LTG) is currently indicated as adjunctive therapy for focal and generalized tonic-clonic seizures and for treatment of bipolar disorder and neuropathic pain. A common concern with LTG in children is the frequency of appearance of skin rash. The intensity of this adverse effect can vary from transient mild rash to Stevens-Johnson syndrome (SJS), which can be fatal mainly when LTG is coadministered with valproic acid (VPA). Hereby, we present the case of an 8-year-old boy who suffered from SJS and other complications two weeks after LTG was added to his VPA treatment in order to control his seizures. VPA is known to decrease LTG clearance via reduced glucuronidation. In this case, the minor elimination pathway of LTG would play a more important role, and the formation of an arene oxide metabolite would be enhanced. As this reactive metabolite is detoxified mainly by enzymatic reactions, involving microsomal epoxide hydrolase and/or GSH-S-transferases and these enzymes are polymorphically expressed in humans, arene oxide toxicity is increased when epoxide hydrolase or GSH-S-transferases is either defective or inhibited or a depletion of intracellular glutathione levels is taking place. VPA can cause inhibition of epoxide hydrolase enzymes and/or depletion of glutathione levels leading to adverse cutaneous reactions.
| S-EPMC6136509 | biostudies-literature
Project description: Not available
| S-EPMC10577827 | biostudies-literature
Project description:Immune checkpoint inhibitors (ICIs) have been widely applicated in clinical therapy in recent years. Skin-related adverse reaction is one of the most common adverse events for ICIs. Stevens-Johnson syndrome (SJS) is one of the serious cutaneous reactions threatening the life. Here, we reported a case of 76-year-old male patient with poorly differentiated metastatic lung adenocarcinoma, after 9 weeks exposure of sintilimab (3 doses) combined with paclitaxel liposome after concurrent chemotherapy/radiotherapy, experienced Stevens-Johnson syndrome involving limbs, trunk, lip and the oral mucosa. Biopsy of the skin tissue showed infiltration of CD4 and CD8 positive T lymphocytes. We also found PD-L1 expression in the glands and the basal layer of the skin. This finding is distinct from the previously reported expression of PD-L1 on the surface of epidermal keratinocytes in patients with SJS due to immunotherapy.
| S-EPMC10540079 | biostudies-literature
Project description:Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening mucocutaneous adverse drug reactions characterized by massive epidermal detachment. Cytotoxic T cells and associated effector molecules are known to drive SJS/TEN pathophysiology, but the contribution of innate immune responses is not well understood. We describe a mechanism by which neutrophils triggered inflammation during early phases of SJS/TEN. Skin-infiltrating CD8+ T cells produced lipocalin-2 in a drug-specific manner, which triggered the formation of neutrophil extracellular traps (NETs) in early lesional skin. Neutrophils undergoing NETosis released LL-37, an antimicrobial peptide, which induced formyl peptide receptor 1 (FPR1) expression by keratinocytes. FPR1 expression caused keratinocytes to be vulnerable to necroptosis that caused further release of LL-37 by necroptotic keratinocytes and induced FPR1 expression on surrounding keratinocytes, which likely amplified the necroptotic response. The NETs-necroptosis axis was not observed in less severe cutaneous adverse drug reactions, autoimmune diseases, or neutrophil-associated disorders, suggesting that this was a process specific to SJS/TEN. Initiation and progression of SJS/TEN keratinocyte necroptosis appear to involve a cascade of events mediated by innate and adaptive immune responses, and understanding these responses may contribute to the identification of diagnostic markers or therapeutic targets for these adverse drug reactions.
| S-EPMC9392155 | biostudies-literature