Even patients with clear histories of preexisting dermatoses tend to have biopsies that are not diagnostic when they present with erythroderma.2, Laboratory evaluation of patients with erythroderma is generally not very helpful in determining a specific diagnosis. Erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. Indian J Dermatol. Overall, T cells are the central player of these immune-mediated drug reactions. Anticoagulation therapy. Dent Clin North Am. When it precedes cutaneous T-cell lymphoma lesions, exfoliative dermatitis becomes the presenting sign of the underlying malignancy. sharing sensitive information, make sure youre on a federal Unfortunately, the clinical picture does not contribute to an understanding of the underlying cause. It is not recommended to use prophylactic antibiotic therapy. Hence, the apparent increase in cases of exfoliative dermatitis may be related to the introduction of many new drugs. Takahashi R, et al. . It is advised against the use of silver sulfadiazine because sulphonamide can be culprit agents. 2012;366(26):2492501. exfoliative conditions. The SCORTEN scale is based on a minimal set of parameters as described in the following table. Initial symptoms could be aspecific, as fever, stinging eyes and discomfort upon swallowing, occurring few days before the onset of mucocutaneous involvement. Epilepsia. Granulysin: Granulysin is a pro-apoptotic protein that binds to the cell membrane by means of charge interaction without the need of a specific receptor, producing a cell membrane disruption, and leading to possible cell death. Main discriminating factors between EMM, SJS, SJS-TEN, TEN and SSSS is summarized in Table3 [84]. Consultation with an oncologist who is well-versed in treatment of cutaneous T-cell lymphoma is advisable once the disease progresses to the tumor stage. journal.pds.org.ph 2000;22(5):4137. Mild to severe alopecia and transient or permanent nail dystrophy also may be encountered. Clinical and Molecular Allergy Drug induced exfoliative dermatitis (ED) are a group of rare and severe drug hypersensitivity reactions (DHR) involving skin and usually occurring from days to several weeks after drug exposure. Wetter DA, Davis MD. 7 DRUG INTERACTIONS 7.1 PDE-5-Inhibitors and sGC-Stimulators 7.2 Ergotamine 8 USE IN SPECIFIC POPULATIONS 8.1 Pregnancy 8.2 Lactation 8.4 Pediatric Use 8.5 Geriatric Use 10 OVERDOSAGE 10.1 Signs and Symptoms, Methemoglobinemia 10.2 Treatment of Overdosage 11 DESCRIPTION 12 CLINICAL PHARMACOLOGY 12.1 Mechanism of Action 12.2 Pharmacodynamics 12. . It should be used only in case of a documented positivity of cultural samples. Br J Dermatol. Staphylococcal Scalded Skin Syndrome: criteria for Differential Diagnosis from Lyells Syndrome. The approach to treatment should include discontinuation of any potentially causative medications and a search for any underlying malignancy. Role of nanocrystalline silver dressings in the management of toxic epidermal necrolysis (TEN) and TEN/StevensJohnson syndrome overlap. Paquet P, et al. Drugs that have been implicated in the causation of LPP include captopril, cinnarizine, ramipril, simvastatin, PUVA, and antituberculous medications. 2005;62(4):63842. [113] retrospectively compared mortality in 64 patients with ED treated either with iv or oral Cys A (35mg/kg) or IVIG (25g/Kg). This hypermetabolic state is also furtherly increased by the inflammation present in affected areas. Recombinant granulocyte colony-stimulating factor in the management of toxic epidermal necrolysis. A slow acetylator genotype is a risk factor for sulphonamide-induced toxic epidermal necrolysis and StevensJohnson syndrome. Dermatitis - Diagnosis and treatment - Mayo Clinic FDA Drug information Palynziq Read time: 10 mins Marketing start date: 04 Mar 2023 . Incidence and drug etiology in France, 1981-1985. Tohyama M, et al. Google Scholar. Article Ther Apher Dial. Polak ME, et al. Med Sci Monit. Arch Dermatol. The authors concluded that they couldnt demonstrate corticosteroids efficacy in monotherapy, but the use of steroid alone is not linked to an increased risk of mortality due to infective complications [108, 109]. Erythema multiforme (EM), StevensJohnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. The most common of these are psoriasis, atopic dermatitis, seborrheic dermatitis, contact dermatitis and pityriasis rubra pilaris. PubMed 2004;59(8):80920. J Am Acad Dermatol. 2. 2015;13(7):62545. Nat Med. In more severe cases continuous iv therapy can be necessary. Ibuprofen Zentiva can be prescribed with OTC Recipe - self-medication. Exfoliative dermatitis (ED) is defined as diffuse erythema and scaling of the skin involving more than 90% of the total body skin surface area. In order to rule out autoimmune blistering diseases, direct immune fluorescence staining should be additionally performed to exclude the presence of immunoglobulin and/or complement deposition in the epidermis and/or the epidermal-dermal zone, absent in ED. Journal of Pharmaceutical Research and health Care. 2018 Jan 28;2018:9095275. doi: 10.1155/2018/9095275. Downey A, et al. Allergic rhinitis and atopic dermatitis. Medical search. Web Wikizero - Basal-cell carcinoma Common acute symptoms include abdominal pain or cramps, nausea, vomiting, and diarrhea, jaundice, skin rash and eyes dryness and therefore could mimic the prodromal and early phase of ED. Erythema multiforme and toxic epidermal necrolysis: a comparative study. It is also recommended to void larger vesicles with a syringe. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. In most severe cases the suggested dosage is iv 11.5mg/kg/day. CAS AQUACEL Ag in the treatment of toxic epidermal necrolysis (TEN). In general, they occur more frequently in women, with a male to female ratio of 0.6 [22]. Systemic corticosteroids: These are the most common used drugs because of their known anti-inflammatory and immunosuppressive effect through the inhibition of activated cytotoxic T-cells and the production of cytokines. Current Perspectives on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis. Clinical features, diagnosis, and treatment of erythema multiforme: a review for the practicing dermatologist. volume14, Articlenumber:9 (2016) More than moderate, unresponsive to treatment, and which interferes with the Soldier's perfor-mance of duty. Targeting keratinocyte apoptosis in the treatment of atopic dermatitis and allergic contact dermatitis. J Am Acad Dermatol. Drug induced exfoliative dermatitis: state of the art, https://doi.org/10.1186/s12948-016-0045-0, http://creativecommons.org/licenses/by/4.0/, http://creativecommons.org/publicdomain/zero/1.0/. Generalized exfoliative dermatitis, or erythroderma, is a severe inflammation of the entire skin surface. Tang YH, et al. Summary: Drug induced interstitial nephritis, hepatitis and exfoliative dermatitis. Law EH, Leung M. Corticosteroids in StevensJohnson Syndrome/toxic epidermal necrolysis: current evidence and implications for future research. Each of these physiologic disruptions is potentially life-threatening. Am J Dermatopathol. Br J Dermatol. Other cases are ultimately classifiable as another dermatosis. and transmitted securely. Mona-Rita Yacoub. Harr T, French LE. Bookshelf Exfoliative dermatitis is a dangerous form of CADR which needs immediate withdrawl of all the four drugs. It has a wide spectrum of severity, and it is divided in minor and major (EMM). Fas-FasL interaction: Fas is a membrane-bound protein that after interaction with Fas-ligand (FasL) induces a programmed cell death, through the activation of intracellular caspases. Drug induced exfoliative dermatitis (ED) are a group of rare and severe drug hypersensitivity reactions (DHR) involving skin and usually occurring from days to several weeks after drug. Exfoliative dermatitis has been reported in association with hepatitis, acquired immunodeficiency syndrome, congenital immunodeficiency syndrome (Omenn's syndrome) and graft-versus-host disease.2,1517, In reviews of erythroderma, a significant percentage of patients (about 25 percent) do not receive a specific etiologic diagnosis. Skin manifestations of drug allergy. The fluid of blisters from TEN patients was found to be rich in TNF-, produced by monocytes/macrophages present in the epidermis [42], especially the subpopulation expressing CD16, known to produce higher levels of inflammatory cytokines [43]. Defective regulatory T cells in patients with severe drug eruptions: timing of the dysfunction is associated with the pathological phenotype and outcome. Efficacy of plasmapheresis for the treatment of severe toxic epidermal necrolysis: is cytokine expression analysis useful in predicting its therapeutic efficacy? Ko TM, et al. Ramirez GA, Yacoub MR, Ripa M, Mannina D, Cariddi A, Saporiti N, Ciceri F, Castagna A, Colombo G, Dagna L. Biomed Res Int. The most common causes of exfoliative dermatitis are preexisting dermatoses, drug reactions, malignancies and other miscellaneous or idiopathic disorders. Drug induced exfoliative dermatitis (ED) are a group of rare and severe drug hypersensitivity reactions (DHR) involving skin and usually occurring from days to several weeks after drug exposure. Drug-induced Exfoliative Dermatitis & Eosinophils Increased: Causes 2016;2:14. Correspondence to Br J Dermatol. Am J Dermatopathol. Ganciclovir and cidofovir should be used when polymerase-chain reactions (PCR) on peripheral blood or other biological sample identifies a viral reactivation (HHV6, HHV7, EBV and CMV). 2000;115(2):14953. Skin testing in delayed reactions to drugs. Annu Rev Pharmacol Toxicol. (adult rickets), anticonvulsant-induced rickets and osteomalacia, osteoporosis, renal osteodystrophy . Nature. Fitzpatricks dermatology in general medicine. 2013;27(3):35664. Adverse cutaneous drug reaction. Clinical features; Delayed type hypersensitivity; Drug hypersensitivity; Erythema multiforme; Exfoliative dermatitis; Lyells syndrome; Pathogenesis; StevensJohnson syndrome; Therapy; Toxic epidermal necrolysis. In addition to all these mechanisms, alarmins, endogenous molecules released after cell damage, were found to be transiently increased in SJS/TEN patients, perhaps amplifying the immune response, including -defensin, S100A and HMGB1 [47]. Painkiller therapy. Beneficial effect of plasma exchange in the treatment of toxic epidermal necrolysis: a series of four cases. Mayes T, et al. Kavitha Saravu. The most notable member of this group is mycosis fungoides. 2015;56(4):298302. Rifampin, paracetamol, metronidazole, paclitaxel, erythromycin, and ibuprofen have all been reported to cause bullous FDE. Google Scholar. 2011;50(2):2214. 1998;37(7):5203. Antiepileptic medications, antihypertensive medications, antibiotics, calcium channel blockers and a variety of topical agents (Table 2)2,3,69 can cause exfoliative dermatitis, but theoretically, any drug may cause exfoliative dermatitis. 2012;13(1):4954. Kostal M, et al. Su SC, Hung SI, Fan WL, Dao RL, Chung WH. Granulysin is a key mediator for disseminated keratinocyte death in StevensJohnson syndrome and toxic epidermal necrolysis. Ethambutol Induced Exfoliative Dermatitis - academia.edu Stevens-Johnson syndrome and toxic epidermal necrolysis due to anticonvulsants share certain clinical and laboratory features with drug-induced hypersensitivity syndrome, despite differences in cutaneous presentations. Springer Nature. It is also extremely important to obtain within the first 24h cultural samples from skin together with blood, urine, nasal, pharyngeal and bronchus cultures. More recently, carcinomas of the fallopian tube,12 larynx13 and esophagus14 have been reported as causes of exfoliative dermatitis. Patients must be cleaned in the affected areas until epithelization starts. Provided by the Springer Nature SharedIt content-sharing initiative. In patients with SJS/TEN increased serum levels of retinoid acid have been found. Acute processes usually favor large scales, whereas chronic processes produce smaller ones. (scFv) (directed against Dsg1/3) or AK23 (directed against Dsg3) with (as a control) or without exfoliative toxin A (ETA). CAS Robyn A. McMenamin, L M. Davies and P. W. Craswell, Aust. 3. (See paras 3 - 42 and 3- 43.) Br J Clin Pharmacol. 2. California Privacy Statement, The administration of a single dose of 5mg/kg was able to stop disease progression in 24h and to induce a complete remission in 614days. StevensJohnson syndrome and toxic epidermal necrolysis: assessment of medication risks with emphasis on recently marketed drugs. The dermo-epidermal junction and epidermis are infiltrated mostly by CD8+ T lymphocytes whereas dermal infiltrate, mainly made from CD4+ T lymphocytes, is superficial and mostly perivascular [20, 51]. The syndrome has been described previously in association with phenindione administration, leptospirosis and heavy metal poisoning. Manage cookies/Do not sell my data we use in the preference centre. The serum levels of granulysin were also found to be increased in the early stage of SJS/TEN, but not in other cutaneous DHR [40]. Anti-tubercular therapy (ATT) induced exfoliative dermatitis-A case Kirchhof MG et al. Case Rep Dermatol. Exanthematous drug eruptions. 2012;66(6):e22936. Toxic epidermal necrolysis: Part I Introduction, history, classification, clinical features, systemic manifestations, etiology, and immunopathogenesis. 2002;146(4):7079. Recurrent erythema multiforme in association with recurrent Mycoplasma pneumoniae infections. Granulysin as a marker for early diagnosis of the StevensJohnson syndrome. Ann Pharmacother. 2009;29(3):51735. J Clin Apher. Ann Intern Med. The incidence of cutaneous adverse drug reactions (CADRs) is high in HIV-infected persons; however, there are large gaps in knowledge about several aspects of HIV-associated CADRs in Africa, which carries the biggest burden of the disease. 2011;71(5):67283. 2001;108(5):83946. Death ligand TRAIL, secreted by CD1a+and CD14+cells in blister fluids, is involved in killing keratinocytes in toxic epidermal necrolysis. See permissionsforcopyrightquestions and/or permission requests. They usually have fever, are dyspneic and cannot physiologically feed. Australas J Dermatol. Semin Dermatol. Palynziq PEGVALIASE 20 mg/mL BioMarin Pharmaceutical Inc. Yamada H, Takamori K. Status of plasmapheresis for the treatment of toxic epidermal necrolysis in Japan. Immunophenotypic studies with the use of advanced antibody panels may be useful in the differential diagnosis of these two forms.10 Reticulum cell sarcoma is another form of cutaneous T-cell lymphoma that may cause exfoliative dermatitis. While nearly any medication can, in theory, cause a reaction if you're sensitive, medications linked to exfoliative dermatitis include: sulfa drugs; penicillin and certain other antibiotics . 2012;43:10115. Drug induced exfoliative dermatitis (ED) are a group of rare and severe drug hypersensitivity reactions (DHR) involving skin and usually occurring from days to several weeks after drug. Interleukin (IL)-1, IL-2, IL-8, intercellular adhesion molecule 1 (ICAM-1), tumor necrosis factor and interferon gamma are the cytokines that may have roles in the pathogenensis of exfoliative dermatitis.2. Harr T, French LE. Allergy. Allergy. 2012;53(3):16571. Exfoliative Dermatitis: Symptoms, Causes, and Treatment - WebMD It is necessary to obtain as soon as possible a central venous access and to start a continuous monitoring of vital signs. Exfoliative Dermatitis - StatPearls - NCBI Bookshelf J Allergy Clin Immunol. 1996;44(2):1646. Toxic epidermal necrolysis: Part II Prognosis, sequelae, diagnosis, differential diagnosis, prevention, and treatment. . Exfoliative Dermatitis Treatment & Management: Medical Care - Medscape 2013;69(4):37583. Mockenhaupt M, et al. As written before, Sassolas B. et al. What are Drug Rashes? Sequelae of exfoliative dermatitis are not widely reported. Ann Allergy Asthma Immunol. 1997;19(2):12732. Barbaud A. Add 1 cup (about 236 milliliters) of vinegar to a bathtub filled with warm water. Patient must be placed in an antidecubitus fluidized bed and room temperature must be kept at 3032C in order to slow catabolism and reduce the loss of calories through the skin [89]. Drug-Induced Kidney Injury & Exfoliative Dermatitis Symptom Checker: Possible causes include Gold Salt. HLA-A* 3101 and carbamazepine-induced hypersensitivity reactions in Europeans. Accessibility In serious cases invasive ventilation can be necessary for ARDS. In postmarketing reports, cases of drug-induced hepatotoxicity have been reported in the first month, and in some cases, the first 2 months of NSAID therapy. Nassif A, et al. CD94/NKG2C is a killer effector molecule in patients with Stevens-Johnson syndrome and toxic epidermal necrolysis. ACE inhibitor-induced cough should be considered in the differential diagnosis of cough. It is a reaction pattern and cutaneous manifestation of a myriad of underlying ailments, including psoriasis and eczema, or a reaction to the consumption of . The lesions consist of pruritic, annular papules, vesicles, and bullae that are found in groups, clinically it is similar to dermatitis herpetiformis, without a gluten-sensitive enteropathy [85]. Disasters. 19 Key critical interactions are discussed below for each mpox antiviral. Poor relevance of a lymphocyte proliferation assay in lamotrigine-induced StevensJohnson syndrome or toxic epidermal necrolysis. tion in models of the types of systemic disease for S. aureus pathogenesis research is also expected to receive which anti-virulence drugs would be most desirable. 2010;2(3):18994. It often precedes or is associated with exfoliation (skin peeling off in scales or layers), when it may also be known as exfoliative dermatitis (ED). Exfoliative dermatitis is also a risk factor for epidemic spread of methicillin-resistant Staphylococcus aureus.6,20. The taper of steroid therapy should be gradual [93]. [Stevens-Johnson Syndrom and Toxic Epidermal Necrolysis--based on literature]. Drug induced exfoliative dermatitis - yxw_88 - | (5.7, 8.1, 8.3) ADVERSE REACTIONS The most commonly reported adverse drug reactions (ADRs), reported in more than 20% of the patients and greater than placebo were skin reactions and diarrhea . Carbamazepine and phenytoin induced StevensJohnson syndrome is associated with HLA-B* 1502 allele in Thai population. 2002;109(1):15561. Kirchhof MG, et al. This compressed maturation process results in an overall greater loss of epidermal material, which is manifested clinically as severe scaling and shedding. Clin Exp Dermatol. 1990;126(1):437. PMC Pathophysiology DIP. Considered variables in SCORTEN are shown in Table2. MRY, MGS, EN and GC designed the study, selected scientifically relevant information, wrote and revised the manuscript. Pehr K. The EuroSCAR study: cannot agree with the conclusions. [81]. Contact Dermatitis. Incidence of hypersensitivity skin reactions. Medical search. Frequent A catabolic state thus ensues, which is often responsible for significant weight loss. Liver injury and exfoliative dermatitis caused by nifuratel[J]. Rabelink NM, Brakman M, Maartense E, Bril H, Bakker-Wensveen CA, Bavinck JN. 2013;69(2):187. Grieb G, et al. Sokumbi O, Wetter DA. Delayed reactions to drugs show levels of perforin, granzyme B, and Fas-L to be related to disease severity. 2011;3(1):e2011004. It was used with success in different case reports [114116]. 583-587. A significant number of these patients eventually progress to cutaneous T-cell lymphoma.8, Clinically, the first stage of exfoliative dermatitis is erythema, often beginning as single or multiple pruritic patches, involving especially the head, trunk and genital region. Nutr Clin Pract. Association of HLA-B*1502 allele with carbamazepine-induced toxic epidermal necrolysis and StevensJohnson syndrome in the multi-ethnic Malaysian population. Drugs causing erythroderma | DermNet Toxic epidermal necrolysis: Part I Introduction, history, classification, clinical features, systemic manifestations, etiology, and immunopathogenesis. Bullous FDE. 22 Abacavir-induced hypersensitivity syndrome is strongly associated with HLA-B*5701 during treatment . A promising and complementary in vitro tool has been used by Polak ME et al. 2013;168(3):55562. Bethesda, MD 20894, Web Policies Overall, T cells are the central player of these immune-mediated drug reactions. For carbamazpine, several studies have found a common link between specific HLAs and different kinds of cutaneous adverse reactions, as for HLA-A*3101 in Japanese [30] and Europeans [31]. Skin eruptions caused by CBZ occur in 24% of the patients on this therapy and include pruritic and erythematous rashes, urticaria, photosensitivity reactions, alterations in skin pigmentation, exfoliative dermatitis, and toxic epidermal necrolysis View on Wiley ncbi.nlm.nih.gov Save to Library Create Alert Cite 12 Citations Citation Type T and NK lymphocytes can produce FasL that eventually binds to target cells. Students also viewed Nostra aetate - Summary Theology: the basics Principles of Risk Management and Insurance Chapters 1-4 Umbilical cord mesenchymal stem cell transplantation in drug-induced StevensJohnson syndrome. Br J Dermatol. 1996;35(4):2346. If cutaneous pathology also mimics cutaneous T-cell lymphoma, it can be very difficult to differentiate a drug-induced skin condition from exfoliative dermatitis associated with a malignancy.2,9. In recent years, clinicians have come to believe that this condition is secondary to a complicated interaction of cytokines and cellular adhesion molecules. Pharmacogenet Genom. The authors wish to thank Dr. Gary White for the picture of EM showed in Fig. The timing of the rash can also vary. J Allergy Clin Immunol. It is not completely clear whether EM and SJS are separate clinical entities or if they represent two different expressions of a single disease process. DailyMed - DICLOFENAC SODIUM- diclofenac sodium solution Also a vesical catheter should be placed to avoid urethral synechiae and to have a precise fluid balance. Schneck J, et al. Schopf E, et al. Minerva Stomatol. Stamp LK, Chapman PT. Exposure to anticonvulsivants (phenytoin, phenobarbital, lamotrigine), non-nucleoside reverse transcriptase inhibitors (nevirapine), cotrimoxazole and other sulfa drugs (sulfasalazine), allopurinol and oxicam NSAIDs [2] confers a higher risk of developing SJS/TEN. 1995;14(6):5589. Int J Dermatol. Fritsch PO. Acute and chronic leukemia may also cause exfoliative dermatitis. J Burn Care Res. J Am Acad Dermatol. Open trial of ciclosporin treatment for StevensJohnson syndrome and toxic epidermal necrolysis. It is recommended to use 1.5mg/kg hydrocortisone. asiatic) before starting therapies with possible triggers (e.g. If it is exfoliative dermatitis that's drug induced, it's easy to treat . These measures include bed rest, lukewarm soaks or baths, bland emollients and oral antihistamines.2527, In patients with chronic idiopathic erythroderma, emollients and topical steroids may be effective. 1995;333(24):16007. Clin Exp Allergy. Exfoliative Dermatitis: Definition, Causes, Treatments and More 1). Cancer Diagnosis & Prognosis J Am Acad Dermatol. Patients with carcinoma of the colon, lung, prostate and thyroid have presented with erythroderma. 2008;128(1):3544. This has been called the nose sign.18, Once the erythema is well established, scaling inevitably follows (Figure 1). Abstract Acute interstitial nephritis associated with hepatitis, exfoliative dermatitis, fever and eosinophilia is uncommon. De Araujo E, et al. Drug reactions are one of the most common causes of exfoliative dermatitis. Dermatol Clin. J Invest Dermatol. Fritsch PO. 2008;53(1):28. PDF Drug induced exfoliative dermatitis: state of the art N Engl J Med. Kano Y, et al. doi: 10.4103/0019-5154.39732. 2012;97:14966. In: Eisen AZ, Wolff K, editors. It is a clinical manifestation and usually associated with various underlying cutaneous disorders, drug induced reactions and malignancies. Shared and restricted T-cell receptor use is crucial for carbamazepine-induced Stevens-Johnson syndrome. Typical laboratory values include mild anemia, leukocytosis, eosinophilia, elevated erythrocyte sedimentation rate, abnormal serum protein electrophoresis with a polyclonal elevation in the gamma globulin region, and elevated IgE levels.13,68. Prevalence is low, with mortality of roughly 512.5% for SJS and 50% for TEN [1, 2]. Careers. 2010;31(1):1004. Terms and Conditions, Mediterr J Hematol Infect Dis. Scientific evidences suggest a role for HLAs and drug-induced SJS/TEN, although some racial differences have been found that can be due to variation of frequencies of these alleles and to the presence of other susceptibility genes [26]. 12 out of 17 studies concluded for a positive role of IVIG in ED. Chung and colleagues found an high expression of this molecule in TEN blister fluid [39] and confirmed both in vitro and in vivo its dose-dependent cytotoxicity [39]. Bastuji-Garin S, et al. 2009;151(7):5145. Drug reaction with Eosinophilia and systemic symptoms (DRESS) syndrome can mimic SJS and TEN in the early phases, since ED can occur together with the typical maculo-papular rash. Cite this article. When less than 10% of the body surface area (BSA) is involved, it is defined SJS, when between 10 and 30% of BSA it is defined overlapping SJS/TEN, when more than 30% of BSA, TEN [2] (Additional file 1: Figure S1, Additional file 2: Figure S2). (in Chinese) . J Dermatol. A recently published meta-analysis by Huang [110] and coworkers on IVIG in SJS/SJS-TEN/TEN reviewed 17 studies with 221 patients and compared the results obtained with high-dosage IVIG (>2g/kg) compared to lower-dosage IVIG (<2g/kg). 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