drug induced exfoliative dermatitisdrug induced exfoliative dermatitis

Article 2012;2012:915314. SSSS is characterized by periorificial face scabs, de-epithelialization of friction zones and conspicuous desquamation after initial erythroderma. Two Cases in Adult Patients. Energy requirements of pediatric patients with StevensJohnson syndrome and toxic epidermal necrolysis. PubMed These levels could reflect the interaction between culprit drugs and aldehyde dehydrogenase that is the enzyme which metabolizes retinoid acid. 1995;14(6):5589. 1994;331(19):127285. Curr Opin Allergy Clin Immunol. Download Free PDF. Erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. Anticoagulation therapy. Erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. Med J Armed Forces India. 1998;37(7):5203. Erythema multiforme, StevensJohnson syndrome and toxic epidermal necrolysis in northeastern Malaysia. What are Drug Rashes? https://doi.org/10.1186/s12948-016-0045-0, DOI: https://doi.org/10.1186/s12948-016-0045-0. Other dermatoses associated with erythroderma are listed in Table 1.2,3,68. doi: 10.4103/0019-5154.39732. 2014;71(2):27883. The most common causes of exfoliative dermatitis are preexisting dermatoses, drug reactions, malignancies and other miscellaneous or idiopathic disorders. doi: 10.1111/dth.15416. Patients with carcinoma of the colon, lung, prostate and thyroid have presented with erythroderma. 2013;27(5):65961. The taper of steroid therapy should be gradual [93]. Anyone you share the following link with will be able to read this content: Sorry, a shareable link is not currently available for this article. Oral hygiene with antiseptic and painkiller mouthwash (chlorhexidine+lidocaine+aluminum hydroxide) together with aerosol therapy with saline and bronchodilators can reduce upper airways symptoms. In particular, drug induced exfoliative dermatitis (ED) are a group of rare and more severe drug hypersensitivity reactions (DHR) involving skin and mucous membranes and usually occurring from days to several weeks after drug exposure [2]. Theoretically, any drug can trigger a reaction, but the medications most associated with this disorder are: Allopurinol; Antiepileptic medications; Barbiturates Herpes simplex virus (HSV) 1 and 2 are the main triggers in young adults (>80% of cases), followed by Epstein-Barr virus (EBV), and Mycoplasma pneumonia [5558]. Both hyperthermia and hypothermia are reported. A slow acetylator genotype is a risk factor for sulphonamide-induced toxic epidermal necrolysis and StevensJohnson syndrome. Oral manifestations of erythema multiforme. Liver injury and exfoliative dermatitis caused by nifuratel[J]. 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. Schwartz RA, McDonough PH, Lee BW. Toxic epidermal necrolysis associated with Mycoplasma pneumoniae infection. Joint Bone Spine. Although the etiology is. Exp Dermatol. Oliveira L, Zucoloto S. Erythema multiforme minor: a revision. 2005;94(4):41923. 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. 2023 Jan 30;11(2):346. doi: 10.3390/microorganisms11020346. Yacoub, MR., Berti, A., Campochiaro, C. et al. Death ligand TRAIL, secreted by CD1a+and CD14+cells in blister fluids, is involved in killing keratinocytes in toxic epidermal necrolysis. Affiliated tissues include skin, liver and bone marrow. Arch Dermatol. 1990;126(1):437. Erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. Exfoliative dermatitis (ED) is defined as diffuse erythema and scaling of the skin involving more than 90% of the total body skin surface area. Mild to severe alopecia and transient or permanent nail dystrophy also may be encountered. Indian J Dermatol. Fritsch PO. Google Scholar. In EM a lymphocytic infiltrate (CD8+ and macrophages), associated with vacuolar changes and dyskeratosis of basal keratinocytes, is found along the dermo-epidermal junction, while there is a moderate lymphocytic infiltrate around the superficial vascular plexus [20]. 2002;118(4):72833. ACE inhibitor-induced cough should be considered in the differential diagnosis of cough. Once ED has occurred, it has to be managed in the adequate setting with a multidisciplinary approach, and every effort has to be made to identify and avoid the trigger and to prevent infectious and non-infectious complications. Ann Intern Med. Exfoliative Dermatitis is a serious skin cell disorder that requires early diagnosis and treatment. Here we provide a systematic review of frequency, risk factors, molecular and cellular mechanisms of reactions, clinical features, diagnostic work-up and therapy approaches to drug induced ED. 2013;27(3):35664. 2004;428(6982):486. Aminoglutethimide: Aminoglutethimide may lead to a loss of corticosteroid-induced adrenal suppression. Australas J Dermatol. PubMed Wetter DA, Davis MD. Karnes JH, Miller MA, White KD, Konvinse KC, Pavlos RK, Redwood AJ, Peter JG, Lehloenya R, Mallal SA, Phillips EJ. Drug-induced Exfoliative Dermatitis & Eosinophils Increased Symptom Checker: Possible causes include Exfoliative Dermatitis. J Am Acad Dermatol. Paulmann M, Mockenhaupt M. Severe drug-induced skin reactions: clinical features, diagnosis, etiology, and therapy. Jarrett P, 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. Gastric protection. Immunoregulatory effector cells in drug-induced toxic epidermal necrolysis. Toxic epidermal necrolysis: review of pathogenesis and management. Ibuprofen Zentiva can be prescribed with OTC Recipe - self-medication. All the linen must be sterile. Infliximab was used in cases refractory to high-dosage steroid therapy and/or IVIG. In HIV patients, the risk of SJS and TEN have been reported to be thousand-fold higher, roughly 1 per 1000 per year [19]. HLA-B* 5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol. 1995;5(4):2558. (adult rickets), anticonvulsant-induced rickets and osteomalacia, osteoporosis, renal osteodystrophy . The most notable member of this group is mycosis fungoides. The approach to treatment should include discontinuation of any potentially causative medications and a search for any underlying malignancy. Careers. 2011;20(5):103441. Khalil I, et al. doi: 10.1016/j.jaad.2013.05.003. 2. 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. Abstract Acute interstitial nephritis associated with hepatitis, exfoliative dermatitis, fever and eosinophilia is uncommon. Br J Dermatol. 2012;66(3):1906. A marker for StevensJohnson syndrome: ethnicity matters. Li X, et al. eCollection 2018. It is not recommended to use prophylactic antibiotic therapy. Corticosteroids could also reduce the amount of keratinocytes apoptosis and the activation of caspases [105]. J Invest Dermatol. PubMedGoogle Scholar. 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. For these reasons, patients should be admitted to intensive burn care units or in semi-intensive care units where they may have access to sterile rooms and to dedicated medical personnel [49, 88]. The exact role of FasL in the pathogenesis of toxic epidermal necrolysis is still questionable especially because a correlation between serum FasL levels and disease severity has not been established and because its levels have been found to be increased also in drug-induced hypersensitivity syndrome and maculopapular eruption [36]. 2008;159(4):9814. . 2010;125(3):70310. Although the final result of this dual interaction is still under investigation, it seems that the combination of TNF-, IFN- (also present in TEN patients) and the activation of other death receptors such as TWEAK can lead to apoptosis of keratinocytes [44]. Erythema multiforme (EM), StevensJohnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. Google Scholar. IBUPROFENE ZENTIVA is indicated for the symptomatic treatment of headaches, migraines, dental pain, back pain, dysmenorrhea, muscle pain, neuralgia . Since cutaneous function as a multiprotective barrier is so disrupted in exfoliative dermatitis, the body loses heat, water, protein and electrolytes, and renders itself much more vulnerable to infection. J Allergy Clin Immunol. 2011;50(2):2214. Talk to our Chatbot to narrow down your search. Br J Dermatol. 2013;69(2):1734. volume14, Articlenumber:9 (2016) Barbaud A. In SJS, SJS/TEN and TEN the efficacy of corticosteroids is far from being demonstrated. Nassif A, et al. In the acute phase, before determination of the etiology, treatment consists of measures to soothe the inflamed skin. Soak for 5 to 10 minutes and rinse off before patting dry. Clin Exp Dermatol. 2010;163(4):84753. Strom BL, et al. The exact source of FasL production has not been yet identified as different groups have postulated that the production might be sought in keratinocytes themselves [33] or in peripheral blood mononuclear cells [34]. 2008;53(1):28. The diagnosis of GVDH requires histological confirmation [87]. 2013;133(5):1197204. Abe R, et al. 2014;70(3):53948. Morel E, et al. Tumor necrosis factor : TNF- seems also to play an important role in TEN [41]. Google Scholar. Volume 8, Issue 1 Pages 1-90 (August 1994). Granulysin is a key mediator for disseminated keratinocyte death in StevensJohnson syndrome and toxic epidermal necrolysis. J Dermatol. Not responsive to therapy. Morel E, et al. Its also characterized by a cell-poor infiltrate, where macrophages and dendrocytes with a strong TNF- immunoreactivity predominate [6, 50]. 2010;88(1):608. An increased metabolism is typical of patients with extended disepithelizated areas. 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. Erythema multiforme and toxic epidermal necrolysis: a comparative study. In recent years, clinicians have come to believe that this condition is secondary to a complicated interaction of cytokines and cellular adhesion molecules. TEN is characterized by full-thickness epidermal necrosis with an evident epidermal detachment and sloughing caused by necrosis of keratinocytes following apoptosis [49, 52]. 2008;128(1):3544. J Am Acad Dermatol. 1997;19(2):12732. CAS Ther Apher Dial. Incidence and drug etiology in France, 1981-1985. Verma R, Vasudevan B, Pragasam V. Severe cutaneous adverse drug reactions. Gonzalez-Delgado P, et al. Br J Dermatol. Medicines have been linked to every type of rash, ranging from mild to life-threatening. Ned Tijdschr Geneeskd. Br J Dermatol. It should be used only in case of a documented positivity of cultural samples. Sequelae of exfoliative dermatitis are not widely reported. Pharmacogenomics J. Dermatol Clin. Google Scholar. First of all, Sassolas and coauthors proposed an algorithm of drug causality (ALDEN) in order to improve the individual assessment of drug causality in TEN and SJS [71]. Since the earliest descriptions of exfoliative dermatitis, medications have been known to be important causative agents. The induction dosage in EMM is usually 1mg/kg/day that should be maintained until a complete control of the skin is obtained. 12 out of 17 studies concluded for a positive role of IVIG in ED. Staphylococcal Scalded Skin Syndrome: criteria for Differential Diagnosis from Lyells Syndrome. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. Notably, Agr inhibitors have not yet been more rigorous pre-clinical testing using the established analyzed using rigorous testing with systemic applica standards for drug development. 2011;38(3):23645. J Dermatol Sci. Erythema multiforme (photo reproduced with, Erythema multiforme (photo reproduced with permission of Gary White, MD): typical target lesions, Mortality rate of patients with TEN has shown to be directly correlated to, Management of patients with a suspected drug induced exfoliative dermatitis, MeSH Kirchhof MG et al. Su SC, Hung SI, Fan WL, Dao RL, Chung WH. The velocity of infusion should be regulated according to patients arterial pressure with the aim of 30mL/h urinary output (1mL/kg/h in case of a child). Posadas SJ, et al. A systematic review of treatment of drug-induced StevensJohnson syndrome and toxic epidermal necrolysis in children. Drugs that have been implicated in the causation of LPP include captopril, cinnarizine, ramipril, simvastatin, PUVA, and antituberculous medications. Clinical classification of cases of toxic epidermal necrolysis, StevensJohnson syndrome, and erythema multiforme. Infectious agents are the major cause of EM, in around 90% of cases, especially for EM minor and in children. Utility of the lymphocyte transformation test in the diagnosis of drug sensitivity: dependence on its timing and the type of drug eruption. Ayangco L, Rogers RS 3rd. 2005;102(11):41349. Samim F, et al. Heat loss is another major concern that accompanies a defective skin barrier in patients with exfoliative dermatitis. Garza A, Waldman AJ, Mamel J. It is challenging to diagnose this syndrome due to the variety . Tang YH, et al. 2010;85(2):131138. 1996;44(2):1646. Patients should be educated to avoid any causative drugs. Sekula P, et al. 2013;69(2):173174. Science. Chang CC, et al. 2011;20(2):10712. Drug-induced LPP. 2008;12(5):3559. Generalized. One of the most common malignancies associated with exfoliative dermatitis is cutaneous T-cell lymphoma, which may not manifest for months or even years after the onset of the skin condition. Carrozzo M, Togliatto M, Gandolfo S. Erythema multiforme. 2010;62(1):4553. Br J Dermatol. The enhanced activation of CD8 T cells seems also to be influenced by the impaired function of CD4+CD25+FoxP3+Treg cells found in the peripheral blood of TEN patients in the acute phase [46]. Applications of Immunopharmacogenomics: Predicting, Preventing, and Understanding Immune-Mediated Adverse Drug Reactions. 2007;48(5):10158. In this study, 965 patients were reviewed. HLA-B1502, HLA-B5701, HLA-B5801 and carbamazepine, abacavir, and allopurinol, respectively). Unlike EMM, SJS and TEN are mainly related to medication use. An official website of the United States government. J Am Acad Dermatol. Man CB, et al. Medical genetics: a marker for StevensJohnson syndrome. On the other hand, it has been demonstrated that genetic predisposition may increase the risk for sulphonamide-induced [24] and carbamazepine-induced TEN and SJS [25]. N Engl J Med. Article N Engl J Med. exfoliative conditions. Both DRESS and SJS may have increased liver enzymes and hepatitis, but they occur in only 10% of cases of SJS compared to 80% of DRESS. 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. As described in Table3, major differential diagnosis of EM and SJS/TEN are (1) staphylococcal scalded skin syndrome (SSSS), (2) autoimmune blistering diseases and disseminated fixed bullous drug eruption, (3) others severe delayed DHR [6, 70, 82] (4) Graft versus host disease. -. 2009;182(12):80719. The efficacy of intravenous immunoglobulin for the treatment of toxic epidermal necrolysis: a systematic review and meta-analysis. A promising and complementary in vitro tool has been used by Polak ME et al. Drug-induced exfoliative dermatitis is usually short-lived once the inciting medication is withdrawn and appropriate therapy is administered. Paradisi et al. Annu Rev Pharmacol Toxicol. 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). 2007;56(5 Suppl):S1189. 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). Intravenous administration is recommended. Hospitalization and dermatologic consultation are indicated in most cases to ensure that all of the necessary cutaneous, laboratory and radiologic investigations and monitoring are performed. loss of taste Derm: stevens-johnson syndrome, toxic epidermal necrolysis, rash, exfoliative dermatitis, hair . Part of This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP. Bourgeois GP, et al. Pharmacogenet Genom. Drug rashes are the body's reaction to a certain medicine. Considered variables in SCORTEN are shown in Table2. Check the full list of possible causes and conditions now! Erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. Case Rep Dermatol. Gastrointest Endosc. They usually have fever, are dyspneic and cannot physiologically feed. Bullous FDE. Wu PA, Cowen EW. 2011;128(6):126676. Autologous transplantation of mesenchymal umbilical cord cells seems also to be highly efficacious [102]. Overall, T cells are the central player of these immune-mediated drug reactions. 2008;14(12):134350. Infliximab: chimeric IgG monoclonal anti-TNF- antibody. Kreft B, et al. In the 5 studies that concluded negatively for IVIG, the dosage was below 0.4g/kg/day and treatment was maintained for less than 5days. Mittmann N, et al. J Am Acad Dermatol. More than moderate, unresponsive to treatment, and which interferes with the Soldier's perfor-mance of duty. This has been called the nose sign.18, Once the erythema is well established, scaling inevitably follows (Figure 1). 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. Recurrence occurs in around one-third of cases [15] and there is a genetic predisposition for certain Asian groups [16]. Szary syndrome, the leukemic variant of mycosis fungoides, is also associated with exfoliative dermatitis. Mockenhaupt M, et al. Also, physicians should be vigilant about possible secondary infection, whether cutaneous, pulmonary or systemic. If there is a high suspicion of infection without a documented source of infection, broad range empiric therapy should be started. 2012;43:10115. Schopf E, et al. Wolkenstein P, et al. 1996;135(2):3056. [71] realized an algorhitm named ALDEN (algorithm of drug causality for epidermal necrolysis) which helps to establish a cause/effect relationship as probable or very probable in 70% of cases. 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 . Orton PW, et al. Rifampin, paracetamol, metronidazole, paclitaxel, erythromycin, and ibuprofen have all been reported to cause bullous FDE. asiatic) before starting therapies with possible triggers (e.g. Allergy. 1991;127(6):8318. It recommended to used G-CSF in patients with febrile neutropenia [94, 95]. The most common causes of death in patients with exfoliative dermatitis are pneumonia, septicemia and heart failure. 2016;2:14. J Allergy Clin Immunol. Detection of a herpes simplex viral antigen in skin lesions of erythema multiforme. Initial symptoms could be aspecific, as fever, stinging eyes and discomfort upon swallowing, occurring few days before the onset of mucocutaneous involvement. Erythema multiforme and toxic epidermal necrolysis. 2002;146(4):7079. New York: McGraw-Hill; 2003. pp. Exanthematous drug eruptions. Chemicals and Drugs 61. Paul C, et al. Also a vesical catheter should be placed to avoid urethral synechiae and to have a precise fluid balance. Vasoactive amines may be necessary in case of shock. Furosemide or ethacrynic acid may be required to maintain an adequate urinary output [90]. Burns. Locharernkul C, et al. Erythema multiforme and latent herpes simplex infection. . Erythema multiforme StevensJohnson syndrome and toxic epidermal necrolysis. In contrast with DRESS, eosinophilia and atypical lymphocytes are not described in patients with SJS or TEN. Rarely, Mycoplasma pneumoniae, dengue virus, cytomegalovirus, and contrast media may be the causative agent of SJS and TEN [22, 6567]. Effects of treatments on the mortality of StevensJohnson syndrome and toxic epidermal necrolysis: a retrospective study on patients included in the prospective EuroSCAR Study. J Eur Acad Dermatol Venereol. Typical target lesions consist of three components: a dusky central area or blister, a dark red inflammatory zone surrounded by a pale ring of edema, and an erythematous halo on the periphery. Overall, T cells are the central player of these immune-mediated drug reactions. 22 Abacavir-induced hypersensitivity syndrome is strongly associated with HLA-B*5701 during treatment . . [113] retrospectively compared mortality in 64 patients with ED treated either with iv or oral Cys A (35mg/kg) or IVIG (25g/Kg). Case Report Toxic epidermal necrolysis and StevensJohnson syndrome. Paradisi A, et al. Article 1993;129(1):926. Contact Dermatitis. Theoretically, any drug may cause exfoliative dermatitis. Options include use of PUVA light therapy, total-body electron beam irradiation, topical nitrogen mustard, systemic chemotherapy and extracorporeal photopheresis. Toxic epidermal necrolysis: Part I Introduction, history, classification, clinical features, systemic manifestations, etiology, and immunopathogenesis. After 24 hours, split formation was evident in hematoxylin and eosin-stained sections of HOSCs treated . Hepatobiliary: jaundice, hepatitis, including . The .gov means its official. Wolkenstein P, et al. Mardani M, Mardani S, Asadi Kani Z, Hakamifard A. Dermatol Ther. In general, they occur more frequently in women, with a male to female ratio of 0.6 [22]. 2008;52(3):1519. It characteristically demonstrates diffuse erythema and scaling of greater than 90% of the body surface area. J Invest Dermatol. If after 4days there is not an improvement it is advised to consider the association of steroid or its replacement with one of the following drugs [49, 93]: Intravenous immunoglobulins (IVIG): play their role through the inhibition of FasFas ligand interaction that it is supposed to be the first step in keratinocytes apoptosis [33]. 2012;42(2):24854. Tohyama M, et al. Arch Dermatol. Linear IgA dermatosis most commonly presents in patients older than 30years. By using this website, you agree to our Bethesda, MD 20894, Web Policies J Invest Dermatol. (2.4, 5.6) Embryo-fetal Toxicity: Can cause fetal harm. Malignancies are a major cause of exfoliative dermatitis. Hum Mol Genet. Apoptosis as a mechanism of keratinocyte death in toxic epidermal necrolysis. 2011;364(12):113443. A case of anti-BP230 antibody-positive dyshidrosiform bullous pemphigoid secondary to dipeptidyl peptidase-4 inhibitor in a 65-year-old Filipino female 2012;97:14966. Grosber M, et al. Allergol Immunopathol (Madr). Von Hebra first described erythroderma (exfoliative dermatitis) in 1868. 1. The most commonly used steroids were methylprednisolone, prednisolone and dexamethasone. Bickle K, Roark TR, Hsu S. Autoimmune bullous dermatoses: a review. N Engl J Med. 2023 BioMed Central Ltd unless otherwise stated. Mawson AR, Eriator I, Karre S. StevensJohnson syndrome and toxic epidermal necrolysis (SJS/TEN): could retinoids play a causative role? 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].

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