Erythema multiforme (EM), StevensJohnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. Erythema multiforme to amoxicillin with concurrent infection by Epstein-Barr virus. Drug-induced LPP. It might be. HHS Vulnerability Disclosure, Help In EMM lesions typically begin on the extremities and sometimes spread to the trunk. 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. 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. Stamp LK, Chapman PT. Li X, et al. 2010;5:39. Tumor necrosis factor : TNF- seems also to play an important role in TEN [41]. Antiviral therapy. Chemicals and Drugs 61. See permissionsforcopyrightquestions and/or permission requests. Early sites of skin involvement include trunk, face, palms and soles and rapidly spread to cover a variable extension of the body. In postmarketing reports, cases of drug-induced hepatotoxicity have been reported in the first month, and in some cases, the first 2 months of therapy, but can occur at any time during treatment with diclofenac. Springer Nature. 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]. A pseudolymphoma reaction with fever, arthralgias, lymphadenopathy, hepatosplenomegaly, anemia and erythroderma may develop as a result of hypersensitivity to dapsone or antiepileptic drugs. Ann Pharmacother. Etanercept: monoclonal antibody against the TNF- receptor. Check the full list of possible causes and conditions now! The EuroSCAR-study. exfoliative dermatitis. 1996;35(4):2346. Inhibition of toxic epidermal necrolysis by blockade of CD95 with human intravenous immunoglobulin. Allergy. Options include use of PUVA light therapy, total-body electron beam irradiation, topical nitrogen mustard, systemic chemotherapy and extracorporeal photopheresis. Among the anti-tubercular drugs exfoliative dermatitis is reported with rifampicin, isoniazid, ethambutol, pyrazinamide, streptomycin, PAS either singly or in combination of two drugs in some cases. Tohyama M, et al. volume14, Articlenumber:9 (2016) Allergol Immunopathol (Madr). Joint Bone Spine. 1998;282(5388):4903. A systematic review of treatment of drug-induced StevensJohnson syndrome and toxic epidermal necrolysis in children. The SCORTEN scale is based on a minimal set of parameters as described in the following table. Erythema multiforme, StevensJohnson syndrome and toxic epidermal necrolysis in northeastern Malaysia. Usually, but not always, the palms of the hands, the soles of the feet and the mucous membranes are spared. ALDEN has shown a good accuracy to assess drug causality compared to data obtained by pharmacovigilance method and casecontrol results of the EuroSCAR casecontrol analysis for drugs associated with TEN. J Am Acad Dermatol. Gastric protection. Article J. Huff JC. Acute and chronic leukemia may also cause exfoliative dermatitis. PubMed Central 2009;29(3):51735. 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. 2001;108(5):83946. Man CB, et al. Am J Clin Dermatol. PubMed Central 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. 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. HLA-B* 5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol. Ann Intern Med. Erythroderma (literally, "red skin"), also sometimes called exfoliative dermatitis, is a severe and potentially life-threatening condition that presents with diffuse erythema and scaling involving all or most of the skin surface area (90 percent, in the most common definition). Napoli B, et al. exfoliative conditions. J Am Acad Dermatol. Hung S-I, et al. Exfoliative dermatitis, also known as erythroderma, is an uncommon but serious skin disorder that family physicians must be able to recognize and treat appropriately. Descamps V, Ranger-Rogez S. DRESS syndrome. In acute phase it is crucial to assess the culprit agent, in particular when the patient was assuming several drugs at time of DHR. 2023 Jan 30;11(2):346. doi: 10.3390/microorganisms11020346. A catabolic state thus ensues, which is often responsible for significant weight loss. Unlike EMM, SJS and TEN are mainly related to medication use. 2004;59(8):80920. Medical genetics: a marker for StevensJohnson syndrome. Ann Allergy Asthma Immunol. 1999;48(5):21726. Carbamazepine and phenytoin induced StevensJohnson syndrome is associated with HLA-B* 1502 allele in Thai population. Cookies policy. 2018 Jan 28;2018:9095275. doi: 10.1155/2018/9095275. Paquet P, et al. N Engl J Med. 1992;11(3):20710. 2010;163(4):84753. Erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. Partial to full thickness epidermal necrosis, intraepidermal vesiculation or subepidermal blisters, due to spongiosis and to the cellular damage of the basal layer of the epidermis, can be present in the advanced disease [49] Occasionally, severe papillary edema is also present [20]. Wetter DA, Camilleri MJ. [Stevens-Johnson Syndrom and Toxic Epidermal Necrolysis--based on literature]. Locharernkul C, et al. Corticosteroids could also reduce the amount of keratinocytes apoptosis and the activation of caspases [105]. 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. Incidence and antecedent drug exposures. Gonzalez-Delgado P, et al. 2023 BioMed Central Ltd unless otherwise stated. Bookshelf Drug-induced Exfoliative Dermatitis & Eosinophils Increased Symptom Checker: Possible causes include Exfoliative Dermatitis. A slow acetylator genotype is a risk factor for sulphonamide-induced toxic epidermal necrolysis and StevensJohnson syndrome. Cutaneous drug eruptions are one of the most common types of adverse reaction to medications, with an overall incidence of 23% in hospitalized patients [1]. Systemic derangements may occur with exfoliative. 2004;114(5):120915. Cho YT, et al. Allergy. Recently, a meta-analysis based on 6 retrospective studies evaluating the role of corticosteroids alone or together with IVIG has been published [107]. 2011;20(5):103441. Continue Reading. The syndrome has been described previously in association with phenindione administration, leptospirosis and heavy metal poisoning. It should be considered only once the patient is stable and if the skin damage is still ongoing and doesnt respond to other conventional therapies (corticosteroids or IVIG). 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. Hypervolemia can also occur in patients with exfoliative dermatitis, contributing to the likelihood of cardiac failure.2124, In most patients with erythroderma, skin biopsies show nonspecific histopathologic features, such as hyperkeratosis, parakeratosis, acanthosis and a chronic perivascular inflammatory infiltrate, with or without eosinophils. Oral manifestations of erythema multiforme. Some anti-seizure medicines have also been known to cause exfoliative dermatitis. Some of these patients undergo spontaneous resolution. Hence, the apparent increase in cases of exfoliative dermatitis may be related to the introduction of many new drugs. 2022 May;35(5):e15416. Rheumatology (Oxford). 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. These patches tend to spread until, after a matter of days or weeks, most of the skin surface is covered with an erythematous, pruritic eruption. Manganaro AM. 2011;50(2):2214. Possible involvement of CD14+CD16+monocyte lineage cells in the epidermal damage of StevensJohnson syndrome and toxic epidermal necrolysis. Exfoliative dermatitis is also a risk factor for epidemic spread of methicillin-resistant Staphylococcus aureus.6,20. PubMed Tohyama M, et al. It is advised against the use of silver sulfadiazine because sulphonamide can be culprit agents. Wetter DA, Camilleri MJ. The timing of the rash can also vary. Generalized exfoliative dermatitis, or erythroderma, is a severe inflammation of the entire skin surface. Jang E, Park M, Jeong JE, Lee JY, Kim MG. Sci Rep. 2022 May 12;12(1):7839. doi: 10.1038/s41598-022-11505-0. 2008;4(4):22431. Although the etiology is often unknown, exfoliative dermatitis may be the result of a drug reaction or an underlying malignancy. 2005;102(11):41349. Usually the amount of calories is 15002000kcal/day and the velocity of infusion is gradually increased based on patients tolerability [92]. PubMed Central StevensJohnson syndrome and toxic epidermal necrolysis: a review of the literature. Patch testing in severe cutaneous adverse drug reactions, including StevensJohnson syndrome and toxic epidermal necrolysis. Drug specific cytotoxic T-cells in the skin lesions of a patient with toxic epidermal necrolysis. If there is a high suspicion of infection without a documented source of infection, broad range empiric therapy should be started. J Am Acad Dermatol. Exfoliative dermatitis accounts for about 1 percent of all hospital admissions for dermatologic conditions.3, Although the disease affects both men and women, it is more common in men, with an average male-to-female ratio of 2.3:1. Manage cookies/Do not sell my data we use in the preference centre. Rzany B, et al. Kirchhof MG, et al. GULIZ KARAKAYLI, M.D., GRANT BECKHAM, M.D., IDA ORENGO, M.D., AND TED ROSEN, M.D. The induction dosage in EMM is usually 1mg/kg/day that should be maintained until a complete control of the skin is obtained. Guidelines for the management of drug-induced liver injury[J]. 2013;69(4):37583. J Clin Apher. 2008;59(5):8989. Other dermatoses associated with erythroderma are listed in Table 1.2,3,68. Most common used drugs are: morphine, fentanyl, propofol and midazolam. EMM is characterizes by target lesions, circular lesions of 1-2cm of diameter, that are defined as typical or atypical that tends to blister. 2009;182(12):80719. It is also recommended to void larger vesicles with a syringe. This content is owned by the AAFP. Do this 2 to 3 times a week. Also, physicians should be vigilant about possible secondary infection, whether cutaneous, pulmonary or systemic. MalaCards based summary: Exfoliative Dermatitis is related to holocarboxylase synthetase deficiency and dermatitis, and has symptoms including exanthema An important gene associated with Exfoliative Dermatitis is SPINK5 (Serine Peptidase Inhibitor Kazal Type 5). Toxic epidermal necrolysis and StevensJohnson syndrome. Prevalence is low, with mortality of roughly 512.5% for SJS and 50% for TEN [1, 2]. 2007;56(5 Suppl):S1189. 1984;101(1):4850. Fischer M, et al. Chung W-H, et al. government site. J Invest Dermatol. A severity-of-Illness score for toxic epidermal necrolysis (SCORTEN) has been proposed and validated to predict the risk of death at admission [81]. By using this website, you agree to our 2011;71(5):67283. 2010;2(3):18994. . 1997;19(2):12732. The balance of fluids and electrolytes should be closely monitored, since dehydration or hypervolemia can be problems. Viard I, et al. -. 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]. J Invest Dermatol. Patients present an acute high-grade of skin and mucosal insufficiency that obviously leads to great impairment in the defenses against bacteria that normally live on the skin, increasing the high risk of systemic infections. Given the different histopathological features of the EM, SJS and TEN, we decided to discuss them separately. 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]. 2015;13(7):62545. Hospitalization is usually necessary for initial evaluation and treatment. Takahashi R, et al. Chung WH, Hung SI. Anti-Allergic Agents Immunoglobulin E Allergens Cetirizine Histamine H1 Antagonists, Non-Sedating Histamine H1 Antagonists Loratadine Emollients Nasal Decongestants Dermatologic Agents Leukotriene Antagonists Antigens, Dermatophagoides Ointments Histamine Antagonists Eosinophil Cationic Protein Adrenal Cortex Hormones Terfenadine Antipruritics Antigens, Plant . Adverse cutaneous drug reaction. Rabelink NM, Brakman M, Maartense E, Bril H, Bakker-Wensveen CA, Bavinck JN. Barbaud A, et al. A drug eruption may start as a rash but eventually progress to more generalized exfoliative dermatitis. 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). Wolkenstein P, et al. Australas J Dermatol. Dent Clin North Am. Next vol/issue The former is usually a recurring, localized eruption of the skin characterized by pathognomonic target or iris lesions, with minimal or no mucosal involvement (Fig. Dermatologist and/or allergist should confirm the diagnosis, individuate the culprit agent, give indications about skin management and necessity to obtain theconsultationofthe ENT specialist, the gynecologist/urologist, the ophthalmologist and/or the pulmonologist in the case of mucosal involvement. Current Perspectives on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis. It is a clinical manifestation and usually associated with various underlying cutaneous disorders, drug induced reactions and malignancies. Retrospective review of StevensJohnson syndrome/toxic epidermal necrolysis treatment comparing intravenous immunoglobulin with cyclosporine. Antitumour necrosis factor-alpha antibodies (infliximab) in the treatment of a patient with toxic epidermal necrolysis. Smith SD, et al. Paulmann M, Mockenhaupt M. Severe drug-induced skin reactions: clinical features, diagnosis, etiology, and therapy. Narita YM, et al. Pharmacogenetics studies have found an association between susceptibility to recurrent EM in response to several stimuli and human leukocyte antigen (HLA) haplotypes of class II, in particular HLA DQB1*0301 [23]. Fritsch PO. Erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. Abe J, et al. Erythroderma is the term used to describe intense and usually widespread reddening of the skin due to inflammatory skin disease. Hum Mol Genet. FDA Drug information Dupixent Read time: 6 mins Marketing start date: 04 Mar 2023 . The drug level peaks after 1- 4 h in plasma after ingestion with 95% protein binding. Here we provide a systematic review on frequency, risk factors, pathogenesis, clinical features and management of patients with drug induced ED. Correspondence to . J Am Acad Dermatol. Incidence of toxic epidermal necrolysis and StevensJohnson Syndrome in an HIV cohort: an observational, retrospective case series study. This is due to a reaction to certain medicines, a pre-existing skin condition, and sometimes cancer. Effects of treatments on the mortality of StevensJohnson syndrome and toxic epidermal necrolysis: a retrospective study on patients included in the prospective EuroSCAR Study. Among drug related cases, the main triggering factors are sulfonamides, nonsteroidal anti-inflammatories (NSAIDs), penicillins, and anticonvulsants (Table1) [59]. Am J Infect Dis. A useful sign for differential diagnosis is the absence of mucosal involvement, except for conjunctiva. Szary syndrome, the leukemic variant of mycosis fungoides, is also associated with exfoliative dermatitis. Skin manifestations of drug allergy. Ko TM, et al. 1994;331(19):127285. Analysis for circulating Szary cells may be helpful, but only if the cells are identified in unequivocally large numbers. of Internal Medicine, University of Bari, Bari, Italy, Andrea Nico,Elisabetta Di Leo,Paola Fantini&Eustachio Nettis, You can also search for this author in The approach to treatment should include discontinuation of any potentially causative medications and a search for any underlying malignancy. c. Amyloidosis. Drugs such as paracetamol, other non-oxicam NSAIDs and furosemide, bringing a relatively low risk of SJS/TEN a priori, are also highly prevalent as putative culprit agents in large SJS/TEN registries, due to their widespread use in the general population [63, 64] (Table1). 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. Kreft B, et al. Moreover, the time necessary for cells to mature and travel through the epidermis is decreased. Google Scholar. Fournier S, et al. An official website of the United States government. Curr Opin Allergy Clin Immunol. All Rights Reserved. However, patchy, diffuse areas of postinflammatory hyperpigmentation and hypopigmentation may occur, especially in patients with darker skin.1,4 One case of posterythrodermic generalized vitiligo beginning six weeks after the onset of exfoliative dermatitis has been reported.29,30 Residual eruptive nevi and keloid formation are rare sequelae. Hypothermia can result in ventricular flutter, decreased heart rate and hypotension. 2018 Feb;54(1):147-176. doi: 10.1007/s12016-017-8654-z. Efficacy of plasmapheresis for the treatment of severe toxic epidermal necrolysis: is cytokine expression analysis useful in predicting its therapeutic efficacy? 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. Mardani M, Mardani S, Asadi Kani Z, Hakamifard A. Dermatol Ther. Autologous transplantation of mesenchymal umbilical cord cells seems also to be highly efficacious [102]. Although the etiology is. Drug eruptions that initially present as morbilliform, lichenoid or urticarial rashes may progress to generalized exfoliative dermatitis. Its also characterized by a cell-poor infiltrate, where macrophages and dendrocytes with a strong TNF- immunoreactivity predominate [6, 50]. Acute interstitial nephritis associated with hepatitis, exfoliative dermatitis, fever and eosinophilia is uncommon. (See paras 3 - 42 and 3- 43.) Albeit the lack of epidemiologic data regarding EM, its reported prevalence is less than 1% [710]. Morel E, et al. Kaffenberger BH, Rosenbach M. Toxic epidermal necrolysis and early transfer to a regional burn unit: is it time to reevaluate what we teach? [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. Sequelae of exfoliative dermatitis are not widely reported. Proc Natl Acad Sci USA. doi: 10.4065/mcp.2009.0379. It is not recommended to use prophylactic antibiotic therapy. 1998;37(7):5203. [113] retrospectively compared mortality in 64 patients with ED treated either with iv or oral Cys A (35mg/kg) or IVIG (25g/Kg). The lymphocyte transformation test in the diagnosis of drug hypersensitivity. New York: McGraw-Hill; 2003. p. 585600. Interstitial nephritis is common in DRESS syndrome, occurring roughly in 40% of cases, whereas pre-renal azotemia may occur in SJS and TEN. Drugs.com provides accurate and independent information on more than . In an open trial on cyclosporine in 29 patients with TEN, the use of Cys A for at least 10days led to a rapid improvement without infective complications [112]. In SJS and TEN mucosal erosions on the lips, oral cavity, upper airways, conjunctiva, genital tract or ocular level are frequent [60, 6870]. Erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. In EMM their efficacyis demonstrated in controlling the evolution of the disease [106]. 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]. New York: McGraw-Hill; 2003. p. 54357. Several authors reported also an increased incidence for aminopenicillins, cephalosporins, and quinolones [61, 62]. Arch Dermatol. Ethambutol Induced Exfoliative Dermatitis. Umbilical cord mesenchymal stem cell transplantation in drug-induced StevensJohnson syndrome. 2015;64(3):2779. Toxic epidermal necrolysis treated with cyclosporin and granulocyte colony stimulating factor. Increased level of retinoid acid could be responsible for keratinocytes apoptosis [99]. Google Scholar. Aminoglutethimide: Aminoglutethimide may lead to a loss of corticosteroid-induced adrenal suppression. Abe R. Toxic epidermal necrolysis and StevensJohnson syndrome: soluble Fas ligand involvement in the pathomechanisms of these diseases. A case of anti-BP230 antibody-positive dyshidrosiform bullous pemphigoid secondary to dipeptidyl peptidase-4 inhibitor in a 65-year-old Filipino female Interferon alfa (Roferon-A, Intron A, Alferon N), Isoniazid (Laniazid, Nydrazid; also in Rifamate, Rimactane), Isosorbide dinitrate (Isordil, Sorbitrate), Para-amino salicylic acid (Sodium P.A.S. Check the full list of possible causes and conditions now! Barbaud A. 2013;52(1):3444. 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. Von Hebra first described erythroderma (exfoliative dermatitis) in 1868. Would you like email updates of new search results? J Am Acad Dermatol. 2012;97:14966. 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. 2013;168(3):55562. In patients with this disorder, the mitotic rate and the absolute number of germinative skin cells are higher than normal. Tang YH, et al. It is challenging to diagnose this syndrome due to the variety . (in Chinese) . 2015;56(4):298302. Shiga S, Cartotto R. What are the fluid requirements in toxic epidermal necrolysis? 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. Skin conditions. Recent advances in the genetics and immunology of StevensJohnson syndrome and toxic epidermal necrosis. Avoid rubbing and scratching. In general, they occur more frequently in women, with a male to female ratio of 0.6 [22]. Genome-wide association study identifies HLA-A* 3101 allele as a genetic risk factor for carbamazepine-induced cutaneous adverse drug reactions in Japanese population. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. Adapted from Ref. Theoretically, any drug can trigger a reaction, but the medications most associated with this disorder are: Allopurinol; Antiepileptic medications; Barbiturates Google Scholar.
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