drug induced exfoliative dermatitis

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). A catabolic state thus ensues, which is often responsible for significant weight loss. Exfoliative dermatitis is a disease process in which most, and sometimes all, of the skin is involved in erythematous inflammation resulting in massive scaling.1 A variety of diseases and other exogenous factors may cause exfoliative dermatitis. Erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. HLA-B1502, HLA-B5701, HLA-B5801 and carbamazepine, abacavir, and allopurinol, respectively). The Nikolskys sign is not specific for SJS/TEN, in fact it is present also in auto-immune blistering diseases like pemphigus vulgaris. Article Erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. Here we provide a systematic review on frequency, risk factors, pathogenesis, clinical features and management of patients with drug induced ED. 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. Medicines have been linked to every type of rash, ranging from mild to life-threatening. In: Eisen AZ, Wolff K, editors. It is important to take into consideration the mechanism of action of the different drugs in the pathogenesis of ED [104]. J Pharm Health Care Sci. Toxic epidermal necrolysis treated with cyclosporin and granulocyte colony stimulating factor. Toxic epidermal necrolysis associated with Mycoplasma pneumoniae infection. Moreover, transpiration and thermoregulation are greatly impaired with an elevated loss of fluids, proteins and electrolytes through the damaged skin and mucosae. Pehr K. The EuroSCAR study: cannot agree with the conclusions. 1995;5(4):2558. Rifampin, paracetamol, metronidazole, paclitaxel, erythromycin, and ibuprofen have all been reported to cause bullous FDE. 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]. This is particularly true for patients with many comorbidities and poli-drug therapy, where it is advisable to monitor liver and kidney toxicity and to avoid Vitamin A excess [99]. Kano Y, et al. PubMed Toxic epidermal necrolysis and StevensJohnson syndrome. 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. A population-based study of StevensJohnson syndrome. Oral manifestations of erythema multiforme. Topical treatment. (in Chinese) . (sometimes fatal), erythema multiforme, Stevens-Johnson syndrome, exfoliative dermatitis, bullous dermatitis, drug rash with eosinophilia and systemic symptoms (DRESS . A drug eruption may start as a rash but eventually progress to more generalized exfoliative dermatitis. Mucosal involvement could achieve almost 65% of patients [17]. 2014;71(2):27883. Bickle K, Roark TR, Hsu S. Autoimmune bullous dermatoses: a review. Many people have had success using a dilute vinegar bath rather than a bleach bath. Grosber M, et al. 2005;102(11):41349. Epub 2022 Mar 9. 2016 Nov 15;17(11):1890. doi: 10.3390/ijms17111890. . SJS/TEN syndrome is associated with severe blistering, mucocutaneous peeling, and multi-organ damage and could be life threatening. Drug specific cytotoxic T-cells in the skin lesions of a patient with toxic epidermal necrolysis. Hepatobiliary: jaundice, hepatitis, including . 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. Among drug related cases, the main triggering factors are sulfonamides, nonsteroidal anti-inflammatories (NSAIDs), penicillins, and anticonvulsants (Table1) [59]. Erythema multiforme: a review of epidemiology, pathogenesis, clinical features, and treatment. In SJS, SJS/TEN and TEN the efficacy of corticosteroids is far from being demonstrated. Rzany B, et al. 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. exfoliative dermatitis. Antitumour necrosis factor-alpha antibodies (infliximab) in the treatment of a patient with toxic epidermal necrolysis. Chung WH, Hung SI. 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. The most common causes of death in patients with exfoliative dermatitis are pneumonia, septicemia and heart failure. exfoliative conditions. 2010;31(1):1004. A switch to oral therapy can be performed once the mucosal conditions improve. It is important to protect the damaged skin with sterile fat dressing especially in the genital area. Ko TM, et al. It is also recommended to void larger vesicles with a syringe. By using this website, you agree to our 2010;85(2):131138. 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. Dent Clin North Am. Download. Exfoliative dermatitis (ED) is defined as diffuse erythema and scaling of the skin involving more than 90% of the total body skin surface area. 2008;58(1):3340. A severity-of-Illness score for toxic epidermal necrolysis (SCORTEN) has been proposed and validated to predict the risk of death at admission [81]. Abe R. Toxic epidermal necrolysis and StevensJohnson syndrome: soluble Fas ligand involvement in the pathomechanisms of these diseases. 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. 2013;69(2):173174. N Engl J Med. Adverse cutaneous drug reaction. 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]. Energy requirements of pediatric patients with StevensJohnson syndrome and toxic epidermal necrolysis. Recently, a meta-analysis based on 6 retrospective studies evaluating the role of corticosteroids alone or together with IVIG has been published [107]. Nat Med. Napoli B, et al. Check the full list of possible causes and conditions now! 1996;135(1):611. Erythroderma is an intense and widespread reddening of the skin due to inflammation which may often be associated with peeling of skin termed as exfoliative dermatitis. In more severe cases corneal protective lens can be used. In: Eisen AZ, Wolff K, editors. Supportive and specific care includes both local and systemic measures, as represented in Fig. Acute interstitial nephritis associated with hepatitis, exfoliative dermatitis, fever and eosinophilia is uncommon. Careers. 2008;159(4):9814. 2011;71(5):67283. As written before, Sassolas B. et al. 1996;44(2):1646. Drug-induced erythroderma invariably recovers completely with prompt initial management and removal of the offending drug. Accurate eye cleaning with saline solution is fundamental for the prevention of synechiae and for reducing corneal damage. T and NK lymphocytes can produce FasL that eventually binds to target cells. Previous vol/issue. 2. 1995;333(24):16007. PubMed Central Other patients may warrant PUVA (psoralen plus ultraviolet A) phototherapy, systemic steroids (if psoriasis has been ruled out), retinoids (for exfoliative dermatitis secondary to psoriasis and pityriasis rubra pilaris), or immunosuppressive agents such as methotrexate (Rheumatrex) and azathioprine (Imuran).2527, When used as adjunctive therapy, behavior modification designed to eliminate persistent scratching has been successful in reducing the rate of excoriation and increasing the rate of healing.28. Robyn A. McMenamin, L M. Davies and P. W. Craswell, Aust. Posadas SJ, et al. Main discriminating factors between EMM, SJS, SJS-TEN, TEN and SSSS is summarized in Table3 [84]. The clinical course of patients with malignancies depends on the type of malignancy and the response to appropriate therapy. Malignancies are a major cause of exfoliative dermatitis. It has a wide spectrum of severity, and it is divided in minor and major (EMM). The diagnosis of GVDH requires histological confirmation [87]. PubMed Central Advise of potential risk to a fetus and use of effective contraception. Roujeau JC, et al. Adapted from Ref. These molecules may play a role in amplifying the immune response and in increasing the release of other toxic metabolites from inflammatory cells [48]. 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. 2018 Feb;54(1):147-176. doi: 10.1007/s12016-017-8654-z. In approximately 25% of people, there is no identifiable cause. Huang YC, Li YC, Chen TJ. Google Scholar. 2015;56(4):298302. f. Arch Dermatol. A serious cutaneous adverse drug reaction namely exfoliative dermatitis (erythroderma) is associated with isoniazid use . The approach to treatment should include discontinuation of any potentially causative medications and a search for any underlying malignancy. Drug-induced Exfoliative Dermatitis & Eosinophils Increased Symptom Checker: Possible causes include Exfoliative Dermatitis. 2008;4(4):22431. 2011;364(12):113443. Erythroderma is a rare but severe Adverse Drug Reaction (ADR) of phenytoin. 2012;27(4):21520. The relative risk of leukemia inducing erythroderma is highly variable, ranging from 11 to 50 percent.11, Internal (visceral) malignancies cause about 1 percent of all cases of exfoliative dermatitis.11 Frequently, erythroderma is the presenting sign of the malignancy. Erythema multiforme and latent herpes simplex infection. 22 Abacavir-induced hypersensitivity syndrome is strongly associated with HLA-B*5701 during treatment . 2010;163(4):84753. MRY, MGS, EN and GC designed the study, selected scientifically relevant information, wrote and revised the manuscript. Rare dermatological side effects such as alopecia, exfoliative dermatitis, xeroderma, pruritus have been reported. Smith SD, et al. Given the different histopathological features of the EM, SJS and TEN, we decided to discuss them separately. Intravenous administration is recommended. 2003;21(1):195205. Clin Pharmacol Ther. Shared and restricted T-cell receptor use is crucial for carbamazepine-induced Stevens-Johnson syndrome. Ned Tijdschr Geneeskd. Erythema multiforme (EM), StevensJohnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. Huang SH, et al. d. Cysts and tumors. 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. HLA-A* 3101 and carbamazepine-induced hypersensitivity reactions in Europeans. (See paras 3 - 42 and 3- 43.) See permissionsforcopyrightquestions and/or permission requests. 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. Genome-scale investigation of drug-induced termination codon-readthrough in a model system of epidermolysis bullosa . Erythema multiforme (photo reproduced with permission of Gary White, MD): typical target lesions (white arrows) together with atypical two-zoned lesions (black arrows). Yamada H, Takamori K. Status of plasmapheresis for the treatment of toxic epidermal necrolysis in Japan. The lymphocyte transformation test in the diagnosis of drug hypersensitivity. Carbamazepine and phenytoin induced StevensJohnson syndrome is associated with HLA-B* 1502 allele in Thai population. Also a vesical catheter should be placed to avoid urethral synechiae and to have a precise fluid balance. 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 . Wetter DA, Davis MD. J Eur Acad Dermatol Venereol. Proc Natl Acad Sci USA. Garza A, Waldman AJ, Mamel J. In vitro diagnostic assays are effective during the acute phase of delayed-type drug hypersensitivity reactions. Paulmann M, Mockenhaupt M. Severe drug-induced skin reactions: clinical features, diagnosis, etiology, and therapy. CAS [80], which consists of the determination of IFN and IL4 by ELISpot (Enzyme-linked immunospot assay), allowing to increase the sensitivity of LTT during acute DHR (82 versus 50% if compared to LPA). [3] The causes and their frequencies are as follows: Idiopathic - 30% Drug allergy - 28% Seborrheic dermatitis - 2% Contact dermatitis - 3% Atopic dermatitis - 10% Lymphoma and leukemia - 14% Psoriasis - 8% Treatment [ edit] Corticosteroids could also reduce the amount of keratinocytes apoptosis and the activation of caspases [105]. N Engl J Med. Arch Dermatol. The SJS histology is characterized by a poor dermal inflammatory cell infiltrate and full thickness necrosis of epidermis [20, 49]. A rare case of toxic epidermal necrolysis with unexpected Fever resulting from dengue virus. 8600 Rockville Pike Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS): Focus on the Pathophysiological and Diagnostic Role of Viruses. Wolkenstein P, et al. PubMed Combination of infliximab and high-dose intravenous immunoglobulin for toxic epidermal necrolysis: successful treatment of an elderly patient. Not responsive to therapy. 2012;366(26):2492501. 2014;81(1):1521. Int J Mol Sci. Four cases are described, two of which were due to phenindione sensitivity. 2012;51(8):889902. Generalized. It is a clinical manifestation and usually associated with various underlying cutaneous disorders, drug induced reactions and malignancies. Fritsch PO. Manganaro AM. 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. 2009;145(2):15762. Exfoliative dermatitis is characterized by generalized erythema with scaling or desquamation affecting at least 90% of the body surface area. 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]. Drug rashes are the body's reaction to a certain medicine. 1996;134(4):7104. . The taper of steroid therapy should be gradual [93]. It characteristically demonstrates diffuse erythema and scaling of greater than 90% of the body surface area. Schwartz RA, McDonough PH, Lee BW. Clin Exp Dermatol. Br J Dermatol. J Allergy Clin Immunol. Br J Dermatol. Current Perspectives on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis. The therapeutic approach of EMM, SJS, TEN depends on extension of skin, mucosal involvement and systemic patients conditions. 2010;125(3):70310. Br J Clin Pharmacol. 2012;12(4):37682. 2011;38(3):23645. Google Scholar. Tumor necrosis factor : TNF- seems also to play an important role in TEN [41]. 2013;69(2):187. Next vol/issue 1999;48(5):21726. volume14, Articlenumber:9 (2016) 2010;88(1):608. government site. Gastrointestinal: pancreatitis, glossitis, dyspepsia. The syndrome has been described previously in association with phenindione administration, leptospirosis and heavy metal poisoning. Once established the percentage of the involved skin, lactate Ringer infusion of 12mL/Kg/% of involved skin must be started during the first 24h [91]. New York: McGraw-Hill; 2003. pp. Blood counts and bone marrow studies may reveal an underlying leukemia. Science. Plasmapheresis may have a role in the treatment of ED because it removes Fas-L [96], other cytokines known to be implied in the pathogenesis (IL-6, IL-8, TNF-) [97, 98]. SJS and TEN are two overlapping syndromes resembling severe burn lesions and characterized by skin detachment. Exfoliative dermatitis is also a risk factor for epidemic spread of methicillin-resistant Staphylococcus aureus.6,20. Terms and Conditions, The SCORTEN scale is based on a minimal set of parameters as described in the following table. Ibuprofen Zentiva can be prescribed with OTC Recipe - self-medication. Read this article to find out all its symptoms, causes and treatments. Toxic epidermal necrolysis: Part II Prognosis, sequelae, diagnosis, differential diagnosis, prevention, and treatment. 2002;146(4):7079. In patients with this disorder, the mitotic rate and the absolute number of germinative skin cells are higher than normal. 583-587. Grieb G, et al. Hence, the apparent increase in cases of exfoliative dermatitis may be related to the introduction of many new drugs. Nutr Clin Pract. Systemic and potentially life-threatening complications include fluid and electrolyte imbalance, thermoregulatory disturbance, fever, tachycardia, high-output failure, hypoalbuminemia, and septicemia. EM is a self-limited skin condition mainly associated with infections and drugs [53, 54]. . [16] Drug-induced Liver Disease Study Group,Chinese Society of Hepatology,Chinese Medical Association. Moreover, after granulysin depletion, they observed an increase in cell viability. Erythema multiforme StevensJohnson syndrome and toxic epidermal necrolysis. Article 00 Comments Please sign inor registerto post comments. 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]. 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. Recurrent erythema multiforme: clinical characteristics, etiologic associations, and treatment in a series of 48 patients at Mayo Clinic, 2000 to 2007. -. doi: 10.1016/j.jaad.2013.05.003. Google Scholar. Joint Bone Spine. 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. It is not recommended to use prophylactic antibiotic therapy. Part of Archivio Istituzionale della Ricerca Unimi, Nayak S, Acharjya B. Bethesda, MD 20894, Web Policies Their occurrence can be prevented by avoiding drug over-prescription and drug associations that interfere with the metabolism of the most frequent triggers [118]. Hospitalization is usually necessary for initial evaluation and treatment. StevensJohnson syndrome and toxic epidermal necrolysis: assessment of medication risks with emphasis on recently marketed drugs. In recent years, clinicians have come to believe that this condition is secondary to a complicated interaction of cytokines and cellular adhesion molecules. Mardani M, Mardani S, Asadi Kani Z, Hakamifard A. Dermatol Ther. They found that the inhibition of these molecules could attenuate the cytotoxic effect of lymphocytes toward keratinocytes. Jarrett P, et al. Article Early sites of skin involvement include trunk, face, palms and soles and rapidly spread to cover a variable extension of the body. 2008;23(5):54750. 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. Clin Exp Dermatol. J Allergy Clin Immunol. 2000;115(2):14953. https://doi.org/10.1186/s12948-016-0045-0, DOI: https://doi.org/10.1186/s12948-016-0045-0. J Dermatol. 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]. Severe Cutaneous Adverse Reactions: The Pharmacogenomics from Research to Clinical Implementation. Pharmacogenomics J. A systematic review of treatment of drug-induced StevensJohnson syndrome and toxic epidermal necrolysis in children. If necessary, it can be repeated every 68h. NSAIDs should be avoided as they can induce ED as well. 2010;62(1):4553. J Dtsch Dermatol Ges. J Am Acad Dermatol. Recurrent erythema multiforme in association with recurrent Mycoplasma pneumoniae infections. Verma R, Vasudevan B, Pragasam V. Severe cutaneous adverse drug reactions. Prevalence is low, with mortality of roughly 512.5% for SJS and 50% for TEN [1, 2]. 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. Beneficial effect of plasma exchange in the treatment of toxic epidermal necrolysis: a series of four cases. Download Free PDF. Genotyping is recommended in specific high-risk ethnic groups (e.g. Bullous FDE. Am Fam Physician. PubMed 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. 2008;12(5):3559. 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]. CAS StevensJohnson syndrome and toxic epidermal necrolysis. 2013;69(4):37583. Fournier S, et al. Risk factors for the development of ocular complications of StevensJohnson syndrome and toxic epidermal necrolysis. 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). Provided by the Springer Nature SharedIt content-sharing initiative. 2011;128(6):126676. 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. Abe J, et al. eCollection 2018. Article Google Scholar. Exfoliative dermatitis is a dangerous form of CADR which needs immediate withdrawl of all the four drugs. A heterogeneous pathologic phenotype. Cho YT, et al. Article Association of HLA-B*1502 allele with carbamazepine-induced toxic epidermal necrolysis and StevensJohnson syndrome in the multi-ethnic Malaysian population. Immune-histopathological features allow to distinguish generalized bullous drug eruption from SJS/TEN [36]. 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. The action of antithyroid drugs may be delayed in amiodarone-induced thyrotoxicosis because of substantial quantities of preformed thyroid hormones stored in the gland. Lin YT, et al. Patients can be extremely suffering because of the pain induced by skin and mucosal detachment. The prognosis of cases associated with malignancy typically depends on the outcome of the underlying malignancy. Infliximab: chimeric IgG monoclonal anti-TNF- antibody. No uniformity of opinion exists concerning the best treatment for cutaneous T-cell lymphoma. Immunoregulatory effector cells in drug-induced toxic epidermal necrolysis. In most severe cases the suggested dosage is iv 11.5mg/kg/day. In more severe cases antiviral therapies should be given together with intravenous immunoglobulins [93]. To avoid the appearance of gastric stress ulcer it is recommended to start a therapy with intravenous proton pump inhibitors. Applications of Immunopharmacogenomics: Predicting, Preventing, and Understanding Immune-Mediated Adverse Drug Reactions. Here we provide a systematic review on frequency, risk factors, pathogenesis, clinical features and management of patients with drug induced ED. Vasoactive amines may be necessary in case of shock. Clinical, etiologic, and histopathologic features of StevensJohnson syndrome during an 8-year period at Mayo Clinic. Mockenhaupt M, et al. Mortality rate of patients with TEN has shown to be directly correlated to SCORTEN. In a hemodialysis patient with active pulmonary tuberculosis, early withdrawl followed by prompt rechallenging to identify the causative agent and then to achieve cure of pulmonary tuberculosis is an interesting therapeutic challenge. 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. The efficacy of intravenous immunoglobulin for the treatment of toxic epidermal necrolysis: a systematic review and meta-analysis. Overall, T cells are the central player of these immune-mediated drug reactions. In EMM lesions typically begin on the extremities and sometimes spread to the trunk. Allergy. Please enable it to take advantage of the complete set of features! . Exfoliative dermatitis may happen as a complication of other skin issues. 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. Ozeki T, et al. Contact Dermatitis. FOIA Painkiller therapy. Epub 2018 Aug 22. In the hospital, special attention must be given to maintaining temperature control, replacing lost fluids and electrolytes, and preventing and treating infection. A useful sign for differential diagnosis is the absence of mucosal involvement, except for conjunctiva. Huff JC. Valeyrie-Allanore L, et al. Clinical clues of a drug-induced etiology include: Abrupt onset, previous morbilliform eruption, multiple, varied cutaneous morphologic lesions present together Extensive erythema is followed in 2-6 days by exfoliative scaling Pruritus can be severe, leading to scratching and lichenification in more chronic processes 2008;53(1):28. A marked increase in serum soluble Fas ligand in drug-induced hypersensitivity syndrome. In this study, 965 patients were reviewed. Curr Allergy Asthma Rep. 2014;14(6):442. The management of toxic epidermal necrolysis. Ther Apher Dial. Trautmann A, et al. A marker for StevensJohnson syndrome: ethnicity matters. Adverse cutaneous drug reaction. This hypermetabolic state is also furtherly increased by the inflammation present in affected areas. It is a clinical manifestation and usually associated with various underlying cutaneous disorders, drug induced reactions and malignancies. Allergy. Ayangco L, Rogers RS 3rd. Some anti-seizure medicines have also been known to cause exfoliative dermatitis. A multicentre study to determine the value and safety of drug patch tests for the three main classes of severe cutaneous adverse drug reactions. A central role in the pathogenesis of ED is played by CD8+ lymphocytes and NK cells. Correspondence to Shiga S, Cartotto R. What are the fluid requirements in toxic epidermal necrolysis? J Dermatol Sci. Theoretically, any drug can trigger a reaction, but the medications most associated with this disorder are: Allopurinol; Antiepileptic medications; Barbiturates 1998;37(7):5203. Exfoliative dermatitis is a rare inflammatory skin condition that is characterized by desquamation and erythema involving more than 90% of the body surface area. Trigger is an exotoxin released by Staphylococcus aureus [83]. Linear IgA dermatosis most commonly presents in patients older than 30years. It is necessary to obtain as soon as possible a central venous access and to start a continuous monitoring of vital signs. Drug-induced LPP. Bullous pemphigoid is characterized by large, tense bullae, but may begin as an urticarial eruption. Summary: Drug induced interstitial nephritis, hepatitis and exfoliative dermatitis. Incidence and drug etiology in France, 1981-1985. A case of anti-BP230 antibody-positive dyshidrosiform bullous pemphigoid secondary to dipeptidyl peptidase-4 inhibitor in a 65-year-old Filipino female 1998;282(5388):4903. The authors concluded for a potential beneficial effect of Cys A and a possible improvement in survival compared to IVIG. PMC 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. StevensJohnson syndrome and toxic epidermal necrolysis: a review of the literature. Lonjou C, et al. The most common causes of exfoliative dermatitis are preexisting dermatoses, drug reactions, malignancies and other miscellaneous or idiopathic disorders. Because a certain degree of cross-reactivity between the various aromatic anti-epileptic drugs exists, some HLAs have been found to be related to SJS/TEN with two drugs, as the case of HLA-B*1502 with both phenytoin and oxcarbazepine [32]. Harr T, French LE. 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.

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