drug induced exfoliative dermatitis

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. Anti-tubercular therapy (ATT) induced exfoliative dermatitis-A case [113] retrospectively compared mortality in 64 patients with ED treated either with iv or oral Cys A (35mg/kg) or IVIG (25g/Kg). Prevalence is low, with mortality of roughly 512.5% for SJS and 50% for TEN [1, 2]. Int J Dermatol. McCormack M, et al. Guidelines for the management of drug-induced liver injury[J]. TEN is also known as Lyell syndrome, since it was first described by Alan Lyell in 1956 [2, 60]. 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). Br J Dermatol. 8600 Rockville Pike Huff JC, Weston WL, Tonnesen MG. Erythema multiforme: a critical review of characteristics, diagnostic criteria, and causes. Li X, et al. 2011;3(1):e2011004. In SJS, SJS/TEN and TEN the efficacy of corticosteroids is far from being demonstrated. 2012;53(3):16571. A population-based study of StevensJohnson syndrome. Exfoliative Dermatitis - StatPearls - NCBI Bookshelf Allergy. J Am Acad Dermatol. In spared areas it is necessary to avoid skin detachment. 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. 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. 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. The more common forms of erythroderma, such as eczema or psoriasis, may persists for months or years and tend to relapse. The scales may be small or large, superficial or deep. Br J Dermatol. The erythrodermic form of mycosis fungoides and the Szary syndrome may also be difficult to distinguish from benign erythroderma. When it precedes cutaneous T-cell lymphoma lesions, exfoliative dermatitis becomes the presenting sign of the underlying malignancy. The authors declare that they have no competing interests. Unfortunately, the clinical picture does not contribute to an understanding of the underlying cause. Nature. Corticosteroids could also reduce the amount of keratinocytes apoptosis and the activation of caspases [105]. 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. Acute and chronic leukemia may also cause exfoliative dermatitis. AQUACEL Ag in the treatment of toxic epidermal necrolysis (TEN). Schopf E, et al. Iv bolus of steroid (dexamethasone 100300mg/day or methylprednisolone 2501000mg/day) for 3 consecutive days with a gradual taper steroid therapy is sometimes advised. In patients with SJS/TEN increased serum levels of retinoid acid have been found. See permissionsforcopyrightquestions and/or permission requests. 2002;146(4):7079. Epidemiological studies on EM, SJS and TEN syndromes report different results, probably related to several biases, such as ethnical differences, diagnostic criteria and drug consumption patterns in different socio-economic systems. Interstitial nephritis is common in DRESS syndrome, occurring roughly in 40% of cases, whereas pre-renal azotemia may occur in SJS and TEN. 19 Key critical interactions are discussed below for each mpox antiviral. Also, physicians should be vigilant about possible secondary infection, whether cutaneous, pulmonary or systemic. Apoptosis as a mechanism of keratinocyte death in toxic epidermal necrolysis. 1990;126(1):3742. California Privacy Statement, EMM is characterizes by target lesions, circular lesions of 1-2cm of diameter, that are defined as typical or atypical that tends to blister. Indian J Dermatol. 2022 May;35(5):e15416. Case Rep Dermatol. . Chemicals and Drugs 61. Von Hebra first described erythroderma (exfoliative dermatitis) in 1868. 2008;34(1):636. Copyright 2023 American Academy of Family Physicians. Cyclosporine A (Cys A): Cys A works through the inhibition of calcineurin, that is fundamental for cytotoxic T lymphocytes activation. Hypersensitivity, Delayed Drug Hypersensitivity Radiodermatitis Drug Eruptions Skin Diseases Hypersensitivity Hand-Foot Syndrome Hypersensitivity, Immediate Dermatitis, Contact Erythema Foot Dermatoses Hand Dermatoses Skin Neoplasms Dermatitis, Allergic Contact Alveolitis, Extrinsic Allergic Acneiform Eruptions Dentin Sensitivity Dermatitis Both hyperthermia and hypothermia are reported. 2013;69(2):1734. Palynziq PEGVALIASE 20 mg/mL BioMarin Pharmaceutical Inc. 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. Panitumumab Induced Forearm Panniculitis in Two Women With Metastatic Erythema multiforme, StevensJohnson syndrome and toxic epidermal necrolysis in northeastern Malaysia. However, according to a consensus definition [54], EMM syndrome has been separated from SJS/TEN spectrum. CD94/NKG2C is a killer effector molecule in patients with Stevens-Johnson syndrome and toxic epidermal necrolysis. 2010;85(2):1318. Medication-Induced Erythroderma | SpringerLink 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. Barbaud A. Chapter 23. Exfoliative Dermatitis | Fitzpatrick's Dermatology in 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. Vasoactive amines may be necessary in case of shock. Bethesda, MD 20894, Web Policies Recurrence occurs in around one-third of cases [15] and there is a genetic predisposition for certain Asian groups [16]. 1). . (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 . Nayak S, Acharjya B. 2008;4(4):22431. SSSS is characterized by periorificial face scabs, de-epithelialization of friction zones and conspicuous desquamation after initial erythroderma. [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. 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 . [81]. J Eur Acad Dermatol Venereol. 1984;101(1):4850. Antibiotics: amoxicillin, ampicillin, ciprofloxacin, demeclocycline , doxycycline , minocycline, nalidixic acid, nitrofurantoin, norfloxacin, penicillin , rifampicin, streptomycin, tetracycline , tobramycin, trimethoprim, trimethoprim + sulphamethoxazole, vancomycin Anticonvulsants : barbiturates, carbamazepine For SJS/TEN, corticosteroids are the cornerstone of treatment albeit efficacy remains unclear. . official website and that any information you provide is encrypted Oral hygiene with antiseptic and painkiller mouthwash (chlorhexidine+lidocaine+aluminum hydroxide) together with aerosol therapy with saline and bronchodilators can reduce upper airways symptoms. Allergol Immunopathol (Madr). . 2015;49(3):33542. CAS AB, CC, ET, GAR, AN, EDL, PF performed a critical revision on the current literature about the described topic, wrote and revised the manuscript. Sequelae of exfoliative dermatitis are not widely reported. Sokumbi O, Wetter DA. Grieb G, et al. MRY, MGS, EN and GC designed the study, selected scientifically relevant information, wrote and revised the manuscript. The efficacy of intravenous immunoglobulin for the treatment of toxic epidermal necrolysis: a systematic review and meta-analysis. 2009;151(7):5145. Theoretically, any drug may cause exfoliative dermatitis. Perforin/granzyme B pathway: Nassif and colleagues have proposed a role for perforin/grazyme B in keratinocyte death [37]. A serious cutaneous adverse drug reaction namely exfoliative dermatitis (erythroderma) is associated with isoniazid use . Unable to load your collection due to an error, Unable to load your delegates due to an error, 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 SCORTEN. Yamada H, Takamori K. Status of plasmapheresis for the treatment of toxic epidermal necrolysis in Japan. Toxic epidermal necrolysis and StevensJohnson syndrome. Google Scholar. 1997;22(3):1467. Liver injury and exfoliative dermatitis caused by nifuratel[J]. 1998;282(5388):4903. Hydration and hemodynamic balance. Indian J Dermatol. Even though exfoliative dermatitis is a complex disorder involving many factors, the underlying disease is usually the key determinant of the course and prognosis. Still, treatment indication, choice and dosage remain unclear, and efficacy yet unproven. Drug-induced hypersensitivity syndrome (DiHS) or drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a severe adverse drug-induced reaction characterized by various symptoms: skin rash, fever, lymph node enlargement and internal organ involvement, which starts within 2 weeks to 3 months after drug initiation. Huff JC. Paquet P, et al. The management of toxic epidermal necrolysis. It is also extremely important to obtain within the first 24h cultural samples from skin together with blood, urine, nasal, pharyngeal and bronchus cultures. Gastrointestinal: pancreatitis, glossitis, dyspepsia. Science. 2011;38(3):23645. Four main pathways have been found to play important roles in the pathogenesis of keratinocyte death: (1) Fas-FasL interaction, (2) Perforin/granzyme B pathway, (3) Granulysin and (4) Tumor necrosis factor (TNF-) [26]. N.Z. 2014;70(3):53948. Diclofenac sodium topical solution, like other NSAIDs, can cause serious systemic skin side effects such as exfoliative dermatitis, SJS, and TEN, which may result in hospitalizations . The taper of steroid therapy should be gradual [93]. Barbaud A. Inhibition of toxic epidermal necrolysis by blockade of CD95 with human intravenous immunoglobulin. Google Scholar. PDF Drug induced exfoliative dermatitis: state of the art Erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the main clinical presentations of drug induced ED. doi: 10.4103/0019-5154.39732. Khalil I, et al. DRUG- Induced- Dermatologic-RXNS lam University St. John's University Course Drug induced disease (CPP 6102) Academic year2023/2024 Helpful? Each of these physiologic disruptions is potentially life-threatening. Drug-induced Exfoliative Dermatitis & Eosinophils Increased Symptom Checker: Possible causes include Exfoliative Dermatitis. Fluid balance is a main focus. 2012;66(3):1906. ), Phenolphthalein (Agoral, Alophen, Modane), Rifampin (Rifadin, Rimactane; also in Rifamate), Trimethoprim (Trimpex; also in Bactrim, Septra). asiatic) before starting therapies with possible triggers (e.g. Analysis for circulating Szary cells may be helpful, but only if the cells are identified in unequivocally large numbers. Exfoliative dermatitis, including Stevens-Johnson syndrome, drug rash with eosinophilia and systemic symptoms, and toxic epidermal necrolysis, has occurred with anti-PD-1/PD-L1 treatments. Amphotericin B injection and potassium-depleting agents: When corticosteroids are administered concomitantly with potassium-depleting agents (ie, amphotericin B, diuretics), patients should be observed closely for development of hypokalemia.There have been cases reported in which concomitant . 1996;134(4):7104. government site. See this image and copyright information in PMC. 49th Annual Meeting of the Arbeitsgemeinschaft Dermatologische Exanthematous drug eruptions. No uniformity of opinion exists concerning the best treatment for cutaneous T-cell lymphoma. Recently, a meta-analysis based on 6 retrospective studies evaluating the role of corticosteroids alone or together with IVIG has been published [107]. A multidisciplinary team is fundamental in the therapeutic management of patients affected by exfoliative DHR. Here we provide a systematic review on frequency, risk factors, pathogenesis, clinical features and management of patients with drug induced ED. 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. Management of patients with a suspected drug induced exfoliative dermatitis, acute generalized exanthematous pustulosis, algorithm of drug causality for epidermal necrolysis, European registry of severe cutaneous adverse reactions to drugs. 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. 2023 BioMed Central Ltd unless otherwise stated. Correspondence to 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. J Dtsch Dermatol Ges. Patch testing in severe cutaneous adverse drug reactions, including StevensJohnson syndrome and toxic epidermal necrolysis. Clinical, etiologic, and histopathologic features of StevensJohnson syndrome during an 8-year period at Mayo Clinic. d. Cysts and tumors. Cite this article. It characteristically demonstrates diffuse erythema and scaling of greater than 90% of the body surface area. Ther Apher Dial. Not responsive to therapy. Strom BL, et al. These levels could reflect the interaction between culprit drugs and aldehyde dehydrogenase that is the enzyme which metabolizes retinoid acid. Schwartz RA, McDonough PH, Lee BW. The drug level peaks after 1- 4 h in plasma after ingestion with 95% protein binding. Karnes JH, Miller MA, White KD, Konvinse KC, Pavlos RK, Redwood AJ, Peter JG, Lehloenya R, Mallal SA, Phillips EJ. New York: McGraw-Hill; 2003. p. 585600. 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).