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• W2078605136 abstract "PresentationMost of the severe systemic toxicities of amiodarone are well known. Yet, a more obscure but equally lethal toxicity occurred in a 74-year-old woman who was administered amiodarone for atrial fibrillation with a rapid ventricular response. Within 72 hours of beginning treatment with the antiarrhythmic agent, she developed a diffuse, desquamative rash involving her trunk, limbs, and face (Figure 1). Her mucous membranes were spared.AssessmentA dermatology consultation was requested, and a subsequent skin biopsy revealed liquefaction in the basal layer of the epidermis and necrotic keratinocytes, predominantly in the basal layer (Figure 2). Bullous formation was noted, as was a mild inflammatory infiltrate consisting mainly of lymphocytes with occasional neutrophils.Figure 2This is a biopsy sample from one of the patient's skin lesions (40x magnification). Partial separation of the epidermis from the underlying dermis layer was noted (thick black arrow). Bullae were present on the epidermis (thin black arrow). Neither necrosis nor dyskeratosis of the epidermis was present. The underlying dermis contained a small amount of inflammatory cells, which are denoted by the asterisk.View Large Image Figure ViewerDownload Hi-res image Download (PPT)DiagnosisOverall, the pathology findings were consistent with a diagnosis along the spectrum of Stevens-Johnson syndrome and toxic epidermal necrolysis. The patient had large contiguous patches of epidermal sloughing, and the extensive nature of the skin involvement favored the more severe diagnosis of toxic epidermal necrolysis, a rare but potentially deadly acute epidermolytic dermopathy.Toxic epidermal necrolysis is distinct from other bullous skin diseases, such as staphylococcal scalded skin syndrome or erythema multiforme major. The nomenclature for these skin disorders can appear indistinct because there are shared characteristics among them. However, the general consensus is that toxic epidermal necrolysis is related to Stevens-Johnson syndrome but is more severe. A proposed classification scheme distinguishes toxic epidermal necrolysis from Stevens-Johnson syndrome primarily based upon greater body surface area involvement and greater confluence of skin lesions.1Bastuji-Garin S. Rzany B. Stern R.S. Shear N.H. Naldi L. Roujeau J.C. Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme.Arch Dermatol. 1993; 129: 92-96Crossref PubMed Scopus (1298) Google Scholar Our patient's clinical presentation fulfilled the criteria for toxic epidermal necrolysis because she had contiguous skin lesions over more than 30% of her body surface area. Notably, she did not experience any of the systemic symptoms that are often associated with toxic epidermal necrolysis, including fever, dysphagia, or lymphadenopathy.In toxic epidermal necrolysis, apoptosis or programmed cell death of keratinocytes between the epidermis and dermis leads to widespread full-thickness epidermal sloughing.2Sluysmans T. De Bont B. Cornu G. Acute epidermal necrolysis or Lyell syndrome.Eur J Pediatr. 1987; 146: 199-200Crossref PubMed Scopus (3) Google Scholar Apoptosis is mediated via a cell-signaling cascade; evidence suggests that keratinocyte death in toxic epidermal necrolysis is triggered by binding of the Fas ligand, a peptide in the tumor necrosis factor family, to its Fas receptor on the targeted cells.3Viard I. Wehrli P. Bullani R. et al.Inhibition of toxic epidermal necrolysis by blockade of CD95 with human intravenous immunoglobulin.Science. 1998; 282: 490-493Crossref PubMed Scopus (979) Google Scholar Cytotoxic lymphocytes appear to play a critical role in mediating this process via granzyme B, a protease released by cytotoxic T cells and natural killer cells that hydrolyzes peptide bonds.4Nassif A. Bensussan A. Boumsell L. et al.Toxic epidermal necrolysis: effector cells are drug-specific cytotoxic T cells.J Allergy Clin Immunol. 2004; 114: 1209-1215Abstract Full Text Full Text PDF PubMed Scopus (316) Google Scholar Granulysin has been identified as another key cytolytic protein.5Chung W.H. Hung S.I. Yang J.Y. et al.Granulysin is a key mediator for disseminated keratinocyte death in Stevens-Johnson syndrome and toxic epidermal necrolysis.Nat Med. 2008; 14: 1343-1350Crossref PubMed Scopus (547) Google ScholarMost cases of toxic epidermal necrolysis are related to drug ingestion and typically occur 1-3 weeks after initial use of the offending agent.6Schwartz R.A. Toxic epidermal necrolysis.Cutis. 1997; 59: 123-128PubMed Google Scholar Medications that have been reported to cause the condition include, but are not limited to, sulfonamides, antiepileptic drugs, allopurinol, tetracyclines, cancer chemotherapeutic agents, and nonsteroidal anti-inflammatory agents.6Schwartz R.A. Toxic epidermal necrolysis.Cutis. 1997; 59: 123-128PubMed Google ScholarSome genetic correlations with development of drug-induced toxic epidermal necrolysis have been noted in certain ethnic groups. For example, 1 study demonstrated a strong association between the HLA-B*1502 gene and carbamazepine-induced Stevens-Johnson syndrome in Han Chinese.7Chung W.H. Hung S.I. Hong H.S. et al.Medical genetics: a marker for Stevens-Johnson syndrome.Nature. 2004; 428: 486Crossref PubMed Scopus (1341) Google ScholarAlthough the multiorgan toxicities of amiodarone are well-known, toxic epidermal necrolysis related to amiodarone is rare.8Bencini P.L. Crosti C. Sala F. Bertani E. Nobili M. Toxic epidermal necrolysis and amiodarone treatment.Arch Dermatol. 1985; 121: 838Crossref PubMed Scopus (17) Google Scholar The temporal relationship between amiodarone administration and our patient's development of the rash, combined with clinical improvement after drug withdrawal, indicates that amiodarone was the likely etiology. None of her concurrent medications were known to cause toxic epidermal necrolysis.Mortality from toxic epidermal necrolysis is attributed mainly to sepsis and multisystem organ failure. Other problems that may arise include hypovolemic shock, gastrointestinal hemorrhage, and respiratory failure. The average reported mortality rate for toxic epidermal necrolysis is 25-35%.9Roujeau J.C. Stern R.S. Severe adverse cutaneous reactions to drugs.N Engl J Med. 1994; 331: 1272-1285Crossref PubMed Scopus (1454) Google Scholar The prognosis can be evaluated using the SCORe of Toxic Epidermal Necrosis (SCORTEN) severity-of-illness system, which consists of 7 parameters: age older than 40 years, malignancy, tachycardia (> 120 beats/min), initial percentage of epidermal detachment (> 10%), elevated serum blood urea nitrogen (> 10 mmol/L), elevated serum glucose (> 250 mg/dL), and reduced bicarbonate level (< 20 meq/L).10Bastuji-Garin S. Fouchard N. Bertocchi M. Roujeau J.-C. Revuz J. Wolkenstein P. SCORTEN: a severity-of-illness score for toxic epidermal necrolysis.J Invest Dermatol. 2000; 115: 149-153Crossref PubMed Scopus (785) Google Scholar The presence of 5 or more of these risk factors predicts a risk for mortality exceeding 90%.ManagementGenerally, patients with a SCORTEN score of at least 3 should be managed in an intensive care unit. Prompt withdrawal of the offending medication is essential and supportive care with fluid and electrolyte repletion is the cornerstone of management. Due to disparate findings from several clinical trials and uncertainty about the optimal steroid treatment regimen, the use of systemic steroids is controversial.11Kardaun S.H. Jonkman M.F. Dexamethasone pulse therapy for Stevens-Johnson syndrome/toxic epidermal necrolysis.Acta Derm Venereol. 2007; 87: 144-148Crossref PubMed Scopus (176) Google Scholar, 12Schneck J. Fagot J.P. Sekula P. Sassolas B. Roujeau J.C. Mockenhaupt M. Effects of treatments on the mortality of Stevens-Johnson syndrome and toxic epidermal necrolysis: a retrospective study on patients included in the prospective EuroSCAR Study.J Am Acad Dermatol. 2008; 58: 33-40Abstract Full Text Full Text PDF PubMed Scopus (375) Google Scholar Several trials have suggested a mortality benefit with the use of high dose intravenous immunoglobulin.13Rajaratnam R. Mann C. Balasubramaniam P. et al.Toxic epidermal necrolysis: retrospective analysis of 21 consecutive cases managed at a tertiary centre.Clin Exp Dermatol. 2010; 35: 853-862Crossref PubMed Scopus (71) Google Scholar, 14Stella M. Clemente A. Bollero D. Risso D. Dalmasso P. Stella M. Clemente A. Bollero D. Risso D. Dalmasso P. Toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS): experience with high-dose intravenous immunoglobulins and topical conservative approach A retrospective analysis.Burns. 2007; 33: 452-459Abstract Full Text Full Text PDF PubMed Scopus (84) Google Scholar An open, phase II trial suggested a mortality benefit from cyclosporine therapy versus a prognostic model.15Valeyrie-Allanore L. Wolkenstein P. Brochard L. et al.Open trial of ciclopsorin treatment for Stevens-Johnson syndrome and toxic epidermal necrolysis.Br J Dermatol. 2010; 163: 847-853Crossref PubMed Scopus (189) Google Scholar Data addressing the use of tumor necrosis factor antagonists, cyclophosphamide, and plasmapheresis are too limited to reasonably allow assessments of their efficacy. A randomized, placebo-controlled trial suggested that use of thalidomide is associated with increased mortality in patients with toxic epidermal necrolysis, so its use is not recommended.16Wolkenstein P. Latarjet J. Roujeau J.C. et al.Randomised comparison of thalidomide versus placebo in toxic epidermal necrolysis.Lancet. 1998; 352: 1586-1589Abstract Full Text Full Text PDF PubMed Scopus (362) Google ScholarAs noted, subsequent to the diagnosis of toxic epidermal necrolysis, a review of our patient's medications indicated amiodarone was the likely culprit. The drug was stopped, and the patient was transferred to a burn intensive care unit for precautionary measures. The patient remained hemodynamically stable, and her skin lesions improved with supportive care while the offending medication was withheld. No other medication was given in its place because her atrial fibrillation continued to be rate-controlled. She was discharged in good condition with resolution of her rash and no further recurrences.This case highlights another potential adverse event associated with amiodarone. Clinicians should be aware of this possible complication if a patient on amiodarone develops a rash. Albeit rare, amiodarone-induced toxic epidermal necrolysis can be an acutely life-threatening condition. PresentationMost of the severe systemic toxicities of amiodarone are well known. Yet, a more obscure but equally lethal toxicity occurred in a 74-year-old woman who was administered amiodarone for atrial fibrillation with a rapid ventricular response. Within 72 hours of beginning treatment with the antiarrhythmic agent, she developed a diffuse, desquamative rash involving her trunk, limbs, and face (Figure 1). Her mucous membranes were spared. Most of the severe systemic toxicities of amiodarone are well known. Yet, a more obscure but equally lethal toxicity occurred in a 74-year-old woman who was administered amiodarone for atrial fibrillation with a rapid ventricular response. Within 72 hours of beginning treatment with the antiarrhythmic agent, she developed a diffuse, desquamative rash involving her trunk, limbs, and face (Figure 1). Her mucous membranes were spared. AssessmentA dermatology consultation was requested, and a subsequent skin biopsy revealed liquefaction in the basal layer of the epidermis and necrotic keratinocytes, predominantly in the basal layer (Figure 2). Bullous formation was noted, as was a mild inflammatory infiltrate consisting mainly of lymphocytes with occasional neutrophils. A dermatology consultation was requested, and a subsequent skin biopsy revealed liquefaction in the basal layer of the epidermis and necrotic keratinocytes, predominantly in the basal layer (Figure 2). Bullous formation was noted, as was a mild inflammatory infiltrate consisting mainly of lymphocytes with occasional neutrophils. DiagnosisOverall, the pathology findings were consistent with a diagnosis along the spectrum of Stevens-Johnson syndrome and toxic epidermal necrolysis. The patient had large contiguous patches of epidermal sloughing, and the extensive nature of the skin involvement favored the more severe diagnosis of toxic epidermal necrolysis, a rare but potentially deadly acute epidermolytic dermopathy.Toxic epidermal necrolysis is distinct from other bullous skin diseases, such as staphylococcal scalded skin syndrome or erythema multiforme major. The nomenclature for these skin disorders can appear indistinct because there are shared characteristics among them. However, the general consensus is that toxic epidermal necrolysis is related to Stevens-Johnson syndrome but is more severe. A proposed classification scheme distinguishes toxic epidermal necrolysis from Stevens-Johnson syndrome primarily based upon greater body surface area involvement and greater confluence of skin lesions.1Bastuji-Garin S. Rzany B. Stern R.S. Shear N.H. Naldi L. Roujeau J.C. Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme.Arch Dermatol. 1993; 129: 92-96Crossref PubMed Scopus (1298) Google Scholar Our patient's clinical presentation fulfilled the criteria for toxic epidermal necrolysis because she had contiguous skin lesions over more than 30% of her body surface area. Notably, she did not experience any of the systemic symptoms that are often associated with toxic epidermal necrolysis, including fever, dysphagia, or lymphadenopathy.In toxic epidermal necrolysis, apoptosis or programmed cell death of keratinocytes between the epidermis and dermis leads to widespread full-thickness epidermal sloughing.2Sluysmans T. De Bont B. Cornu G. Acute epidermal necrolysis or Lyell syndrome.Eur J Pediatr. 1987; 146: 199-200Crossref PubMed Scopus (3) Google Scholar Apoptosis is mediated via a cell-signaling cascade; evidence suggests that keratinocyte death in toxic epidermal necrolysis is triggered by binding of the Fas ligand, a peptide in the tumor necrosis factor family, to its Fas receptor on the targeted cells.3Viard I. Wehrli P. Bullani R. et al.Inhibition of toxic epidermal necrolysis by blockade of CD95 with human intravenous immunoglobulin.Science. 1998; 282: 490-493Crossref PubMed Scopus (979) Google Scholar Cytotoxic lymphocytes appear to play a critical role in mediating this process via granzyme B, a protease released by cytotoxic T cells and natural killer cells that hydrolyzes peptide bonds.4Nassif A. Bensussan A. Boumsell L. et al.Toxic epidermal necrolysis: effector cells are drug-specific cytotoxic T cells.J Allergy Clin Immunol. 2004; 114: 1209-1215Abstract Full Text Full Text PDF PubMed Scopus (316) Google Scholar Granulysin has been identified as another key cytolytic protein.5Chung W.H. Hung S.I. Yang J.Y. et al.Granulysin is a key mediator for disseminated keratinocyte death in Stevens-Johnson syndrome and toxic epidermal necrolysis.Nat Med. 2008; 14: 1343-1350Crossref PubMed Scopus (547) Google ScholarMost cases of toxic epidermal necrolysis are related to drug ingestion and typically occur 1-3 weeks after initial use of the offending agent.6Schwartz R.A. Toxic epidermal necrolysis.Cutis. 1997; 59: 123-128PubMed Google Scholar Medications that have been reported to cause the condition include, but are not limited to, sulfonamides, antiepileptic drugs, allopurinol, tetracyclines, cancer chemotherapeutic agents, and nonsteroidal anti-inflammatory agents.6Schwartz R.A. Toxic epidermal necrolysis.Cutis. 1997; 59: 123-128PubMed Google ScholarSome genetic correlations with development of drug-induced toxic epidermal necrolysis have been noted in certain ethnic groups. For example, 1 study demonstrated a strong association between the HLA-B*1502 gene and carbamazepine-induced Stevens-Johnson syndrome in Han Chinese.7Chung W.H. Hung S.I. Hong H.S. et al.Medical genetics: a marker for Stevens-Johnson syndrome.Nature. 2004; 428: 486Crossref PubMed Scopus (1341) Google ScholarAlthough the multiorgan toxicities of amiodarone are well-known, toxic epidermal necrolysis related to amiodarone is rare.8Bencini P.L. Crosti C. Sala F. Bertani E. Nobili M. Toxic epidermal necrolysis and amiodarone treatment.Arch Dermatol. 1985; 121: 838Crossref PubMed Scopus (17) Google Scholar The temporal relationship between amiodarone administration and our patient's development of the rash, combined with clinical improvement after drug withdrawal, indicates that amiodarone was the likely etiology. None of her concurrent medications were known to cause toxic epidermal necrolysis.Mortality from toxic epidermal necrolysis is attributed mainly to sepsis and multisystem organ failure. Other problems that may arise include hypovolemic shock, gastrointestinal hemorrhage, and respiratory failure. The average reported mortality rate for toxic epidermal necrolysis is 25-35%.9Roujeau J.C. Stern R.S. Severe adverse cutaneous reactions to drugs.N Engl J Med. 1994; 331: 1272-1285Crossref PubMed Scopus (1454) Google Scholar The prognosis can be evaluated using the SCORe of Toxic Epidermal Necrosis (SCORTEN) severity-of-illness system, which consists of 7 parameters: age older than 40 years, malignancy, tachycardia (> 120 beats/min), initial percentage of epidermal detachment (> 10%), elevated serum blood urea nitrogen (> 10 mmol/L), elevated serum glucose (> 250 mg/dL), and reduced bicarbonate level (< 20 meq/L).10Bastuji-Garin S. Fouchard N. Bertocchi M. Roujeau J.-C. Revuz J. Wolkenstein P. SCORTEN: a severity-of-illness score for toxic epidermal necrolysis.J Invest Dermatol. 2000; 115: 149-153Crossref PubMed Scopus (785) Google Scholar The presence of 5 or more of these risk factors predicts a risk for mortality exceeding 90%. Overall, the pathology findings were consistent with a diagnosis along the spectrum of Stevens-Johnson syndrome and toxic epidermal necrolysis. The patient had large contiguous patches of epidermal sloughing, and the extensive nature of the skin involvement favored the more severe diagnosis of toxic epidermal necrolysis, a rare but potentially deadly acute epidermolytic dermopathy. Toxic epidermal necrolysis is distinct from other bullous skin diseases, such as staphylococcal scalded skin syndrome or erythema multiforme major. The nomenclature for these skin disorders can appear indistinct because there are shared characteristics among them. However, the general consensus is that toxic epidermal necrolysis is related to Stevens-Johnson syndrome but is more severe. A proposed classification scheme distinguishes toxic epidermal necrolysis from Stevens-Johnson syndrome primarily based upon greater body surface area involvement and greater confluence of skin lesions.1Bastuji-Garin S. Rzany B. Stern R.S. Shear N.H. Naldi L. Roujeau J.C. Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme.Arch Dermatol. 1993; 129: 92-96Crossref PubMed Scopus (1298) Google Scholar Our patient's clinical presentation fulfilled the criteria for toxic epidermal necrolysis because she had contiguous skin lesions over more than 30% of her body surface area. Notably, she did not experience any of the systemic symptoms that are often associated with toxic epidermal necrolysis, including fever, dysphagia, or lymphadenopathy. In toxic epidermal necrolysis, apoptosis or programmed cell death of keratinocytes between the epidermis and dermis leads to widespread full-thickness epidermal sloughing.2Sluysmans T. De Bont B. Cornu G. Acute epidermal necrolysis or Lyell syndrome.Eur J Pediatr. 1987; 146: 199-200Crossref PubMed Scopus (3) Google Scholar Apoptosis is mediated via a cell-signaling cascade; evidence suggests that keratinocyte death in toxic epidermal necrolysis is triggered by binding of the Fas ligand, a peptide in the tumor necrosis factor family, to its Fas receptor on the targeted cells.3Viard I. Wehrli P. Bullani R. et al.Inhibition of toxic epidermal necrolysis by blockade of CD95 with human intravenous immunoglobulin.Science. 1998; 282: 490-493Crossref PubMed Scopus (979) Google Scholar Cytotoxic lymphocytes appear to play a critical role in mediating this process via granzyme B, a protease released by cytotoxic T cells and natural killer cells that hydrolyzes peptide bonds.4Nassif A. Bensussan A. Boumsell L. et al.Toxic epidermal necrolysis: effector cells are drug-specific cytotoxic T cells.J Allergy Clin Immunol. 2004; 114: 1209-1215Abstract Full Text Full Text PDF PubMed Scopus (316) Google Scholar Granulysin has been identified as another key cytolytic protein.5Chung W.H. Hung S.I. Yang J.Y. et al.Granulysin is a key mediator for disseminated keratinocyte death in Stevens-Johnson syndrome and toxic epidermal necrolysis.Nat Med. 2008; 14: 1343-1350Crossref PubMed Scopus (547) Google Scholar Most cases of toxic epidermal necrolysis are related to drug ingestion and typically occur 1-3 weeks after initial use of the offending agent.6Schwartz R.A. Toxic epidermal necrolysis.Cutis. 1997; 59: 123-128PubMed Google Scholar Medications that have been reported to cause the condition include, but are not limited to, sulfonamides, antiepileptic drugs, allopurinol, tetracyclines, cancer chemotherapeutic agents, and nonsteroidal anti-inflammatory agents.6Schwartz R.A. Toxic epidermal necrolysis.Cutis. 1997; 59: 123-128PubMed Google Scholar Some genetic correlations with development of drug-induced toxic epidermal necrolysis have been noted in certain ethnic groups. For example, 1 study demonstrated a strong association between the HLA-B*1502 gene and carbamazepine-induced Stevens-Johnson syndrome in Han Chinese.7Chung W.H. Hung S.I. Hong H.S. et al.Medical genetics: a marker for Stevens-Johnson syndrome.Nature. 2004; 428: 486Crossref PubMed Scopus (1341) Google Scholar Although the multiorgan toxicities of amiodarone are well-known, toxic epidermal necrolysis related to amiodarone is rare.8Bencini P.L. Crosti C. Sala F. Bertani E. Nobili M. Toxic epidermal necrolysis and amiodarone treatment.Arch Dermatol. 1985; 121: 838Crossref PubMed Scopus (17) Google Scholar The temporal relationship between amiodarone administration and our patient's development of the rash, combined with clinical improvement after drug withdrawal, indicates that amiodarone was the likely etiology. None of her concurrent medications were known to cause toxic epidermal necrolysis. Mortality from toxic epidermal necrolysis is attributed mainly to sepsis and multisystem organ failure. Other problems that may arise include hypovolemic shock, gastrointestinal hemorrhage, and respiratory failure. The average reported mortality rate for toxic epidermal necrolysis is 25-35%.9Roujeau J.C. Stern R.S. Severe adverse cutaneous reactions to drugs.N Engl J Med. 1994; 331: 1272-1285Crossref PubMed Scopus (1454) Google Scholar The prognosis can be evaluated using the SCORe of Toxic Epidermal Necrosis (SCORTEN) severity-of-illness system, which consists of 7 parameters: age older than 40 years, malignancy, tachycardia (> 120 beats/min), initial percentage of epidermal detachment (> 10%), elevated serum blood urea nitrogen (> 10 mmol/L), elevated serum glucose (> 250 mg/dL), and reduced bicarbonate level (< 20 meq/L).10Bastuji-Garin S. Fouchard N. Bertocchi M. Roujeau J.-C. Revuz J. Wolkenstein P. SCORTEN: a severity-of-illness score for toxic epidermal necrolysis.J Invest Dermatol. 2000; 115: 149-153Crossref PubMed Scopus (785) Google Scholar The presence of 5 or more of these risk factors predicts a risk for mortality exceeding 90%. ManagementGenerally, patients with a SCORTEN score of at least 3 should be managed in an intensive care unit. Prompt withdrawal of the offending medication is essential and supportive care with fluid and electrolyte repletion is the cornerstone of management. Due to disparate findings from several clinical trials and uncertainty about the optimal steroid treatment regimen, the use of systemic steroids is controversial.11Kardaun S.H. Jonkman M.F. Dexamethasone pulse therapy for Stevens-Johnson syndrome/toxic epidermal necrolysis.Acta Derm Venereol. 2007; 87: 144-148Crossref PubMed Scopus (176) Google Scholar, 12Schneck J. Fagot J.P. Sekula P. Sassolas B. Roujeau J.C. Mockenhaupt M. Effects of treatments on the mortality of Stevens-Johnson syndrome and toxic epidermal necrolysis: a retrospective study on patients included in the prospective EuroSCAR Study.J Am Acad Dermatol. 2008; 58: 33-40Abstract Full Text Full Text PDF PubMed Scopus (375) Google Scholar Several trials have suggested a mortality benefit with the use of high dose intravenous immunoglobulin.13Rajaratnam R. Mann C. Balasubramaniam P. et al.Toxic epidermal necrolysis: retrospective analysis of 21 consecutive cases managed at a tertiary centre.Clin Exp Dermatol. 2010; 35: 853-862Crossref PubMed Scopus (71) Google Scholar, 14Stella M. Clemente A. Bollero D. Risso D. Dalmasso P. Stella M. Clemente A. Bollero D. Risso D. Dalmasso P. Toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS): experience with high-dose intravenous immunoglobulins and topical conservative approach A retrospective analysis.Burns. 2007; 33: 452-459Abstract Full Text Full Text PDF PubMed Scopus (84) Google Scholar An open, phase II trial suggested a mortality benefit from cyclosporine therapy versus a prognostic model.15Valeyrie-Allanore L. Wolkenstein P. Brochard L. et al.Open trial of ciclopsorin treatment for Stevens-Johnson syndrome and toxic epidermal necrolysis.Br J Dermatol. 2010; 163: 847-853Crossref PubMed Scopus (189) Google Scholar Data addressing the use of tumor necrosis factor antagonists, cyclophosphamide, and plasmapheresis are too limited to reasonably allow assessments of their efficacy. A randomized, placebo-controlled trial suggested that use of thalidomide is associated with increased mortality in patients with toxic epidermal necrolysis, so its use is not recommended.16Wolkenstein P. Latarjet J. Roujeau J.C. et al.Randomised comparison of thalidomide versus placebo in toxic epidermal necrolysis.Lancet. 1998; 352: 1586-1589Abstract Full Text Full Text PDF PubMed Scopus (362) Google ScholarAs noted, subsequent to the diagnosis of toxic epidermal necrolysis, a review of our patient's medications indicated amiodarone was the likely culprit. The drug was stopped, and the patient was transferred to a burn intensive care unit for precautionary measures. The patient remained hemodynamically stable, and her skin lesions improved with supportive care while the offending medication was withheld. No other medication was given in its place because her atrial fibrillation continued to be rate-controlled. She was discharged in good condition with resolution of her rash and no further recurrences.This case highlights another potential adverse event associated with amiodarone. Clinicians should be aware of this possible complication if a patient on amiodarone develops a rash. Albeit rare, amiodarone-induced toxic epidermal necrolysis can be an acutely life-threatening condition. Generally, patients with a SCORTEN score of at least 3 should be managed in an intensive care unit. Prompt withdrawal of the offending medication is essential and supportive care with fluid and electrolyte repletion is the cornerstone of management. Due to disparate findings from several clinical trials and uncertainty about the optimal steroid treatment regimen, the use of systemic steroids is controversial.11Kardaun S.H. Jonkman M.F. Dexamethasone pulse therapy for Stevens-Johnson syndrome/toxic epidermal necrolysis.Acta Derm Venereol. 2007; 87: 144-148Crossref PubMed Scopus (176) Google Scholar, 12Schneck J. Fagot J.P. Sekula P. Sassolas B. Roujeau J.C. Mockenhaupt M. Effects of treatments on the mortality of Stevens-Johnson syndrome and toxic epidermal necrolysis: a retrospective study on patients included in the prospective EuroSCAR Study.J Am Acad Dermatol. 2008; 58: 33-40Abstract Full Text Full Text PDF PubMed Scopus (375) Google Scholar Several trials have suggested a mortality benefit with the use of high dose intravenous immunoglobulin.13Rajaratnam R. Mann C. Balasubramaniam P. et al.Toxic epidermal necrolysis: retrospective analysis of 21 consecutive cases managed at a tertiary centre.Clin Exp Dermatol. 2010; 35: 853-862Crossref PubMed Scopus (71) Google Scholar, 14Stella M. Clemente A. Bollero D. Risso D. Dalmasso P. Stella M. Clemente A. Bollero D. Risso D. Dalmasso P. Toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS): experience with high-dose intravenous immunoglobulins and topical conservative approach A retrospective analysis.Burns. 2007; 33: 452-459Abstract Full Text Full Text PDF PubMed Scopus (84) Google Scholar An open, phase II trial suggested a mortality benefit from cyclosporine therapy versus a prognostic model.15Valeyrie-Allanore L. Wolkenstein P. Brochard L. et al.Open trial of ciclopsorin treatment for Stevens-Johnson syndrome and toxic epidermal necrolysis.Br J Dermatol. 2010; 163: 847-853Crossref PubMed Scopus (189) Google Scholar Data addressing the use of tumor necrosis factor antagonists, cyclophosphamide, and plasmapheresis are too limited to reasonably allow assessments of their efficacy. A randomized, placebo-controlled trial suggested that use of thalidomide is associated with increased mortality in patients with toxic epidermal necrolysis, so its use is not recommended.16Wolkenstein P. Latarjet J. Roujeau J.C. et al.Randomised comparison of thalidomide versus placebo in toxic epidermal necrolysis.Lancet. 1998; 352: 1586-1589Abstract Full Text Full Text PDF PubMed Scopus (362) Google Scholar As noted, subsequent to the diagnosis of toxic epidermal necrolysis, a review of our patient's medications indicated amiodarone was the likely culprit. The drug was stopped, and the patient was transferred to a burn intensive care unit for precautionary measures. The patient remained hemodynamically stable, and her skin lesions improved with supportive care while the offending medication was withheld. No other medication was given in its place because her atrial fibrillation continued to be rate-controlled. She was discharged in good condition with resolution of her rash and no further recurrences. This case highlights another potential adverse event associated with amiodarone. Clinicians should be aware of this possible complication if a patient on amiodarone develops a rash. Albeit rare, amiodarone-induced toxic epidermal necrolysis can be an acutely life-threatening condition." @default.
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• W2078605136 title "A Dire Reaction: Rash after Amiodarone Administration" @default.
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• W2078605136 cites W1942477582 @default.
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• W2078605136 cites W2010296185 @default.
• W2078605136 cites W2031125773 @default.
• W2078605136 cites W2045391651 @default.
• W2078605136 cites W2049902892 @default.
• W2078605136 cites W2062608493 @default.
• W2078605136 cites W206445102 @default.
• W2078605136 cites W2109696646 @default.
• W2078605136 cites W2136481244 @default.
• W2078605136 cites W2152226036 @default.
• W2078605136 cites W2317624504 @default.
• W2078605136 cites W3116890861 @default.
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