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in particular in cases of long immobilization or Wegener granulomatosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0075"><span class="elsevierStyleSup">5&#8211;7</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">We present the case of a 24-year-old woman with a history of a personality disorder and occasional consumption of cocaine and amphetamines who was found unconscious in her home&#46; She had taken multiple pills from her regular medication supply &#40;topiramate&#44; duloxetine&#44; quetiapine&#44; and clorazepate&#41;&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">On arrival at the emergency department&#44; she had a low level of consciousness &#40;score 6 on the Glasgow Coma Scale&#41;&#44; pale skin&#44; and reactive mydriatic pupils&#46; Partial improvement &#40;Glasgow Coma Scale 10&#41; was observed following physical stimulation&#44; and the patient was treated with oxygen&#44; fluid therapy&#44; gastric lavage&#44; and activated charcoal&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">There was no evidence of acute intracranial lesions on the computed tomography scan&#46; The laboratory workup showed a serum creatine kinase level of 5590<span class="elsevierStyleHsp" style=""></span>U&#47;L and normal kidney function&#46; The urine drug screening test showed high levels of benzodiazepines&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">During her first 24<span class="elsevierStyleHsp" style=""></span>hours in hospital&#44; the patient developed asymptomatic skin lesions located mainly on bony prominences&#46; The physical examination showed tense clear fluid-filled blisters on well-delimited erythematous plaques &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>A&#44;B&#41;&#46; The lesions had an artifactual morphology and were characteristically located on pressure points &#40;metacarpophalangeal joints on the right hand&#44; right hip&#44; and left knee&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">The histopathologic examination showed a subepidermal blister with foci of reepithelialization &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41; and focal epithelial necrosis of eccrine coils&#44; with periglandular infiltration of neutrophils &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>A&#41;&#46; Additional findings included dermal&#44; perivascular&#44; and periadnexal infiltrates&#44; which were predominantly neutrophilic&#44; together with foci of fibrinoid necrosis in the walls of the small dermal capillaries and neutrophilic infiltration of the walls &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>B&#41;&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0035" class="elsevierStylePara elsevierViewall">Administration of topical antibiotics led to resolution of the lesions within 3 weeks&#44; and there were no signs of scarring or recurrence&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">The clinical presentation and histopathologic findings were consistent with a diagnosis of coma blisters&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Clinically&#44; coma blisters are characterized by tense clear or hemorrhagic blisters that develop on erythematous-violaceous macules or plaques of varying size&#46; The lesions typically appear within 24<span class="elsevierStyleHsp" style=""></span>hours of the intake of drugs and within 48 to 72<span class="elsevierStyleHsp" style=""></span>hours of the loss of consciousness&#46; They primarily develop on pressure points&#44; such as fingers and toes&#44; elbows&#44; knees&#44; ankles&#44; and heels&#46; They are self-limiting and heal within days or weeks&#44; without causing scarring or atrophy&#46; The only treatment indicated thus is topical treatment to prevent secondary infections&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2&#44;8</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Multiple factors have been implicated in the etiology and pathogenesis of coma blisters&#44; including local pressure or friction&#44; generalized hypoxia and tissue ischemia&#44; direct toxicity due to drugs excreted in sweat&#44; immune mechanisms&#44; and vasomotor changes in comatose states&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">Although a diagnosis can be established on clinical grounds only&#44; a histopathologic study can be of great use&#46; The main histopathologic findings are subepidermal or intraepidermal blisters and eccrine gland necrosis&#44; mainly affecting the secretory portion&#46; The secretory coils and ducts of the eccrine glands show a granular eosinophilic cytoplasm&#44; ghost nuclei&#44; and irregular membranes&#46; However&#44; the absence of necrosis in these glands does not necessarily rule out a diagnosis of coma blisters&#46; Other possible findings are neutrophil exocytosis&#44; necrosis of dermal or subcutaneous tissue or epidermal appendages&#44; predominantly neutrophilic perivascular infiltrates&#44; focal fibrinoid necrosis of the walls of small capillaries and arterioles&#44; and thrombi in the lumen of dermal vascular structures&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">The vascular damage observed in drug-induced coma blisters is probably a consequence rather than a cause of the blisters&#46; Furthermore&#44; the absence of an epidermal infiltrate and the presence of thrombi in the dermal vessels are mainly observed in coma blisters not induced by drugs&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">Direct immunofluorescence studies performed in certain cases of coma blisters have shown patched intercellular staining for immunoglobulin &#40;Ig&#41; G&#44; IgA&#44; and C3&#44; together with IgG&#44; IgM&#44; and C3 deposits in dermal vessel walls and epidermal keratinocytes&#46; These findings&#44; however&#44; are nonspecific and are not considered to result from an immune-mediated response&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">4&#44;10</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">In conclusion&#44; coma blisters are a benign&#44; self-limiting condition that should be suspected in patients who develop pressure blisters several hours after an altered state of consciousness&#46; Although the diagnosis is mainly clinical&#44; correlation of clinical and pathologic findings is necessary to rule out other blistering dermatoses&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of Interest</span><p id="par0075" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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Case and Research Letters
Coma Blisters After an Overdose of Central Nervous System Depressants
Ampollas del coma tras sobredosis de fármacos depresores del sistema nervioso central
I. Vázquez-Osorioa,
Autor para correspondencia
rogivaos@gmail.com

Corresponding author.
, P. Gonzalvo-Rodríguezb, E. Rodríguez-Díaza
a Servicio de Dermatología, Hospital Universitario de Cabueñes, Gijón, Asturias, Spain
b Servicio de Anatomía Patológica, Hospital Universitario de Cabueñes, Gijón, Asturias, Spain
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    "titulo" => "Coma Blisters After an Overdose of Central Nervous System Depressants"
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">A&#44; Focal epithelial necrosis in the eccrine coils with neutrophilic periglandular infiltration &#40;hematoxylin-eosin&#44; original magnification &#215;20&#41;&#46; B&#44; Predominantly neutrophilic perivascular and periadnexal infiltrates and foci of fibrinoid necrosis in the walls of dermal capillaries&#44; with neutrophilic infiltration of the walls &#40;hematoxylin-eosin&#44; original magnification &#215;20&#41;&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">The term <span class="elsevierStyleItalic">coma blisters</span> refers to a condition that occurs in patients who lose consciousness&#46; It was first described in 1812 by Larrey<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> in soldiers with carbon monoxide poisoning&#46; Since then&#44; it has been mainly associated with overdose of drugs and nervous system depressants&#44; such as barbiturates&#44; tricyclic antidepressants&#44; opiates and alcohol&#59; neurological disorders&#44; such as meningoencephalitis&#44; cerebrovascular disease&#44; and cranioencephalic trauma&#59; and metabolic disorders&#44; such as hyperkalemia&#44; hypoglycemia&#44; and diabetic ketoacidosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2&#8211;4</span></a> Coma blisters&#44; however&#44; have also been described in patients without an altered state of conscience&#44; in particular in cases of long immobilization or Wegener granulomatosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0075"><span class="elsevierStyleSup">5&#8211;7</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">We present the case of a 24-year-old woman with a history of a personality disorder and occasional consumption of cocaine and amphetamines who was found unconscious in her home&#46; She had taken multiple pills from her regular medication supply &#40;topiramate&#44; duloxetine&#44; quetiapine&#44; and clorazepate&#41;&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">On arrival at the emergency department&#44; she had a low level of consciousness &#40;score 6 on the Glasgow Coma Scale&#41;&#44; pale skin&#44; and reactive mydriatic pupils&#46; Partial improvement &#40;Glasgow Coma Scale 10&#41; was observed following physical stimulation&#44; and the patient was treated with oxygen&#44; fluid therapy&#44; gastric lavage&#44; and activated charcoal&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">There was no evidence of acute intracranial lesions on the computed tomography scan&#46; The laboratory workup showed a serum creatine kinase level of 5590<span class="elsevierStyleHsp" style=""></span>U&#47;L and normal kidney function&#46; The urine drug screening test showed high levels of benzodiazepines&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">During her first 24<span class="elsevierStyleHsp" style=""></span>hours in hospital&#44; the patient developed asymptomatic skin lesions located mainly on bony prominences&#46; The physical examination showed tense clear fluid-filled blisters on well-delimited erythematous plaques &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>A&#44;B&#41;&#46; The lesions had an artifactual morphology and were characteristically located on pressure points &#40;metacarpophalangeal joints on the right hand&#44; right hip&#44; and left knee&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">The histopathologic examination showed a subepidermal blister with foci of reepithelialization &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41; and focal epithelial necrosis of eccrine coils&#44; with periglandular infiltration of neutrophils &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>A&#41;&#46; Additional findings included dermal&#44; perivascular&#44; and periadnexal infiltrates&#44; which were predominantly neutrophilic&#44; together with foci of fibrinoid necrosis in the walls of the small dermal capillaries and neutrophilic infiltration of the walls &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>B&#41;&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0035" class="elsevierStylePara elsevierViewall">Administration of topical antibiotics led to resolution of the lesions within 3 weeks&#44; and there were no signs of scarring or recurrence&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">The clinical presentation and histopathologic findings were consistent with a diagnosis of coma blisters&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Clinically&#44; coma blisters are characterized by tense clear or hemorrhagic blisters that develop on erythematous-violaceous macules or plaques of varying size&#46; The lesions typically appear within 24<span class="elsevierStyleHsp" style=""></span>hours of the intake of drugs and within 48 to 72<span class="elsevierStyleHsp" style=""></span>hours of the loss of consciousness&#46; They primarily develop on pressure points&#44; such as fingers and toes&#44; elbows&#44; knees&#44; ankles&#44; and heels&#46; They are self-limiting and heal within days or weeks&#44; without causing scarring or atrophy&#46; The only treatment indicated thus is topical treatment to prevent secondary infections&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2&#44;8</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Multiple factors have been implicated in the etiology and pathogenesis of coma blisters&#44; including local pressure or friction&#44; generalized hypoxia and tissue ischemia&#44; direct toxicity due to drugs excreted in sweat&#44; immune mechanisms&#44; and vasomotor changes in comatose states&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">Although a diagnosis can be established on clinical grounds only&#44; a histopathologic study can be of great use&#46; The main histopathologic findings are subepidermal or intraepidermal blisters and eccrine gland necrosis&#44; mainly affecting the secretory portion&#46; The secretory coils and ducts of the eccrine glands show a granular eosinophilic cytoplasm&#44; ghost nuclei&#44; and irregular membranes&#46; However&#44; the absence of necrosis in these glands does not necessarily rule out a diagnosis of coma blisters&#46; Other possible findings are neutrophil exocytosis&#44; necrosis of dermal or subcutaneous tissue or epidermal appendages&#44; predominantly neutrophilic perivascular infiltrates&#44; focal fibrinoid necrosis of the walls of small capillaries and arterioles&#44; and thrombi in the lumen of dermal vascular structures&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">The vascular damage observed in drug-induced coma blisters is probably a consequence rather than a cause of the blisters&#46; Furthermore&#44; the absence of an epidermal infiltrate and the presence of thrombi in the dermal vessels are mainly observed in coma blisters not induced by drugs&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">Direct immunofluorescence studies performed in certain cases of coma blisters have shown patched intercellular staining for immunoglobulin &#40;Ig&#41; G&#44; IgA&#44; and C3&#44; together with IgG&#44; IgM&#44; and C3 deposits in dermal vessel walls and epidermal keratinocytes&#46; These findings&#44; however&#44; are nonspecific and are not considered to result from an immune-mediated response&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">4&#44;10</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">In conclusion&#44; coma blisters are a benign&#44; self-limiting condition that should be suspected in patients who develop pressure blisters several hours after an altered state of consciousness&#46; Although the diagnosis is mainly clinical&#44; correlation of clinical and pathologic findings is necessary to rule out other blistering dermatoses&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of Interest</span><p id="par0075" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; V&#225;zquez-Osorio I&#44; Gonzalvo-Rodr&#237;guez P&#44; Rodr&#237;guez-D&#237;az E&#46; Ampollas del coma tras sobredosis de f&#225;rmacos depresores del sistema nervioso central&#46; Actas Dermosifiliogr&#46; 2017&#59;108&#58;81&#8211;83&#46;</p>"
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ISSN: 15782190
Idioma original: Inglés
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