SEARCH · PubMed Health

Results for “EPIDERMAL NECROLYSIS, TOXIC”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1991

Toxic epidermal necrolysis.

Toxic epidermal necrolysis is a rapidly progressive dermatologic condition associated with high mortality. Several factors have been implicated in the development of toxic epidermal necrolysis including drugs, vaccinations, infections, and neoplasia. Toxic epidermal necrolysis therapy has been compared with partial-thickness burn injury treatment. The absence of burned tissue can dampen fluid requirements and metabolic needs of toxic epidermal necrolysis in comparison to equivalent burn injury. In the following case report, a 69-year-old woman with multiple medical problems developed toxic epidermal necrolysis after treatment with metolazone and phenytoin. Her measured energy expenditure (3360 kcal) was considerably higher than previously reported caloric expenditure in toxic epidermal necrolysis patients (2500 kcal).

Aged↗

PubMed1998

Hypopharyngeal stenosis and dysphagia complicating toxic epidermal necrolysis.

Toxic epidermal necrolysis is a severe dermatologic disorder clinically characterized by the acute onset of erythema and tenderness of the skin. Destruction of the epidermal barrier results in significant morbidity and mortality. Large erosions of mucous membrane, including the mouth and oral mucosa, are typical of toxic epidermal necrolysis. After ingesting naproxen sodium (Aleve) and aspirin, a previously healthy 43-year-old woman developed toxic epidermal necrolysis that resulted in hypopharyngeal stenosis complicated by dysphagia and recurrent aspiration.

Adult↗

PubMed2003

Suspected lamotrigine-induced toxic epidermal necrolysis.

Toxic epidermal necrolysis and Stevens-Johnson syndrome are rare, life treating cutaneous reactions. Most cases of toxic epidermal necrolysis are drug induced. The drugs with the highest estimated incidence include co-trimoxazloe (trimethoprim-sulfamethoxazole), sulfadoxine-pyrethamine, and carbamazepine. Among other drugs, the reported reaction rates are relatively low for lamotrigine and sulbactam-ampicillin. We describe a patient who developed toxic epidermal necrolysis after either administration of lamotrigine or of ampicillin.

Adult↗

PubMedDate not supplied

Use of Biobrane in the treatment of toxic epidermal necrolysis.

Toxic epidermal necrolysis syndrome is an exfoliative dermatologic disorder of unknown origin resulting in the loss of epidermis in a sheetlike fashion at the dermoepidermal junction. The resulting wound renders the patient vulnerable to potential septic complications, fluid and protein losses, and severe pain. During the past decade treatment of toxic epidermal necrolysis syndrome has incorporated the basic tenets of burn care: appropriate fluid resuscitation, nutritional support, infection surveillance and treatment, and optimal care of the open wound. Biobrane, a readily available and effective biosynthetic skin substitute, has been successfully used in the treatment of toxic epidermal necrolysis syndrome and provides a safe and reliable method to achieve wound closure. Its successful use requires a thorough understanding of application and removal techniques. Once adherent, it avoids the cost and pain associated with repeated dressing changes.

Biocompatible Materials↗

PubMed2002

Drug specific cytotoxic T-cells in the skin lesions of a patient with toxic epidermal necrolysis.

Toxic epidermal necrolysis is an extremely severe drug reaction, manifesting itself by widespread apoptosis of keratinocytes, generally considered to result from Fas/CD95-FasLigand interaction, but of unknown primary mechanism. We looked at the role of cells present in the skin blisters as probable effectors of this immune reaction. In a patient suffering from cotrimoxazole-induced toxic epidermal necrolysis, blister fluid cells were phenotyped by FACS and tested without prior restimulation for cytotoxicity on autologous and allogeneic cells in the presence of the drug. Blister fluid lymphocytes were predominantly CD8+, DR+, CLA+, CD56+ T lymphocytes, perforin positive and expressing preferentially two Vbeta chains of the T cell receptor repertoire. These lymphocytes were cytotoxic only in the presence of the drug towards autologous EBV transformed lymphocytes and towards allogeneic cells sharing HLA-Cw4. Cytotoxicity occurred in the presence of either cotrimoxazole, sulfamethoxazole, or the nitroso metabolite of sulfamethoxazole, but not with the hydroxylamine metabolite of sulfamethoxazole. The lysis was blocked by an anti-MHC class I monoclonal antibody. It was abolished by EGTA and CMA, but neither by anti-fas, brefeldin A, nor by anti-TRAIL receptor monoclonal antibodies, strongly suggesting perforin/granzyme-mediated cytotoxicity, without implication of Fas or TRAIL at this stage. This is direct evidence that T lymphocytes present within the lesions of toxic epidermal necrolysis may exhibit, without any re-stimulation, a drug-specific cytotoxicity against autologous cells. Harboring the markers of classical CTL and MHC class I restriction these lymphocytes reacted against the parent drug and one of its reactive metabolites. These results challenge several current concepts and could support new therapeutic approaches.

Anti-Infective Agents↗

PubMed1979

Toxic epidermal necrolysis.

Toxic epidermal necrolysis (TEN) is a disorder characterized by the sudden onset of widespread erythema and tenderness of the skin with rapid progression to desquamation of sheets of epidermis, resembling scalding. Although the clinical picture is similar in many instances, toxic epidermal necrolysis is subdivided into two main clinicopathologic types, those due to staphylococcal infections, and the nonstaphylococcal variant. It occurs as the result of a number of causes, including specific exfoliative toxin-producing staphylococci, drugs, vaccines, and the graft vs. host reaction. Differentiation of these types is important, both for therapeutic and prognostic reasons.

Adult↗

PubMed2004

Evaluation of the potential role of cytokines in toxic epidermal necrolysis.

Toxic epidermal necrolysis is a rare disease observed as a consequence of adverse reactions to drugs. It results in the widespread apoptosis of epidermal cells and has a high mortality rate. The mechanisms leading to this apoptosis are not yet elucidated. We investigated whether the cytokines present in the blister fluid, which accumulates under necrotic epidermis, originated from T lymphocytes and may play a role in the propagation of keratinocyte apoptosis. Interferon gamma (IFN-gamma), soluble tumor necrosis factor alpha (TNF-alpha), soluble Fas ligand (sFas-L) were present in much higher concentration in the blister fluids of 13 toxic epidermal necrolysis (TEN) patients than in control fluids from burns. The results of RT-PCR studies, however, indicated that only IFN-gamma and to a lesser extent interleukin (IL)-18 were produced by mononuclear cells present in the fluid. That suggests that the other cytokines also present (TNF-alpha, sFas-L, IL-10) rather originated from activated keratinocytes. Fas-L was indeed overexpressed on the membranes of keratinocytes in lesional skin in situ. The Th1 profile of T lymphocyte activation found in the blister fluid of patients with TEN is consistent with a key role for drug-specific cytotoxic T lymphocytes (CTL) as previously reported, the activation of keratinocytes by IFN-gamma making them sensitive to cell-mediated cytolysis. We propose the hypothesis that the production of Fas-L, TNF-alpha, and IL-10 by keratinocytes could be a defense mechanism against CTL rather than a way of propagating apoptosis among epidermal cells.

Apoptosis↗

PubMed1999

Progressive bronchial obstruction associated with toxic epidermal necrolysis.

Toxic epidermal necrolysis (TEN) is an acute life-threatening condition, characterized by erosion of the mucous membranes, extensive detachment of the epidermis, and severe constitutional symptoms. Pulmonary complications of TEN are reported as rare, but are one of the most common causes of death. Our report focuses on an unusual case of toxic epidermal necrolysis which showed multiple bronchial obliteration during the chronic phase of the disease. Biopsied tissue of the obliterated bronchi demonstrated non-specific granulation. To improve the obliterated ventilatory function, we tried to reopen the bronchial obliteration using a balloon catheter under the guidance of fibreoptic bronchoscopy, however rapid restenosis of the bronchi ensued.

Adult↗

PubMed1981

Ethambutol-induced toxic epidermal necrolysis.

Toxic epidermal necrolysis (TEN) is a severe cutaneous reaction that most commonly is related to drug exposure and that clinically can be confused with other bullous dermatoses, particularly staphylococcal scalded skin syndrome (SSSS) and erythema multiforme major (the Stevens-Johnson syndrome). We report the first case, to our knowledge, of TEN associated with ethambutol hydrochloride administration. Toxic epidermal necrolysis can be partially differentiated from other bullous dermatoses by history and clinical presentation. Microbiological results (eg, the isolation of Staphylococcus aureus in SSSS) and immunological studies (eg, the demonstration of immune complexes in the Stevens-Johnson syndrome) may aid in differentiation, but ultimately the diagnosis depends on histopathological examination of involved skin.

Aged↗

PubMed1978

Burn unit management of toxic epidermal necrolysis.

Toxic epidermal necrolysis is the name given to a group of dermatologic disorders characterized by a separation of epidermis and dermis with a subsequent skin slough. The denuded areas have the appearance of a second-degree burn. The complications of infection, negative nitrogen balance, severe pain, and emotional instability are identical to those seen in the patient with major burns. There are difficulties in patient management and advantages in burn unit care. As with the major burn, care of the patient with skin loss from toxic epidermal necrolysis is extremely complex, requiring the expertise of a burn team along with that of the dermatologist.

Adult↗

PubMed1988

Survival after a second episode of toxic epidermal necrolysis.

Toxic epidermal necrolysis resulting from severe hypersensitivity to medication has a reported mortality of up to 66%. A patient surviving two episodes with more than a 50% skin loss is unprecedented in the medical literature. Mortality has been associated with many factors, including delayed reepithelialization, persistent skin slough, coagulopathy, severe hypoproteinemia, and sepsis. It may be possible to decrease morbidity and mortality by preventing the shearing of epidermis, thereby limiting the denuded areas. This case report describes the successful management of our patient's second episode of toxic epidermal necrolysis. The treatment of this patient in our specialized burn center consisted of careful fluid and electrolyte management, nutritional support, standard topical antimicrobials, and new modalities of local wound management.

Adult↗

PubMedDate not supplied

Ecthyma gangrenosum in a patient with toxic epidermal necrolysis.

Toxic epidermal necrolysis and Stevens-Johnson syndrome are a spectrum of disease characterized by a delayed hypersensitivity reaction that involves the skin and mucous membranes and typically is associated with either recent upper respiratory infection or with certain medications. Ecthyma gangrenosum is a rare necrotizing vasculitis that most commonly affects immunocompromised and burn patients and is often a sequela of Pseudomonas aeruginosa bacteremia. The cutaneous lesions of ecthyma gangrenosum are characterized by an erythematous halo surrounding a dark gray or black nodule. P. aeruginosa preferentially invades the venules, resulting in secondary thrombosis of the arterioles, tissue edema, and separation of the epidermis. Management of ecthyma gangrenosum includes systemic treatment with antipseudomonal antibiotics and débridment of the lesions, as well as improving the patient's immune status if possible. We present a case of a patient admitted to the burn unit for toxic epidermal necrolysis who developed pseudomonal bacteremia with ecthyma gangrenosum.

Anti-Infective Agents↗

PubMedDate not supplied

A 10-year experience with toxic epidermal necrolysis.

Toxic epidermal necrolysis is a devastating medication-induced desquamation disorder with a reported mortality rate of 30% to 60% in adults. Data from previously reported series suggest that age, delay in referral to a burn center, total body surface area (TBSA) involvement, and systemic steroid treatment are poor prognostic indicators. We reviewed the records of 39 patients treated in our burn center over the past 10 years and found that the mortality rate was significantly correlated with age, thrombocytopenia, and delay in presentation. Steroid treatment and TBSA involvement were not significantly related to the mortality rate. Thirty-nine adult patients with greater than 20% TBSA epithelial necrosis were cared for in our center from January 1987 to March 1998. Wounds were treated with topical antimicrobial medications and porcine xenografts in a bacteria-controlled nursing unit. We reviewed the records of these patients for 28 clinical characteristics and looked for clinical correlates of mortality by single analysis of variance. The mortality rate was 44% (17 of 39 patients); the cause of death was most commonly multiple-organ dysfunction syndrome, for which a microbial etiologic agent was not always identified. Autopsies were performed on 11 of the 17 patients who died; there was evidence of multiple-organ damage. The patients who survived and the patients who died did not differ significantly in TBSA epithelial necrosis (66%+/-6% vs 72%+/-5%, respectively), admission platelets, number of nosocomial infections, number of complications, preadmission exposure to steroids, or extent of mucosal involvement. When compared with the patients who died, the patients who survived were (1) 20 years younger (47.5+/-4.2 years vs 64.5+/-5.3 years), (2) admitted to the hospital sooner after the onset of their rash (3.5+/-0.4 days vs 5.9+/-1.0 days), (3) much less likely to experience early thrombocytopenia (platelet nadir, 154+/-24 vs 70+/-18), (4) more likely to be febrile on presentation, and (5) less likely to have been treated with antibiotics before referral to our unit. These differences were statistically significant. The most common etiologic agents were antibiotics, anticonvulsants, and nonsteroidal anti-inflammatory drugs. Our results for a group of older patients with toxic epidermal necrolysis with extensive skin involvement suggest that age, delay in hospitalization, thrombocytopenia, and early empiric antibiotic treatment are associated with a poor prognosis.

Adult↗

PubMed1980

Toxic epidermal necrolysis.

Toxic epidermal necrolysis is one of the rarest events -- a dermatologic emergency. The clinical presentation is characteristic -- disseminate erythema and widespread bullous necrosis of the epidermis and mucous membranes. Toxicity is universal and mortality is substantial even with prompt and intensive therapy. Drugs are the most commonly incriminated agents and therapy remains controversial, the majority favoring high-dose systemic corticosteroids.

Diagnosis, Differential↗

PubMed1999

Thalidomide-induced toxic epidermal necrolysis.

Toxic epidermal necrolysis (TEN) is a severe dermatologic disorder associated with mortality of up to 30%. Withdrawal of the causative agent is crucial in its management. Although thalidomide-induced dermatologic disorders rarely were reported before thalidomide was administered to patients positive for the human immunodeficiency virus, hypersensitivity reactions including rash are the agent's major dose-limiting toxicities in this population. As it is prescribed for other immunosuppressed patients, such as those with malignancies, the frequency of dermatologic reactions (including TEN) may increase. A 62-year-old woman developed TEN after approximately 5 weeks of thalidomide therapy for the treatment of a glioblastoma.

Angiogenesis Inhibitors↗

PubMed1984

Esophageal stricture secondary to drug-induced toxic epidermal necrolysis.

Toxic epidermal necrolysis is a cutaneous disorder with high morbidity and mortality. Esophageal stricture has rarely been reported following recovery from this abnormality. A case is presented demonstrating the occurrence of an esophageal stricture following successful therapy. New methods of treatment are changing the mortality and morbidity such that esophageal stricture will be observed more frequently.

Amoxicillin↗

PubMedDate not supplied

Toxic epidermal necrolysis.

Toxic epidermal necrolysis (TEN) is a life-threatening condition in which the epidermis blisters and peels in large sheets. The clinical syndrome and diagnosis are reviewed. Current treatment and prevention of complications are discussed. The key to low morbidity and mortality in TEN is early intervention. Physicians should be knowledgeable about TEN and the appearance of the skin in its initial presentation.

Humans↗

PubMed2000

Toxic epidermal necrolysis.

Toxic epidermal necrolysis (TEN) is a rare but life-threatening adverse drug reaction. Implicated drugs are sulfonamides, anticonvulsants, allopurinol, and pyrazolone derivatives. Recently, advances in pathogenesis have been made in two directions. It is now known that (1) most patients with TEN have an abnormal metabolism to the culprit drug; and (2) the mechanism leading to epidermal necrolysis seems to be a cell-mediated cytotoxic reaction. The treatment remains symptomatic.

Humans↗