Drugs as etiologic factors in the Stevens-Johnson syndrome

Bianchine, Joseph R.; Macaraeg, Placido V. J.; Lasagna, Louis; Azarnoff, Daniel L.; Brunk, S.fred; Hvidberg, Eigill F.; Owen, John Andrew

doi:10.1016/0002-9343(68)90110-1

Cited by 134 publications

(40 citation statements)

References 86 publications

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“…Fluid and electrolyte imbalance and septicemia account for the mortality associated with the disease. Inflamma tion and erosions of the conjunctiva, mucous mem brane of the stomach and the genitalia occur as do erosions of the mucous membranes of the trachea and the esophagus [2][3][4][5][6][7], Erosive lesions of the bronchial and gastrointestinal tract have been only sparsely re ported [3,6,7]. We are aware of only a few reports that contain but short remarks on the histology of these extracutaneous lesions [6].…”

Section: Introductionmentioning

confidence: 99%

Toxic Epidermal Necrolysis with Extensive Mucosal Erosions of the Gastrointestinal and Respiratory Tracts

Roupe¹,

Ahlmén²,

Fagerberg³

et al. 1986

Int Arch Allergy Immunol

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Toxic epidermal necrolysis with epidermal shedding over almost the entire body occurred in a patient with classical rheumatoid arthritis treated with sulindac, penicillamine and a combination analgesic containing paracetamol and chlormezanone. Erosions in the lower respiratory tract and the intestine contributed to a lethal outcome of the disease and showed a microscopical picture similar to that of the skin involved. The histopathological picture of these extracutaneous lesions have been only briefly reported previously.

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Section: Introductionmentioning

confidence: 99%

Toxic Epidermal Necrolysis with Extensive Mucosal Erosions of the Gastrointestinal and Respiratory Tracts

Roupe¹,

Ahlmén²,

Fagerberg³

et al. 1986

Int Arch Allergy Immunol

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“…In addition to the non-specific skin irritation resulting by the defatting action, severer generalized dermatitis with hepatitis, which includes Stevens-Johnson syndrome and toxic epidermal necrolysis, sometimes occurs after exposure to trichloroethylene [3][4][5][6][7][8][9][10] . Such dermatitis is generally known to occur subsequent to the administration of various medicines and infections-i.e., antibiotics such as sulfonamides, anticonvulsives such as carbamazepine and phenobarbital, anti-inflammatory medications such as acetylsalicylic acid and paracetamol, anti-parasitic medications such as albendazole and tinidazole, viruses, mycoplasma, and other bacterial infections [11][12][13][14][15] . As for other types of chemical exposure, there have been a few case reports on the dermatitis, that of a young woman who used pesticide spray 16) , and students who were exposed to 9-bromofluorene in a lab setting 17) .…”

mentioning

confidence: 99%

Generalized Skin Reactions in Relation to Trichloroethylene Exposure: A Review from the Viewpoint of Drug‐Metabolizing Enzymes

Nakajima

Yamanoshita

Kamijima

et al. 2003

Journal of Occupational Health

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Generalized Skin Reactions in Relation to Trichloroethylene Exposure: A Review from the Viewpoint of Drug-metabolizing Enzymes: Tamie NAKAJIMA, et al. Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine-The literature was reviewed to study cases of intoxication with systemic dermatitis associated with exposure to trichloroethylene. The average age of patients in the reports reviewed to date was twenty-nine; these diseases were found in relatively young persons and no difference was found according to gender. Many cases occurred within one month after the onset of exposure to trichloroethylene, and were accompanied by hepatitis, jaundice, hepatomegaly or hepatosplenomegaly. Most of the patients had no history of drug abuse or herpes infection. The level of exposure to trichloroethylene was not recorded in many cases, but ranged from less than 9 ppm to 800 ppm. In the severest cases, the lesions involved mucous membranes such as the conjunctiva and oral cavity, and the patients were diagnosed with Stevens-Johnson syndrome, but the etiology of the disease after trichloroethylene exposure remains unclear. Since several drugs have also been shown to cause systemic dermatitis with hepatitis, susceptibility factors are discussed. Many patients were found to have the slow acetylator genotype of Nacetyltransferase (NAT) 2, suggesting that the NAT2 genotype is a susceptibility factor. This hypothesis may also be applicable to trichloroethylene because NAT is involved in the glutathione-mediated metabolism. (J Occup Health 2003; 45: 8-14)

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“…Severe ery thema multiforme (Stevens-Johnson syn- drome) usually affects buccal, conjunctival and pharyngeal mucous membranes but is rarely more disseminated [21] and case re ports ofintestinal damage are few [22]. Toxic epidermal necrolysis, thought by some to be a variant of erythema multiforme, may, how ever, cause very severe upper intestinal mu cosal destruction, and in association with se vere skin loss carries a high mortality [23].…”

Section: Blistering Disordersmentioning

confidence: 99%

The Gut in Skin Disease: Gastro-Intestinal Manifestations of Selected Skin Disorders

Barkley¹,

Gawkrodger²

1985

Dig Dis

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Drugs as etiologic factors in the Stevens-Johnson syndrome

Cited by 134 publications

References 86 publications

Toxic Epidermal Necrolysis with Extensive Mucosal Erosions of the Gastrointestinal and Respiratory Tracts

Toxic Epidermal Necrolysis with Extensive Mucosal Erosions of the Gastrointestinal and Respiratory Tracts

Generalized Skin Reactions in Relation to Trichloroethylene Exposure: A Review from the Viewpoint of Drug‐Metabolizing Enzymes

The Gut in Skin Disease: Gastro-Intestinal Manifestations of Selected Skin Disorders

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