Toxic epidermal necrolysis in two patients with pustular psoriasis

Rogers, S.; McKee, Phillip H.

doi:10.1111/j.1365-2133.1977.tb06146.x

Cited by 8 publications

(4 citation statements)

References 9 publications

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“…Th17 cells might be involved in inflammation and tissue damage through regulation of the recruitment of neutrophils and other inflammatory leukocytes. Th17 cells also profoundly participate in the pathogenesis of psoriasis and patients with pustular psoriasis sometimes develop severe cutaneous side effects to drugs (5,6). although we could not estimate the Th17 frequency in peripheral blood in our patient due to DIC, the association of psoriasis and possible Th17 elevation might underlie the pathomechanism of a rare severe TEN caused by cefozopran in this case.…”

Section: Discussionmentioning

confidence: 73%

Fatal Case of Toxic Epidermal Necrolysis Caused by Cefozopran and Associated with Psoriasis

Sawada¹,

Kabashima-Kubo²,

Hino³

et al. 2014

Acta Derm Venerol

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Cefozopran is a fourth-generation cephem antibiotics and has a broad spectrum of antibacterial activity, inhibiting most of the gram-negative and gram-positive organisms and is used as an antibiotic agent for the empirical treatment of bacterial infections in febrile neutropenia patients (1). There have been several case reports of mild cutaneous side effects, such as exanthema, due to cefozopran, however, no severe drug eruption by cefozopran has been documented in English literature. Herein, we report the first case of toxic epidermal necrolysis (TEN) caused by cefozopran.CasE REpoRT a 71-year-old woman was referred to our department for evaluation of a generalised eruption. she had been treated for psoriasis with narrowband ultraviolet B light intermittently for 10 years. Because of pyelonephritis and septicaemia, she received cefozopran, which gradually improved her general condition. However, 7 days after intravenous administration of 1 mg cephozopran twice daily, she developed a widespread skin eruption accompanied with a high fever, 39°C. she had no medication other than cefozopran and no history of allergy to any medicine. on physical examination, erosions and scaly crusts spread widely on the chest (Fig. 1), back, and extremities involving more than 70% of body surface area. The oral mucosa was also affected and Nikolsky sign was positive. Laboratory examination revealed C-reactive protein 14.53 mg/dl (normal < 0.2 mg/dl), fasting serum glucose 469 mg/dl (normal 126 mg/dl), blood urea nitrogen (BUN) 39 mg/dl (normal 8-22 mg/dl). Her SCORTEN score was 4 points (age > 40 years, serum BUN > 27 mg/dl, blistering body surface > 10%, serum glucose > 250 mg/dl). We performed lymphocyte stimulation test with cefozopran as described previously (2, 3). 3 H-thymidine incorporation was significantly increased by the addition of 1.6×10 -7 M cefozopran (corresponding to C max for intravenous dosing) to the peripheral lymphocyte culture with a stimulation index of 4.2 (Fig. 2). Three normal volunteers showed negative results. Histological evaluation was difficult for this patient because of the detached epidermis in skin biopsy specimen. The patient did not give consent to another biopsy, and direct immunofluorescence could not be performed. We diagnosed her eruption as TEN caused by cefozopran. Although Fig. 1. Erosive and ulcerative lesions on the chest 7 days after starting cefozopran.Fig. 2. The patient's peripheral blood mononuclear cells (2×10 5 /well) taken at the initial visit and were cultured for 72 h in a 96-well plate with cefozopran at 3 different concentrations.

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Section: Discussionmentioning

confidence: 73%

Fatal Case of Toxic Epidermal Necrolysis Caused by Cefozopran and Associated with Psoriasis

Sawada¹,

Kabashima-Kubo²,

Hino³

et al. 2014

Acta Derm Venerol

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“…), and viral (herpesviruses, vaccinia virus, varicella-zoster virus) infections resemble SSSS. Isolated cases of diffuse cutaneous mastocytosis (195), Kawasaki disease (79), psoriasis (217), and TSS (66) have been reported to mimic SSSS.…”

Section: Differential Diagnosismentioning

confidence: 99%

Clinical, Microbial, and Biochemical Aspects of the Exfoliative Toxins Causing Staphylococcal Scalded-Skin Syndrome

et al. 1999

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SUMMARY The exfoliative (epidermolytic) toxins of Staphylococcus aureus are the causative agents of the staphylococcal scalded-skin syndrome (SSSS), a blistering skin disorder that predominantly affects children. Clinical features of SSSS vary along a spectrum, ranging from a few localized blisters to generalized exfoliation covering almost the entire body. The toxins act specifically at the zona granulosa of the epidermis to produce the characteristic exfoliation, although the mechanism by which this is achieved is still poorly understood. Despite the availability of antibiotics, SSSS carries a significant mortality rate, particularly among neonates with secondary complications of epidermal loss and among adults with underlying diseases. The aim of this article is to provide a comprehensive review of the literature spanning more than a century and to cover all aspects of the disease. The epidemiology, clinical features, potential complications, risk factors, susceptibility, diagnosis, differential diagnoses, investigations currently available, treatment options, and preventive measures are all discussed in detail. Recent crystallographic data on the toxins has provided us with a clearer and more defined approach to studying the disease. Understanding their mode of action has important implications in future treatment and prevention of SSSS and other diseases, and knowledge of their specific site of action may provide a useful tool for physiologists, dermatologists, and pharmacologists.

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“…Other chemicals that must be considered are boric acid (Rubenstein & Musher, 1970), ethylene oxide (Biro et ai, 1974), acrylonitrile with carbon tetrachloride fumigant spray (Radimer et ai, 1974), tribromofiuorene (Cavendish, 1940;De Feo, 1966) and monosulfiram (Copeman, 1968). A TEN-like phase occurs rarely in psoriasis (Rogers & McKee, 1977) with or without the use ofmethotrexate or other drugs (Stille, 1967). The histopathology in my experience shows a sub-corneal split, the space being packed with polymorph neutrophils, as in the von Zumbusch type of pustular psoriasis, of which this is probably a variant.…”

Section: Diagnosismentioning

confidence: 99%