History
A 38-year-old woman presented with a lump in her breast and was diagnosed with peripheral T-cell non-Hodgkin’s lymphoma stage 3A. She underwent six cycles of CHOP-21 chemotherapy; however, a PET (positron emission tomography) scan revealed residual disease in her mediastinal lymph nodes. During a planned admission for a BEAM autolo-gous stem cell transplantation she developed a widespread, mildly pruritic skin eruption.
The rash started on her upper body and spread distally over 24 hours. She had received pre-conditioning chemotherapy and prophylactic antimicrobials (azithromycin, penicil-lin, fluconazole, aciclovir) 4 days prior to the onset of the eruption.
Examination
There are multiple erythematous macules and papules scattered diffusely over her trunk and limbs (Fig. 19.1), with relative sparing of her face. There are no pustules, blisters or scaling. The eruption blanches on pressure.
Questions
• What is the diagnosis?
• What is the most likely cause of her sudden-onset rash?
• How would you manage this patient?
The patient has developed a drug rash called toxic erythema; this was confirmed histo-logically from the skin biopsy. This is the most common type of cutaneous drug eruption.
Classically, it spreads in a craniocaudal direction and is mildly pruritic. The rash is sym-metrical and consists of a myriad of very small erythematous papules and macules. The individual lesions blanch on pressure. There are no blisters or pustules, the palms and soles are spared. Toxic erythema usually starts within two weeks of taking a new medica-tion. Sudden-onset widespread rashes are usually ‘reactive’ with the two most common underlying causes being ‘drugs or bugs’. The key to identifying the culprit drug is the taking of a detailed history of the patient’s medications and the time course over which each was started in relation to the onset of the rash. In this case the drug responsible is penicillin. If possible, the culprit drug should be stopped; however, if the drug is vital for the patient’s underlying condition then toxic erythema can be managed with a moderately potent topical steroid and emollients.
Usually the rash fades over a few weeks with desquamation.
KEY POINTS
• Toxic erythema is the most common type of drug rash.
• The rash spreads in a craniocaudal direction and consists of erythematous macules and papules.
• Common culprit drugs include antibiotics, anticonvulsants, allopurinol, non-steroidal anti-inflammatories, and thiazides.
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