‘Sandpaper’ rash spreading over torso, limbs in a 15-year-old female
Click Here to Manage Email Alerts
A 15 year-old girl presented to our pediatric dermatology clinic with a 1-month history of a “rash all over.” The rash started on the abdomen and spread to involve the chest, back, arms and legs with sparing of the face, palms and soles (Figure). The patient complains of moderate pruritus. Two weeks before the rash started, she had a sore throat and fever of 101.5°F for 3 days and a “sandpaper-like” rash on her trunk and arms. Her pediatrician performed a throat culture and then prescribed a 10-day course of oral amoxicillin, which made her feel much better. The family is not sure what the throat culture showed. She denies cough, headache, nausea, rhinorrhea, joint aches or pains and abnormal movements.
On exam, the patient is an afebrile, well-appearing teen in no distress. She has no conjunctival injection, no nasal discharge and a normal oropharynx. She has no murmurs or organomegaly. Discrete, salmon-pink plaques with overlying adherent silvery scale were found scattered diffusely over her trunk, arms and legs. Notably, the lesions involve her umbilicus and gluteal cleft. Her tongue is normal, and she did not exhibit nail pitting.
Case Discussion
This eruption is a classic example of (C) guttate psoriasis in association with recent streptococcal pharyngitis. Guttate psoriasis is diagnosed on clinical examination by the finding of numerous, “drop-like,” (ie, gestate) 2 to 6 mm lesions of psoriasis, characterized by sharply demarcated pink to red papules and plaques with overlying micaceous (ie, silvery) scale. The lesions tend to favor the trunk and proximal extremities. Similar to chronic plaque psoriasis, the lesions may be pruritic or painful. Involvement of the umbilicus and/or gluteal cleft is common. Geographic tongue and nail pitting may be present, but tend to be more closely associated with plaque-type psoriasis.
The majority of guttate psoriasis cases are related to a recent streptococcal infection — typically pharyngitis — ranging in incidence from 56% to 97% depending on the study. This relationship was initially described more than 50 years ago and has continued to be supported by more recent studies. Recent streptococcal infection can be proven by throat culture or by elevated antistreptolysin O, anti-DNase B or streptozyme titers. While group A streptococci were initially implicated in psoriasis pathogenesis, groups C and G streptococci also may play a role. Tonsillar or pharyngeal infections are most frequently implicated, but perianal streptococcal infections also can trigger the development of guttate psoriasis.
Up to 40% of pediatric patients who initially present with guttate psoriasis will subsequently develop chronic plaque psoriasis, while the remainder will spontaneously clear. The relationship of streptococcal infections to chronic plaque psoriasis is less clear than its relationship to guttate psoriasis. Patients with chronic plaque psoriasis are more likely than controls to be tonsillar carriers of beta-hemolytic streptococci, suggesting there is a role for streptococci in the pathogenesis and exacerbations of chronic psoriasis.
The other answer choices can be differentiated from guttate psoriasis based on the clinical presentation. The eruption of streptococcal scarlet fever is a diffuse, ill-defined eruption of tiny, rough erythematous papules that is concurrent with the symptoms of fever and acute pharyngitis. Rheumatic fever, while also temporally distanced from the streptococcal infection, is associated with the cutaneous findings of erythema marginatum and subcutaneous nodules. The viral exanthem of mononucleosis is nonspecific and can be petechial, scarlatiniform, macular, urticarial or erythema multiforme-like.
Our patient was treated with medium-potency topical corticosteroids twice a day for 2 weeks straight with marked improvement. Her recent streptococcal pharyngitis was appropriately treated with a full course of amoxicillin, and her follow-up throat culture was negative.
- References:
- Fry L, et al. Clin Dermatol. 2007;doi:10.1016/j.clindermatol. 2007.08.015.
- Gudjonsson JE, et al. Br J Dermatol. 2003;doi:10.1046/j.1365-2133.2003.05552.x.
- Herbst RA, et al. J Am Acad Dermatol. 2000; 42:885-887.
- McFadden JP, et al. Br J Dermatol. 2009;doi:10.1111/j.1365-2133.2009.09102.x.
- For more information:
- Emily Osier, MD, is a clinical research fellow in pediatric dermatology at Rady Children’s Hospital, San Diego. She can be reached at ejosier@gmail.com.
- Andrew C. Krakowski, MD, is an attending physician at Rady Children’s Hospital, San Diego.