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Granuloma Annulare

Patient Story

A 3-year-old boy presents with an annular eruption on the dorsum of his foot for 6 months. Prior to this visit the child was treated with multiple topical antifungal creams prescribed by other health care providers for presumed tinea corporis. The absence of significant scaling and the failure to respond to topical antifungals point to the diagnosis of granuloma annulare (GA). Also, this is a common location for GA. A KOH preparation was also negative for hyphae. The diagnosis was discussed with the parents and the decision was made to try a mid-potency corticosteroid topically for treatment. While intralesional steroids are more effective this is not a viable option for 3-year-old child.


GA is a common dermatologic condition that presents as small, light-red, dermal papules coalescing into annular plaques without scale. As the previous vignette describes, it is often mistaken as nummular eczema or tinea corporis. Distribution, pattern, and lack of scale are important diagnostic clues.


  • GA affects twice as many females than males.1

  • The four presentations of GA are localized, disseminated/generalized, perforating, and subcutaneous.

  • Of the four variations, the localized form is seen most often.1

Etiology and Pathophysiology

  • Benign cutaneous, inflammatory disorder of unknown origin.1

  • Disease may be self-limiting, but may persist for many years.

  • There is a reported association between type 1 diabetes and subcutaneous granuloma annulare in children. One retrospective study looked at 34 children less than 10 years of age with subcutaneous granuloma annulare and found 2 of these children (5.9%) had type 1 diabetes.2,3 While this is much higher than the prevalence of childhood type 1 diabetes, this does not prove causality.

  • Reported associations include viral infections (including HIV), Borrelia and streptococcal infections, insect bites, lymphoma, tuberculosis, and trauma.4,5

  • One proposed mechanism for GA is a delayed-type hypersensitivity reaction as a result of T-helper–type cell (Th)-1 lymphocytic differentiation of macrophages. These macrophages become effector cells that express tumor necrosis factor (TNF)-α and matrix metalloproteinases. The activated macrophages are responsible for dermal collagen matrix degradation.6

  • An association between high expression of gil-1 oncogene and granulomatous lesions of the skin, including GA, has been established.7

Risk Factors

The only identifiable risk factor is being a female. There are several associations, but nothing has been shown to be causative.

Clinical Features

Annular lesions have raised borders that are skin-colored to erythematous (Figures 148-1 and 148-2). The rings may become hyperpigmented or violaceous (Figure 148-3). There is often a central depression within the ring. These lesions range from 2 mm to 5 cm. Although the classical appearance of GA is annular, the lesions may be arcuate instead ...

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