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Granuloma Annulare

PATIENT STORY

A 39-year-old woman presents with raised rings on her right hand. Not knowing the correct diagnosis, another physician prescribed topical steroids and antifungal medicines with no benefit. The diagnosis of granuloma annulare (GA) was made by the typical clinical appearance, and the patient was offered intralesional steroids. Triamcinolone acetonide was injected as seen in Figure 182-1A. The patient noted improvement over the subsequent weeks, but within a month new lesions began to appear on her other hand (Figure 182-1B). Additional injections were provided and 1 month later the patient had regression of the treated lesions but had new lesions on the right arm (Figure 182-2A). At the next visit, the patient had new lesions on her feet as well (Figure 182-2B). The diagnosis of disseminated GA was made and systemic treatment was started.

FIGURE 182-1

A. GA in a 42-year-old woman. Intralesional steroids were administered on the first visit with resolution of the injected lesions. B. Same patient months later with new annular lesions on the opposite hand. She requested additional injections. (Reproduced with permission from Richard P. Usatine, MD.)

FIGURE 182-2

A. Same patient as in Figure 182-1 1 month later with new crops of lesions on the arms and feet. She has disseminated GA. Note the area of hypopigmentation secondary to a previous steroid intralesional steroid injection. B. Disseminated GA on the foot of the same patient. The rings are flatter and many are conjoined. (Reproduced with permission from Richard P. Usatine, MD.)

INTRODUCTION

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

EPIDEMIOLOGY

  • GA affects twice as many women as men.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.

  • Reported associations include diabetes mellitus, viral infections (including HIV), Borrelia and streptococcal infections, insect bites, lymphoma, tuberculosis, and trauma.2,3

  • 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.4

  • An association between high expression of gil-1 oncogene and granulomatous lesions ...

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