Granuloma annulare
GA; localised / generalised / perforating / subcutaneous granuloma annulare
Granuloma annulare is a benign granulomatous dermatosis presenting most commonly as skin-coloured to pink-violaceous annular papules and plaques on the dorsal hands, feet and elbows. It is a frequent differential / biopsy target in skin-oncology clinic — annular plaques are interpreted as superficial BCC, dermatofibroma, cutaneous sarcoidosis or even mycosis fungoides. Four main variants are recognised — localised, generalised, perforating, and subcutaneous. Most cases self-resolve over months to years; generalised disease may be associated with hyperlipidaemia and (more weakly) diabetes mellitus.
Clinical variants
- Localised GA — commonest. Single or several annular skin-coloured / pink plaques on dorsal hands, feet, elbows; 1–5 cm. Typically self-resolves over 1–2 years.
- Generalised GA — > 10 lesions distributed over trunk and extremities; often refractory; associations with hyperlipidaemia and diabetes are debated (modest in modern series).
- Perforating GA — umbilicated or crusted papules with transepidermal elimination of necrobiotic collagen; hands.
- Subcutaneous GA (pseudorheumatoid nodule) — children; firm subcutaneous nodules on pretibia, scalp, sacrum; can mimic rheumatoid nodule.
- Patch GA — erythematous patches without obvious annular border; truncal; commonly misdiagnosed.
Dermoscopy
- Pink-orange structureless background with peripheral linear / dotted vessels.
- White / yellow structureless areas in older lesions.
- Absence of pearly margin, arborising vessels and blue-grey nests argues against BCC.
Histology
- Interstitial pattern — histiocytes between collagen bundles, focal mucin deposition (alcian blue +).
- Palisading pattern — histiocytes around an area of necrobiotic collagen / mucin (classical pattern); fewer plasma cells than necrobiosis lipoidica.
- Differential on histology — necrobiosis lipoidica (more diffuse necrobiosis, sclerosing change, plasma cells), sarcoidosis (no necrobiosis, naked granulomas), rheumatoid nodule (fibrinoid necrosis), foreign-body granuloma.
Systemic associations
- Hyperlipidaemia — modest association in generalised GA; check lipid profile.
- Diabetes mellitus — historical association now considered weaker than once thought; check FBG / HbA1c in atypical cases.
- Thyroid disease — autoimmune.
- HIV — generalised GA reported.
- Malignancy — case reports of paraneoplastic GA with solid and haematological cancers; routine cancer workup not warranted without other clues.
- Drugs — TNF-α inhibitors, ICI, anti-EGFR; consider drug-induced GA in temporal association.
Management
- Localised disease — observation; potent topical corticosteroid; intralesional triamcinolone; cryotherapy.
- Generalised disease — broader options:
- Phototherapy — narrowband UVB or PUVA.
- Hydroxychloroquine 200 mg twice daily.
- Tetracyclines (minocycline, doxycycline) combined with topical steroid.
- Methotrexate, ciclosporin, fumarates in refractory.
- TNF-α inhibitors / biologics — limited evidence.
- Reassurance about benign nature is often the most useful intervention; self-resolution is the rule.
References
- Piette EW, Rosenbach M. Granuloma annulare — clinical and histologic variants, epidemiology and update on therapy. J Am Acad Dermatol; 2016.
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