What does granuloma annulare look like and where does it appear?

The classic appearance is firm, skin-coloured to pink or red-brown papules that merge into ring-shaped plaques with a raised border and central clearing. There is no scale — this helps distinguish it from tinea (ringworm) or psoriasis. The most common locations are the dorsal hands and fingers, dorsal feet, extensor ankles, and elbows. Lesions are usually one to five centimetres across and are mostly asymptomatic, though around 30% of people notice mild itching. The subcutaneous subtype in children presents as deep firm nodules under normal-looking skin, most often on the shins or scalp.

Does granuloma annulare always need treatment?

Not always. Around 50% of localised lesions resolve spontaneously within two years, so watchful waiting with reassurance and a baseline photograph is a reasonable first approach. When treatment is desired, a potent topical corticosteroid — such as betamethasone dipropionate 0.05% or mometasone furoate 0.1% ointment — applied under overnight occlusion for six to eight weeks is the most practical option in general practice. Individual stubborn lesions can be treated with intralesional triamcinolone or cryotherapy by a dermatologist. Generalised disease is harder to clear and often requires dermatology-led phototherapy or systemic treatment.

Why does granuloma annulare need a diabetes check?

Generalised granuloma annulare is associated with type 2 diabetes, dyslipidaemia, thyroid disease, and (less commonly) HIV and hepatitis B or C. A 2014 case-control study in JAMA Dermatology found roughly double the rate of type 2 diabetes in people with granuloma annulare compared with controls, with similar associations for dyslipidaemia and thyroid disease. For localised disease in a young person, routine blood tests are not mandatory. For any adult with generalised disease, checking HbA1c, fasting lipids, TSH, and HIV and hepatitis B and C serology is recommended.

What conditions can mimic granuloma annulare?

The most important differential is tinea corporis (ringworm), which has a scaly advancing border and a positive skin scrape with KOH preparation. Necrobiosis lipoidica appears on the shins with an atrophic yellow-brown centre and telangiectasias, and is strongly associated with diabetes. Sarcoidosis produces similar annular lesions but shows 'apple-jelly' colour on diascopy and non-caseating granulomas on biopsy. Erythema migrans from tick-borne disease can produce an expanding ring, particularly with a travel or outdoor exposure history. Discoid lupus affects sun-exposed skin, produces scarring, and has follicular plugging on dermoscopy or biopsy.

Are there warning signs that need urgent attention?

Granuloma annulare itself is benign, but generalised disease appearing suddenly in an older adult — especially with unintentional weight loss, night sweats, or enlarged lymph nodes — warrants a paraneoplastic workup including a chest X-ray and age-appropriate cancer screening. Very rapidly spreading, tender, or ulcerated lesions should be reviewed by a dermatologist promptly to exclude other diagnoses. New generalised disease in any adult is also an opportunity to check HIV status, since HIV is a recognised association even without other risk factors.

Granuloma annulare

Granuloma annulare: ring-shaped skin lesions — the AU general practice approach

By Dr HB Lo, FACRRM Reviewed 27 October 2026 9 min read

Granuloma annulare is a benign, non-infectious skin condition producing ring-shaped papules and plaques, most often on dorsal hands, feet, and ankles. Around 50% of localised cases clear within two years without treatment; for most patients, confident clinical diagnosis and reassurance suffices. Potent topical corticosteroids under occlusion are the most practical first-line treatment when the appearance is bothersome. Generalised disease warrants screening for type 2 diabetes, dyslipidaemia, thyroid disease, HIV, and hepatitis B and C, and referral to dermatology.

What granuloma annulare is

Granuloma annulare (GA) is a benign, non-infectious, granulomatous skin condition characterised by firm ring-shaped papules and plaques with central clearing. It is not contagious, not cancerous, and in the majority of localised cases will resolve on its own. The condition affects around 0.1–0.4% of the general population, affects women about twice as often as men, and has a bimodal age distribution — one peak in childhood and another in adults aged 30–50.

The underlying mechanism is a Th1-mediated delayed hypersensitivity response to an unidentified antigen, producing a lymphohistiocytic infiltrate that surrounds and degrades dermal collagen with mucin deposition — the hallmark histological pattern. The trigger is not known in most cases, though associations with trauma, UV exposure, medications, and systemic disease have been described.

The word “granuloma” in the name relates to the microscopic pattern, not to infection. “Annulare” refers to the ring-shaped clinical appearance. Explaining this to patients prevents unnecessary alarm.

A. Core clinical — the AU general-practice framework

Clinical subtypes

The Australasian College of Dermatologists recognises five main clinical subtypes, each with different implications:

Localised GA (~75%) is the most common form — single or a few annular lesions on the dorsal hands, fingers, dorsal feet, extensor ankles, or wrists. Lesions are firm, skin-coloured to pinkish, one to five centimetres across, and largely asymptomatic. About 50% resolve spontaneously within two years.

Generalised GA (~15%) involves more than ten widespread lesions on the trunk and extremities. It predominantly affects adults over 50, runs a chronic relapsing course, and carries systemic associations (see below). This subtype is the one that requires investigation.

Subcutaneous GA is rare and predominantly paediatric, presenting as deep firm nodules under normal-looking skin on the shins, scalp, or buttocks. It clinically resembles a rheumatoid nodule and requires biopsy.

Perforating GA is a rare variant where papules develop central umbilication as degenerated collagen is extruded through the epidermis.

Patch or macular GA presents as diffuse erythematous patches without a raised papular border, often on the trunk, and may be misdiagnosed as eczema or early cutaneous lymphoma.

History

Lesion onset and evolution — gradual ring formation over weeks to months; central clearing develops as the lesion expands outward.
Symptoms — mostly asymptomatic; mild pruritus in about 30%; rarely tender.
Distribution — localised to hands/feet suggests localised GA; widespread trunk and limb involvement suggests generalised GA.
Past medical history — diabetes, thyroid disease, dyslipidaemia, HIV risk factors, hepatitis exposure.
Medications — TNF inhibitors (paradoxically both cause and treat GA), allopurinol, amlodipine, ACE inhibitors, vemurafenib, vaccinations in the preceding weeks.
Psychosocial — visible lesions on the dorsal hands are cosmetically distressing and have a measurable impact on quality of life.
Constitutional symptoms — weight loss, night sweats, fever suggest paraneoplastic workup.

Examination

The lesions of localised GA are firm annular plaques with no scale — the absence of scale is a key distinguishing feature from tinea, psoriasis, and eczema. The border is raised and well-defined; the centre shows partial or complete clearing. Look for diabetic stigmata (acanthosis nigricans, necrobiosis lipoidica) in adults with generalised disease.

Differential diagnosis

Condition	Key distinguishing feature
Tinea corporis	Scaly border; KOH preparation positive
Necrobiosis lipoidica	Pretibial; atrophic yellow-brown centre; telangiectasias; diabetes association
Sarcoidosis	“Apple-jelly” on diascopy; systemic features; non-caseating granulomas on biopsy
Erythema migrans	Rapid expansion; tick exposure history; single lesion typical
Annular psoriasis	Silvery scale; extensor distribution; nail changes
Discoid lupus	Photodistribution; follicular plugging; scarring; photosensitivity
Erythema annulare centrifugum	Trailing inner scale; more transient
Mycosis fungoides (early)	Epidermal change; chronic; biopsy required

Investigation

Localised GA — clinical diagnosis is sufficient in the typical presentation. No routine blood tests are required in a young patient with typical lesions.

Generalised GA in any adult — screen for systemic associations:

HbA1c and fasting glucose — type 2 diabetes association approximately double population risk (Wang JAMA Dermatol 2014)
Fasting lipid profile
TSH — autoimmune thyroid disease is associated (Erfurt-Berge Eur J Dermatol 2014)
HIV serology
Hepatitis B and C serology

Subcutaneous GA in a child — skin biopsy is required to exclude rheumatoid nodule. Consider rheumatoid factor and anti-CCP if histology is equivocal.

Biopsy is indicated when the diagnosis is uncertain, lesions are atypical, or generalised disease warrants histological confirmation. Palisading granulomas with central mucin and collagen degeneration are diagnostic when correlated with the clinical picture.

Paraneoplastic workup — if explosive generalised onset occurs in a patient over 50, perform a chest X-ray, lymph node examination, and age-appropriate cancer screening per the RACGP Red Book.

B. Evidence appraisal — treatment options and what works

First-line — localised GA

Per eTG Dermatology, the recommended first-line approach for localised GA involves:

Watchful waiting — 50% resolve spontaneously within two years. Reassurance with baseline photography is appropriate management in many cases.
Potent topical corticosteroid under occlusion — betamethasone dipropionate 0.05% or mometasone furoate 0.1% ointment applied twice daily, covered with cling wrap overnight, for six to eight weeks. This is the most accessible general practice treatment. Warn about skin thinning with prolonged use.
Topical tacrolimus 0.1% ointment — off-label, but small case series support its use, particularly for the face or areas where corticosteroid atrophy is concerning.
Intralesional triamcinolone acetonide (5–10 mg/mL) — for stubborn or cosmetically significant individual lesions; typically administered by a dermatologist.
Cryotherapy (liquid nitrogen, single freeze-thaw cycle) — for individual lesions in patients with fair skin; 80% clearance in one case series. Counsel darker-skinned patients regarding the risk of post-inflammatory dyspigmentation.

Second-line and generalised GA — dermatology-led

For generalised or refractory disease, referral to dermatology is appropriate. Evidence is based on case series rather than randomised controlled trials:

Narrowband UVB or PUVA phototherapy — 50–70% improvement in observational series; typically two to three sessions weekly for two to three months.
Hydroxychloroquine 200–400 mg daily — off-label; baseline ophthalmology review required, with six-monthly visual field and OCT monitoring.
Pentoxifylline 400 mg three times daily — anti-TNF effect; modest case-series evidence.
Dapsone, isotretinoin, methotrexate, ciclosporin — used in refractory cases under specialist supervision.
TNF inhibitors (adalimumab, infliximab) — a paradox exists: anti-TNF therapy is used to treat refractory GA, yet is also a recognised trigger for de novo GA in patients receiving these drugs for psoriasis or inflammatory bowel disease.

Treating associated comorbidities

Treating underlying type 2 diabetes, dyslipidaemia, or thyroid disease is clinically important in its own right and may contribute to improved skin disease in generalised GA, though direct evidence for skin improvement with metabolic control is observational only.

C. Natural history and recurrence

Localised GA has a favourable natural history — around half resolve within two years without intervention. Generalised GA is more persistent, often following a chronic relapsing course over years. After apparent clearance, recurrence is possible in both subtypes.

There is no evidence that any specific diet, supplement, or complementary therapy changes the natural history of granuloma annulare. Patients searching online will encounter many claims to the contrary; supporting them to evaluate these claims with good information is part of effective care.

Koebner phenomenon — new lesions appearing at sites of skin trauma — has been described. Patients with active disease should avoid unnecessary skin trauma.

Photoprotection is sensible in the photo-distributed variant, which appears on sun-exposed skin and may be triggered or worsened by UV exposure.

D. Australian operations

MBS items

General practice consultations — MBS items 23 (standard), 36 (long), and 44 (prolonged).
Telehealth — items 91790 and 92029 for established patients.
Skin biopsy — MBS item 30071 (small lesion excision for histology); histopathology under the 72800-series items.
Pathology — HbA1c 66541; fasting lipids 66536; TFT 66719; HIV and hepatitis serology when clinically indicated.
Mental Health Care Plan — MBS 2715 is appropriate when visible disease causes significant psychosocial distress.
Dermatology referral — MBS 105.

PBS medicines

Betamethasone dipropionate 0.05% ointment — PBS general schedule.
Mometasone furoate 0.1% cream and ointment — PBS general schedule.
Triamcinolone acetonide injection — supplied in-clinic for intralesional use.
Tacrolimus 0.1% ointment — PBS Authority for atopic dermatitis only; off-label private prescription for GA.
Hydroxychloroquine 200 mg — PBS general schedule; requires ophthalmology baseline.
Dapsone 100 mg — PBS Authority; G6PD screen required before initiation.

Referral pathways

Dermatology — generalised disease requiring phototherapy or systemic therapy; diagnostic uncertainty; biopsy under local anaesthesia; cosmetically significant refractory localised disease.
Endocrinology — newly diagnosed type 2 diabetes identified on screening.
Sexual health or infectious diseases — newly identified HIV on screening.
Paediatric dermatology or paediatric rheumatology — subcutaneous GA in a child to exclude rheumatoid nodule.

E. Special populations

Paediatric patients — Localised GA in children is common and has an excellent prognosis, with most resolving without treatment. Subcutaneous GA in children requires biopsy and specialist review to exclude juvenile idiopathic arthritis-related rheumatoid nodules. Topical corticosteroids are used cautiously on children’s skin — limit potent formulations to short courses on small areas.

Older adults — Generalised GA appearing for the first time in a patient over 50 warrants a thorough investigation for associated metabolic and haematological conditions, and a paraneoplastic screen if the clinical picture is atypical. Skin biopsy is more likely to be needed in this age group for diagnostic certainty.

Darker skin tones — Post-inflammatory dyspigmentation from cryotherapy or even natural healing is a significant concern. Set realistic expectations, prefer topical corticosteroids over cryotherapy when possible, and document the discussion.

Immunocompromised patients — HIV-associated generalised GA may respond to effective antiretroviral therapy. The broader immunosuppressed population (organ transplant recipients, patients on TNF inhibitors for other indications) has increased risk of de novo and treatment-paradoxical GA.

People taking TNF inhibitors — GA can appear as a paradoxical reaction in patients being treated with anti-TNF agents for rheumatoid arthritis, psoriasis, or inflammatory bowel disease. If temporally related, consider whether the drug can be switched or tapered in consultation with the treating specialist.

When to escalate

Refer or escalate when:

Generalised GA requires dermatology assessment for phototherapy or systemic treatment
The diagnosis is uncertain and biopsy is needed
Subcutaneous GA in a child requires specialist evaluation
New generalised disease in an older adult suggests paraneoplastic aetiology
Newly identified systemic disease (diabetes, HIV, hepatitis) requires specialist management
Significant psychological distress from visible disease warrants psychology via a Mental Health Care Plan

What this article is and is not

This is general health information drawn from current Australian dermatology and general practice references — Australasian College of Dermatologists, Therapeutic Guidelines (eTG), DermNet NZ, and the RACGP Red Book. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about investigation, treatment, and specialist referral are made with your own GP and treating clinicians.

For consumer-friendly information: HealthDirect — skin conditions and the Better Health Channel.

Sources cited

Frequently asked questions

What does granuloma annulare look like and where does it appear?

The classic appearance is firm, skin-coloured to pink or red-brown papules that merge into ring-shaped plaques with a raised border and central clearing. There is no scale — this helps distinguish it from tinea (ringworm) or psoriasis. The most common locations are the dorsal hands and fingers, dorsal feet, extensor ankles, and elbows. Lesions are usually one to five centimetres across and are mostly asymptomatic, though around 30% of people notice mild itching. The subcutaneous subtype in children presents as deep firm nodules under normal-looking skin, most often on the shins or scalp.
Does granuloma annulare always need treatment?

Not always. Around 50% of localised lesions resolve spontaneously within two years, so watchful waiting with reassurance and a baseline photograph is a reasonable first approach. When treatment is desired, a potent topical corticosteroid — such as betamethasone dipropionate 0.05% or mometasone furoate 0.1% ointment — applied under overnight occlusion for six to eight weeks is the most practical option in general practice. Individual stubborn lesions can be treated with intralesional triamcinolone or cryotherapy by a dermatologist. Generalised disease is harder to clear and often requires dermatology-led phototherapy or systemic treatment.
Why does granuloma annulare need a diabetes check?

Generalised granuloma annulare is associated with type 2 diabetes, dyslipidaemia, thyroid disease, and (less commonly) HIV and hepatitis B or C. A 2014 case-control study in JAMA Dermatology found roughly double the rate of type 2 diabetes in people with granuloma annulare compared with controls, with similar associations for dyslipidaemia and thyroid disease. For localised disease in a young person, routine blood tests are not mandatory. For any adult with generalised disease, checking HbA1c, fasting lipids, TSH, and HIV and hepatitis B and C serology is recommended.
What conditions can mimic granuloma annulare?

The most important differential is tinea corporis (ringworm), which has a scaly advancing border and a positive skin scrape with KOH preparation. Necrobiosis lipoidica appears on the shins with an atrophic yellow-brown centre and telangiectasias, and is strongly associated with diabetes. Sarcoidosis produces similar annular lesions but shows 'apple-jelly' colour on diascopy and non-caseating granulomas on biopsy. Erythema migrans from tick-borne disease can produce an expanding ring, particularly with a travel or outdoor exposure history. Discoid lupus affects sun-exposed skin, produces scarring, and has follicular plugging on dermoscopy or biopsy.
Are there warning signs that need urgent attention?

Granuloma annulare itself is benign, but generalised disease appearing suddenly in an older adult — especially with unintentional weight loss, night sweats, or enlarged lymph nodes — warrants a paraneoplastic workup including a chest X-ray and age-appropriate cancer screening. Very rapidly spreading, tender, or ulcerated lesions should be reviewed by a dermatologist promptly to exclude other diagnoses. New generalised disease in any adult is also an opportunity to check HIV status, since HIV is a recognised association even without other risk factors.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.