eMedicine Specialties > Dermatology > Reactive & Inflammatory Dermatoses
Granuloma Annulare
Updated: Aug 26, 2009
Introduction
Background
Granuloma annulare (GA) is a benign inflammatory dermatosis. T. Colcott Fox first described granuloma annulare in 1895; however, not until 1902 did Radcliffe-Crocker label it as granuloma annulare.
Granuloma annulare is relatively common disease that occurs in all age groups, but it is rare in infancy. Granuloma annulare is characterized clinically by dermal papules and annular plaques. The precise cause of granuloma annulare is unknown. Histological examination reveals foci of degenerative collagen associated with palisaded granulomatous inflammation.
The following clinical variants are recognized:
- Localized granuloma annulare: This is the most common form. Localized granuloma annulare is characterized by skin-colored to violaceous lesions up to 5 cm in diameter. Usually, the epidermis has attenuated surface markings. Annular rings with solitary firm papules or nodules may be present. Localized granuloma annulare has a predilection for the feet, ankles, lower limbs, and wrists.
- Generalized granuloma annulare: This form occurs predominantly in adults. The trunk is usually involved, as well as the neck, extremities, face, scalp, palms, and soles. Lesions range from widespread papules to annular plaques to large, discolored patches with a variety of coloration from yellow to violaceous.
- Subcutaneous granuloma annulare1,2 : This form occurs predominantly in children. Subcutaneous granuloma annulare is characterized by firm or hard asymptomatic nodules in the deep dermis or subcutaneous tissues, with individual lesions measuring from 5 mm to 4 cm in diameter. They are prevalent on the anterotibial plateau, ankles, dorsal feet, buttocks, hands, scalp, and eyelids.
- Perforating granuloma annulare3 : This form is very rare. Perforating granuloma annulare is usually localized to the dorsal hands and fingers or may be generalized on the trunk and extremities. A variety of superficial umbilicated papules develop, with or without a discharge, that heal with scarring.
- Arcuate dermal erythema: This is an uncommon form of granuloma annulare that manifests as infiltrated erythematous patches that may form large, hyperpigmented rings with central clearing.
Pathophysiology
Proposed pathogenic mechanisms for granuloma annulare include cell-mediated immunity (type IV), immune complex vasculitis, and an abnormality of tissue monocytes. Some other possible mechanisms include primary degeneration of connective tissue leading to granulomatous inflammation, lymphocyte-mediated immune reaction with macrophage activation, and cytokine-mediated degradation of connective tissue.
Frequency
International
The frequency of granuloma annulare is in the general population is unknown. Granuloma annulare does not favor a particular race, ethnic group, or geographical area.
- Localized granuloma annulare is the most common among the various subtypes.
- Of all patients with granuloma annulare, 9-15% have the generalized variant.
- Perforating granuloma annulare has been reported to have a prevalence of 5% among granuloma annulare subtypes; further, reports suggest that this variant may be more common in the Hawaiian Islands.
Mortality/Morbidity
Most cases of granuloma annulare resolve without adverse medical sequelae.
Sex
Women are affected by granuloma annulare twice as often as men.
Age
- Localized granuloma annulare is most commonly found in children and in adults younger than 30 years.
- Generalized granuloma annulare demonstrates a bimodal age distribution, occurring in patients younger than 10 years and in patients aged 30-60 years.
- Although subcutaneous granuloma annulare can occur in adults, it is predominantly a disease of otherwise healthy children, who are typically aged 2-10 years.
- Similarly, perforating granuloma annulare most often affects children.
Clinical
History
- Both localized and generalized granuloma annulare lesions usually manifest as asymptomatic cutaneous lesions. Lesions may improve in winter and worsen in summer.
- Subcutaneous granuloma annulare most often manifests as a large, asymptomatic soft tissue mass. Although nodules are usually stable for months, they may rapidly enlarge over the course of weeks.
Physical
- Patients with localized granuloma annulare commonly present with groups of 1- to 2-mm papules that range in color from flesh-toned to erythematous, often in an annular arrangement over distal extremities.
- Grouped lesions may expand into arciform or annular plaques measuring 1-5 cm in diameter.
- Centers of lesions may be slightly hyperpigmented and depressed relative to their borders, which may be solid or composed of numerous dermal papules.
- Lesions most commonly manifest on the dorsal surfaces of the feet, hands, and fingers, and on the extensor aspects of the arms and legs.
- Rarely, lesions appear on the face, scalp, or penis.
- Patients with generalized granuloma annulare characteristically present with a few to thousands of 1- to 2-mm papules or nodules that range in color from flesh-toned to erythematous and involve multiple body regions.
- Lesions may coalesce into annular plaques, which measure 3-6 cm in diameter and which may enlarge centrifugally over weeks to months.
- Although any part of the cutaneous surface may be involved, lesions tend to be symmetrically disposed over acral areas and the trunk.
- Rarely, the head, palms, soles, and mucous membranes are involved.
- Patients with subcutaneous granuloma annulare present with a firm, nontender, flesh-colored or pinkish nodule without overlying epidermal alteration.
- Lesions are typically solitary but may occur in clusters.
- The most commonly reported site of involvement is the lower extremities (65% of cases), often on the pretibial surface.
- Other typical sites include the fingers and palms and the dorsa of the feet.
- The buttocks, forehead, and scalp are less commonly affected.
- Deep dermal or subcutaneous nodules on the extremities are attached to fascia and are often therefore mobile, whereas lesions on the scalp are attached to underlying periosteum and are therefore fixed or only slightly mobile.
- Patients with perforating granuloma annulare present with 1 to hundreds of grouped 1- to 4-mm papules that range in color from flesh-toned to erythematous.
- Papules often coalesce to form annular plaques.
- In some patients, the erythematous papules may evolve into yellowish pustular lesions that subsequently exude a thick and creamy or clear and viscous fluid, forming umbilicating, crusting, or scaling papular lesions that heal, leaving atrophic hypopigmented or hyperpigmented scars.
- Larger and more ulcerated plaques are common in middle-aged and elderly patients.
- Lesions affect all areas of the body but have a predilection for the extensor surfaces of extremities and the dorsa of hands and fingers.
- Arcuate dermal erythema is an uncommon form of granuloma annulare that manifests as infiltrated erythematous patches that may form large, hyperpigmented rings with central clearing. Papules are a less prominent feature in this variant. Patches typically appear on the trunk and may spread centrifugally over weeks to months.
- Patients with actinic annulare present with 1-10 plaques, which tend to be annular or serpiginous areas with raised erythematous borders.
- Lesions may be hypopigmented centrally; the epidermis is otherwise spared.
- Plaques are typically distributed over sun-exposed areas, such as the arms, neck, face, and dorsa of the hands.
- Other than by their location on heat- or sun-damaged skin, actinic annulare lesions are difficult to distinguish clinically from eruptions of granuloma annulare.
Causes
The etiology of granuloma annulare is usually unknown, and the pathogenetic mechanisms are poorly understood, with a vast majority of granuloma annulare cases occurring in patients who are otherwise healthy. The range of predisposing events and associated diseases is diverse, and granuloma annulare is thought to represent a reaction pattern with many different initiating factors.
Granuloma annulare has been hypothesized to be associated with tuberculosis, insect bites, trauma, sun exposure, thyroiditis, vaccinations, and viral infections, including HIV, Epstein-Barr virus, hepatitis B virus, hepatitis C virus, and herpes zoster virus. However, these suggested etiologic factors remain unproven.
Familial cases of granuloma annulare observed in identical twins and siblings in several generations, along with an association of granuloma annulare with HLA phenotypes, suggest the possibility of a hereditary component in some cases. The HLA-B8 level has been reported to be increased in localized granuloma annulare; HLA-A29 and HLA-BW35 levels are reported to be increased in generalized granuloma annulare.
Some reports associate chronic stress with granuloma annulare as a trigger of the disease. Granuloma annulare also has some predilection for the sun-exposed areas and photodamaged skin. Photosensitive granuloma annulare has been found in association with HIV infection. Finally, some cases of granuloma annulare or granuloma annulare–like reactions have been reported after gold therapy and treatment with allopurinol, diclofenac, quinidine, calcitonin, amlodipine, ACE inhibitors, daclizumab,5 and calcium channel blockers.
Relationship to systemic diseases
Granuloma annulare has been associated primarily with type I diabetes mellitus, but it is only rarely associated with type II diabetes mellitus and thyroid disease, based on an increased number of granuloma annulare patients with these diseases in small case series.6
Small case series have reported granuloma annulare to occur in association with malignancy, AIDS, and herpes zoster lesions. Although no definite patterns relating granuloma annulare and systemic disease have been thoroughly established, it has been suggested that an atypical histologic (vasculopathy or extravascular neutrophilia) or clinical presentation (unusual appearance or location) may indicate an associated disease. In the case of malignancy, a 2003 study by Li et al reviewed classic cases in the literature and could find no definite relationship between granuloma annulare and malignant neoplasms.7
Relationship with malignant diseases
Certain malignancies are accompanied by different mucocutaneous paraneoplastic syndromes. Lesions that mimic granuloma annulare or are histologically confirmed as granuloma annulare have occurred in association with:
- Non-Hodgkin lymphoma
- Hodgkin lymphoma
- Acute myelogenous leukemia
- Chronic lymphocytic leukemia
- Myelomonocytic leukemia
- Large granular lymphocytic leukemia
- Myelodysplastic syndrome
- T-cell lymphoma
- Follicular lymphoma
- Lennert lymphoma
- Solid tumors:
- Breast tumors
- Cervical cancer
- Colon cancer
- Lung cancer
- Prostate cancer
- Testicular tumors
- Thyroid cancer
Differential Diagnoses
Erythema Annulare Centrifugum
Erythema Elevatum Diutinum
Lichen Planus
Other Problems to Be Considered
Localized granuloma annulare
Annular lichen planus
Acute febrile neutrophilic dermatosis
Erythema annulare centrifugum
Erythema elevatum diutinum
Erythema migrans of Lyme disease
Fat necrosis
Giant cell arteritis8
Hansen disease (leprosy)
Mucocutaneous paraneoplastic syndrome
Necrobiosis lipoidica diabeticorum
Neonatal lupus erythematosus
Subacute cutaneous lupus erythematosus
Tinea corporis
Generalized granuloma annulare
Cutaneous metastases
Cutaneous paraneoplastic syndrome
Lichen myxedematous
Lichen planus
Sarcoidosis
Subcutaneous granuloma annulare
Dermoid cyst
Erythema nodosum
Rheumatoid nodule
Perforating granuloma annulare
Elastosis perforans serpiginosa
Foreign body granuloma
Insect bites
Molluscum contagiosum
Pityriasis lichenoides
Perforating collagenosis
Actinic granuloma annulare
Erythema annulare centrifugum
Necrobiosis lipoidica diabeticorum
Sarcoidosis
Workup
Laboratory Studies
- Laboratory studies are largely noncontributory in patients with granuloma annulare (GA). With a classic history and unremarkable physical examination findings (other than the presenting lesion[s]), no additional workup is necessary.
- If, however, a thorough history is not available or systemic disease is considered likely, appropriate laboratory evaluations should be performed to exclude other diagnostic possibilities.
- For example, in subcutaneous granuloma annulare, a CBC count, an erythrocyte sedimentation rate, and a rheumatoid factor study may assist in excluding other possible causes for nodules.
Imaging Studies
- Imaging studies are not generally necessary in diagnosing granuloma annulare. However, radiographs, CT scans, or MRIs may be helpful in the evaluation of atypical subcutaneous lesions.
- Radiographs of subcutaneous granuloma annulare show a nonspecific soft tissue mass without calcification.
- On CT scans, subcutaneous granuloma annulare appears as a poorly defined mass with variable attenuation and variable contrast enhancement.
- On MRIs, subcutaneous granuloma annulare appears as a mass with poorly defined margins that is limited to subcutaneous tissue. MRI findings may be suggestive of, but not diagnostic of, subcutaneous granuloma annulare.9,10
Procedures
- Biopsy is recommended for a subcutaneous lesion and for an atypical presentation with respect to history (ie, rapid enlargement, pain) or location of lesion.
Histologic Findings
Early interstitial or incomplete granuloma annulare lesions show an interstitial pattern characterized by lymphocytes around vessels of the superficial and deep plexuses and by macrophages scattered between reticular dermal collagen bundles that are separated by mucin within which mast cells may be found. Mucin in granuloma annulare is hyaluronic acid and is visible in sections stained with hematoxylin and eosin as faintly basophilic stringy material. Its presence can be confirmed by staining with colloidal iron or Alcian blue at pH 2.5.
Fully evolved granuloma annulare lesions and deep subcutaneous granuloma annulare nodules demonstrate palisaded granulomatous dermatitis or a septal and lobular panniculitis, respectively. Macrophages surround acellular necrobiotic areas in which collagen bundles are thinned, or they sometimes have a pale, homogeneous, light-blue appearance, the latter of which is due to the presence of mucin.
In many cases of subcutaneous granuloma annulare, and in some dermal infiltrates, the centers of granulomas contain degenerated, homogeneous-appearing collagen and are deeply eosinophilic. In some sections, necrotic small vessels in the centers of palisaded foci are surrounded by nuclear dust. Presence of fibrinogen can be shown by direct immunofluorescence in the centers of palisaded granulomas. In perforating lesions, necrobiotic material is extruded through focal perforations. Epidermal hyperplasia at the edge of the perforation forms a pseudochannel communicating with an underlying necrobiotic granuloma.
Rare cases of nonnecrobiotic, sarcoidal, or tuberculoid granuloma annulare are also described.
Actinic annulare, also known as annular elastolytic giant cell granuloma, may lack the classic palisaded arrangement observed in granuloma annulare. Although elastosis is abundant in the mid dermis outside the granuloma, elastic tissue is absent from the center of the annulus. Giant cells frequently abut elastotic tissue, and phagocytosed elastotic fibers are noted in histiocytic cells at the advancing edge. Collagen has a normal appearance outside the lesion but a finely fibrillar pattern within the annulus. Mucin deposition is not increased as it is in granuloma annulare. Thus, actinic annulare can be distinguished histologically from granuloma annulare by a preponderance of giant cells in relation to elastotic tissue, by absence of mucin, and, occasionally, by absence of palisading histiocytes around granulomas.
Treatment
Medical Care
Localized granuloma annulare
Localized granuloma annulare (GA) is not often symptomatic and it has a tendency towards spontaneous resolution. Reassurance is often all that is necessary. Painful or disfiguring lesions have been treated by various methods, although the level of evidence supporting these methods is low.
Localized lesions have been treated with potent topical corticosteroids with or without occlusion for 4-6 weeks, as well as with intralesional corticosteroids with varying total doses of steroid.
Cryotherapy using liquid nitrogen or nitrous oxide as refrigerants has been shown in a prospective, uncontrolled trial to be an effective treatment for localized granuloma annulare. Secondary dyschromia may be a complication of cryotherapy.11
Other anecdotes of therapeutic efficacy in both localized and generalized granuloma annulare involve tacrolimus and pimecrolimus12,13,14 and imiquimod cream.15,16
Generalized granuloma annulare
Generalized granuloma annulare tends to be more persistent and unsightly. Treatment of the generalized disease is unfortunately fraught with a lack of consistently effective options. While the treatment of choice remains to be defined, the available literature supports the use of isotretinoin or phototherapy with oral psoralen and UV-A (PUVA) as first-line options for generalized granuloma annulare.17,18
Piaserico et al report successful therapy for long-standing generalized granuloma annulare using methyl aminolevulinate photodynamic therapy.19 Weisenseel et al reported moderate success with photodynamic therapy using 20% 5-aminolevulinic acid (ALA) gel.20
Marcus et al report on 6 patients with granuloma annulare that was refractory to standard treatment. The patients were treated with monthly combination therapy including rifampin at 600 mg, ofloxacin at 400 mg, and minocycline hydrochloride at 100 mg monthly for 3 months. Three to 5 months after the initiation of treatment, the plaques were cleared completely. Postinflammatory hyperpigmentation was reported by some patients. Although the treatment was successful, the authors suggested further studies may be needed to confirm this combination therapy as a successful option for recalcitrant granuloma annulare.21
Other anecdotal reports and small series describe successful treatment with dapsone, systemic steroids, pentoxifylline, hydroxychloroquine, cyclosporine, fumaric esters, interferon-gamma, potassium iodide, nicotinamide, etanercept, infliximab, adalimumab, and efalizumab.22,23
Consultations
A clinical guideline summary, Diabetic foot disorders: a clinical practice guideline, from the American College of Foot and Ankle Surgeons may be helpful.24
Medication
Therapies that may be considered as initial approaches for patients seeking therapy for localized granuloma annulare include intralesional corticosteroids, potent topical corticosteroids alone or under occlusion, and cryotherapy.
Patients with generalized granuloma annulare may accept more aggressive treatment because of the chronicity or pronounced cosmetic disfigurement associated with the disease. Generalized granuloma annulare may be treated initially with isotretinoin or PUVA, if not otherwise contraindicated.
Corticosteroids
Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
Clobetasol (ointment, cream, lotion) 0.05% (Temovate, Olux)
For inflammatory dermatoses responsive to steroids. Decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability. Affects production of lymphokines and has inhibitory effect on Langerhans cells.
Dosing
Adult
Apply thin film bid/qid to response; not to exceed 50 g/wk
Pediatric
Administer as in adults with caution
Interactions
None reported
Contraindications
Documented hypersensitivity; paronychia, cellulitis, impetigo, angular cheilitis, erythrasma, erysipelas, rosacea, perioral dermatitis, acne, or fungal skin infections
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Can cause atrophy of groin, face, and axillae; may cause striae distensae, rosacealike eruption with telangiectasia, acneiform eruption, and pigmentary changes; may increase skin fragility; rarely may suppress HPA axis; if infection develops and is not responsive to antibiotic treatment, discontinue until infection is under control
Triamcinolone acetonide (Aristocort, Kenalog)
For inflammatory dermatoses responsive to steroids. Decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability. Affects production of lymphokines and has inhibitory effect on Langerhans cells.
Dosing
Adult
10 mg/mL concentration injected intralesionally
Pediatric
Not established
Interactions
None reported
Contraindications
Documented hypersensitivity; bacterial, viral, or fungal skin infections
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Multiple complications (eg, severe infections, hyperglycemia, edema, atrophy and thinning of nearby skin, telangiectasia, pigmentary changes, delayed pain, scarring, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression) may occur; abrupt discontinuation of glucocorticoids may cause adrenal crisis
Prednisone (Deltasone, Orasone)
Synthetic corticosteroid, strong immunosuppressant, and anti-inflammatory drug with proven effects in cutaneous inflammatory disorders.
Dosing
Adult
60 mg/d; taper over 3-4 wk.
Pediatric
Not established
Interactions
Contraindications
Peptic ulcer, osteoporosis, psychoses or severe psychoneuroses; usually contraindicated in presence of acute infection; administration of live-virus vaccines, including smallpox, contraindicated in patients receiving immunosuppressive doses because expected serum antibody response may not be obtained
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Because of multiple and serious short-and long-term adverse effects, use precaution prior to administration; expert in the field must be consulted prior to any administration
Retinoids
Vitamin A derivatives have many roles. They encourage cellular differentiation, are antiproliferative, and serve as immunomodulators.
Isotretinoin (Accutane)
Oral agent that treats serious dermatologic conditions. Synthetic 13-cis isomer of the naturally occurring tretinoin (trans -retinoic acid). Both agents are structurally related to vitamin A. Should be prescribed only by physicians experienced and/or trained in its use.
A US Food and Drug Administration–mandated registry is now in place for all individuals prescribing, dispensing, or taking isotretinoin. For more information on this registry, see iPLEDGE. This registry aims to further decrease the risk of pregnancy and other unwanted and potentially dangerous adverse effects during a course of isotretinoin therapy.
Dosing
Adult
0.5-1 mg/kg/d PO
Pediatric
Not established
Interactions
Toxicity may occur with vitamin A coadministration; pseudotumor cerebri or papilledema may occur when coadministered with tetracyclines or other drugs associated with pseudotumor cerebri; may reduce plasma levels of carbamazepine
Contraindications
Absolute: Pregnancy, likely to become pregnant, or intends to become pregnant; females who cannot use reliable contraception while undergoing treatment; noncompliance with contraception; breastfeeding; concurrent use of methotrexate (increased liver toxicity) or tetracyclines (pseudotumor cerebri); documented hypersensitivity
Relative: Leukopenia; moderate-to-severe cholesterol or triglyceride elevation, significant hepatic or renal dysfunction
Precautions
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
May decrease night vision; inflammatory bowel disease may occur; may be associated with development of hepatitis; occasional exaggerated healing response of acne lesions (excessive granulation with crusting) may occur
Diabetes patients may experience problems in controlling their blood glucose while on isotretinoin; avoid exposure to UV light or sunlight until tolerance achieved; discontinue treatment if rectal bleeding, abdominal pain, or severe diarrhea occur; mood swings or depression may occur; caution if history of depression
Psoralen phototherapy agents
These agents inhibit cell proliferation.
Methoxsalen plus UVA (8-MOP, Oxsoralen)
Inhibits mitosis by binding covalently to pyrimidine bases in DNA when photoactivated by UV-A. May have a direct cytotoxic effect on activated histiocytes, fibroblasts, and lymphocytes in dermal infiltrate of lesions. May control lymphokine production through modulation of activated lymphocytes.
Dosing
Adult
Doses based on lean body weight
Oxsoralen, crystalline: 0.6 mg/kg 1.5-2 h before exposure to UV light, at least 48 h apart
Oxsoralen ultra, liquid: 0.3-0.4 mg/kg 1.5-2 h before exposure to UV light, at least 48 h apart
Pediatric
Not established
Interactions
Toxicity increases with phenothiazines, griseofulvin, nalidixic acid, tetracyclines, thiazides, and sulfanilamides
Contraindications
Documented hypersensitivity; squamous cell cancer; cataracts; light-sensitive diseases (eg, lupus, porphyria); ingestion of photosensitizing drugs; hepatitic disease; arsenic therapy; lactation
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Severe burns may occur from sunlight or UVA if dose or treatment frequency exceeded; use only if response to other forms of therapy is inadequate; long-term use may increase risk of skin cancer; patients should have a pretreatment eye examination to evaluate for presence of cataracts, repeat q6mo thereafter while undergoing PUVA therapy
Follow-up
Complications
- Gass et al report a 70-year-old man with disseminated granuloma annulare (GA) in a photosensitive distribution, who, after successful systemic and topical treatment, developed milia and scarring. This is purported to be the first report of scarring and milia formation after successful treatment of granuloma annulare.25
Prognosis
- Spontaneous resolution of localized granuloma annulare has occurred within 2 years in 50% of cases, although lesions may last weeks to decades. Recurrence, often at the same site, is noted in 40% of cases.
- Generalized granuloma annulare has a more chronic course, with rare spontaneous resolution, poor response to treatment, and frequent relapses.
- Subcutaneous granuloma annulare lesions often spontaneously regress. Local or distant recurrences have been reported in 20-75% of cases in different studies.
Patient Education
- Patients and families should be reassured about the typically benign nature and course of granuloma annulare.
Miscellaneous
Medicolegal Pitfalls
- Because most cases of granuloma annulare resolve without adverse medical sequelae, the risk of medical/legal liability is minimal. Complications resulting from treatment may be a more likely cause of litigation.
References
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Penas PF, Jones-Caballero M, Fraga J, Sanchez-Perez J, Garcia-Diez A. Perforating granuloma annulare. Int J Dermatol. May 1997;36(5):340-8. [Medline].
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O'Brien JP, Regan W. Actinically degenerate elastic tissue is the likely antigenic basis of actinic granuloma of the skin and of temporal arteritis. J Am Acad Dermatol. Feb 1999;40(2 Pt 1):214-22. [Medline].
De Maeseneer M, Vande Walle H, Lenchik L, Machiels F, Desprechins B. Subcutaneous granuloma annulare: MR imaging findings. Skeletal Radiol. Apr 1998;27(4):215-7. [Medline].
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Blume-Peytavi U, Zouboulis CC, Jacobi H, Scholz A, Bisson S, Orfanos CE. Successful outcome of cryosurgery in patients with granuloma annulare. Br J Dermatol. Apr 1994;130(4):494-7. [Medline].
Harth W, Linse R. Topical tacrolimus in granuloma annulare and necrobiosis lipoidica. Br J Dermatol. Apr 2004;150(4):792-4. [Medline].
Jain S, Stephens CJ. Successful treatment of disseminated granuloma annulare with topical tacrolimus. Br J Dermatol. May 2004;150(5):1042-3. [Medline].
Rigopoulos D, Prantsidis A, Christofidou E, Ioannides D, Gregoriou S, Katsambas A. Pimecrolimus 1% cream in the treatment of disseminated granuloma annulare. Br J Dermatol. Jun 2005;152(6):1364-5. [Medline].
Kuwahara RT, Naylor MF, Skinner RB. Treatment of granuloma annulare with topical 5% imiquimod cream. Pediatr Dermatol. Jan-Feb 2003;20(1):90. [Medline].
Badavanis G, Monastirli A, Pasmatzi E, Tsambaos D. Successful treatment of granuloma annulare with imiquimod cream 5%: a report of four cases. Acta Derm Venereol. 2005;85(6):547-8. [Medline].
Kerker BJ, Huang CP, Morison WL. Photochemotherapy of generalized granuloma annulare. Arch Dermatol. Mar 1990;126(3):359-61. [Medline].
Looney M, Smith KM. Isotretinoin in the treatment of granuloma annulare. Ann Pharmacother. Mar 2004;38(3):494-7. [Medline].
Piaserico S, Zattra E, Linder D, Peserico A. Generalized granuloma annulare treated with methylaminolevulinate photodynamic therapy. Dermatology. 2009;218(3):282-4. [Medline].
Weisenseel P, Kuznetsov AV, Molin S, Ruzicka T, Berking C, Prinz JC. Photodynamic therapy for granuloma annulare: more than a shot in the dark. Dermatology. 2008;217(4):329-32. [Medline].
Marcus DV, Mahmoud BH, Hamzavi IH. Granuloma annulare treated with rifampin, ofloxacin, and minocycline combination therapy. Arch Dermatol. Jul 2009;145(7):787-9. [Medline].
Weber HO, Borelli C, Rocken M, Schaller M. Treatment of disseminated granuloma annulare with low-dose fumaric acid. Acta Derm Venereol. 2009;89(3):295-8. [Medline].
Rosmarin D, LaRaia A, Schlauder S, Gottlieb AB. Successful treatment of disseminated granuloma annulare with adalimumab. J Drugs Dermatol. Feb 2009;8(2):169-71. [Medline].
[Guideline] Frykberg RG, Zgonis T, Armstrong DG, et al. Diabetic foot disorders. A clinical practice guideline (2006 revision). J Foot Ankle Surg. Sep-Oct 2006;45(5 Suppl):S1-66. [Medline].
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Keywords
granuloma annulare, GA, dermatosis, dermal papules, annular plaques, localized granuloma annulare, generalized granuloma annulare, subcutaneous granuloma annulare, perforating granuloma annulare, arcuate dermal erythema, actinic granuloma, AG, annular elastolytic giant cell granuloma, Miescher granuloma, type IV cell-mediated immunity, immune complex vasculitis
Contributor Information and Disclosures
Author
Ruby Ghadially, MBChB, FRCP(C)Derm, Professor, Department of Dermatology, University of California, San Francisco, School of Medicine
Ruby Ghadially, MBChB, FRCP(C)Derm is a member of the following medical societies: American Academy of Dermatology, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Coauthor(s)
Akos Z Szabo, MD, Resident Physician, Department of Plastic and Hand Surgery, Freiburg University Medical Center
Disclosure: Nothing to disclose.
Amit Garg, MD, Director of Clinical Elective in Dermatology, Assistant Professor, Department of Internal Medicine, Division of Dermatology, University of Massachusetts Medical School
Amit Garg, MD is a member of the following medical societies: American Academy of Dermatology and American Medical Student Association/Foundation
Disclosure: Abbott Immunology Honoraria Speaking and teaching; Centocor Grant/research funds Other; RegenRx Grant/research funds Other
Medical Editor
James J Nordlund, MD, Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine
James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Pharmacy Editor
Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.
Managing Editor
Rosalie Elenitsas, MD, Herman Beerman Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System
Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology and American Society of Dermatopathology
Disclosure: Nothing to disclose.
CME Editor
Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.
Chief Editor
Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.