Annular plaques on the foot, shin, hand - Clinical Advisor

Annular plaques on the foot, shin, hand

Slideshow

  • 2014 October Dermatology Clinic

A woman, aged 26 years, presents with circular rashes that developed 3 months earlier. She reported that the rashes first appeared as raised pink bumps, but soon after they formed a more circular shape.

Her primary-care physician treated the rashes for ringworm with the topical antifungal ketoconazole, but they did not improve. The patient is otherwise healthy, taking only an oral contraceptive for the last two years.

Examination of the rashes revealed firm dermal papules coalescing to annular plaques with central clearing. These were located on the left dorsal foot, right anterior shin, and right dorsal hand. There was no mucosal involvement.


This Clinical Advisor CME activity consists of 3 articles.To obtain credit, read fluid-filled lesion on a child’s leg and new growth on the forehead. Then take the post-test here.


Granuloma annulare (GA) is a relatively common and benign inflammatory condition that presents as a raised annular rash. It occurs in all age groups, but is rare in infancy.1Although its cause is unknown, GA is thought to be a cell-mediated...

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Granuloma annulare (GA) is a relatively common and benign inflammatory condition that presents as a raised annular rash. It occurs in all age groups, but is rare in infancy.1

Although its cause is unknown, GA is thought to be a cell-mediated type-IV immune response. Cases of GA have been reported following malignancy, infection, and trauma.2 The condition has also been associated with diabetes mellitus, but the link is controversial.3

Clinically, GA presents as flesh-colored or erythematous papules that are grouped and annular plaques. In localized disease, which is the most common form of the disease, only one or a few lesions are present. Typical sites of presentation are the dorsal hands and the lateral and dorsal fingers, elbows, feet, and ankles. Localized GA is most common in children and young adults. Females are affected twice as often as males.1

Another subtype of this condition is generalized or disseminated GA, which presents with diffuse and symmetrical lesions.1 These are usually seen on the neck, upper trunk, and proximal upper extremities. Individual lesions may last 3 to 4 years, whereas the overall eruption can last up to 10 years. The rate of recurrence is higher in generalized GA.

A less-common subtype of GA is the subcutaneous type, also known as deep GA or pseudorheumatoid nodules. Subcutaneous GA is limited to toddlers and young children. Soft subcutaneous nodules grow on the trunk and extremities, and some of these nodules may rapidly enlarge. These often appear after trauma to the affected area.

The rarest form of GA is the perforating subtype, which presents as papules with a central crust or ulceration that may resemble a pustule and typically appears on the dorsal hands.4

Most patients are asymptomatic, but some report mild pruritus or describe progression of the rash after scratching. This is consistent with the tendency of GA to exhibit the Koebner phenomenon, in which lesions form in the lines of trauma and injury.

The differential diagnosis of GA includes other annular and granulomatous disease, such as tinea corporis, erythema migrans of Lyme disease, erythema multiforme, subacute cutaneous lupus erythematosus, necrobiosis lipoidica, sarcoidosis, and rheumatoid nodules.5 When examining any rash, especially annular ones, it is important to examine for the presence of scale and other surface changes to reduce the number of possible differential diagnoses.

Localized and generalized GA is usually diagnosed clinically, but a skin biopsy should be taken in cases that are questionable or suspected to be subcutaneous or perforating subtypes. Special stains, such as colloidal iron or Alcian blue, may be needed to aid in the diagnosis. Histologic examination of GA will show a granulomatous inflammatory pattern with palisading of histiocytes around an anuclear dermis. The deposition of mucin is also often seen.

Localized GA is generally self-limiting, resolving spontaneously in 1 to 2 years, usually without any evidence of scarring.6 Therefore, no treatment is necessary. Many patients report resolution of the lesions even after a skin biopsy has been performed.7

Nevertheless, many patients request treatment, often just for a cosmetic benefit. Potent topical corticosteroids, such as clobetasol propionate, may be applied with or without occlusion to papular lesions for 4 to 6 weeks. Small amounts of triamcinolone (2.5-5 mg/mL) may be injected into the raised borders of GA lesions. Cryotherapy and electrodessication may also be beneficial, but these carry a higher risk of atrophy and postinflammatory pigment alteration.

Generalized GA has a more chronic course and should be treated, but there is no consensus as to which is the best treatment option. Isotretinoin, an oral retinoid, has been shown to be effective, although it does carry the risk of blood count, cholesterol, and liver abnormalities.8

The antibiotic dapsone, the antimalarial agent hydroxychloroquine, and the immunosuppressant cyclosporine have also been used, but again, each of these has risks of serious systemic adverse effects.9 These medications should be considered only in consultation with a dermatologist experienced with their use.

The patient in this case was educated regarding the diagnosis of GA and the tendency for the rashes to resolve on their own within 1 to 2 years. After discussing all treatment options, including benign neglect, the patient requested treatment with topical clobetasol ointment. She used the ointment without occlusion every evening for 4 weeks and reported that the rash faded moderately. She did not wish to try other options.

Esther Stern, NP-C, is a family nurse practitioner at Advanced Dermatology & Skin Surgery, P.C., in Lakewood, N.J.


This Clinical Advisor CME activity consists of 3 articles.To obtain credit, read fluid-filled lesion on a child’s leg and new growth on the forehead. Then take the post-test here.


References

  1. Muhlbauer JE. Granuloma annulare. J Am Acad Dermatol. 1980;3(3):217-230.
  2. Hu SW, Kaplan J, Patel RR, Kamino H. Trauma-related papular granuloma annular. Dermatology Online Journal. 2013;19(12):20719. Available at escholarship.org/uc/item/7615b2nn
  3. Katsarou A, Vavouli C, Balamoti E, et al. Granuloma annulare in children. J Am Acad Dermatol. 2014;70(5 Suppl 1):AB145.
  4. Samlaska CP, Sandberg GD, Maggio KL, Sakas EL. Generalized perforating granuloma annulare. J Am Acad Dermatol. 1992;27(2 Pt 2):319-322.
  5. Hsu S, Le EH, Khoshevis MR. Differential diagnosis of annular lesions. Am Fam Physician. 2001;64(2):289-296. Available at aafp.org/afp/2001/0715/p289.html
  6. Thornsberry LA, English JC 3rd. Etiology, diagnosis, and therapeutic management of granuloma annulare: an update. Am J Clin Dermatol. 2013;14(4):279-290.
  7. James WD, Berger T, Elston D, eds. Macrophage/monocyte disorders. Andrews’ Diseases of the Skin: Clinical Dermatology. 10th ed. Philadelphia, Pa.: Elsevier Saunders; 2006:705.
  8. Schleicher SM, Milstein HJ, Lim SJ, Stanton CD. Resolution of disseminated granuloma annulare with isotretinoin. Int J Dermatol. 1992;31(5):371-372.
  9. Lebwohl M, Heymann W, Berth-Jones J, Coulson I. Granuloma annulare. In: Treatment of Skin Disease. 1st ed. Philadelphia, Pa.: Elsevier Saunders; 2002:275-277.

All electronic documents accessed on October 1, 2014.

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