The aetiopathogenesis of keratoacanthoma (KA) remains controversial, and surgical excision represents the mainstay of management.[1] However, tumour size, problematic sites and underlying dermatoses often pose difficulties for surgery approach. We report the use of imiquimod as treatment for a giant KA arising on a background of lupus vulgaris (LV).

A 72-year-old man presented with a 4-month history of a giant nodule on his face. On physical examination, a reddish crateriform nodule, measuring 50 × 50 mm, with a central keratotic plug, was seen on the patient's cheek (Fig. 1a). The lesion had developed over the atrophic centre of a red-brown infiltrated and sharply demarcated plaque, involving both cheeks, which had been present for 15 years. Using diascopy, an ‘apple-jelly’ appearance was seen. The lesion was provisionally diagnosed as KA arising on a background of LV.


Figure 1. (a) A giant keratoacanthoma arising over the atrophic centre of an infiltrated and sharply demarcated plaque of lupus vulgaris (LV); (b) partial remission of the tumour after 12 weeks of imiquimod enabled surgical intervention; (c) satisfactory outcome after surgery. There was also a marked beneficial effect of antibiotic treatment on the LV lesions.

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Further investigations were carried out, including chest radiography, thoracic computer tomography, sputum cultures, and bacteriological examination of urine. A dermal tuberculin test (DTT) was peformed, and the reaction measured 20 × 20 mm. Skin biopsies were taken from the tumour and the underlying plaque.

On histological examination of the plaque, a granulo-matous inflammation was seen, with lymphocytes, histiocytes, epithelioid cells and Langerhans giant cells, but no areas of caseation necrosis (Fig. 2a). These findings were in keeping with the diagnosis of LV. The histological findings for the nodule included a crateriform architecture, with marked hyperkeratosis, acanthosis and papillomatosis. The elongated hyperplastic rete ridges consisted of well-differentiated keratinocytes with a brightly eosinophilic glassy cytoplasm, surrounding a core filled with cornified material (Fig. 2b). These findings confirmed the diagnosis of KA. Laboratory and imaging investigations did not reveal any signs of active systemic infection.


Figure 2. (a) Granulomatous inflammation with lymphocytes, histiocytes, epithelioid cells and Langerhans giant cells, with no areas of caseation necrosis, confirming the diagnosis of lupus vulgaris (LV). (b) Crateriform architecture, with marked hyperkeratosis, acanthosis and papillomatosis, and elongated hyperplastic rete ridges consisting of well-differentiated keratinocytes with a brightly eosinophilic glassy cytoplasm, surrounding a core filled with cornified material ((haematoxylin and eosin, original magnification × 20). These findings established the diagnosis of KA.

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Following consultations with the respiratory physicians and cardiothoracic surgeons, the patient was started on quadruple anti-tuberculosis therapy for 2 months, plus isioniazid and rifampicin for another 4 months. Simultaneously, the KA was managed with imiquimod 5% 5 days per week for 12 weeks, resulting in partial tumour remission (Fig. 1b). A severe inflammatory reaction appeared during the imiquimod treatment. Sub-sequently, the patient underwent surgery to excise the tumour (Fig. 1c).

KA is known to arise in the background of scarring dermatoses such as discoid lupus erythematosus and lichen planus.[2] Randazzo reported KA arising on a background of LV,[3] and our case is similar. These cases indicate that LV may represent another possible inflammatory process that can trigger the development of KA.

Management of KAs arising on inflammatory lesions is challenging, as surgical excision may be troublesome and too destructive when performed on an inflammatory background; consequently, the cosmetic and functional outcomes are uncertain. Imiquimod has been suggested as an alternative option for treatment of KAs, and satisfying results have been reported.[4] In our patient, 12 weeks of imiquimod did not result in complete remission. This might be related to the tumour size or to the underlying tuberculosis, as none of the KAs previously reported to have cleared with imiquimod had developed in a patient with an inflammatory condition. However, given that KAs spontaneously resolve, it is difficult to be confident that the excellent results reported previously for imiquimod were actually due to the drug and not the natural history. Although imiquimod did not result in clearance of our patient's KA, it did produce a marked reduction in tumour size, facilitating subsequent surgery. Imiquimod has been used for pretreatment of nodular basal cell carcinomas in order to reduce the extent of surgery required.[5] The current report represents an indication that it might also be used in a similar way for difficult KAs.

In conclusion, we report a patient with LV who developed KA on an LV lesion. LV should be added to the inflammatory substrates on which KA may arise. In such cases, and especially when the tumour size is problematic, imiquimod may represent a useful neo-adjuvant method of facilitating subsequent surgery.


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