4 months later, follow up – no signs of recurrence of the disease



removal of sutures at day 10


Histology report came back with a diagnosis revised to squamous cell carcinoma.

化驗報告結果 – 鱗狀細胞皮膚癌

Follow up at 1 month’s time. Rapid recurrence of the tumour and excision was done with a 4 mm margin.



化驗報告結果 – 角化棘皮瘤 角化棘皮瘤 Keratoacanthoma


角化棘皮瘤主要發生在皮膚曝曬陽光的部位(臉部、前臂、及手背),是一種單一且快速生長的低惡性腫瘤;其約有百分之六的病灶,在本質上根本是鱗狀上皮細胞癌(squanous cell carcinoma)。角化棘皮瘤的發生與長期紫外線照射及人類乳突病毒(human papilloma virus)感染有關;一般咸信角化棘皮瘤是由毛囊頸部的細胞變異分化而來。 角化棘皮瘤一般較常發生在老年人(平均年齡64歲),病灶的特點是單一圓形的拱頂型突起及明顯的中央凹陷(類似火山口);其凹陷中央充滿角質鱗屑,外緣則是平滑、發炎、且充血的皮膚。角化棘皮瘤的病理特徵為棘層增生的鱗狀上皮突起,併有壞死性角質細胞、嗜中性白血球,及充滿角蛋白的中央質塊;由於包含未分化細胞,因此不易與鱗狀上皮癌細胞分辨。 角化棘皮瘤的生長非常快速,可以在數週內達到數公分大小,接著可能壞死、結痂;因為其惡性腫瘤的本質(又被稱為分化良好的鱗狀上皮細胞癌),因此需積極治療。角化棘皮瘤的最佳治療方式為完整的手術切除,有時還可能需要輔助性的放射線治療。


Introduction The case I am going to present is an 89 year old fragile lady. She had a 7-week history of a rapidly enlarging right facial skin lump. Presentation The lesion arouse from the centre of a well circumscribed homogenous brownish macule (probably a solar lentigo). It grew rapidly in about seven weeks from a small papule to become a dome-shaped, symmetrical papule/plaque, surrounded by a smooth wall of inflamed skin, and capped with keratin scales and debris. There was a little bit necrotic debris on the surface when I first saw her. It was neither painful nor itchy. It did not bleed and was 1.3 cm in diameter. According to her daughter, the lesion might have shrunk a little bit before the lady came to see me. The short history, the clinical appearance and the fact that the tumour size had shrunk highly suggested the diagnosis of keratoacanthoma(KA), although a squamous cell carcinoma(SCC) could not be excluded. There were many well circumscribed homogenous brown macules on her face and back of her hands and extensor surface of both of her forearms. They all looked like normal solar lentigines. She was a farmer for 10 years and was a construction site worker for another 20 years. She did not put on any sun-block when she worked out-door. She had no history of skin diseases/skin cancer. No family history of skin cancer. She suffered from chronic diseases for more than 15 years. She had diabetes mellitus, hypertension, heart disease and impaired renal function. A clinical diagnosis of KA was made and I needed to make a decision whether I chose to 1) Be conservative – medical observation and wait for the lesion to regress by itself or 2) Do a shave biopsy – electrodessication and curettage – to make a more definite diagnosis and also be therapeutic or 3) Refer to a dermatologist for excisional biopsy or a plastic surgeon for Mohs’ surgery. Management I chose to do a shave biopsy because 1) Spontaneous resolution of KA was not uncommon and the lesion had shrunk a little bit, 2) KA can be differentiated from SCC, 3) KA only very rarely developed into invasive SCC 4) The lady was old and fragile and her family did not want her to suffer too much and strongly requested a less invasive approach to the skin disease. However, making a clear diagnosis of KA is not easy as both clinical and histological features of KA resemble those of SCC. The histology came back and showed proliferation of lobules of squamous cells in the dermis. The squamous cells show no cellular atypia. The overall features are those of an epidermal proliferation best characterized as KA. There is no definite evidence of malignancy. The wound healed up quickly and nicely and left minimal scar. I arranged follow-ups for the lady every 2 weeks for the first 3 months and then every 2 months for the next one year. If there was recurrence of the diseases, referral to a dermatologist or a plastic surgeon would be needed.

Discussion Epidemiology The peak incidence of solitary KA occurs between the ages of 50 and 69 years, however, KA has been reported in all age groups. Studies on gender distribution show that there is a slight predilection for males. The true incidence of KA is unknown, mainly because some of the lesions regress spontaneously, and are therefore not treated by physicians. In addition, most of these lesions, when seen by physicians, are considered to be SCCs and are treated as such.[1] A seasonal presentation has also been documented, where the peak incidence appears to correlate with the sunny months.[1] Several etiologic factors have been implicated in the formation of KA. These are ultraviolet light (major), chemical carcinogens (tar, pitch), mineral oil, cigarettes, trauma, immunosuppression, human papillomavirus, genetic predisposition (Ferguson-Smith-type multiple KAs, autosomal dominant Muir-Torre syndrome), etc.[1] Life history of KA Three clinical stages observed in the natural history of KA [2] 1. Proliferative stage: a rapidly enlarging firm, smooth and hemispheric papules for 2 to 4 weeks. 2. Mature stage: a bud- or dome-shaped or berry-shaped, skin coloured or red tumour with central, often unbilicated, keratinous core. It is not fixed to underlying structures and its base is not indurated. 3. Involutional stage: takes place after a few months. It becomes necrotic and resorbs and the central keratotic plug expelled. This leaves a puckered hypopigmented scar. Treatment options for KAs[3] Surgical (curettage and cautery, standard excision, MMS) Cryotherapy Radiotherapy Laser(argon, erbium:yttrium–aluminium–garnet, CO2) Photodynamic treatment Intralesional(5-fluorouracil, methotrexate, steroids, bleomycin, interferon-a) Systemic(retinoids, methotrexate, cyclophosphamide) Topical(5-fluorouracil, imiquimod) Conservative watch and wait Malignant transformation uncommon KA can be seen as an “abortive malignancy which only rarely progresses into an invasive SCC." A study of 39 KAs in 35 patients is noteworthy; careful histologic examination revealed six with perineural invasion and one with vascular invasion. During a follow-up period ranging from 4 to 8 years, none of these histologically disturbing findings was associated with metastases. Even invasion of medium-sized veins does not suggest malignant transformation.[2] Spontaneous regression of KA Although many authors advocate complete excision of KA (due to the fear of confusion with SCC), Griffiths found almost 1000 published cases (of different qualities) of observing KA to spontaneously regress. Only one recurred after spontaneous regression[4]. Griffiths observed and photographed 14 patients. All KAs underwent spontaneous resolution. The mean duration of the lesion at presentation was 9 weeks, and the mean time to resolution from appearance was 27 weeks. Mean follow-up after resolution was 3 years 5 months. No recurrences occurred[4]. Need for Intervention Although KA usually involutes spontaneously, biopsy and treatment are undertaken for several important reasons. Biopsy establishes the diagnosis and serves to rule out SCC. Treatment provides hastened resolution or cure, prevention of rapid enlargement or impingement on important structures, and improvement in overall cosmetic result.[2] Problem of distinguishing KA from SCC Short history, with a plateau of growth and resolution of the tumour, is distinctive of KA. Histology remains the gold standard for the diagnosis of KA. Even with a well-performed excisional biopsy, however, the diagnosis of KA remains challenging as a result of the lack of sufficient sensitive or specific histologic features to distinguish it from SCC. In two studies, after examining more than 300 KA and SCC biopsies, it was concluded that many of the criteria commonly used for the differential diagnosis of SCC and KA are not reliable.[1] KA can be differentiated from SCC Weedon pointed out that KA is a distinctive skin tumour which should not be included as SCC. Intravenous invasion and perineural invasion are seen uncommonly and these phenomenons do not portend an adverse outcome. Very rarely, cases of metastasis of KA have been reported (might be due to an initial incorrect diagnosis, ‘rogue’ behaviour of rare tumours, immunosuppression, etc), but Weedon himself has not seen a single case with such behaviour in his personal series of approximately 5000 cases.[3] Weedon pointed out that the histological pattern of keratinization of KA is distinctive and allowed an unequivocal diagnosis to be made in most shaves biopsies and punch biopsies and in all excision specimens. He commanded on a paper by Cribier who looked at the histopathological criteria differentiating SCC from KA. He pointed out that Cribier did not mention this important pattern of keratinization as a criterion. But he agreed with Cribier that the other relevant criteria of KA were an epithelial lip (buttressing) and sharp outline between tumour and stroma. And those of SCC were ulceration, numerous mitoses and marked pleomorphism/anaplasia. Weedon suggested that pathologists who worked in those parts of the world in which there was a significant risk of a KA transforming into a SCC need to qualify their reports on superficial shave specimens to accommodate this phenomenon. In a more recent study by Ko [6], they also studied the clinical and histopathological features of regressing KAs. Tumours that displayed rapid growth and crateriform architecture underwent partial biopsy. The biopsy was examined for features of KA. Tumours with evidence of clinical regression at follow-up were classified as KA and those without were SCCs. A common finding in all regressing KAs was persistent crateriform architecture over time, clinically and histopathologically, with central hyperkeratosis rimmed by a banal epidermis of variable thickness and underlying fibroplasia. The lesion is likely to be a regressing KA Regression has been suggested by Magalhaes as the gold stand for the diagnosis of a KA.[7] Criteria set by Griffiths for making a confident clinical diagnosis of KA were a short history of a few weeks, and that the lesion had been larger, had reached a plateau and was now getting smaller, and the appearance of raised edges with a central keratin plug progressively fragmenting to leave a crater appearance, with or without hair growth in it.[4] The lesion of my patient had morphology very similar to KA and it had shrunk before the patient came to see me so I was fairly confident that this was a regressing KA. Follow-up of the patient Close follow-up is needed no matter the lesion is treated by shave biopsy (plus electrodessication and curettage) (as in the present case) or by conventional complete excision. Schwartz pointed out that surgical excision is often desirable for the solitary KA. Although quantification of KA treatment data is lacking, recurrence of classic KA after excision is a well-known phenomenon, seen in approximately 4% to 8% of them.[5] Another author, Griffiths, after reviewing some papers, concluded that recurrences of KA after various types of surgical excision or other intervention (including Mohs’ surgery) during the phase of proliferation, occur swiftly within a few weeks. This may be more likely if ablation of the lesion has been incomplete such as with curettage. Rates of recurrence are 3–8%, depending on the method used.[4] Karaa pointed out that if recurrence occurs within a few weeks after surgery, this may be the result of incomplete curettage or excision. Recurrence of the tumour months after intervention is proof enough to revise the diagnosis of KA to SCC.[1] Conclusion I do not propose that shave biopsy with electrodessication and curettage be done in every patient, especially in physically fit patients. In these situations, radical surgical excision should still be the gold standard. In the essay, I pointed out some features of keratoacanthosis which suggest that the lesion will likely undergo regression. However, I don’t suggest observation even though all the features are present, as this might provoke anxiety in the patient. These features merely serve as indictor that the lesion is more benign than malignant. Only in some rare situations e.g. patient being very old and fragile, these features can act as a guidance to management e.g. shave biopsy plus electrodessication and curettage instead of wide margin excision.


1.       Karaa A, Khachemoune A. Keratoacanthoma: a tumor in search of a classification. International Journal of Dermatology 2007, 46, 671–678 2.       Schwartz RA. Keratoacanthorna. Journal of the American Academy of Dermatology 1994. Volume 30 Number 1 3.       Weedon D. Keratoacanthoma: a personal perspective. Current Diagnostic Pathology (2003) 9, 259—265 4.       Griffiths RW. Keratoacanthoma observed. The British Association of Plastic Surgeons (2004) 57, 485–501 5.       Schwartz RA. Keratoacanthoma: A Clinico-Pathologic Enigma. Dermatol Surg 2004;30:326–333 6.       Ko CJ, et al. Keratoacanthoma: Clinical and histopathologic features of regression. J Am Acad Dermatol 2012;67:1008-12. 7.       Magalhaes RF, Cruvinel GT, Cintra GF, et al. Diagnosis and follow-up of keratoacanthoma-like lesions: clinical-histologic study of 43 cases. J Cutan Med Surg 2008;12:163-73.


皮膚癌學術研究 – 角化棘皮瘤 (鱗狀細胞皮膚癌) -  keratoacanthoma turning into squamous cell carcinoma

皮膚癌 – 鱗狀細胞皮膚癌


監督及指導機構 – 英國威爾斯大學/卡的夫大學皮膚科