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Case 1: A 58-year-old man presented with a solitary asymptomatic nodule on his thumb (Figure A). After trauma with a rusty nail approximately 20 years ago, he had developed a small papule, which had enlarged gradually for a few days initially before stabilizing. His personal and family medical histories were unremarkable. Dermatologic examination revealed a 1-cm crater-like nodule on the left palmar area. This was a firm and nontender lesion that was fixed to the overlying skin but moved freely from underlying structures. There were no similar lesions elsewhere on his body. Case 2: A 52-year-old man presented with a nodular lesion on the left palmar surface of his thumb. The 0.8-cm lesion was lightly colored, with a central cup-shaped epidermal depression and thin epidermis. The patient described an insect bite to the area 15 years earlier as the precipitating event. The firm and nontender lesion was fixed to the overlying skin but moved freely from underlying structures (Figure B). Case 3: A 36-year-old man consulted for a nodular lesion, located on his left palmar surface, that had not enlarged or changed since appearing 3 years ago. He described mechanical trauma to the area as precipitating the lesion. Clinical examination revealed a 0.6-cm, well-circumscribed nodule, with a dome shape and colored skin. Clinically, the nodular lesion appeared to be a benign tumor (Figure C). In each case, the nodule was excised totally and histopathologic examination revealed a well-circumscribed, nonencapsulated nodule within the mid-dermis. Thick, acellular collagen bundles were arranged randomly in short fascicles through the center of the lesion. Cellular areas consisting of histiocytes and fibroblasts with a storiform pattern at the periphery of lesion were observed, but nuclear atypia and mitotic activity were not. Results of immunohistochemical stain with CD34 were negative, but in all cases were strongly positive for Factor XIIIa. Slight epidermal hyperplasia was present with orthokeratotic hyperkeratosis and flattened rete ridges in the overlying epidermis (Figure A-1, Figure B-1, Figure C-1). The subcutaneous fat and adjacent skin were normal. No folliculosebaceous units at the periphery of the lesion were seen, but a few eccrine sweet glands were noted. No recurrence appeared in 18 months of follow-up.
Figure Figure. (A-C) Palmar dermatofibromas. (A-1–C-1) Sections show thick, cellular collagen bundles arranged randomly in short fascicles through the center of each lesion; other cellular areas consist of histiocytes and fibroblasts with a storiform pattern at the lesion periphery (hematoxylineosin stain, original magnification ×100).
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The clinical diagnosis of dermatofibroma is usually quite easy, depending on the appearance and location of the lesion. In some cases, because the lesion occurs at unusual sites, is relatively large, or appears as multiple lesions, diagnosis may be more difficult. Although dermatofibromas are usually found on the extremities of young people, these lesions can be rarely detected on the hand or foot. To our knowledge, there have been only 2 previous reports of dermatofibroma on the hand. One described children with multiple palmar and plantar lesions1 and the other with subungual dermatofibroma on the thumb.2 Similar reports of hand lesions have described either a malignant fibrous histiocytoma or fibrous histiocytoma of the tendon sheath.3 Keloid and leiomyomas are 2 benign tumors that can be distinguished on clinical grounds, the former showing a shiny surface in special locations such as the chest and ear lobes, and the latter being painful with pressure or cold.3 Fibrous histiocytoma of the tendon sheath is a distinct entity with nodules adherent to tendons primarily on the hands.4
Malignant fibrous histiocytoma, usually appearing on the head and neck of older individuals, tends to be larger than the usual dermatofibroma.3,5 Desmoplastic melanoma is asymmetric without presenting a dell-like depression over the nodule.5,6
When a dermatofibroma is composed predominantly of fibroblasts or myofibroblasts, has cytologic atypia, or extends to the subcutaneous tissue, it can be difficult to distinguish histologically from the other benign lesions (eg, cellular digital fibromas) or malignant soft tissue tumors (eg, dermatofibrosarcoma protuberans or malignant fibrous histiocytoma).3 Histopathologically, dermatofibrosarcoma protuberans has a monomorphous appearance with thin spindle cells and no or mild nuclear atypia, with fewer secondary elements (eg, giant and inflammatory cells) than either benign or malignant fibrohistiocytoma. The spindle cells are arranged in short interweaving fascicles, giving rise to a storiform appearance. Involvement of subcutaneous tissue with pseudoseptae formation (honeycomb appearance) is a striking feature. Malignant fibrous histiocytoma is not often confused with dermatofibrosarcoma protuberans because of the histiocytoma's rapid growth; the occurrence of far more nuclear pleomorphism, mitotic activity, and necrosis; and typical deep location that affects muscle.7 Digital angiofibromas, fibrokeratomas, and dermatofibromas stain predominately for Factor XIIIa, with little or no staining for CD34.
On the other hand, cellular digital fibromas are characterized by a dense cellular proliferation of CD34-positive spindle cells. Awareness of this digital fibroma variant and its staining pattern is critical in preventing misdiagnosis as dermatofibrosarcoma protuberans, particularly in superficial biopsies.8 Factor XIIIa, which stains most dermatofibromas, is only focally positive in a small number of cases of dermatofibrosarcoma protuberans.9 In the present cases, histologic diagnosis was rather easy based on hematoxylin-and-eosin-stained sections; the findings of a well-circumscribed nodule limited to mid-dermis, coarse bundles of collagen arranged randomly, and vascularized fibrohistiocytic areas in storiform pattern at the periphery of the lesion were characteristic of a late-stage dermatofibroma. The spindle cells in all cases stained strongly for Factor XIIIa, but not CD34.
The etiology of dermatofibroma remains unclear. Whether the lesion represents a reactive hyperplasia or a true neoplasm is debated.6 One researcher has proposed that dermatofibroma develops as a response to injury, which may be external as is the case with punctures or insect bites, or internal from ruptured follicles or follicular cysts.5 A report has described papillomavirus in 2 fibromatous dermal nodules; these nodules were similar to those present in the caudal fold skin of the tail in 25 of 145 beef cattle that underwent tuberculin testing 3 months earlier.10 Bovine warts were endemic on the property and the authors hypothesized that a virus-contaminated tuberculin syringe introduced the papilloma virus intradermally. Warts may be precursor lesions to dermatofibroma, produced as a result of secondary trauma to the underlying dermis from pressure or wart-removal therapy, including electrodessication, cryotherapy, and surgical excision.
In our cases, histories of a puncture support an etiology related to local injury. On the other hand, although the palms and soles are commonly traumatized areas, they are rarely the site of dermatofibromas.11 For that reason, future research into the etiopathogenesis of dermatofibromas should look at factors other than injury.