Atypical junctional melanocytic proliferations in benign lichenoid keratosis
ABSTRACT Melanocytic lesions with lichenoid regression may mimic a benign lichenoid keratosis (BLK) histologically. A total of 336 BLKs were reviewed and deeper sections obtained to determine the frequency of this phenomenon. Two cases (0.6%) showed at least 1 melanocytic nest or junctional multinucleated melanocyte (starburst melanocyte) on deeper sections confirmed by MART-1 immunostaining. Both of these cases demonstrated solar elastosis, and 1 case had an effaced rete ridge pattern. Not included in the histological study are 5 additional cases in which the initial slide showed only lichenoid dermatitis, but deeper sections obtained before to the initial sign-out revealed a melanocytic proliferation. These 5 cases would have been signed out as "consistent with BLK" if deeper sections had not been obtained. Fluorescent in situ hybridization (FISH) was performed on 3 cases; in each case, the melanocytes demonstrated a loss of chromosome 9p21 DNA copy number. The finding of nests of genetically altered melanocytes on severely sun-damaged skin strongly suggests that these cases represent lichenoid regression of melanoma in situ. Pathologists should approach a diagnosis of BLK cautiously in the setting of severely sun-damaged skin.
Article: Mechanisms of RegressionClinical Medicine & Research 06/2004; 2(2):85-8. DOI:10.3121/cmr.2.2.85
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ABSTRACT: Benign lichenoid keratosis, otherwise known as lichen planus-like keratosis, is a common, cutaneous entity that is often confused with cutaneous malignancy. Few studies have examined the multiple clinical and pathologic guises of this entity, particularly within the context of clinical pathologic correlation or magnitude of this study. We examined the epidemiologic, clinical, and pathologic attributes of 1040 consecutive cases of benign lichenoid keratosis referred for pathologic examination at a busy laboratory over an entire year. Clinical parameters assessed included the age, anatomic location, gender, and multiplicity of the lesions. Pathologic attributes were assessed yielding discernment of five different subtypes that included a classic type, bullous type, atypical type with cytologically atypical lymphocytes, an early or interface type, and a late regressed or atrophic type. The results yielded an average age at presentation of 59.5 years with an age range of 36 to 87 years. The gender frequency was 76% female, 24% male. The trunk was the most common location (76%), followed by the extremities (33%) and head and neck (7%); 8% of patients presented with two lesions and less than 1% with three lesions prompting consideration of lichen planus. The classic, atypical, and bullous forms of the disease clinically presented with erythematous papule/plaque(s). The early or interface type showed erythematous to hyperpigmented brown macules and the regressed or atrophic type presented as violaceous papules or irregularly distributed macular pigmentation; 81% of the lesions showed the classic histology consisting of epidermal acanthosis with a band-like lichenoid lymphocytic infiltrate. Variable numbers of plasma cells, eosinophils, and neutrophils were identified as well as epidermal parakeratosis distinguishing these lesions from typical lichen planus. The bullous variant showed intraepidermal or subepidermal bullous cavities with a dense associated lymphocytic infiltrate and increased numbers of necrotic basilar layer keratinocytes. The atypical variant showed features of the classic type with scattered enlarged CD-3, CD-30 (+) lymphocytes possessing hyperchromatic, irregular nuclei. The early interface type showed single lymphocytes aligned along the dermoepidermal junction without epidermal acanthosis and adjacent lentigo. The regressed or atrophic variant showed epidermal atrophy with papillary dermal scarring, patchy lymphocytic infiltrates and melanin incontinence. The clinicopathologic spectrum of benign lichenoid keratosis is broad and encompasses several unrelated entities. An awareness of its expanded presentation is essential to avoid misdiagnosis and may serve as an important forerunner of pathogenic discernment.American Journal of Dermatopathology 11/2005; 27(5):387-92. DOI:10.1097/01.dad.0000175533.65486.84 · 1.43 Impact Factor
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ABSTRACT: Lichenoid keratosis (LK) is a well-described entity which has been proposed to represent an immunological or regressive response to pre-existing epidermal lesions such as solar lentigines or seborrhoeic keratoses. To evaluate the dermoscopic criteria of a series of cases of LK with remaining areas of seborrhoeic keratosis which were both dermoscopically and histologically diagnosed. Pigmented lesions with dermoscopic areas of seborrhoeic keratosis and LK in the same tumour were consecutively diagnosed and prospectively included in the study. All pigmented lesions were examined and registered using DermLite Foto equipment (3Gen, LLC, Dana Point, CA, U.S.A.), at 10-fold magnification, at the Dermatology Department of Hospital de Sant Pau i Santa Tecla (Tarragona, Spain), between 1 January 2003 and 31 December 2005. In total, 24 cases of lesions with dermoscopic areas of seborrhoeic keratosis and LK were collected. In four lesions (17%), the clinical differential diagnosis without dermoscopy included malignant melanoma and in seven lesions (29%), basal cell carcinoma. The diagnosis of LK was clinically considered without dermoscopy in only six cases (25%). A granular pattern was observed to be distributed throughout the LK areas of the lesions. This pattern consisted of the presence of brownish-grey, bluish-grey or whitish-grey coarse granules that formed, in 11 cases (46%), globules and/or short lines. In one lesion, located on the face, these short lines produced annular or rhomboid structures as seen in lentigo maligna melanoma. Dermoscopy is a useful tool which assists in the correct clinical recognition of LK, which may also potentially illuminate the pathogenesis of these tumours, showing the intermediate stage of regressing epidermal lesions in an LK.British Journal of Dermatology 09/2007; 157(2):266-72. DOI:10.1111/j.1365-2133.2007.07963.x · 4.10 Impact Factor