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Inverted follicular keratosis, a benign tumor of the skin believed to arise from the infundibular portion of the hair follicle that can involve perioral skin, has a unique histologic picture. It can be confused with forms of skin cancer; with knowledge of this entity, oral and maxillofacial surgeons may be able to avoid unnecessary surgery. The clinical and microscopic findings of 12 cases of inverted follicular keratosis are reported.
Keratosis obturans is characterized by the accumulation of desquamated keratinous material in the bony portion of the external auditory canal. Classically, it is reported to present with severe otalgia, conductive hearing loss and global widening of the external auditory canal. Extensive erosion of the bony meatus, with exposure of the facial nerve, has been previously reported, but no case of facial nerve palsy has as yet been published. We report the first published case, to our knowledge, of a unilateral facial nerve palsy secondary to neglected keratosis obturans.
BACKGROUND: A variety of dermatopathologic entities are histologically defined by the presence of follicular differentiation. Follicular differentiation confined to the epidermis may follow induction from dermal mesenchymal proliferations, as in a nevus sebaceus of Jadassohn, or represent endogenous proliferations such as the tumor of the follicular infundibulum or trichilemmoma. METHODS: We report on five cases of a histologically distinct form of benign keratosis showing variable follicular differentiation. Clinicopathologic correlation and analysis of a potential human papilloma virus pathogenesis was investigated. RESULTS: Each of the cases arose on the trunk or extremities of three men and two women with a mean age at presentation of 66.6 years. All of the lesions showed variable follicular differentiation, with germinative basaloid cells, matrical cells with matrical keratinization, inner root sheath with trichohyalin granules, or glycogenated lower outer root sheath. Immunohistochemical staining for human papilloma virus was negative in each case. CONCLUSIONS: There exists a distinct entity, histologically defined as a keratosis with variable follicular differentiation, which has not been previously described. These lesions do not appear to be pathogenically related to human papilloma virus infection.
p16INK4a is involved in many important regulatory events in the cell and the expression and function is closely associated with the retinoblastoma protein (Rb). Earlier, we have in colorectal cancer and in basal cell carcinoma showed that p16INK4a is upregulated at the invasive front causing cell cycle arrest in infiltrative tumor cells via a functional Rb. This role for p16INK4a as a regulator of proliferation when tumor cells infiltrate might besides a general cyclin-dependent kinase (cdk) inhibitory effect explain why p16INK4a is deregulated in many tumor forms. The expression pattern of p16INK4a in relation to Rb-function in squamous cancer and precancerous forms of the skin has not been fully detailed. We therefore characterized the expression of p16INK4a, Rb-phosphorylation and proliferation in actinic keratosis, squamous cell carcinoma in situ and invasive squamous cell carcinoma with special reference to infiltrative behavior. The expression of p16INK4a varied between the lesions, with weak and cytoplasmic p16INK4a expression and functional Rb in actinic keratosis. Strong nuclear and cytoplasmic p16INK4a expression was observed in all carcinomas in situ in parallel with lack of Rb-phosphorylation but high proliferation indicating a nonfunctional Rb. Invasive squamous carcinoma showed a mixed p16INK4a expression pattern where some tumors had strong cytoplasmic p16INK4a expression, large fraction of Rb-phosphorylated cells and high proliferation. Interestingly, despite this disability of p16INK4a to inhibit proliferation there was an upregulation of cytoplasmic p16INK4a in infiltrative cells compared to tumor cells towards the tumor center. A similar scenario but strong and combined nuclear and cytoplasmic p16INK4a expression in infiltrative cells, was observed in other invasive squamous cancers. This suggests that the p16INK4a upregulation in infiltrative cells is governed independently of the subcellular localization or of the potential to affect proliferation via Rb, and suggests a potentially proliferation independent function for p16INK4a in infiltrative behavior.
Benefit and harm associated with treating actinic keratosis (AK) with the immune response modifier imiquimod was assessed using published randomized-controlled trials. Five randomized double-blind trials lasted 12-16 weeks and treated 1,293 patients. Complete clearance occurred in 50% of patients treated with imiquimod, compared to 5% treated with vehicle, and the number needed to treat (NNT) for one patient to have their keratosis completely cleared after 12-16 weeks was 2.2 (95% confidence interval 2.0-2.5). For partial (>/=75%) clearance the NNT was 1.8 (1.7-2.0). The proportion of patients with any adverse event, any local adverse event, or any treatment-related adverse event was substantially higher with imiquimod than with vehicle, and numbers needed to harm for one additional adverse event with imiquimod over 12-16 weeks ranged from 3.2 to 5.9. Particular local adverse events with imiquimod included erythema (27%), scabbing or crusting (21%), flaking (9%), erosion (6%), edema (4%), and weeping (3%). Imiquimod 5% cream was effective in the treatment of AK, preventing potential development of squamous cell carcinoma. Future investigation might be aimed at elucidating optimal dosing to minimize adverse events without detriment to efficacy, and evaluating long-term recurrence.
We report a patient with a 17-year history of reticulated keratotic papules on the trunk and limbs, and telangiectatic eruption on the face, in whom the diagnosis of keratosis lichenoides chronica was first established. However, the biopsies showed an epidermotropic infiltrate of small irregular CD4+ lymphocytes, and detection of a T-cell clone in the lesions by polymerase chain reaction confirmed the diagnosis of mycosis fungoides. Thus, keratosis lichenoides chronica can be an unusual and potentially misleading presentation of mycosis fungoides.
We biopsied longitudinal erythronychia in 16 subjects, and found an onychopapilloma in 14 cases and Bowen's disease in the remaining two. Shared clinical features in addition to erythronychia (or sometimes an interrupted line made up of splinter haemorrhages) were typically a longitudinal marked ridge of the nail bed expanded at the distal nail bed as subungual keratosis, and associated localized onycholysis. The presentation of Bowen's disease in this pattern has not been previously reported. In all cases of onychopapilloma of the nail bed, acanthosis and papillomatosis were evident, and were associated with a keratogenous zone identical to the nail matrix. In addition, we found multinucleate giant cells in two onychopapillomas. We have therefore suggested that the term 'localized, distal, subungual keratosis with multinucleate cells' should be replaced by 'onychopapilloma' (nail-producing papilloma).
Stucco keratosis is a skin disorder with papular warty lesions that usually appear on the lower limbs in elderly people. The aetiology, pathogenesis and treatment is still a matter of debate. We report a 75-year-old non-immunosuppressed man with extensive lesions all over his body, which had not responded to curettage or electrodesiccation. To determine the possible role of human papillomavirus (HPV) in stucco keratosis, we used nested polymerase chain reaction (PCR) to identify HPV DNA in the lesions. To include a broad range of both cutaneous and mucosal HPV types, PCR was performed with two sets of degenerate primers. Using this approach we detected HPV types 9, 16, 23b, DL322 and a variant of HPV type 37 in multiple stucco keratoses. Imiquimod (5% cream), a new compound that modifies the immune response by stimulating production of cytokines, applied overnight, three times a week for 5 weeks, resulted in resolution of all treated lesions.
Actinic keratosis in the most common premalignant keratotic tumour of sun-exposed skin. A 66-year-old man developed a large actinic keratosis on his scalp, which did not respond to conventional treatment. Fractionated radiotherapy with a cumulative dose of 28 Gy resulted in complete remission without relapse during a 14-month follow-up. In older subjects in whom conventional treatment fails, low-dose fractionated radiation therapy is an effective alternative method.
OBJECTIVE: This article describes a new subtype of actinic keratosis that exhibits proliferative characteristics both histologically and clinically. We describe three representative cases occuring in the presence of infiltrative squamous cell carcinoma (SCC) and/or basal cell carcinoma (BCC). METHODS: Histories of each lesion in the three cases discussed were obtained. The lesions were removed by Mohs micrographic surgery. Permanent sections, stained with hematoxylin and eosin, were examined and studied under light microscopy. RESULTS: All three lesions had failed conventional treatment with liquid nitrogen and/or 5-fluorouracil (5-FU). Histologic examination of the lesions revealed sheets of dysplastic cells growing along the basal layer of the epidermis and migrating down hair follicles and sweat ducts. An associated infiltrative SCC and/or BCC was found in each case. CONCLUSIONS: Proliferative actinic keratosis is resistant to standard therapies because of deep migration of abnormal cells along hair follicles and sweat ducts. It has a strong propensity to develop infiltrative SCC and may occur concomitantly with BCC.
BACKGROUND: Most seborrheic keratoses may be readily clinically differentiated from skin cancer, but occasional lesions resemble atypical melanocytic neoplasms. OBJECTIVE: To evaluate the frequency, cost, and intensity of procedures performed that result in the removal and histopathologic evaluation of seborrheic keratoses. METHODS: Episodes of surgical removal of lesions that were identified as seborrheic keratoses by histologic identification were determined using Medicare Current Beneficiary Survey data from 1998 to 1999. These episodes were defined by a histopathology procedure code that is associated with a diagnosis code for seborrheic keratosis. We then identified what procedure(s) generated the histopathology specimen. Biopsy and shave procedures were considered "low intensity," whereas excision and repair procedures were considered "high intensity." RESULTS: Dermatologists managed 85% of all episodes of seborrheic keratoses. Dermatologists managed 89% of seborrheic keratosis episodes using low-intensity procedures compared with 51% by other specialties. For nondermatologists, 46% of the treatment cost (9 million US dollars) to Medicare was generated from high-intensity management compared with 15% by dermatologists (6 million US dollars). CONCLUSION: There is a significant difference in the management of suspicious pigmented lesions between dermatologists and other specialists. This affects both the cost and quality of care.
BACKGROUND: Actinic keratoses are premalignant lesions and are a sensitive and important manifestation of sun-induced skin damage. Studies in animals have shown that dietary fat influences the incidence of sun-induced skin cancer, but the effect of diet on the incidence of actinic keratosis in humans is not known. METHODS: We randomly assigned 76 patients with nonmelanoma skin cancer either to continue their usual diet (control group) or to eat a diet with 20 percent of total caloric intake as fat (dietary-intervention group). For 24 months, the patients were examined for the presence of new actinic keratoses by physicians unaware of their assigned diets. RESULTS: At base line, the mean (+/- SD) percentage of caloric intake as fat was 40 +/- 4 percent in the control group and 39 +/- 3 percent in the dietary-intervention group. After 4 months of dietary therapy the percentage of calories as fat had decreased to 21 percent in the dietary-intervention group, and it remained below this level throughout the 24-month study period. The percentage of calories as fat in the control group did not fall below 36 percent at any time. The cumulative number of new actinic keratoses per patient from months 4 through 24 was 10 +/- 13 in the control group and 3 +/- 7 in the dietary-intervention group (P = 0.001). CONCLUSIONS: In patients with a history of nonmelanoma skin cancer, a low-fat diet reduces the incidence of actinic keratosis.
We report a case of malignant melanoma associated with seborrheic keratosis. This has been reported rarely in the literature, with disagreement regarding whether it is coincidental or whether malignant transformation occurs. Because seborrheic keratoses are common and association with malignant melanoma is very rare, we conclude that the association is coincidental. However, because of the association of other malignancies, a biopsy of any suspect or changing seborrheic keratosis is essential.
Keratosis pilaris is found commonly in isolation as well as associated with other conditions. We describe a family with keratosis pilaris and hereditary koilonychia, with an autosomal dominant pattern of inheritance. These two findings have only been previously found in the context of monilethrix. The coexistence of the two disorders suggests a close association of their genetic pathogenesis.
The microscopic spectrum of benign lichenoid keratosis (BLK) was studied by examination of 30 examples. BLK consists of a segment of hyperplastic epidermis accompanied by a lymphoid infiltrate in the papillary dermis. Although termed "lichen planus-like," saw-tooth acanthosis predominated in only seven lesions, whereas irregular acanthosis was widespread in 23. The infiltrate had both a band-like (lichenoid) and perivascular arrangement, but a lichenoid appearance predominated in only half the specimens. Liquefaction of the basal layer was widespread, and hydropic change often involved the midepidermis. Mild cytologic atypicality was present in each case, but other features of actinic keratosis were lacking. Changes of senile lentigo were observed adjacent to 17 lesions. Partial involution was present in several cases. BLK often is confused clinically with a variety of other cutaneous tumors. Nevertheless, the diagnosis usually can be made on histologic grounds alone when the history indicates a solitary lesion.
The expression of human placental type glutathione S-transferase (GST-pi) was investigated in human cutaneous carcinoma in situ, that is, actinic keratosis and Bowen's disease, and compared with that in normal skin, using Northern blot and immunohistochemical analysis. In Northern blot examination, the expression of GST-pi transcript was recognized in all instances. Carcinoma in situ showed significantly higher expressions of GST-pi than normal skin. In the immunohistochemical examination, nuclear staining of GST-pi was noticed in some dysplastic cells of carcinoma in situ, especially in Bowen's disease. In actinic keratosis, a framework appearance was noticed in the staining pattern at a lower magnification because the lower part of the cytoplasm of dysplastic cells lining the stratum basale was positive for GST-pi, and all cells of the stratum granulosum and more cells of the stratum spinosum showed stronger GST-pi positive reaction than normal skin. In Bowen's disease, GST-pi positive, dysplastic cells existed throughout the epidermis. Because GST-pi positive, dysplastic cells and GST-pi positive, normal looking squamous cells made the GST-pi positive cell nests throughout the epidermis, and GST-pi positive, dysplastic cells, and GST-pi negative, normal looking cells coexisted in the parabasal layer, they showed a sawtooth appearance in the staining pattern at a lower magnification. These findings suggest that GST-pi is involved in the process of carcinogenesis.
Colloid keratosis is characterized by homogeneous eosinophilic masses of variable size and number within the upper layers of squamous epithelia, including epidermis. It has been observed as the characteristic feature of many onychoses and inflammatory conditions of oral epithelium, and as an incidental finding in neoplastic and nonneoplastic lesions in the skin and respiratory tract. Its nature remains obscure, but knowledge at present suggests that it may represent a disorder of an early phase of keratinization. Current evidence supports the hypothesis that colloid keratosis represents a nonspecific cellular reaction pattern of squamous epithelium.
This report describes a case of inverted follicular keratosis in a keratotic nodule found on the thigh of a 58-year-old man. The upper surface of the nodule was papillary, while the lateral aspect was smooth with columnar structures. Histologically, the lesion exhibited primarily exophytic growth, although there was some endophytic growth. There were multiple closely approximated columnar solid tumor nests. Many of these columnar tumor nests had a central funnel-shaped plug of dense parakeratotic keratinous material. The tumor nests were composed of peripheral smaller basaloid cells and central squamoid cells forming squamous eddies. Inflammatory lymphocytic cell infiltration and lytic change were found mainly at the base of the tumor. Several hair follicles transversed the tumor. Ballooning alteration of granular cells and vacuolated keratinocytes, especially within areas of hypergranulosis, were observed in each of the columnar tumor nests. Some cells with ballooning alteration were recognized by papillomavirus common antibody. Ultrastructurally, vacuolated keratinocytes exhibited cytoplasmic vacuoles containing keratohyaline composite granules. Compound structures of membrane-coating granules, which have been associated with outer root sheath keratinization, were noted. The case therefore represents an inverted follicular keratosis manifesting as a distinct hair follicle tumor related to prior infection by papillomavirus.