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PubMed2000

Apocrine acrosyringeal keratosis in association with syringocystoadenoma papilliferum.

We report the clinical and histopathological features of a keratosis that developed in association with syringocystadenoma papilliferum. This tumour shows a pinkish, pedunculated, spherical nodule with a cerebriform surface and visible keratinous plugs. In addition to the typical features of syringocystadenoma papilliferum, the tumour shows many hyperkeratotic columns surrounded by acanthotic epidermis with the characteristics of trichilemmal keratinization and keratohyalin granules. This keratosis seems to be derived from the middle to lower portion of the apocrine acrosyringium, based on the distribution of keratohyalin granules and the direct connection with the apocrine acrosyringium in an early lesion. Accordingly, we propose to identify this rare keratosis as apocrine acrosyringeal keratosis.

Acrospiroma↗

PubMed2003

Eccrine porocarcinoma arising in a seborrheic keratosis evaluated with dermoscopy and treated with Mohs' technique.

A 78-year-old white woman returned for a routine 6-month skin cancer examination. She had a history of actinic keratosis and multiple basal cell carcinomas. She had no personal or family history of dysplastic nevi or melanoma. The patient was asymptomatic and unaware of any new or changing skin lesions. The patient had multiple lentigines, hemangiomas, and actinic and seborrheic keratoses on all sun-exposed areas. There were no less than 10 seborrheic keratoses on the right mid-back, and one was found to have a 1-cm, reddish nodule asymmetrically located within it (Figs 1 and 2). A clear papule on the left preauricular area was found on biopsy to be a basal cell carcinoma. The nodule on the back was still present 1 month later and it was felt that further evaluation was indicated. As melanoma has been reported to develop in seborrheic keratoses, we decided to examine the lesion using digital dermoscopy. With digital dermoscopy, a well-demarcated reddish nodule was asymmetrically located within a brown lesion. It blanched significantly with pressure. Within the nodule, there were dotted and irregular linear vessels (atypical vascular pattern; also known as polymorphous vascular pattern) and regular-appearing brown dots. Surrounding the reddish nodule, there were pale and pigmented, comedo-like openings, fissures, and ridges (brain-like appearance). Some of the follicular openings appeared to be within the wall of the nodule (Figs 3 and 4). Comedo-like openings, fissures, and ridges are primary dermoscopic criteria for the diagnosis of a seborrheic keratosis; however, the vascular pattern seen has not been reported in seborrheic keratosis. Due to the patient's age and the rarity of significant pathology arising in a seborrheic keratosis, a shave biopsy was performed. To our surprise, the specimen was interpreted by an experienced dermatopathologist as a well-differentiated eccrine porocarcinoma. Due to the high local recurrence rate and metastatic potential of this carcinoma, the patient was referred for Mohs' surgery. Both the basal cell carcinoma and the eccrine porocarcinoma were excised in one stage. A metastatic work-up was negative and the patient appears to be doing well.

Aged↗

PubMed2003

Delayed wound healing after three different treatments for widespread actinic keratosis on the atrophic bald scalp.

BACKGROUND: Actinic keratosis is an exceedingly common premalignant lesion that can develop into squamous cell carcinoma. There is an increasing prevalence of actinic keratosis with increasing age. Numerous treatment options are available for the treatment of actinic keratosis on the scalp. Although we know that atrophic skin heals slowly, one should be careful but should not hesitate to treat. OBJECTIVE: We present three patients with widespread actinic keratotic lesions on the atrophic bald scalp who received different treatments. METHODS: Patient 1 was treated with medium-depth chemical peel, patient 2 with cryopeel, and patient 3 with CO2 laser resurfacing. In all patients, the entire surface area was treated. RESULTS: Despite the different treatment methods used, all three patients had severely delayed wound healing as a complication. Remarkably, all patients had a prolonged period of re-epithelialization. CONCLUSION: Care has to be taken in patients with widespread actinic keratosis on the atrophic bald scalp when treating the entire surface area regardless the treatment modality.

Aged↗

PubMed1995

Immunohistochemical localization of keratins and involucrin in solar keratosis and Bowen's disease.

The present study was conducted to determine the patterns of immunohistochemical characterization of keratin (K) and involucrin in solar keratosis and Bowen's disease in order to clarify the abnormal differentiation or maturation of the tumor cells in these precancerous epithelial dermatoses. Seventeen human anti-cytokeratin antibodies and an anti-involucrin antibody were used to examine 15 cases of solar keratosis and 18 cases of Bowen's disease. Formalin-fixed and paraffin-embedded sections were stained with these antibodies by the avidin-biotin-peroxidase technique. In solar keratosis, keratin and involucrin distribution was similar to that in normal epidermis, whereas in Bowen's disease the keratin distribution varied among individual cases. The dyskeratotic cells in Bowen's disease showed a reduction or loss of staining with these antibodies, and they were occasionally positive for keratin 19. These observations suggest that there is a difference in keratin and involucrin expression between solar keratosis and Bowen's disease and that the atypical cells of Bowen's disease exhibit a diversity of differentiation.

Aged↗

PubMed2004

Melan-A: not a helpful marker in distinction between melanoma in situ on sun-damaged skin and pigmented actinic keratosis.

Pigmented actinic keratosis is one of the simulators of early melanoma in situ from severely sun-damaged skin. Close scrutiny of the hematoxylin and eosin stained section does not always allow an unequivocal diagnosis, because it is sometimes difficult to distinguish pigmented keratinocytes from melanocytes. Immunohistochemical stains, such as S-100 and HMB-45, are used routinely to address this problem. Melan-A, also known as MART-1, is an additional melanocytic marker and has proved to be useful in identifying metastatic tumors of melanocytic origin. The usefulness of this marker to discriminate pigmented actinic keratosis from early melanoma in situ, however, has not yet been a subject of investigation. In this study we evaluated Melan-A expression in ten unequivocal cases of pigmented actinic keratosis and compared the staining pattern with that of S-100, HMB-45, and tyrosinase. In all ten cases the number of cells highlighted with Melan-A was by far larger than those labeled with S-100, HMB-45, and tyrosinase. Four cases showed clusters of Melan-A positive cells being suggestive of melanocytic nests. Even areas of normal skin adjacent to the actinic keratosis featured prominent staining of Melan-A, but only inconsistent labeling of intraepidermal melanocytes with S-100, HMB-45, and tyrosinase. We therefore believe that Melan-A is a more sensitive marker for intraepidermal melanocytes than S-100, HMB-45, and tyrosinase. In addition there may be expression of Melan-A in keratinocytes and nonmelanocytic cells. To avoid an erroneous diagnosis of malignant melanoma one should therefore interpret results obtained from Melan-A stained slides carefully and in the context with other melanocytic markers.

Aged↗

PubMed1993

Lichen planus-like keratosis. A clinical and histological reexamination.

Lichen planus-like keratosis (LPLK) is a common skin lesion that has some morphologic features of lichen planus (LP) and lichenoid actinic keratosis (LAK). Although most authors consider LPLK to be a distinct lesion, surgical pathologists are often unfamiliar with it. We examined in detail the clinical and histologic features of LPLK in 100 consecutive cases. In our series, LPLK lesions occurred mostly in late-middle-aged individuals, on the trunk (64%) and extremities (31%) and predominantly in women (73%). Among the 14 histologic parameters that were studied, most LPLK had hyperkeratosis (81%) with hypergranulosis (77%), focal acanthosis (75%), and focal parakeratosis (59%). Solar elastosis was observed in 48% of the cases. Only a few cases had eosinophils (15%) or plasma cells (7%) in the inflammatory infiltrate. The adjacent skin was available for study in 71% of the specimens, and only 26.8% of the cases had an adjacent lesion, most frequently seborrheic keratosis (8.4%), solar lentigo (7%), and actinic keratosis (5.6%). According to our results, the most consistent features observed in LPLK are a lichenoid lymphocytic infiltrate with hyperkeratosis, hypergranulosis, focal acanthosis, and focal parakeratosis, without prominent atypia of keratinocytes.

Atrophy↗

PubMed2005

Benign lichenoid keratosis: a clinical and pathologic reappraisal of 1040 cases.

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.

Adult↗

PubMed1994

Aberrations of the tumor suppressor p53 gene and p53 protein in solar keratosis in human skin.

Aberrations of the p53 gene in 27 solar keratoses were examined by the polymerase chain reaction and single-strand conformation polymorphism and DNA sequencing analyses. In a series of Japanese patients, eight of 27 cases (30%) of solar keratosis showed structural abnormalities of the p53 gene. Six of eight aberrations of p53 gene were determined to be single nucleotide substitutions, and five of these were located at a dipyrimidine site. In solar keratosis, noticeable mutations were C to T in three cases, and one each of C to A and T to C nucleotide changes. p53 protein was detected immunohistochemically in the nuclei of six of 27 cases (22%) of solar keratosis. Nuclear staining for p53 protein was only significantly correlated with the presence of missense mutation of p53 gene (p < 0.01). Aberrations of the p53 gene in solar keratosis may be a marker to predict early cancerous lesions.

Base Sequence↗

PubMed1991

Differentiation disorders of keratinocytes in seborrheic keratosis (acanthotic type).

Since the differential disorder of keratinocytes in seborrheic keratosis remains to be elucidated, the differentiation of seborrheic keratosis (acanthotic type) was examined immunohistochemically using a lectin and two anti-keratin monoclonal antibodies. A lectin, peanut agglutinin (PNA), and anti-keratin monoclonal antibody, 34 beta B4, recognize the whole epidermis except for the basal layer in the normal epidermis. In seborrheic keratosis (acanthotic type), cells unstained with either PNA or 34 beta B4 were found throughout the entire tumor. In the upper part of the tumor, some cells appeared to undergo keratinization without expressing the differential markers recognized by PNA or 34 beta B4. Another anti-keratin monoclonal antibody, 34 beta E12, stained the tissues in the same way as in the normal epidermis. Thus it was indicated that, in seborrheic keratosis (acanthotic type), although differentiation was partially maintained, some cells might undergo maturation without expressing the differentiation markers recognized by PNA or 34 beta B4.

Aged↗

PubMed1993

Trichilemmal carcinoma occurring in a lesion of solar keratosis.

A case of trichilemmal carcinoma occurring in a lesion of solar keratosis was reported. A 92-year-old woman had an erythematous plaque on her face that contained a reddish nodule. Histological examination of the nodule revealed typical features of trichilemmal carcinoma accompanied by those of solar keratosis in the marginal zone. The histological features of the erythematous plaque corresponded with those of solar keratosis. However, in situ the carcinoma developed in the epithelium of a hair follicle as well as in the interfollicular epidermis in the lesion of solar keratosis. We considered it likely that bowenoid malignant transformation occurred in both interadnexal and adnexal epithelium because of actinic damage, and a trichilemmal carcinoma arose. The paper also discussed the histogenesis of trichilemmal carcinoma.

Aged↗

PubMed1998

Occult basal cell carcinoma arising in seborrheic keratosis.

The present study reports a case of an occult basal cell carcinoma that arose in seborrheic keratosis. The patient was a fifty-six-year-old male who presented with a dark brown plaque on his back. Clinically, the lesion demonstrated no nodules or ulcerations suggesting that it was malignant. However, histopathological analysis of the lesion revealed an atypical basaloid cell mass that appeared to be a solid basal cell carcinoma beneath and surrounded by a seborrheic keratosis lesion. Thus, the coexistence of basal cell carcinoma and seborrheic keratosis is possible and should be considered when a malignant change in seborrheic keratosis is apparent.

Basal Cell Carcinoma↗

PubMed2004

Keratosis obturans and external ear canal cholesteatoma: how and why we should distinguish between these conditions.

Keratosis obturans and external ear canal cholesteatomas have been considered as separate entities for the last 20 years, after being regarded as variations of the same disease for at least 87 years. While both disorders are distinct, they do have some overlapping characteristics which may make it difficult to reach a definite diagnosis. This review explores the diagnostic dilemmas which may arise, and discusses the classification, aetiology, pathogenesis and management of these conditions. We concur that external ear canal cholesteatoma and keratosis obturans are different conditions and conclude that the presence of osteonecrosis and focal overlying epithelial loss are the most reliable features favouring the diagnosis of external ear canal cholesteatoma over keratosis obturans. Furthermore, whilst keratosis obturans can be managed successfully by regular aural toilet, external ear canal cholesteatoma may require surgical intervention depending on the extent of the disease.

Cholesteatoma↗

PubMed2005

Topical photodynamic therapy using intense pulsed light for treatment of actinic keratosis: clinical and histopathologic evaluation.

BACKGROUND: Photodynamic therapy (PDT) is suitable for the treatment of actinic keratosis, and, recently, topical PDT using intense pulsed light as a light source has been reported. However, evaluations of its therapeutic effects have been clinically based. OBJECTIVE: The objective of this study was to confirm the histopathologic resolution of actinic keratosis treated by topical PDT using intense pulsed light as a light source. METHODS: Twelve actinic keratosis lesions in seven patients were treated with 5-aminolevulinic acid-PDT using intense pulsed light as a light source. After a single treatment, the clinical response was assessed and histopathologic examinations were performed on clinically resolved lesions. RESULTS: Six of 12 (50%) lesions showed clinical clearance after a single treatment, but histologic examinations showed that only 5 of the 12 (42%) lesions had been removed. No complications, such as pigmentary changes or scarring, were observed. CONCLUSION: Intense pulsed light is potentially an effective light source for PDT. However, the determination of complete remission in actinic keratosis requires caution, and long-term follow-up or histologic confirmation may be required.

Aged↗

PubMed1978

Seborrheic keratosis: an acantholytic variant.

Two elderly women with seborrheic keratoses on the abdomen are reported on because of the peculiar histologic appearance characterized by prominent acantholysis. Although the basic histologic architecture was a papillomatous acanthoma corresponding to that of seborrheic keratosis, the upper portion of the lesions showed extensive acantholytic changes and dyskeratotic cells. Differentiation from seborrheic keratosis with focal acantholytic dyskeratosis, warty dyskeratoma, keratosis senilis and acantholytic squamous cell carcinoma could be made on the basis of clinical as well as histological features. Although the histogenesis is uncertain, it seems logical to propose that this is a rare variant of irritated seborrheic keratosis.

Acantholysis↗

PubMed2001

Seborrheic keratosis with compound nevus, junctional nevus and basal cell carcinoma in the same lesion.

Seborrheic keratosis can be associated with different neoplasms such as basal cell carcinomas, squamous cell carcinomas and melanomas. We describe an unusual case of a man who presented with a brown plaque on his back. The clinical diagnosis was melanoma. Histopathologic examination of the lesion revealed four neoplasms: a compound nevus, a junctional nevus, a superficial basal cell carcinoma and a seborrheic keratosis. Although this association most likely represents a chance phenomenon, we discuss the possibility that the seborrheic keratosis developed from the nevus, and that subsequently the junctional nevus and the basal cell carcinoma developed from the seborrheic keratosis.

Back↗

PubMedDate not supplied

Actinic keratosis. Current treatment options.

Actinic keratoses are hyperkeratotic skin lesions that represent focal abnormal proliferation of epidermal keratinocytes. Some actinic keratoses evolve into squamous cell carcinoma of the skin, while others resolve spontaneously. The conversion rate of actinic keratosis to squamous cell carcinoma is not accurately known, but appears to be in the range of 0.25 to 1% per year. Although there is a low rate of conversion of actinic keratoses to squamous cell carcinoma, 60% of squamous cell carcinomas of the skin probably arise from actinic keratoses. The main cause of actinic keratoses in otherwise healthy Caucasians appears to be the sun. Therapy for actinic keratoses begins with prevention which starts with sun avoidance and physical protection. Sunprotection with sunscreens actually slows the return of actinic keratoses in patients already getting actinic keratoses. Interestingly, a few studies are available that demonstrate that a high fat diet is associated with the production of more actinic keratoses than is a low fat diet. One of the mainstays of therapy has been local destruction of the actinic keratoses with cryotherapy, and curettage and electrodesiccation. A new addition to this group of therapies to treat individual actinic keratoses is photodynamic therapy with topical aminolevulinic acid and light. In patients who have numerous actinic keratoses in an area of severely sun damaged skin, therapies which are applied to the whole actinic keratosis area are used. The goal of treating such an area of skin is to treat all of the early as well as the numerous clinically evident actinic keratoses at the same time. The classical approaches for treating areas of photodamaged skin without treating actinic keratoses individually include: the use of topically applied fluorouracil cream, dermabrasion, and cutaneous peels with various agents like trichloroacetic acid. Both topically as well as orally administered retinoids have been used to treat actinic keratoses but retinoids alone are probably not an optimal monotherapy. Photodynamic therapy with topical aminolevulinic acid and light is a new therapy for actinic keratoses. Aminolevulinic acid is a precursor of protoporphyrin IX (PpIX) which is synthesized in the actinic keratosis when it is treated with aminolevulinic acid, and the PpIX photosensitizes the actinic keratosis so that light exposure can lead to its destruction. Photodynamic therapy with topical aminolevulinic acid is approved in the US to treat multiple individual actinic keratoses on the face and scalp and has similar cure rates to those reported for cryotherapy and fluorouracil therapy.

Humans↗

PubMed2004

The immunopathology of regression in benign lichenoid keratosis, keratoacanthoma and halo nevus.

BACKGROUND: Regression is a phenomenon present in a variety of cutaneous lesions. It is likely that similar immunologic mechanisms explain the phenomenon of spontaneous regression occurring in the various lesions. METHODS: Twenty-seven specimens, nine each of halo nevus, keratoacanthoma, and benign lichenoid keratosis, including three examples each of predominantly early, mid, and late regression were examined with antibodies to HLA-II, CD1a, CD3, CD4, CD8, CD20, CD34, CD56, and CD68. RESULTS: Epidermotropism of inflammatory cells, including CD1a positive, CD68 positive, CD3 positive, and CD8 positive cells, was present in benign lichenoid keratosis and keratoacanthoma, but not in halo nevus. In halo nevus, the nests of halo nevus cells tended to be infiltrated by CD1a positive, CD68 positive, CD3 positive, and CD8 positive cells. The blood vessels exhibited endothelial cell swelling with luminal narrowing and disruption within the dermis of all lesions. The CD1a positive cells were increased in number in lesional epidermis except in keratoacanthoma lesions where the density of CD1a positive cells was increased in the epithelial lip, but decreased within the epithelial portion of the keratoacanthoma proper. Conversely, the CD8 positive cells were scarce in the dermis below the epithelial lip of the keratoacanthoma, but increased in the dermis of the neoplastic epithelium. CD1a positive cells were also seen throughout the dermal portion of the lesion, particularly at the lesion base. In halo nevus, the CD1a positive cells and CD68 positive cells within the lesions were larger than those in non-lesional skin, indicating activation. The composition of the inflammatory infiltrate varied within each lesion type according to stage of regression, but T-lymphocytes predominated. CONCLUSION: Cytotoxic T-cells may be the final common denominator of regression in benign lichenoid keratosis, keratoacanthoma, and halo nevus. In halo nevus, cytotoxic T-cells may play the predominant role in regression. In keratoacanthoma and benign lichenoid keratosis, cytotoxic T-cells play a pivotal role, but additional mechanisms may also be involved in the phenomenon of regression. Benign lichenoid keratoses progress through stages of regression accompanied by varying proportions of inflammatory cells, including CD3, CD4, and CD8 positive T-lymphocytes, natural killer cells, macrophages and Langerhans cells.

Antigens, CD↗

PubMed2000

[Expression of EGFR in keratosis of laryngeal and the correlation with malignant phenotype].

OBJECTIVE: To evaluate the roles of EGFR expression in laryngeal keratosis. METHOD: The ABC immunohistochemical method was performed to investigate the expression of EGFR in 32 cases of laryngeal keratosis tissue. RESULT: The EGFR indices in light, moderate and serious non-typical hyperplasia were 12.5%, 22.5% and 47.8% respectively. There were significant differences between heavy with light and middle non-typical hyperplasia (P < 0.05). CONCLUSION: The EGFR might play some role in the process of carcinogenesis of laryngeal keratosis, and be as an useful marker for the assessment of the behavior and prognosis in the laryngeal premalignant lesions keratosis.

Adult↗