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We describe a patient with multiple fibroepithelial basal-cell carcinoma (FEBCC) associated with seborrheic keratosis distributed in a neviform fashion on the left side of the body and clinically resembling skin tags.
A 67-year-old man noticed on the abdominal skin a coin-sized verrucous plaque, in which a small granulation-like lesion developed several weeks before the first consultation at our clinic. The histology of the biopsied granulation-like lesion showed a well demarcated, but not associated with the collagenous capsule, mass of proliferating eosinophilic cells, consisting of intervening spindle-shaped Schwann cells and mature ganglion cells scattered in the tumor nest. We diagnosed this tumor nest as a ganglioneuroma, which rarely develops in the skin tissue. The simply resected surrounding verrucous lesion was histologically seborrheic keratosis.
A case of arsenical keratosis with multiple lesions of Bowen's disease and squamous cell carcinoma is described. The patient was successfully treated with a combination of acitretin and intralesional 5-fluorouracil. All the lesions resolved after three months of therapy with no side effects and no recurrence during four months of follow-up.
Keratosis lichenoides chronica (KLC) is a rare chronic disease characterized by violaceous, papular and nodular lesions typically arranged in a linear and reticulate pattern. The etiology of KLC is unknown, but it may be associated with internal diseases such as hypothyroidism, glomerulonephritis and lymphoproliferative disorders. Herein, we describe the case of 44-year-old male patient with characteristic lesions of KLC on the trunk and extremities, present for 12 years. The clinical diagnosis was proven by histopathological examination on several occasions. In the years following the diagnosis of KLC, he developed bilateral hilar and multiple mediastinal, cervical and inguinal lymphadenopathies and hepatosplenomegaly. In 2000, diffuse interstitial and then reticulonodular pulmonary infiltrates associated with fever, weight loss, malaise and subcutaneous nodules developed. Biopsies taken from peripheral and mediastinal lymph nodes, pulmonary parenchyma, pleural tissue, bone marrow and skin showed non-necrotizing granulomas, indicating a sarcoidal granulomatous reaction. Characteristic histopathological findings and the absence of atypical cells, clonality and a high proliferative index excluded lymphomas. Furthermore, detailed tests showed no evidence of an infectious granulomatous disease. As far as we know, this is the first reported case of KLC associated with a sarcoidal granulomatous reaction.
Keratosis lichenoides chronica is characterized by violaceous, papular and nodular lesions typically arranged in a linear and reticulate pattern, most marked on the hands and feet, and accompanied by a seborrhoeic dermatitis-like eruption of the face. This rare condition is very refractory to treatment but we report a patient whose eruption responded top photochemotherapy.
We describe two cases in which keratosis pilaris atrophicans faciei (ulerythema oophryogenes) occurred in association with hereditary woolly hair. This association also occurred in the father of case I. In case 2, Noonan's syndrome was also present.
The prevalence of keratosis pilaris and accentuated palmoplantar marking was evaluated in 61 patients with atopic dermatitis, 35 patients with dominant ichthyosis vulgaris and 247 other dermatological cases taken as controls. Our data showed that (1) these features are of no diagnostic significance for atopic dermatitis and (2) they are significantly more frequent in patients with ichthyosis vulgaris without associated eczema than in those with atopic dermatitis. Consequently, they should be considered as part of the phenotype of ichthyosis vulgaris rather than attributed to a concomitant atopic dermatitis as suggested by some. These findings should be taken into account when evaluating atopic dermatitis or ichthyosis. To assess the frequency of scaling under winter weather conditions, 155 control subjects were also examined for evidence of visible desquamation and 25.8% showed slight but definite scaling.
The DNA-synthesizing cells in benign and malignant keratotic diseases including psoriasis, seborrhoeic keratosis, Bowen's disease and basal cell carcinoma were studied. Cells in S-phase were labelled after small pieces of the lesions were incubated in tissue culture medium that contained 5-bromo-2'-deoxyuridine (BrdU). The labelling of DNA was analysed using the labelling index and pattern. Although the malignant diseases tended to show a higher DNA labelling index, neither this nor the loss of polarity alone was associated with malignancy. However, a higher DNA labelling index together with a loss of polarity was characteristic for malignancy.
A questionnaire was sent to 83 patients in the south Buckinghamshire area, in whom a primary diagnosis of keratosis pilaris (KP) had been made within the preceding 20 years. Of the 50 questionnaires returned, one was invalid, and 49 were evaluated. The age range of patients surveyed was 18 months-25 years; 61% were female and 39% male. Age of onset of KP was within the first decade in 51%, second decade in 35%, third decade in 12%, and fourth decade in 2%. Body sites affected were the arms (92%), legs (59%), face (41%), buttocks (30%) and eyebrows (8%). Other family members were affected by KP in 39%; 55% had no family history of KP, and 6% did not know. There was a personal history of atopy in 37%, 16% had associated dry skin, and 47% had neither. A seasonal variation in the severity of KP was noted in 80% of patients; 49% of these improved in the summer and 47% worsened in the winter. Overall, KP had improved with age in 35% of patients, remained unchanged in 43%, and worsened in 22%. The mean age of improvement was 16 years.
BACKGROUND: Although photodynamic therapy (PDT) is becoming an important treatment method for skin lesions such as actinic keratosis (AK) and superficial basal cell carcinoma, there are still discussions about which fluence rate and light dose are preferable. Recent studies in rodents have shown that a low fluence rate is preferable due to depletion of oxygen at high fluence rates. However, these results have not yet been verified in humans. OBJECTIVES: The objective was to investigate the impact of fluence rate and spectral range on primary treatment outcome and bleaching rate in AK using aminolaevulinic acid PDT. In addition, the pain experienced by the patients has been monitored during treatment. PATIENTS/METHODS: Thirty-seven patients (mean age 71 years) with AK located on the head, neck and upper chest were treated with PDT, randomly allocated to four groups: two groups with narrow filter (580-650 nm) and fluence rates of 30 or 45 mW cm(-2), and two groups with broad filter (580-690 nm) and fluence rates of 50 or 75 mW cm(-2). The total cumulative light dose was 100 J cm(-2) in all treatments. Photobleaching was monitored by fluorescence imaging, and pain experienced by the patients was registered by using a visual analogue scale graded from 0 (no pain) to 10 (unbearable pain). The primary treatment outcome was evaluated at a follow-up visit after 7 weeks. RESULTS: Our data showed a significant correlation between fluence rate and initial treatment outcome, where lower fluence rate resulted in favourable treatment response. Moreover, the photobleaching dose (1/e) was found to be related to fluence rate, ranging from 4.5 +/- 1.0 J cm(-2) at 30 mW cm(-2), to 7.3 +/- 0.7 J cm(-2) at 75 mW cm(-2), indicating higher oxygen levels in tissue at lower fluence rates. After a cumulative light dose of 40 J cm(-2) no further photobleaching took place, implying that higher doses are excessive. No significant difference in pain experienced by the patients during PDT was observed in varying the fluence rate from 30 to 75 mW cm(-2). However, the pain was found to be most intense up to a cumulative light dose of 20 J cm(-2). CONCLUSIONS: Our results imply that the photobleaching rate and primary treatment outcome are dependent on fluence rate, and that a low fluence rate (30 mW cm(-2)) seems preferable when performing PDT of AK using noncoherent light sources.
BACKGROUND: DNA of epidermodysplasia verruciformis (EV)-associated human papillomaviruses (HPVs) has been widely detected in lesions of malignant skin tumours, benign tumours and other proliferative diseases of epithelial origin. OBJECTIVES: To investigate the presence of EV-associated HPV DNA in nongenital seborrhoeic keratosis (SK) and to elucidate the prevalence of distinct HPV genotypes. METHODS: We investigated HPV DNA in 55 nongenital SK biopsies, which were compared with 48 normal skin biopsies (healthy controls) using a nested polymerase chain reaction (PCR) using consensus primers CP65/CP70 and CP66/CP69. The positive PCR products were retracted and used to prepare recombination clones with T-vector. Distinct clones were analysed with endonucleases, and HPV genotypes were identified by direct sequencing. RESULTS: EV-associated HPV DNA was detected in 42 of 55 (76%) nongenital SK biopsies vs. only 13 of 48 (27%) healthy controls (chi2 = 22.087; P < 0.005). The prevalence was higher in patients with more than five lesions than in those with only one lesion (P < 0.05). Ten distinct HPV genotypes were detected in the nongenital SK biopsies: HPV 20, 23, 5, renal transplant recipient (RTR) X7, HPV 17, 37, 17b, RTRX4, RTRX4b and strain SK3. HPV 20 was found in 26 of 42 (62%) positive specimens, followed by HPV 23 (11 of 42, 26%) and HPV 5 (six of 42, 14%). Existence of multiple HPV genotypes was observed in 12 of 42 (29%) positive specimens. In healthy controls, five genotypes of EV-associated HPV (HPV 20, 23, 5, 17 and RTRX4) were detected, with the same predominant genotype of HPV 20 (five of 13, 38%). Several distinct HPV genotypes were found to coexist in four of 13 (31%) positive specimens. CONCLUSIONS: This study provides some evidence that EV-associated HPVs might play a part in the pathogenesis of nongenital SK.
The association of contiguous or 'collision' tumours in the same biopsy specimen is not uncommon and is often reported in the literature. The most common association, basal cell carcinoma (BCC) and naevus, is very difficult to diagnose clinically. We describe a 38-year-old woman with a previous history of melanoma, who presented with a modified pigmented lesion of the hip that had begun to change 6 months earlier. Histologically, the lesion was a melanocytic compound naevus and a BCC with a seborrhoeic keratosis. The case was investigated clinically and by focusing on the dermoscopic features and their pathological correlates. Cutaneous collision tumours are extremely difficult to diagnose preoperatively, even with the help of dermoscopy, in particular when one of the lesions is melanocytic.
BACKGROUND: Actinic keratosis (AK) has been defined as a precancerous lesion or an early phase in the evolution of squamous cell carcinoma (SCC) and histological changes seen in the individual cells of an AK are indistinguishable from those seen in SCC, which invade the dermis. Cyclin A is an increasingly utilized proliferation marker that has functions in both S phase (DNA replication) and initiation of mitosis, whereas alterations of beta-catenin, the molecule involved in cell-cell adhesion and in signalling transduction, could promote invasive and proliferative capacities of malignant tumours. OBJECTIVES: To determine cyclin A and beta-catenin expression pattern in cutaneous SCC and in in situ lesions classified as keratinocytic intraepidermal neoplasia (KIN) and, using traditional terms, as AK and Bowen's disease (BD), and to analyse it in relation to SCC differentiation, diameter and thickness. METHODS: Immunohistochemical staining was performed on 110 formalin-fixed paraffin-embedded tissue samples with the streptavidin-biotin technique using antibodies to cyclin A and beta-catenin. On histological examination, 53 lesions were diagnosed as AK, 16 as BD and 41 as SCC-11 well differentiated (WD), 16 moderately differentiated (MD) and 14 poorly differentiated (PD). Using KIN classification, 22 lesions were KIN1, 23 were KIN2 and 24 were KIN3. For cyclin A, distribution and labelling index (LI), and for beta-catenin, level of membranous staining and presence of aberrant (nuclear/cytoplasmic) localization were examined. RESULTS: Diffuse cyclin A presence was observed more frequently in BD than in AK (P < 0.0001) or SCC (P = 0.0002), and in SCC-PD compared with SCC-WD (P < 0.0001) or SCC-MD (P = 0.0003). Differences between KIN3 and KIN2, as well as KIN3 and KIN1 lesions, were statistically significant (P < 0.0001), and the same result appeared when KIN1 and KIN2 cases were grouped and compared with those of KIN3 (P < 0.0001). Cyclin A LI was significantly lower (P < 0.05) in AK than in BD or SCC, but no difference between BD and SCC was found, and LI in BD was even higher than in SCC-WD or SCC-MD, while analysis regarding SCC differentiation and KIN classification revealed the same correlation as for the cyclin A distribution. Reduced or absent beta-catenin membranous staining was found in 90 cases (81.8%), more often in SCC than in AK (P = 0.03) or in AK and BD grouped together (P = 0.02). There was no statistical difference between SCCs of various level of differentiation, or between different KIN grades. Diffuse loss of membranous beta-catenin staining showed 36 lesions (32.7%), more frequently SCC than AK (P = 0.003) or AK and BD grouped (P = 0.006), as well as SCC-PD compared with SCC-WD (P = 0.01) and SCC-MD (P = 0.03), whereas all KIN comparisons remained nonsignificant. Aberrant beta-catenin cellular localization demonstrated 28 lesions (25.5%), most often in the basal or peripheral parts and in the lesions with diffuse beta-catenin loss (P = 0.009), but revealed no correlation with the histological type, SCC level of differentiation or KIN grades. Diffuse loss of membranous beta-catenin staining was found to be significantly more frequent in SCC thicker than 4 mm (P = 0.03), while all other comparisons between cyclin A or beta-catenin with the tumour size remained nonsignificant. Cyclin A LI was higher in cases with diffuse loss of membranous staining (P = 0.001) or with aberrant cellular localization of beta-catenin (P = 0.002). CONCLUSIONS: Cyclin A LI showed greater difference between AK and BD than between BD and SCC, suggesting that increased proliferation (measured by cyclin A LI) characterizes progression of in situ lesions from AK to BD, whereas reduced beta-catenin expression separates more clearly SCC from the in situ lesions. Diffuse pattern of loss of membranous beta-catenin staining correlated better with the type of lesion, SCC differentiation and tumour size than reduced expression in general or aberrant cellular localization of beta-catenin. KIN classification does not seem to be supported by our findings, except when KIN1 and KIN2 lesions (in situ, partial thickness) are grouped.
BACKGROUND: Imiquimod 5% cream is a topically applied immune response modifier that has been shown to give effective treatment of actinic keratosis (AK). The therapeutic effects of imiquimod are likely to involve the provocation of a cutaneous immune response against abnormal cells, an assumption based on a strong correlation between complete clearance rates and the severity of the local skin reactions (erythema, oedema, erosion/ulceration, weeping/exudation and scabbing/crusting); however, no clinical studies have conclusively proved this mechanism. OBJECTIVES: To determine the nature of cellular infiltrates induced by the application of imiquimod to AK lesions and to study cells involved in the cutaneous immune response. METHODS: Eighteen patients participated in this phase I, randomized, double-blind, parallel group, vehicle-controlled study. Enrolled patients were randomized in a 2 : 1 ratio to receive imiquimod cream or vehicle cream and applied study cream to five lesions on the scalp, forearm or upper trunk once daily, three days per week for up to 16 weeks. Each patient had punch biopsies of two distinct AK lesions: a lesion was biopsied before treatment to obtain baseline biomarker levels, and a different lesion was biopsied after 2 weeks of treatment. Biopsy specimens were examined using routine and immunohistochemical staining. RESULTS: The imiquimod group showed statistically significant increases from baseline to week 2 in tissue biomarker levels for CD3, CD4, CD8, CD11c, CD86/CD11c, CD68, HLA-DR and TUNEL. No significant differences were seen for the vehicle group. Complete clearance of all treated AK lesions was achieved in five of 11 (45%) imiquimod patients and in none of six vehicle patients. CONCLUSIONS: Imiquimod stimulates a cutaneous immune response characterized by increases in activated dendritic cells and CD4+ and CD8+ T cells.
BACKGROUND: Tenascin-C (Tn-C) is an extracellular matrix protein with multiple functions that is present at low levels in normal tissues, but which is highly present in various tumours. The mRNA expression and protein level of Tn-C including its various isoforms have not been investigated comprehensively so far in cutaneous squamous cell carcinoma (SCC) and the precursor lesion actinic keratosis (AK). OBJECTIVES: To assess the dysregulated expression and splice variants of Tn-C in cutaneous squamous cell dysplasia and carcinoma. METHODS: Biopsies from 66 patients (or representative subsets) that comprised 25 specimens from normal skin, 19 AK and 22 cutaneous SCC were analysed for Tn-C splice variants using splice-specific primers. The amount of Tn-C mRNA was investigated by quantitative real-time reverse transcription-polymerase chain reaction. In addition, the presence of Tn-C protein was analysed in sections of paraffin-embedded tissues using immunohistochemistry. RESULTS: The large Tn-C splice variant was present in only 5% of normal skin samples, in comparison with 63% of AK (P < 0.001) and 88% of SCC (P < 0.001). Tn-C mRNA expression was significantly increased in AK and SCC compared with normal skin (P < 0.001). The corresponding proteins were rarely detected in cells of the vascular epithelial layers and perifollicular layers of some normal skin specimens, and their spatial localization expanded into the papillary dermis of AK. The largest amount and the widest distribution were found in samples of SCC, in which Tn-C was located in the basal cells at the tumour invasion front and additionally in the papillary dermis and reticular dermis. CONCLUSIONS: Tn-C is present in the dermis, its expression is increased during skin cancer development, and the large splice variant is characteristic for AK and SCC, which may prove useful for diagnostic approaches in cutaneous SCC.
BACKGROUND: The accuracy of clinical diagnosis of nonpigmented, facial actinic keratosis (AK) is often suboptimal, even for experienced clinicians. OBJECTIVES: To investigate the dermoscopic features of nonpigmented AK located on the head/neck that may assist the clinical diagnosis. METHODS: Forty-one nonpigmented AKs on facial sites were examined by dermoscopy for any consistent underlying features. Lesions were gathered from skin cancer centres in Australia, Austria, Italy and the U.S.A. All cases were diagnosed histopathologically. RESULTS: Four essential dermoscopic features were observed in facial AK: (i) erythema, revealing a marked pink-to-red 'pseudonetwork' surrounding the hair follicles (95%); (ii) white-to-yellow surface scale (85%); (iii) fine, linear-wavy vessels surrounding the hair follicles (81%); and (vi) hair follicle openings filled with yellowish keratotic plugs (66%) and/or surrounded by a white halo (100%). These features combined, in 95% of cases, to produce a peculiar 'strawberry' appearance. CONCLUSIONS: A dermoscopic model of 'strawberry' pattern is presented, which may prove helpful in the in vivo diagnosis of nonpigmented, facial AK. A limitation of this study is the lack of testing of the specificity of the described dermoscopic criteria in differentiating nonpigmented AKs from other nonpigmented skin lesions at this site.
BACKGROUND: Various effective therapeutic options are currently available for the treatment of actinic keratosis (AK) and basal cell carcinoma (BCC), but none is perfect. Poor cosmesis resulting from surgical procedures and skin irritation induced by topical agents remain significant problems. OBJECTIVES: To evaluate the cost-effectiveness of a recent approach, methyl aminolaevulinate-based photodynamic therapy (MAL-PDT; Metvix; Galderma, Lausanne, Switzerland) in AK and BCC. METHODS: A medical decision tree was developed for simulation of all possible outcomes associated with the medical decision to apply MAL-PDT or a comparator. The time horizon was 1 year for AK and 5 years for BCC. The comparators were cryotherapy in AK and excision surgery in BCC. Clinical data for the model were obtained from the literature. Data on medical management resulted from a Delphi panel performed among 12 Belgian dermatologists. Based on the model, the cost per full responder was calculated, whereby a responder was defined as a patient with all lesions clinically responding and showing an excellent cosmetic result. RESULTS: MAL-PDT is a more expensive treatment compared with cryotherapy for AK. However, the cost per full responder is comparable with cryotherapy (euro363 and euro379, respectively). Incremental cost per extra full responder is euro401. Incremental cost per full responder is euro469 for nodular BCC and euro251 for superficial BCC, both compared with excision surgery. CONCLUSIONS: The results suggest that MAL-PDT is a cost-effective intervention in AK taking a 1-year time horizon, if society is willing to pay euro1.50 per day of response, and that MAL-PDT is better value for money than excision in BCC, taking a 5-year time horizon.
Three cases of a benign follicular tumour of infundibular origin are reported. The neoplasms were solitary, verrucous, slowly-growing papules or nodules on the face, which were diagnosed clinically as verruca vulgaris or seborrhoeic keratoses. Histologically, several epithelial lobules were seen, mainly above the level of the surface of the surrounding skin, with characteristic funnel-shaped invaginations. The tumours occasionally contained vellus hairs or were connected with sebaceous glands and/or hair follicles at their bases, indicating their follicular origin. The tumour masses consisted of peripherally arranged basaloid and inner squamoid cells. The latter cells contained more glycogen and appeared paler with haematoxylin and eosin (H&E) stains than the normal inter-follicular squamous cells. Neither clear cells nor squamous eddies were observed. Palisading of the basaloid cells was not a prominent feature. The name 'infundibular keratosis' is proposed for such tumours, which probably represent the prototype of infundibular tumours of the hair follicle.