The hallmark of invasive SCC is the extension of atypical keratinocytes beyond the basement membrane and into the dermis. The presence of solar elastosis or keratinocyte atypia at tumor margins suggest that the SCC is actinically derived. Cutaneous SCC shows a significant rate of metastasis 0. So far, staging systems do not allow the assessment of a risk score or a standardized therapeutical approach. The prevalence of lentigo senilis or solar lentigo, or lentigo solaris correlates with increasing age.
They appear most commonly in sun-exposed areas, such as the face and back of the hands. Their presence is a risk factor for melanoma and NMSC. Solar lentigines represent a marker of intermittent high intensity and of cumulative UVR.
They are characterized by epidermal hyperplasia, concerning both keratinocytes and melanocytes. The primary defect could be in either cell type eliciting a secondary proliferative response in the other. Phototoxic doses of PUVA may lead to the development of lentigines 6—8 mo after therapy.
Their appearance has also been associated with UVA tanning bed use for cosmetic tanning. Lentigo solaris is a benign, acquired, circumscribed pigmented macule with a smooth or irregular border that appears in sun-exposed skin, such as face and back of hands. It presents on skin exposed to natural or artificial UVR, but may also appear in sun-protected areas.
Children with xeroderma pigmentosum develop lentigines solaris even in the early months of life after minimal sun exposure. Variants of lentigo senilis with acute onset after intense UVR are sunburn freckles. To differentiate from solar lentigines, ephelids are common genetically determined pigment spots appearing during childhood in a distinct photodistribution.
Multiple lentigines senilis on face of an elderly woman and a seborrheic keratosis on her left cheek. Diagnosis is primarily clinical.
Dermoscopy reveals a uniform reticular network. A solar lentigo can be hard to distinguish from a flat seborrhoic keratosis. It also has to be differentiated from an ephelis, a lentigo simplex, a pigmented actinic keratosis, a pigmented BCC and a lentigo maligna.
A lentigo solaris shows increased basal melanocytes, while an ephelid increased pigmentation but no increase in melanocytes. Lentigo maligna LM is a subtype of melanoma in situ with a prolonged radial growth phase. Lentigo maligna melanoma LMM is the most common subtype of melanoma on the face. Presentation of LMM may be quite subtle, particularly in early stages and delayed diagnosis is common.
They are rarely seen before the age of Epidemiology of these tumors progressively concerns younger patients. LM pathogenesis is thought to be associated with cumulative, and not intermittent, sun exposure.
It is thought that the dysfunctional epidermis in chronically sun-damaged skin may be permissive to aberrant melanocyte proliferation in the early stages of melanoma development. Keratinocytes influence the number, morphology, and proliferation of melanocytes.
An interference in the melanocyte-keratinocyte relationship may contribute to LMM development. Lentigo maligna presents as a flat, slowly enlarging macular lesion with poorly defined irregular borders, prominent asymmetry and pigment variation, persisting for years on chronically sun-exposed skin of elderly individuals Fig.
LMM is frequently larger than LM and may continue to be macular, although a nodular portion is often seen within the macule as the lesion progresses 61 Fig.
A Histologically confirmed lentigo maligna melanoma on left cheek of an elderly male patient, arising from a lentigo maligna after many years.
B Dermoscopic picture of LMM on same patient. Early clinical detection of LM is imperative, though often very difficult.
Differential diagnoses include solar lentigo, early lesions of seborrheic keratosis, lentigo maligna melanoma, lichen planus-like keratosis, pigmented actinic keratosis and melanocytic naevus.
Dermoscopy has been shown to have higher diagnostic accuracy.
Dermoscopically, LM is often associated with one or two pigment colors and few distinctive dermoscopic features. Dermoscopic features of LMM include a large number of colors, an annular-granular pigment pattern, asymmetrical pigmented follicular openings, pigmented rhomboidal structures, obliterated hair follicles, gray pseudo-network.
Also, an increased density of the vascular network, red rhomboidal structures and target-like patterns can be commonly seen in invasive LMMs.
Vertical growth phase-associated dermoscopic criteria ulceration, blue papular areas and black structureless areas are rarely seen 6869 Fig. Dermatoscopic diagnosis of a pigmented skin lesion cannot be based on the presence of a single criterion, and therefore histopathology still remains the gold standard for correct diagnosis. Histological differentiation of LM and LMM can be difficult due to widespread atypical melanocytes that are present in an area of chronically sun damaged skin.
Limited sampling may be inadequate for an accurate diagnosis of pigmented melanocytic lesions on actinically damaged skin. Areas chosen for biopsy may not contain the most advanced areas histologically and may fail to detect foci of invasive melanoma elsewhere within the lesion.
Lentigo maligna may evolve into LMM after many years. Prognosis for invasive lentigo maligna melanoma does not differ from that for other histogenetic types of melanoma after controlling for tumor thickness. For all above mentioned UV-associated skin lesions, prevention of further exposure to UVR and close patient monitoring for melanoma or NMSC development is of greatest importance.
Patient education and increased public awareness may potentially aid in their early detection and treatment. The most effective preventive measure is photoprotection, including broad-spectrum sunscreen use starting from an early age, use of UV-protective clothing, and behavioral adjustments, such as avoidance of tanning beds. Sun avoidance and protection methods should be rigorous. Other preventive measures include treatment of precursor lesions, such as individual actinic keratoses, or field cancerizationHPV transmission prevention, smoking and alcohol consumption cessation.
Patient education is of highest importance. Except for photoprotection, skin self-examination in order to achieve early lesion detection is imperative. After diagnosis of one NMSC all patients should be considered at high risk for developing another tumor. In patients with a history of NMSC, monthly self examination of all skin surfaces is recommended. Individual risk assessment is necessary and should be discussed.
In case of organ transplant patients, patient education should begin at transplantation, whereas in case of xeroderma pigmentosum or albinism, at birth or diagnosis. Patient follow-up is a second-line prevention mechanism for UV-associated skin lesions. In patients with a history of BCC, complete skin examination should occur every 6—12 mo for life.
As for patients with LM, at least an annual skin examination for life is recommended. For invasive LMM, follow-up is recommended according to the stage of the disease. Patients with actinic keratoses, field cancerization or any predisposing risk factors for the development of a NMSC should be monitored on a regular basis, at least annually.
Early diagnosis and therapy of pre-malignant cutaneous lesions is crucial for the secondary prophylaxis of further invasive and highly aggressive skin cancers. In case of field cancerization, field directed therapies are more worthwhile than lesion targeted approaches.
In organ transplant patients, long-term skin surveillance, early diagnosis and aggressive treatment of any suspicious lesion, tapering immunosuppressive treatment or the selection of immunosuppressants with proposed antiangiogenic properties like mTor-inhibitors may help to reduce the multiplicity of subsequent primary skin cancers in high-risk patients.
NMSC chemoprevention is a promising intervention for early management, and has made enormous progresses over the past years due to the large number of research studies including many randomized clinical trials. Chemoprevention with systemic retinoids has demonstrated promise in decreasing the incidence of new primary NMSCs in immunocompromised post-transplantation recipients.
There is limited evidence for the use of systemic retinoids in the non-transplantation patient, indicating that despite short-time effectiveness, systemic retinoids do not prevent tumor recurrence.
Use of oral retinoids acitretin, isotretinoin has been effective in reducing the development of precancerous lesions, but side effects may be significant and therapeutic effects disappear shortly after cessation of the drug.
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Topical tretinoin failed to show a chemopreventive benefit for NMSC. Chemopreventive activity has also been studied in various agents including COX inhibitors, vitamin E forms, green tea extracts and other plant-derived compounds like resveratrol, protocatechuic, ellagic and caffeic acids. Encouraging outcomes were found with most natural extracts.
Previously published online: www. National Center for Biotechnology InformationU. Journal List Dermatoendocrinol v. Author information Copyright and License information Disclaimer. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. This article has been cited by other articles in PMC. Abstract Age-associated skin lesions linked to UV radiation UVR include actinic keratosis, non-melanoma skin cancer—such as basal cell carcinoma and squamous cell carcinoma—lentigo senilis and lentigo maligna.
Keywords: skin aging, carcinogenesis, skin cancer, actinic keratosis, field cancerization, basal cell carcinoma, squamous cell carcinoma, lentigo maligna, photoprotection. Introduction Age-related skin changes are induced by chronological aging, also known as intrinsic aging, and photoaging or extrinsic aging. Actinic Keratosis and Field Cancerization Actinic keratoses or solar keratoses or senile keratoses are intraepithelial skin neoplasms constituted by atypical proliferation of keratinocytes.
Clinical findings AKs are ill-defined pink to skin-colored hyperkeratotic papules found on chronically sun-exposed areas, most frequently on the face, scalp, ears, forearms, décolleté, dorsal hands. Open in a separate window. Diagnosis Diagnosis is primarily made clinically.
Pigmented lesion assay may help avoid unneeded skin biopsies
Clinical findings BCC is a slow-growing, locally invasive epidermal tumor with characteristic clinical features that depend on the clinical subtype. Diagnosis Diagnosis is primarily clinical and is completed with histological confirmation. Histopathology Features vary according to the subtype, but common histological findings include a tumor consisting of proliferating atypical basal cells, which appear large, oval and stain deep blue on hematoxylin-eosin. Disease progression: Prognosis BCC is a slow-developing malignant skin tumor, infiltrating the adjacent tissues.
Squamous cell carcinoma Cutaneous SCC is a malignant neoplasm derived from suprabasal epidermal keratinocytes. Etiology: Pathogenesis While sporadic BCC develops de novo, SCC arises from precursor lesions of actinic keratosis and Bowen's disease, and represents a multistep accumulation of genetic damage.
Clinical findings SCC tends to present as a rapidly growing pink or red nodule or plaque, which may be hyperkeratotic or ulcerated Figs. Diagnosis Clinical suspicion must always be verified by skin biopsy.
Histopathology The hallmark of invasive SCC is the extension of atypical keratinocytes beyond the basement membrane and into the dermis. Lentigo Senilis Epidemiology: Risk factors The prevalence of lentigo senilis or solar lentigo, or lentigo solaris correlates with increasing age. Etiology: Pathogenesis Solar lentigines represent a marker of intermittent high intensity and of cumulative UVR.
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Clinical findings Lentigo solaris is a benign, acquired, circumscribed pigmented macule with a smooth or irregular border that appears in sun-exposed skin, such as face and back of hands.
Diagnosis Diagnosis is primarily clinical. Histopathology A solar lentigo can be hard to distinguish from a flat seborrhoic keratosis. Etiology: Pathogenesis LM pathogenesis is thought to be associated with cumulative, and not intermittent, sun exposure.
Clinical findings Lentigo maligna presents as a flat, slowly enlarging macular lesion with poorly defined irregular borders, prominent asymmetry and pigment variation, persisting for years on chronically sun-exposed skin of elderly individuals Fig.
Diagnosis Early clinical detection of LM is imperative, though often very difficult. Conclusion For all above mentioned UV-associated skin lesions, prevention of further exposure to UVR and close patient monitoring for melanoma or NMSC development is of greatest importance. Disclosure of Potential Conflicts of Interest No potential conflicts of interest were disclosed.
Footnotes Previously published online: www. References 1. Zouboulis CC, Makrantonaki E. Clinical aspects and molecular diagnostics of skin aging. Clin Dermatol. The determinants of periorbital skin ageing in participants of a melanoma case-control study in the U. Br J Dermatol. Apoptosis and immune response are responsible for the site-specific incidence of non-melanoma skin cancer. Med Hypotheses. Review ofactinic keratosis.
Journal of the American Academy of Dermatology. Abstract Epidermoid inclusion cysts are common lesions with unclear etiology.
Chapitre 6 - MST
Le texte complet de cet article est disponible en PDF. Discussion Evidence for viruses causing cysts. Conflicts of interest: None declared. Tous droits réservés. Eosinophilic fasciitis in a female child Alex G. Ortega-Loayza, Bradley G. Merritt, Pamela A. Groben, Dean S. L'accès à l'intégralité du contenu de ce site est reservé uniquement aux professionnels de santé disposant d'un compte.
The mean biopsy specificity was There was a The difference between mean pre-PLA and post-PLA specificity among the dermatologist reached statistical significance P Mean physician confidence score was 3. Vous avez atteint la limite d'articles par visiteur Inscription gratuite Disponible uniquement pour les professionnels de santé Inscrivez-vous gratuitement. Se connecter à votre compte. Continuer via Facebook ou. Créer un compte ou.