光化性角化病 Actinic keratosis - PubMed 文献(第 2 页)
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光化性角化病 的 PubMed 搜索结果(第 2 页)
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What is the most relevent factor causing pain during ALA-PDT? A multi-center, open clinical pain score research trial of actinic keratosis, acne and condylomata acuminata. 导致ALA-PDT过程中疼痛的最相关因素是什么？一项针对光化性角化病、痤疮和尖锐湿疣的多中心、开放性临床疼痛评分研究。
To date, it has been reported that the intrinsic factors(lesions location, lesions area, disease tynpes) and extrinsic factors(fluence rate) contribute to the pain during 5-aminolevulinic acid photodynamic therapy (ALA-PDT). But there are few studies on pain during ALA-PDT and lack of sufficient clinical evidence related to the pain intensity. To investigate pain intensity and its relative factors during ALA-PDT and to provide clinical implication. The pain numeric rating scale (PNRS) score was used to evaluate the patients' pain intensity at different times during ALA-PDT irradiation from 0 to 10 min during treatment. Gender, age, lesions location, lesions area, ALA concentration and fluence rate were recored. The trial enrolled 274 patients in total, including 118 acne patients (in face), 30 actinic keratosis(AK)patients(in face), 126 Condylomatata acuminate patients(in genitalia). The average pain score in PDT was highest in the patients with actinic keratosis(7.3 ± 0.7), and that of condylomata acuminata was the lowest (4.5 ± 1.1) (p < 0.05). The highest pain score in patients with AK, acne and condylomata acuminata was 8, 6 and 6 respectively which occurred at 4 min, 4 min and 6 min respectively. The pain score of males was higher compared with females in all of the three diseases (p < 0.05). The pain score of facial diseases (5.6 ± 1.2) was higher than that of the genitalia (4.5 ± 1.1) (p < 0.05). The lesions area was positively correlated with the pain score (p < 0.05). In facial diseases, the pain score of patients with high fluence rate (7.3 ± 0.7) was higher than patients with low fluence rate (5.1 ± 0.9) (p < 0.05). Intrinsic and extrinsic factors both correlate with pain during PDT. Intrinsic factors are difficult to change, so extrinsic factors are the key point to control. We can reduce the fluence rate and extend the treatment time, relieving pain intensity while still ensuring equivalent efficacy.
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Arsenic and chromium levels in hair correlate with actinic keratosis/non-melanoma skin cancer: results of an observational controlled study. 头发中砷和铬水平与光化性角化病/非黑色素瘤皮肤癌相关：一项观察性对照研究结果。
The role of heavy metals in carcinogenetic process has been widely established; however, information on the most common environmental metals that serve as major risk factors for actinic keratosis (AK)/non-melanoma skin cancer (NMSC) are still lacking. The aim of this study was to evaluate levels of the most common environmental heavy metals in hair of patients with AK/NMSC as compared to healthy controls. Thirty-one patients diagnosed with AK/NMSC and 34 healthy controls were enrolled. Patients were interviewed for heavy metals exposure and underwent hair analysis for detection of arsenic (As), cadmium (Cd), chromium (Cr), nickel (Ni) and lead (Pb). Continuous variables were analyzed using Wilcoxon Non-Parametric Rank Test and proportions were compared by Fisher's Exact Test. Statistical significance was determined by P<0.05. In our cohort we observed 48.4% patients had AKs, 16.1% basal cell carcinoma (BCC), 9.7% squamous cell carcinoma (SCC) and 25.9% of patients presented with a combination of these lesions. There were significantly elevated levels of As and Cr in AK-NMSC group as compared to controls. We identified a strong positive correlation between As and Cr concentration and AK/NMSC adding new clues to the scenery of NMSC risk factors that should be taken under consideration in exposed populations.
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A Natural History of Actinic Keratosis and Cutaneous Squamous Cell Carcinoma Microbiomes. 光化性角化病和皮肤鳞状细胞癌微生物组的自然史。
Cutaneous squamous cell carcinoma (SCC) is the second-most-common cancer in Australia. The majority of SCCs progress from premalignant actinic keratosis (AK) lesions that form on chronically sun-exposed skin. The role of skin microbiota in this progression is not well understood; therefore, we performed a longitudinal microbiome analysis of AKs and SCCs using a cohort of 13 SCC-prone immunocompetent men. The majority of variability in microbial profiles was attributable to subject, followed by time and lesion type. and organisms were relatively more abundant in nonlesional photodamaged skin than in AKs and SCCs. was most commonly associated with lesional skin, in particular, sequences most closely related to Of 11 -like operational taxonomic units (OTUs), six were significantly associated with SCC lesions across seven subjects, suggesting their specific involvement with AK-to-SCC progression. If a causative link exists between certain -like OTUs and SCC etiology, therapeutic approaches specifically targeting these bacteria could be used to reduce SCC. Actinic keratosis (AK) and cutaneous squamous cell carcinoma (SCC) are two of the most common dermatologic conditions in Western countries and cause substantial morbidity worldwide. The role of human papillomaviruses under these conditions has been well studied yet remains inconclusive. One PCR-based study has investigated bacteria in the etiology of these conditions; however, no study has investigated the microbiomes of AK and SCC more broadly. We longitudinally profiled the microbiomes of 112 AK lesions, profiled cross sections of 32 spontaneously arising SCC lesions, and compared these to matching nonlesional photodamaged control skin sites. We identified commonly occurring strains of and at higher relative abundances on nonlesional skin than in AK and SCC lesions, and strains of were relatively more abundant in lesional than nonlesional skin. These findings may aid in the prevention of SCC.
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Real-world approach to actinic keratosis management: practical treatment algorithm for office-based dermatology. 光化性角化病管理的真实世界方法：面向诊所皮肤科的实用治疗算法。
Actinic keratosis (AK) is a chronic skin disease in which multiple clinical and subclinical lesions co-exist across large areas of sun-exposed skin, resulting in field cancerisation. Lesions require treatment because of their potential to transform into invasive squamous cell carcinoma. This article aims to provide office-based dermatologists and general practitioners with simple guidance on AK treatment in daily clinical practice to supplement existing evidence-based guidelines. Novel aspects of the proposed treatment algorithm include differentiating patients according to whether they have isolated scattered lesions, lesions clustered in small areas or large affected fields without reference to specific absolute numbers of lesions. Recognising that complete lesion clearance is rarely achieved in real-life practice and that AK is a chronic disease, the suggested treatment goals are to reduce the number of lesions, to achieve long-term disease control and to prevent disease progression to invasive squamous cell carcinoma. In the clinical setting, physicians should select AK treatments based on local availability, and the presentation and needs of their patients. The proposed AK treatment algorithm is easy-to-use and has high practical relevance for real-life, office-based dermatology.
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Evaluation of Resource Utilization and Treatment Patterns in Patients with Actinic Keratosis in the United States. 美国光化性角化病患者资源利用和治疗模式的评估。
To compare health care resource utilization and treatment patterns between patients with actinic keratosis (AK) treated with ingenol mebutate gel (IngMeb) and those treated with other field-directed AK therapies. A retrospective, propensity-score-matched, cohort study compared refill/repeat and adding-on/switching patterns and outpatient visits and prescriptions (health care resource utilization) over 6 months in patients receiving IngMeb versus those receiving imiquimod, 5-fluorouracil, diclofenac sodium, and methyl aminolevulinate or aminolevulinic acid photodynamic therapy (MAL/ALA-PDT). The final sample analyzed included four matched treatment cohort pairs (IngMeb and comparator; n = 790-971 per treatment arm). Refill rates were similar except for imiquimod (15% vs. 9% for imiquimod and IngMeb, respectively; P < 0.05). MAL/ALA-PDT treatment repetition rates were higher than IngMeb refill rates (20% vs. 10%; P < 0.05). Topical agent add-on/switch rates were comparable. PDT had higher switch rates than did IngMeb (5% vs. 2%; P < 0.05). The IngMeb cohort had a significantly lower proportion of patients with at least one AK-related outpatient visit during the 6-month follow-up than did any other cohort: versus imiquimod (50% vs. 66%; P < 0.0001), versus 5-fluorouracil (50% vs. 69%; P < 0.0001), versus diclofenac sodium (51% vs. 56%; P = 0.034), and versus MAL/ALA-PDT (50% vs. 100%; P < 0.0001). There were significantly fewer AK-related prescriptions among patients receiving IngMeb than among patients in other cohorts. Results based on the first 6 months after treatment initiation suggested that most field-directed AK therapies had clinically comparable treatment patterns except imiquimod, which was associated with higher refill rates, and PDT, which was associated with significantly more frequent treatment sessions and higher switching rates. IngMeb was also associated with significantly fewer outpatient visits than were other field-directed therapies.
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Identification of differentially expressed genes in actinic keratosis samples treated with ingenol mebutate gel. Ingenol mebutate凝胶治疗光化性角化病样本中差异表达基因的鉴定。
Actinic keratosis is a common skin disease that may progress to invasive squamous cell carcinoma if left untreated. Ingenol mebutate has demonstrated efficacy in field treatment of actinic keratosis. However, molecular mechanisms on ingenol mebutate response are not yet fully understood. In this study, we evaluated the gene expression profiles of actinic keratosis lesions before and after treatment with ingenol mebutate using microarray technology. Actinic keratoses on face/scalp of 15 immunocompetent patients were identified and evaluated after treatment with topical ingenol mebutate gel 0.015%, applied once daily for 3 consecutive days. Diagnostic and clearance of lesions was determined by clinical, dermoscopic, and reflectance confocal microscopy criteria. Lesional and non-lesional skin biopsies were subjected to gene expression analysis profiled by Affymetrix microarray. Differentially expressed genes were identified, and enrichment analyses were performed using STRING database. At 8 weeks post-treatment, 60% of patients responded to ingenol mebutate therapy, achieving complete clearance in 40% of cases. A total of 128 differentially expressed genes were identified following treatment, and downregulated genes (114 of 128) revealed changes in pathways important to epidermal development, keratinocyte differentiation and cornification. In responder patients, 388 downregulated genes (of 450 differentially expressed genes) were also involved in development/differentiation of the epidermis, and immune system-related pathways, such as cytokine and interleukin signaling. Cluster analysis revealed two relevant clusters showing upregulated profile patterns in pre-treatment actinic keratoses of responders, as compared to non-responders. Again, differentially expressed genes were mainly associated with cornification, keratinization and keratinocyte differentiation. Overall, the present study provides insight into the gene expression profile of actinic keratoses after treatment with ingenol mebutate, as well as identification of genetic signatures that could predict treatment response.
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P53 staining index and zonal staining patterns in actinic keratoses. 光化性角化病P53染色指数和带状染色模式
Actinic keratoses (AKs) are common dysplastic lesions resulting from chronic excessive ultraviolet exposure. Neither the clinical grade of thickness nor the histological grade of dysplasia seems valid predictors of aggressive potential of AKs. Instead, the mutational status in AKs appears to predict well the clinical course. TP53 gene mutations result in a non-functional protein resistant to degradation, thus immunohistochemical staining for p53 can suggest mutation status. Increased p53 was associated with progression from AK to squamous cell carcinoma. To investigate how the intensity of p53 staining (p53 staining index) varies according to body site, histological subtype and grade dysplasia of AKs. Secondly, we sought to investigate the distribution in the epidermal layers of non-functional p53 (zonal staining patterns). p53 staining index was greater than 50% in 90.7% of AKs. p53 staining index was significantly higher in older age (p < 0.0093) and in facial AKs compared to other body areas (p = 0.03). A significant correlation between p53 staining index and grade of dysplasia was observed (p = 0.006) and between p53 staining index and zonal p53 staining pattern (p = 0.003). No significant differences in p53 staining index among the various histological AK types were observed. No correlation between clinical and histological grade. All AKs, independently from their clinical appearance, should be treated but special attention is required for AKs on severely photodamaged skin on the face and in older patients.
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An overview of Bcl-2 expression in histopathological variants of basal cell carcinoma, squamous cell carcinoma, actinic keratosis and seborrheic keratosis. Bcl-2在基底细胞癌、鳞状细胞癌、光化性角化病和脂溢性角化病组织病理学变异体中表达的概述。
The Bcl-2 protein has been shown to suppress cell death and protects cell against apoptosis induced by different death-inducing signals. In this study the authors have analyzed imunohistochemically the expression of Bcl-2 protein in the histopathological variants of the most common malignant tumors of the skin--basal cell carcinoma (BCC) and squamous cell tumor (SCC), as well as in the precancerous lesion actinic keratosis (AK) and in benign tumor seborrheic keratosis (SK). Bcl-2 expression in solid, adenoid and cystic variants of BCC exhibited immunoreactivity of tumor stroma with more intense staining among peripheral palisading cells. Morphoeic variant demonstrated reduced amount of Bcl-2 expression. Among SCC in all samples, tumor tissue lack to express Bcl-2 positivity. In cases of hypertrophic and atrophic variants of AK, Bcl-2 expression was confined to basal cell layer, as well as in one case of hypertrophic variant in suprabasal cells. In three histological variants of SK expresseion of Bcl-2 protein was in areas of basaloid proliferation, while in areas of squamous differentiation was negative. In clonal variant immunostaining was positive among cells in characteristic "nests" Distribution of Bcl-2 protein expression in solid, adenoid and cystic variant of BCC showed that peripheral proliferating cells are protected against apoptosis what permits tumor growth. In morpheaform variant reduced amount of Bcl-2 expression indicated that this variant of BCC has increased cell proliferation, and in practice shows tendency for recurrence and difficulties to eradicate. Bcl-2 expression supports the observation that tumor cells are derived from basal keratinocytes. In SCC, lack of Bcl-2 expression indicates that origin of tumor cells is from more differentiated suprabasal keratinocytes. In AK results suggest that immunoreactivity is regulated with respect of the keratinocyte's differentiation status, but not closely correlate with proliferative rate.
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Concordance in Distinguishing Actinic Keratosis from Squamous Cell Carcinoma in Situ on Mohs Histological Frozen Sections. 莫氏组织冰冻切片上区分光化性角化病与原位鳞状细胞癌的一致性。
Mohs surgeons routinely encounter squamous cell carcinoma at surgical margins and often base the decision to take another layer on the severity of atypia observed. Currently, no criteria exists for distinguishing borderline histological patterns that could be interpreted differently as actinic keratosis (AK), squamous cell carcinoma in situ (SCCIS), or AK with focal SCCIS. To assess interrater concordance amongst Mohs surgeons in distinguishing AK from SCCIS when evaluating Mohs frozen sections. Seventeen slides were selected and converted into digitally formatted cases. They were compiled into an electronic survey and distributed to the American College of Mohs Surgery. Overall κ was 0.26 corresponding to weak agreement between raters compared to the standard, with κ of 0.34 for AK and 0.37 for SCCIS. There exists notable variability among Mohs surgeons who interpret the spectrum of in situ carcinoma differently. Ongoing learning and consensus building among Mohs surgeons and trainees can aid in quality patient care, even if there may not be agreement on every case. J Drugs Dermatol. 2023;22(2):199-194. doi:10.36849/JDD.7084.
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Impact of interval and combination therapies on the management of actinic keratosis: review and clinical considerations. 间隔治疗和联合治疗对光化性角化病管理的影响：综述与临床考量。
Abstract An increasing body of evidence, including epidemiological data, clinical and histopathologic observations, and molecular biological findings, has highlighted the underlying malignant nature of actinic keratosis (AK). Scientific evidence accumulated over the past decade supports the concept that AK should no longer be considered premalignant but instead is now thought to be the earliest stage of a biologic continuum ending in squamous cell carcinoma. This paradigm shift, coupled with a worldwide increase in the incidence of AK, has changed how dermatologists treat AK. These changes include the development of novel topical and procedural therapies; modification of established topical monotherapy regimens to include interval, sequential, short-course, and short-contact therapies; combining various topical therapies; and combining topical and procedural therapies. This review will examine the mechanisms of action and the safety and efficacy data for emerging interval and combination therapies used to treat AK.