With the increase of the medium lifespan in developing countries, skin aging rise attention more and more. In 2007, Kaya and Saurat rebranded the extreme expression of skin fragility under the name of ‘‘dermatoporosis’’ or chronic cutaneous insufficiency/fragility syndrome. Dermatoporosis is still underused in medical literature and nurses and wound specialists know also about this condition, but they call it “skin tears”. There is obvious confusion cause the nursing literature talks about skin tears while dermatologists write about dermatoporosis. Clinical aspects comprise atrophy, purpura, and pseudo-stellate scars. Firstly, the British dermatologist Thomas Bateman described senile purpura in 1818 as purpuric patches arising in elderly people after minimal trauma, especially on the dorsum of the hands. Furthermore, between 1970 and the full documentation of Kaya and Saurat in 2007, we found medical papers about senile purpura, pseudoscars, skin tears, and so on. Starting from this historical data, they bring valuable information according to clinical aspects, histopathology, ultrasonographic aspects, pathophysiology, and therapeutics. This paper aims to analyze published data for improving the diagnosis and management of dermatoporosis.
Malignant melanoma and urological cancers originate from different tissues and organs, yet several studies highlight connections between these malignancies, including common risk factors, genetic predispositions, and immunological pathways. Evidence from recent studies suggests that a prior diagnosis of melanoma may increase the likelihood of subsequently developing renal cell carcinoma (RCC), and, conversely, patients with RCC appear to face a heightened risk of being diagnosed with melanoma. Shared factors such as a personal or family history of cancer, UV radiation exposure, smoking, and obesity have all been linked to an increased incidence of various cancer types. A major link between malignant melanoma and urological cancers is the presence of shared genetic mutations and familial cancer syndromes. Key mutations, including germline mutations in BRCA1, MITF, CDKN2A, TP53, and alterations in the PI3K/AKT pathway, significantly contribute to the risk of both types of malignancies. Personalized medicine, which tailors prevention and treatment strategies to an individual’s genetic, environmental, and lifestyle factors, has significantly improved cancer care. The primary aim is to select the most effective treatment for each patient, maximizing therapeutic outcomes, reducing side effects, and minimizing the risk of drug resistance. Advances in genomics and immunology are driving the development of personalized therapies that target specific molecular pathways and immune responses common to both melanoma and urological cancers. Angiogenesis inhibitors and checkpoint inhibitors have demonstrated notable success in treating these cancers, with tumor mutational burden serving as a valuable biomarker for predicting the efficacy of immune checkpoint inhibitors.
The process of aging population is increasing the relevance of comprehending age-related changes in skin structure and function, as well as their implications for clinical care. This narrative review explores aspects of the intrinsic and extrinsic mechanisms of skin aging, their molecular and morphological consequences, and their clinical expression, with particular attention to chronic cutaneous insufficiency. The intrinsic aging process is reflecting declining cellular functionality, impaired tissue homeostasis, and endocrine changes, especially regarding estrogen deficiency after menopause. These processes are reducing collagen synthesis, hydration, and elasticity and thus contributing to epidermal and dermal atrophy and barrier dysfunction. On the other hand, extrinsic aging is driven mainly by cumulative ultraviolet exposure, with additional contributions from pollution, smoking, diet, and behavioral and psychosocial factors. Processes such as oxidative stress, inflammation, DNA damage, glycation, and increased matrix metalloproteinase activity promote extracellular matrix degradation, linking the environmental exposure to the photoaging and cutaneous carcinogenesis. Main clinical manifestations include xerosis, chronic pruritus, pigmentary changes, benign lesions, actinic keratoses, and basal cell and squamous cell carcinomas. Inflammatory, allergic, autoimmune, and drug-induced dermatoses, including psoriasis, lichen planus, and bullous pemphigoid, are complicating healthcare in older adults, while systemic comorbidities and medication use are influencing clinical presentation and treatment. Dermatoporosis is characterized by cutaneous atrophy, purpura, pseudoscars, and susceptibility to injury after minor trauma. Reduced hyaluronic acid availability and CD44 expression contribute to impaired hydration and mechanical resilience, potentially leading to ulceration and deep dissecting hematomas. Management measures are emphasizing the role of photoprotection, skin hydration, trauma prevention, and reduction of modifiable exposures, with corticosteroid use warranting reassessment in secondary dermatoporosis. Other discussed approaches are topical hyaluronic acid, retinoids, alpha-hydroxy acids, and vitamin C, but the proposed interventions have limited supporting evidence. Therefore, it is considered that early recognition of these interconnected changes may be supportive for planning prevention, a timely diagnosis, and individualized care, based on considerations like skin fragility, associated disease, and treatment burden in older patients.
