Such a subjective perception of "having fragile skin" should be clearly differentiated from "skin fragility", a well documented disorder, occurring mostly in newborn infants and elderly individuals, leading to skin tears of mechanical origin.
Despite extensive research on the physiologic and pathologic mechanisms leading to skin barrier dysfunction, which may result in perceived skin fragility, there is limited epidemiologic information regarding the prevalence of "fragile skin" in different adult populations.
The accumulation of porphyrins results in severe sun sensitivity, with blistering, increased skin fragility, and scarring on the areas exposed to light.
EDS is a heterogeneous group of inherited connective tissue disorders, with its major manifestations being skin fragility, skin hyperextensibility, and joint hypermobility [2].
Recessive dystrophic epidermolysis bullosa is a severe skin fragility disease caused by loss of functional type VII collagen at the dermal-epidermal junction.
Among the various subtypes of epidermolysis bullosa, recessive dystrophic epidermolysis bullosa (RDEB) is the severest form involving mucosal membrane and systemic diseases such as renal insufficiency as well as abnormal skin fragility [2].
Mutations in hemidesmosome-related genes give rise to skin fragility syndromes called epidermolysis bullosa, whereas aberration in desmosomal genes give rise to variable abnormalities in skin, hair, and heart.
Mutations in more than 80 genes cause monogenic disorders that include severe skin fragility, myopathies, neurodegeneration, and premature ageing, and contribute to polygenic disorders including liver and inflammatory bowel disease.
Patients with dystrophic epidermolysis bullosa (DEB) have incurable skin fragility, blistering, and multiple skin wounds because of mutations in the gene that encodes for type VII collagen (C7), which holds together the epidermal and dermal layers of human skin.
Mutant mice with targeted disruption of the decorin gene (Dcn−/−) exhibit an abnormal collagen architecture in the dermis and reduced tensile strength, collectively leading to a skin fragility phenotype.
This includes the acute attacks of abdominal pain, nausea, vomiting, diarrhea, tachycardia, hypertension and seizures, as well as the cutaneous findings seen in porphyria cutanea tarda (PCT), namely increased skin fragility, bullous lesions after exposure to sunlight and increased scarring.
