KWE is characterized by a number of anomalies affecting the skin.<unk>  causes redness of the skin, which is generally associated with inflammation and irritation. Including<unk>  and hyperkeratosis (thickening of the stratum corneum), naturally occurring<unk>  peeling and scaling, with increased manifestation in<unk> , are prevailing features of the disorder.<unk>  in KWE has been attributed to necrobiosis (cellular death) within the Malpighian layer (the innermost layer of the epidermis). Peeling and scaling are caused by spreading dissection of the stratum corneum, correlating to the underlying necrobiosis. The effects of KWE appear<unk> mittently as patches on the skin of the palms and soles, with these patches appearing on the limbs, buttocks and torso in severe cases. Facial lesions of this type have also been reported with the disorder, though this is considered to be an extremely rare occurrence. Onset and cyclical recurrence of KWE have shown to be associated with the arrival of<unk> , or<unk> -like weather. Worsening of symptoms during this time may be considered as an indicator of recurrent onset in patients known to have the disorder, and age of initial onset can be from early childhood to young adulthood, with attenuation of symptoms sometimes happening after age 30. Patients first exhibiting the disorder at a younger age may also experience worsened symptoms. Currently, no specific correlating factor or reason for<unk> -related manifestation has been established, though the coldness and dryer air common to<unk>  conditions may be suspect.<unk>  onset is, however, considered to be a distinguishing feature of KWE among other<unk> tic skin disorders. When peeling of skin occurs, the newly exposed layer of skin underneath is moist, raw and very sensitive. While this may result in minor discomfort and inconvenience, in severe cases of KWE where large areas of raw skin are present, it is often life-altering and debilitating. KWE is inherited in an autosomal dominant manner. This means that the defective gene responsible for the disorder is located on an autosome (chromosome 8 is an autosome), and one copy of the defective gene is sufficient to cause the disorder when inherited from a parent who also has the disorder. KWE can begin as a spontaneous mutation, first appearing in an individual with no previous family history of the disorder. This may be due to a genetic predisposition for the disorder, possibly connected to the Oudtshoorn ancestral line.
Keratolytic winter erythema
Herpetic whitlow
Papuloerythroderma of Ofuji
Streptococcal intertrigo
Lichenoid eruption
Demodicosis
Cutaneous larva migrans
Granuloma faciale