taking and a comprehensive physical examina-tion are important first steps to establish if the present-ing patient is otherwise healthy or if additional complaints point toward more systemic disease.
Not every cause as outlined above will be covered here.
The goal of this chapter is to introduce the reader to the primary causes of hyperkeratosis within the companion animal population.
10.2 Idiopathic Hyperkeratosis Note that diagnostic investigation of hyperkeratosis may be inconclusive. Cases of nasal and footpad hyperkerato-sis in otherwise asymptomatic canine patients may be idiopathic. These cases most often develop in aged [1, 9, 10, 15]. These dogs may or may not respond to thera-peutic attempts to soften the excessive keratin with petroleum jelly, propylene glycol, salicylic acid, and/or tretinoin gel [1, 5, 16].
10.3 Hereditary Hyperkeratosis Hereditary nasal parakeratosis (HNP) was first described in Labrador retriever and Labrador retriever crosses in two separate studies by Page et al. and Peters et al. in 2003 [9, 16]. Parakeratosis refers to the principle histologic feature that these patients share, parakeratotic hyperker-atosis [9, 16]. This specific type of hyperkeratosis defines the condition by which cells of the stratum corneum pro-liferate extensively and retain their nuclei [9, 16]. The presence of these nucleated squames may reflect incom-plete differentiation or an underlying inflammatory process [16]. In humans, parakeratotic hyperkeratosis is a response to inflammation, as is seen in psoriasis [16].
Whether or not inflammation is an inciting factor in dogs with HNP remains to be determined.
Patients with HNP develop nasal hyperkeratosis as young adults, typically between 6 and 12 months of age [9, 16]. Of the 18 cases that were described by Page, the majority did not have concurrent footpad disease [9].
Dogs with HNP have gray‐to‐brown accumulations of keratin [9]. Concurrent depigmentation of the nasal planum is rare, but possible (see Figures 10.6a, b).
These hyperkeratotic lesions do not appear to worsen with sunlight. Some owners report that they improve after the dog’s nose is moistened by rain or snow [9].
Dogs with HNP are otherwise healthy [9, 16].
HNP does not appear to be sex‐linked in terms of its inheritance: males and females are affected equally. HNP does not also appear to favor certain coat colors [16].
Page et al. proposed an autosomal recessive inheritance, but this has yet to be confirmed [9].
Treatment is not necessary. However, some dogs may response to the use of topical propylene glycol or other emollients, such as petroleum jelly [9, 16]. In these patients, treatment is not curative. Treatment reduces lesions, but must be continued indefinitely to retain ben-eficial effects [16].
A second inherited condition that involves a thickened stratum corneum is digital hyperkeratosis (DH), other-wise referred to as hereditary footpad hyperkeratosis (HFH). HFH is inherited among Irish Terriers as an auto-somal recessive trait [17]. This condition was first described by Binder et al. in 2000 [18]. It has also been described in Kerry Blue Terriers and Dogues de Bordeaux [18–21].
Patients with HFH develop appreciable calluses on the palmar and plantar surfaces of all four feet. As these lesions progress, they are prone to cracking. The result-ant pain causes lameness [18].
Much like HNP, HFH lesions arise as early as 18 weeks of age [18]. By the time the patient is six months old, paw pads are encrusted with keratin [18]. Keratin accumula-tion can be quite extreme, resulting in deposits up to 5 mm deep.
Histopathologic lesions classically reflect orthokera-totic hyperkeratosis. This means that cells are anucleate as compared to those in HNP [17, 18, 22].
In addition, the claws of affected Irish Setters m
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