Is "milk crust" a transient form of golden retriever ichthyosis?

Roethig, Anja; Schildt, Kirsti J M; Welle, Monika Maria; Wildermuth, Brett E; Neiger, Reto; Thom, Nina (2015). Is "milk crust" a transient form of golden retriever ichthyosis? Veterinary dermatology, 26(4), 265-e57. Blackwell Science 10.1111/vde.12216

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BACKGROUND

A recessive inherited form of lamellar ichthyosis is well recognized in golden retrievers. In this breed, young puppies demonstrate a self-limiting scaling disorder which is commonly recognized by breeders, who use the term "milk crust" to describe this syndrome.

HYPOTHESIS/OBJECTIVES

To determine whether "milk crust" is a new keratinization disorder or a self-limiting form of golden retriever ichthyosis.

ANIMALS

A total of 179 golden retriever dogs (21 dams and 158 puppies) were examined.

METHODS

Dermatological examination and assessment of the patatin-like phospholipase-1 (PNPLA1) genotype by PCR testing of buccal mucosal swabs. Skin biopsies from one affected puppy were evaluated for histopathological abnormalities.

RESULTS

Forty-five of 158 (28%) puppies exhibited scaling at 8 weeks of age; 113 of 158 (72%) were dermatologically normal. Of 144 analysed samples, 40 of 144 (28%) puppies demonstrated a homozygous mutation of the PNPLA1 genotype [of which, 36 of 40 (90%) had signs of scaling], 77 of 144 (53%) demonstrated a heterozygous mutation and 27 of 144 (19%) were a normal wild-type. In six of 17 (35%) dams, a homozygous mutation of the PNPLA1 genotype was found, eight of 17 (47%) demonstrated a heterozygous mutation and three of 17 (18%) were normal wild-type. Dams with a homozygous mutation were clinically unaffected. A 1 year follow-up revealed that 23 of 28 (82%) puppies affected with this syndrome failed to develop typical signs of ichthyosis. In five of 28 (18%) dogs there was persistence of mild scaling.

CONCLUSIONS AND CLINICAL IMPORTANCE

We hypothesize that the clinical syndrome termed "milk crust" could represent a transient form of golden retriever ichthyosis. Remission is not fully linked to PNPLA1 genotype, suggesting that unknown factors may contribute to the clinical disease.

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