Cutaneous asthenia are a group of syndromes characterized by defects in collagen production. This results in a variety of clinical signs, including loose, hyperextensible, fragile skin; joint laxity; and other connective tissue dysfunctions. These collagen defects have been described in cats (Himalayan and Domestic shorthair). The mode of inheritance has been demonstrated for Himalayan cats (recessive) and domestic shorthair cats (dominant). These conditions are extremely rare in cats.
Ehlers-Danlos syndrome (EDS)
EDS is characterised bgy an abnormality of the enzyme system procollagen aminopeptidase, and inherited as an autosomal recessive trait[1]. In the cat, two types of EDS have been reported. The extremely rare form, inherited as a recessive trait has been described in the Himalayan breed and is similar EDS VIIc in man and dermatosporaxis in calves and sheep. This form is caused by a defect in procollagen peptidase. The form inherited as a dominant trait results from a biochemical defect referred to as type EDS I-III and has not yet been characterised. No breed predisposition has been observed[2][3].
Clinical features include fragile skin from the time of birth, wounds that heal with thin scars, delayed wound healing, pendulous skin, and haematoma and hygroma formation. In lambs, rupture of the GI tract and arterial aneurysms are features, and the disease is fatal in lambs and calves. In horses, the onset is later and the lesions are well circumscribed, consisting of hyper-extensible and somewhat fragile skin. In dogs and cats, the disease is not fatal, and older animals develop hanging folds of skin and exhibit extensive scarring; some have joint laxity or ocular anomalies. Diagnosis is based on clinical signs and histopathologic studies of the collagen structure, which require age and breed-matched controls[4].
For diagnosis, a skin extensibility index has been developed. Thrombocytopenia has been reported in cats with cutaneous asthenia due to abnormal vessel ultrastructure[5].
There are anecdotal reports of improvement of affected dogs with vitamin C supplementation. The major differential diagnosis in adult cats is feline hyperadrenocorticism with acquired skin fragility.
Differential diagnosis includes other causes of acquired cutaneous hyperfragility (e.g. Cushing’s syndrome, hepatic cholangiocarcinoma, hepatic lipidosis). Prognosis is always guarded since signs usually worsen with time. Only certain forms are compatible with a subnormal life. Life expectancy of cats with EDS type VIIc seems better than in other species. There is no specific treatment, only hygienic measures aimed at avoiding or limiting mechanical stress.
Cutis laxa
Cutis laxa is a rare disease of cats characterized clinically by a flaccid, inelastic skin with excessive folding. It is associated with genetic abnormalities in elastin fibres, especially involving reduced synthesis or destruction of elastin fibres (elastolyse)[6]. Cutis laxa has not yet been reported in the cat.
References
- ↑ Guaguere, E & Prelaud, P (2000) A practical guide to feline dermatology. Merial, France
- ↑ Collier, LL, & Leathers CW (1980) Feline Practice 10:25-36
- ↑ Counts, DF Byers, BF & Holbrook, KA (1980) Invest Dermatol 74:96-99
- ↑ Merck Veterinary Manual
- ↑ August, JR (2006) Consultations in feline internal medicine. Vol 5. Elsevier Saunders, Philadelphia, pp:582-583
- ↑ Ultti, J Fazio, MJ & Christiano, AM (1993) Connective tissue and its heritable disorders. (Ed Royce, PM., Steinmann, B). Willey-Liss, New York, USA pp:409-423