Zinc responsive dermatosis
Zinc responsive dermatosis is a nutritional skin disease that can be categorized as syndromes I or II. Syndrome I is a disease
primarily seen in Siberian huskies and Malamutes. Lesions develop in these breeds despite having adequate zinc in their diets
and most commonly occur in young dogs (1-3 years of age). It has been shown in malamutes that they have a decreased ability
to absorb zinc from the intestines. About half of these patients are pruritic. Clinical signs include hyperkeratosis of the
foot pads and sometimes claw disease (onychomalacia). Other common areas affected are perioral, periocular, pinnal, chin,
mucocutaneous junctions (prepuce, vulva, and anus), elbows, and hocks. Lesions begin as erythema, then progress to alopecia,
crusting, scaling/hyperkeratosis, and suppuration. The coat may be dull and excessive sebaceous secretions are common.
Syndrome II occurs in rapidly growing pups or young dogs that are fed a diet deficient in zinc or with large amounts of components
such as calcium or phytates that bind zinc. Lesions are very similar to syndrome I.
Serum or hair zinc levels may or may not be normal and due to inherent difficulties in zinc analysis, this is not recommended.
Diagnosis is made by history, exam, and skin biopsy. Treatment involves changing the diet in syndrome II dogs and zinc supplementation
in syndrome I dogs. Treatment of secondary bacterial and Malassezia infections is essential. There are many forms of zinc
that can be used but zinc methionine is the form of choice (1.7 mg.kg.day). Pruritic dogs may benefit initially with corticosteroids
to decrease inflammation and pruritus as well as to enhance absorption of zinc from the intestines.
Necrolytic migratory erythema (hepatocutaneous syndrome, superficial necrolytic dermatitis, metabolic epidermal necrosis)
This is a condition that has been recognized in the dog and the cat, but it is exceedingly rare in the cat. The pathogenesis
is ill-defined, but the skin lesions are due to degeneration of the keratinocytes and the foot pads are almost always affected
and are often the first skin lesions to occur. At least 90% of dogs with NME have a hepatopathy with the remaining cases associated
with pancreatic neoplasia (functional glucagonomas). Existing theories on the mechanism of the skin lesions are a direct cytotoxic
effect on the keratinocytes from the excessive circulating glucagon, a profound deficiency in amino acids (hypoaminoacidemia)
leading to epidermal protein depletion and necrosis, concurrent hypoalbuminemia resulting in a lack of ability to carry zinc
and fatty acids to the skin, and an induction of eicosanoid production resulting in skin inflammation.
Hyperkeratotosis of the foot pads with resultant fissuring is the hallmark clinical feature. Over time, there is often scaling
and alopecia of the feet as well. Other skin lesions start as erythema then progress to papules, plaques and crusts with occasional
vesicles or bullae. Other regions affected are the mucocutaneous junctions, elbows, hocks, perineal region, axillae, groin,
nose, and pinnae. The oral cavity is rarely affected.
Dogs with hepatocutaneous syndrome should have elevations in ALP and ALT, and often leukocytosis, anemia, and hypoalbuminemia
. Concurrent diabetes mellitus is common. The vast majority of patients have an abnormal ultrasound with a characteristic
"swiss cheese" or "honey-comb" look to the liver. I have seen some cases of chronic, severe, hepatocutaneous syndrome without
abnormal liver enzyme changes at the time of presentation, but previously these enzymes had been elevated. In these cases,
there are not even enough functional hepatocytes to release excessive ALT .Dogs with glucagonomas generally have hyperglycemia
and mild to moderate (sometimes normal) elevations in ALT and ALP. An ultrasound may or may not be able to identify a pancreatic
The diagnosis of NME can be confirmed with a skin biopsy as there are characteristic findings histologically. Impression smears
should be performed to identify secondary infection with yeast and bacteria. There is almost always secondary infection interdigitally
and this creates a large amount of pruritus and pain for these patients.
Treatment is aimed at controlling the infections and supporting the patient nutritionally. Intravenous amino acids (8.5 –
10% Aminosyn, Abbott Labs) are often used to correct the hypoaminoacidemia. These are ideally delivered through a central
line due to phlebitis (25 ml/kg/bw or 500 mls total) once per week for 4 weeks, then as needed thereafter. Response should
be seen with the first 2 treatments. Another method is to give these treatments for three days in a row and note response.
Supplementation with fatty acids and zinc is also recommended. Before the advent of using IV amino acids, feeding egg yolks
(1 yolk/4.5 kg) was thought to be helpful. Nutritional support of the liver (SAME, etc) may also be beneficial.
If present, surgical removal of the pancreatic neoplasia is the treatment of choice. If this is not possible or there are
metastases, a somatostatin analogue, ocetrotide that inhibits glucagon release has been shown to be effective in a few cases.
This therapy may also prove to be beneficial in liver-asociated cases as well.