[Polyendocrine syndromes in dogs]. / Polyendokrine Syndrome beim Hund.

The autoimmune polyendocrine syndrome (APS) refers to a combination of autoimmune endocrine disorders. It is rarely described in dogs. The most common combinations are hypoadrenocorticism and hypothyroidism, followed by diabetes mellitus, and less often hypoparathyroidism and orchitis. The diagnosis of the APS is based on the diagnosis of each endocrinopathy, as is the therapy, which involves the substitution of deficient hormones. If a patient was previously stable under treatment and is showing further signs (e.g. polyuria, polydipsia, or weight loss), the development of additional endocrinopathies like hypoadrenocorticism or diabetes mellitus should be considered. The diagnosis of the initially diagnosed endocrinopathy should also be critically questioned. This article summarizes some cases of our own animal hospital and selected cases published in the available literature.

Insulin-dependent diabetes mellitus associated with presumed autoimmune polyendocrine syndrome in a mare.

A 5-year-old Thoroughbred-cross mare was diagnosed with insulin-dependent diabetes mellitus. Partial glycemic control and clinical improvement were achieved with daily insulin administration for 18 mo. The mare subsequently developed evidence of hypoadrenocorticism and died. Necropsy findings included lymphocytic infiltration of the pancreas, adrenal cortex, adrenal medulla, and thyroid glands, suggestive of an immune-mediated polyendocrinopathy.

Autoimmune polyendocrine syndrome with hypoadrenocorticism and diabetes mellitus in a dog: A rare case.

BACKGROUND: Autoimmune polyendocrine syndrome, also called polyglandular autoimmune syndrome, is a rare immune-mediated disorder that involves various endocrine glands. PURPOSE: To report autoimmune polyendocrine syndrome in a dog. METHODS: A 9-year-old spayed female miniature poodle diagnosed with insulin-dependent diabetes mellitus emergently visited our clinic for anorexia, severe depression, and vomiting. Hyponatremia, hypochloridemia, and recurrent hypoglycaemia were found. Hypoadrenocorticism was diagnosed based on consistent clinical signs and repeated adrenocorticotropic hormone stimulation tests. RESULTS: After injecting deoxycorticosterone pivalate and increasing the oral prednisolone dose, the patient's systemic condition improved. CONCLUSIONS: To the best of our knowledge, this is the first case report of hypoadrenocorticism concurrent with diabetes mellitus in a dog. Furthermore, we would like to present the probability of an immune-mediated disorder with multiple organs involved, like type IV autoimmune polyendocrine syndrome in humans.

Polyglandular endocrinopathy type II (Schmidt's syndrome) in a Dobermann pinscher.

A three-year-old, female neutered, Dobermann pinscher was presented for investigation of lethargy, episodic collapse, ataxia and myxoedema. Primary hypothyroidism and primary cortisol-deficient hypoadrenocorticism were diagnosed based on history, physical examination and compatible hormonal analysis. Increased serum concentrations of thyroglobulin autoantibodies and 21-hydroxylase autoantibodies indicated an immune-mediated aetiology. The case was complicated by lymphadenopathy with hand-mirror lymphocytes, classically identified in lymphoma. A polymerase chain reaction test for antigen receptor rearrangement indicated polyclonality and therefore reactive lymphadenopathy. The dog's clinical signs resolved following introduction of levothyroxine and prednisolone. Prioritising the problem-based approach in this case facilitated the diagnosis of hypoadrenocorticism in addition to hypothyroidism due to the persistence of clinical signs despite thyroxine replacement. Importantly, atypical adrenal gland dysfunction was not misinterpreted as inadequate therapeutic response to thyroxine supplementation. The observation that polyglandular endocrinopathy type II can occur in dogs suggests that in dogs with a suboptimal response to treatment for hypothyroidism or hypoadrenocorticism comorbid endocrinopathies should be investigated.

Immunity and the endocrine system.

In conclusion, interaction between the immune and endocrine systems is highly complex. Generally, abnormalities of T suppressor cells, a result of HLA antigen genetic abnormalities, result in autoimmunity that causes endocrine gland destruction and hormone deficiency, as seen in lymphocytic thyroiditis of dogs, type I DM, hypoparathyroidism, hypoadrenocorticism, and APS. On the other hand, endocrine deficiency (hypothyroidism, DM) or excess (hyperadrenocorticism) states may cause abnormalities of cell-mediated and antibody-associated immunity, leading to susceptibility to a variety of viral, bacterial, and fungal infections. It is hoped that this article sheds some light on the complex and highly integrated endocrine-immune interactions.