Megaoesophagus and glucocorticoid-deficient hypoadrenocorticism in a dog

A seven-year-old German shepherd dog was referred for acute onset regurgitation. Muscle weakness and severe dermatological disease were present. Thoracic radiographs revealed generalised megaoesophagus. Diagnostic testing revealed glucocorticoid deficiency, and rapid resolution of the megaoesophagus followed appropriate supplementation. The dog made a full recovery. Unique features of this case include a transiently positive antinuclear antibody titre and clinical features of myasthenia gravis.     

Reversible mega-oesophagus in a dog with hypoadrenocorticism

Mega-oesophagus was diagnosed in a nine-month-old male Shar Pei with hypoadrenocorticism in which anorexia persisted despite appropriate initial therapy. Endoscopy confirmed the mega-oesophagus and revealed oesophagitis, gastritis and gastric haemorrhage. There was a dramatic improvement in clinical signs following treatment with metoclopramide and cimetidine and the mega-oesophagus resolved with treatment for the hypoadrenocorticism.     

Primary hypoadrenocorticism in a dog receiving glucocorticoid supplementation

A 5-year-old, spayed, female husky-Labrador retriever cross was diagnosed with primary hypoadrenocorticism, an uncommon endocrine disorder caused by a deficiency of glucocorticoid and mineralocorticoid hormones. Subtle clinical signs and previous treatment with exogenous glucocorticoid drugs required an adrenocorticotropic hormone stimulation test to confirm the diagnosis.     

Non-dexamethasone-suppressible, pituitary-dependent hyperadrenocorticism in a dog

A 5-year-old female dog with hyperadrenocorticism was determined to have pituitary-dependent hyperadrenocorticism even though plasma cortisol concentrations were not suppressed after high-dosage dexamethasone administration. The diagnosis was based on a supranormal response of plasma cortisol to ACTH administration and a lack of suppression of plasma cortisol concentration after administration of 0.1 mg of dexamethasone/kg. Although a higher dosage of dexamethasone (1 mg/kg) did not cause suppression of plasma cortisol, plasma ACTH concentrations in the dog were increased above those in clinically normal dogs, supporting a diagnosis of pituitary-dependent hyperadrenocorticism. During treatment with mitotane, the dog became unconscious and died. Necropsy revealed a pituitary tumor that had compressed and displaced the hypothalamus. Although high-dosage dexamethasone suppression tests often are useful in the differential diagnosis of hyperadrenocorticism, a lack of suppression of plasma cortisol does not necessarily exclude pituitary-dependent hyperadrenocorticism.     

Regression of venous thrombus after trans-sphenoidal hypophysectomy for pituitary-dependent hyperadrenocorticism in a dog

An 8.0-kg 8-year-old male dachshund was presented for surgical treatment of suspected pituitary-dependent hyperadrenocorticism with portal vein thrombosis. Advanced diagnostic imaging revealed a thrombus in the splenic and portal veins. For the portal vein thrombus, CT angiography showed an enhanced timing delay in the lateral right and caudate liver lobes. Blood tests showed a marked increase in the liver panel, including total bile acid. Brain MRI revealed a pituitary mass, suggesting pituitary-dependent hyperadrenocorticism. The mass was completely resected. The preoperative antithrombotic therapy of rivaroxaban (0.66 mg/kg, PO, once per day) and clopidogrel sulphate (1.66 mg/kg, PO, once per day) was continued postoperatively. Six months after resection of the pituitary mass, the thrombus had disappeared. Further studies are required to prove a causal association between the disappearance of the thrombus and the treatments provided.     

Secondary hypoadrenocorticism associated with craniocerebral trauma in a dog

An 11-month-old, neutered female miniature schnauzer presented with a severe head injury. The dog was treated for the acute effects of craniocerebral trauma and was hospitalized for just over a week. Several weeks later, she became weak and lethargic. A diagnosis of hypoadrenocorticism was confirmed with an adrenocorticotropin hormone (ACTH) stimulation test. An endogenous ACTH assay confirmed secondary hypoadrenocorticism. The dog was tested for hypopituitarism with canine thyroid-stimulating hormone and thyroxine serum assays and an insulin-like growth factor assay. These tests could not confirm panhypopituitarism in this dog. The hypoadrenocorticism was treated with prednisone, and the dog remains controlled adequately three years later.     

Chronic hypoglycaemia in a hunting dog clue to secondary hypoadrenocorticism

A six-year-old neutered female pointer was referred for evaluation of seizures that occurred only in association with exercise. A tenacious ocular discharge was also evident and tear production was decreased bilaterally. Diagnostic testing revealed severe hypoglycaemia caused by secondary hypoadrenocorticism. Treatment was instituted with prednisone (5 mg, orally, once daily) and the seizures ceased. Tear production returned to normal without additional treatment. Glucocorticoid deficiency should be considered a cause of hypoglycaemic seizures once other, more common, causes have been ruled out.     

Parapituitary meningioma in a dog with pituitary-dependent hyperadrenocorticism

A dog with constitutional and cutaneous signs of hyperadrenocorticism had central visual impairment caused by an intracranial mass. Irradiation of the presumed pituitary mass did not improve the dog's condition. At necropsy, the intracranial mass was not of pituitary origin, but rather, was a parapituitary meningioma.     

Mycobacterium goodii infection in a dog with concurrent hyperadrenocorticism

Abstract A 9-year-old Boston terrier was diagnosed with multifocal, nodular panniculitis caused by an organism belonging to the Mycobacterium smegmatis group by histological evaluation and bacteriological identification. The mycobacterial species was identified by direct gene sequence analysis and confirmed to be Mycobacterium goodii. Treatment using doxycycline and ciprofloxacin was successfully implemented for the mycobacterial panniculitis over a period of 9 months. Concurrent pituitary-dependent hyperadrenocorticism (Cushing's disease) was also identified using routine diagnostic methods and mitotane therapy was implemented. There was follow-up for 14 months after cessation of antimicrobial therapy with no recurrence of mycobacterial infection. Although cutaneous infections are frequently recognized as complications of canine pituitary-dependent hyperadrenocorticism, concurrent mycobacterial panniculitis due to any rapidly growing mycobacterium has not previously been reported. This is the first confirmed case of mycobacterial panniculitis due to M. goodii infection in a dog and also the first of any rapidly growing mycobacterial infection in a dog with concurrent endogenous Cushing's disease.     

Suspected spontaneous hyperadrenocorticism in a young experimental beagle dog

A 6-month-old female beagle dog, assigned to the low-dose group in a toxicity study, was evaluated for compound toxicity, and spontaneous hyperadrenocorticism was suspected. The animal had an externally apparent distended abdomen on clinical examination upon arrival. Pre-dose clinical pathology showed slightly higher erythroid parameters and stress leukogram on hematology; plasma biochemistry showed higher total protein, gamma-glutamyl transferase, total cholesterol, and triglyceride levels than the reference data. On necropsy, a prominent increase in adipose tissues of the subcutis and abdomen and increased weight of the adrenal gland and liver were observed. Histopathology revealed diffuse hyperplasia of adrenocortical cells in the zona fasciculata and reticularis, cortical atrophy of the thymus, and abundant glycogen accumulation in the hepatocytes. These findings were incidental and not test-substance-related. Electron microscopy of the adrenocortical cells in the zona fasciculata revealed decreased typical translucent lipid droplets, increased electron-dense lipid droplets, and abundant smooth endoplasmic reticulum and lysosomes. Additionally, increased numbers of various sizes and forms of mitochondria with tubular, vesicular, or lamellar cristae compared to that of normal animals were observed. These ultrastructural characteristics of the adrenocortical cells suggested hyperfunction. The pre-dose plasma cortisol levels were slightly higher than those of other females assigned to the toxicity study, while plasma adrenocorticotropic hormone levels were within the normal range. These findings indicate that hyperadrenocorticism is a possible cause of the systemic changes in this case.     

Reversible megaesophagus associated with atypical primary hypoadrenocorticism in a dog.

Megaesophagus, hypercalcemia, and eosinophilia associated with glucocorticoid deficiency were detected in a 5-year-old neutered female Standard Poodle with concurrent hypothyroidism. Clinical and biochemical abnormalities resolved with glucocorticoid replacement treatment, and the dog was normal 29 months after diagnosis. The dog's breed and sex and the existence of a second endocrinopathy supported an underlying immunologic disorder.     

Myopathy associated with hyperadrenocorticism in the dog

Naturally occurring or iatrogenic hyperadrenocorticism was associated with myopathy in six dogs. One dog had muscle weakness and muscle atrophy but normal electromyographic findings. Five dogs had muscle stiffness, proximal appendicular muscle enlargement, and myotonic discharges on electromyography. Histologic, electron microscopic, and histochemical findings in the musculature of dogs that were examined were characteristic of noninflammatory degenerative myopathy. Clinical signs of the myopathy improved to varying degrees in five dogs that were treated for the hyperadrenocorticism.     

Glucocorticoid-dependent hypoadrenocorticism with thrombocytopenia and neutropenia mimicking sepsis in a Labrador retriever dog

Glucocorticoid-deficient hypoadrenocorticism (GDH) with immune-mediated-neutropenia (IMN) and -thrombocytopenia (IMT) were diagnosed in a 3-year-old Labrador retriever dog. Glucocorticoid-deficient hypoadrenocorticism is rare and diagnostically challenging as clinical signs and laboratory abnormalities are often nonspecific. Immune-mediated cytopenias and other autoimmune disorders, as part of an autoimmune polyglandular syndrome have been reported with hypoadrenocorticism in humans. This is the first reported case of hypoadrenocorticism and bicytopenia in a dog.     

Adrenal necrosis in a dog receiving trilostane for the treatment of hyperadrenocorticism

Clinical and biochemical changes suggestive of hypoadrenocorticism were observed in a 10-year-old male neutered Staffordshire bull terrier shortly after beginning therapy with trilostane for the treatment of hyperadrenocorticism. The dog's condition was stabilised with intravenous fluids, fludrocortisone and prednisolone. An exploratory laparotomy and excisional biopsy of the left adrenal gland were performed. Histopathological analysis showed adrenal cortical necrosis with reactive inflammation and fibrosis. Trilostane is a reversible inhibitor of steroid synthesis and this complication has not been reported previously. Clinicians should be aware that trilostane therapy may result in adrenal necrosis but that prompt treatment might correct a life-threatening situation.