CANINE MEDICINE tively confirm VH . Ultrasonographic features reflect hepatic parenchymal remodelling and progression of non-degenerative to degenerative VH with formation of regenerative nodules sometimes associated with dysplastic hepatocellular foci . It is possible that these foci precede the development of hepatic carcinoma as occurs in humans .
Approximately 40 % of Scottish terriers with VH have a broad range of historical , physical , and clinic-pathologic features consistent with typical hyperadrenocorticism . Finding elevated serum ALP activity or VH in a Scottish terrier may thus lead to adrenal function testing that may show an exaggerated adrenal hormone production , which then may be interpreted to represent typical or atypical hyperadrenocorticism . However , one study in 13 Scottish terriers undergoing conventional therapy for hyperadrenocorticism showed no positive outcomes . All treatments were either ineffective or resulted in adverse reactions , such as glucocorticoid insufficiency , hepatotoxicity , and even death . The apparent frailty of the Scottish terrier with VH treated with conventional therapy for hyperadrenocorticism remains unexplained .
As the underlying metabolic abnormality causing VH in the Scottish terrier may be associated with sex hormone – related adrenal gland hyperactivity , treatment with trilostane may thus be ill-advised , considering that studies in dogs have shown that trilostane fosters accumulation of sex hormone precursors , fails to control overproduction of androstenedione , and leads to adrenomegaly . Adrenal gland hyperactivity associated with VH in the Scottish terrier predominantly involves sex hormones ( most notably progesterone and androstenedione ) and may be accompanied by overt adrenomegaly ( unilateral or bilateral ). Despite adrenomegaly , various studies have shown that cortisol assessments ( baseline and post-ACTH stimulation testing , low-dose dexamethasone suppression test , urine cortisol-to-creatinine ratio ) inconsistently verify typical hyperadrenocorticism .
It remains possible that adrenal hyperplasia secondary to chronic stress or illness can account for the increased serum concentrations of cortisol and sex hormones . However , it is plausible that the adrenal gland hyperactivity and associated VH reflect a breed-related genetic disorder affecting adrenal steroid genesis that leads to ALP induction , hepatocellular glycogen accumulation , progressive VH , and ultimately formation of hepatic carcinoma in some dogs . In some Scotties , VH is not always benign , as it may rapidly progress to liver failure with development of small nodular liver , portal hypertension , and ascites . Yet , in other dogs with VH , chronically elevated serum ALP activity ( 3-20 fold ) can persist for > 10 years without apparent clinical deterioration .
The magnitude of elevated serum ALP and ALT activities does not differentiate between dogs with VH with and without hepatic carcinoma and does not predict early death from hepatic failure . Consequently , considering the variable age of syndrome onset and rate of progression , it is impossible to predict relative risk for hepatic failure or development of hepatic carcinoma without sequential patient monitoring .
In conclusion , the Scottish terrier has a breed-specific VH containing glycogen and moderately to severely elevated serum ALP activity . Affected dogs generally have no clinical signs ; show elevated ALP activity ; and increases in one or more non-cortisol steroid hormones can be demonstrated . It is thus recommended that Scottish terriers with elevated serum ALP activity undergo biannual monitoring of serum liver enzyme activities and liver function as well as a yearly hepatic ultrasonographic examination .
Increased surveillance frequency is advised for dogs with sudden marked increases in serum ALP activity or transitioning to a nodular hepatopathy on ultrasonographic evaluation . This strategy would allow early detection of hepatic mass lesions likely to represent surgically excisable hepatic carcinomas and recognition of a subclinical gallbladder mucocele that may allow for uncomplicated cholecystectomy .
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