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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatopathy associated with glucocorticoid therapy or with naturally occurring hyperadrenocorticism was detected retrospectively in hepatic biopsy specimens from 22 of 60 dogs, by histologic review. The hepatopathy was characterized by centrilobular vacuolization, perivacuolar glycogen accumulation within hepatocytes, and focal centrilobular necrosis. The predominant clinical findings were hepatomegaly, increased serum enzyme activity associated with hepatic disease, and increased bromsulphalein retention. The hepatopathy appeared to be reversible.
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PMID:A retrospective study of probable glucocorticoid-induced hepatopathy in dogs. 84 10

A 7-year-old adult male ferret had progressive hair loss that was bilaterally symmetric. Also clinically evident were severe dehydration, polydipsia, muffled heart sounds, weak femoral pulses, hepatomegaly, lethargy, weakness, temporal muscular atrophy, dyspnea, and weakness. The blood profile of the ferret indicated profound leukopenia, eosinopenia, and high phosphorus, BUN, creatinine, and potassium concentrations, as well as high aspartate transaminase activity; the albumin concentration was low. The serum cortisol concentration was 8.1 micrograms/dl. Necropsy and histologic findings confirmed a diagnosis of hyperadrenocorticism, complicated by dilatative cardiomyopathy, chronic active hepatitis, and renal disease.
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PMID:Hyperadrenocorticism in a ferret. 365 2

Of cases of hyperadrenocorticism in small animals 80-85% are the result of adrenocortical hyperplasia. Middle-aged or older Poodles, Dachshunds, Boston Terriers and Boxers are most commonly affected, and cats rarely. Clinical signs include polydipsia, polyuria, alopecia, abdominal distension, lethargy, weakness, hepatomegaly, calcinosis cutis, testicular atrophy and anestrus. Hematologic and biochemical changes may include neutrophilia, lymphopenia, monocytosis, eosinopenia, increased blood levels of alkaline phosphatase, SGPT, cholesterol, Na and glucose, and decreased K and T4 levels. The high-dosage dexamethasone suppression test helps differentiate pituitary-dependent hyperadrenocorticism from that caused by adrenal tumors. The low-dosage dexamethasone suppression test, determination of plasma ACTH levels, and ACTH response test are additional diagnostic aids in the diagnosis of Cushing's disease. Medical treatment involves oral use of mitotane (o,p'-DDD) at 50 mg/kg/day for 7 days and prednisone or prednisolone at 0.05 mg/kg/day. Hypophysectomy has been used with only 5% mortality in cases of pituitary-dependent hyperadrenocorticism. Adrenalectomy is indicated in cases of adrenal neoplasia.
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PMID:Diseases of the adrenal cortex of dogs and cats. 633 May 21

Concurrent diabetes mellitus and hyperadrenocorticism were diagnosed in 30 dogs over a 2-year period. Clinical signs included polyuria, hepatomegaly, polyphagia, abdominal distension, truncal alopecia, anorexia, and vomiting. Because of the similar clinical and laboratory findings for hyperadrenocorticism and diabetes mellitus, hyperadrenocorticism was initially overlooked in some dogs. Insulin resistance, characterized by high daily insulin requirements, developed in the diabetic dogs with untreated hyperadrenocorticism. Therapy with o,p'-DDD resulted in precipitous declines in insulin requirements. By lowering the dosage of o,p'-DDD and supplementing with glucocorticoids during the o,p'-DDD loading period, serious hypoglycemia was avoided. Control of coexisting hyperadrenocorticism lessened the severity of the diabetes mellitus, but insulin therapy remained a necessity in all dogs.
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PMID:Diagnosis and management of concurrent diabetes mellitus and hyperadrenocorticism in thirty dogs. 700 30

Varying degrees of respiratory distress developed in 3 dogs in which hyperadrenocorticism was diagnosed. The respiratory distress was attributed to pulmonary artery thrombosis. Radiography revealed pleural effusion, increased diameter and blunting of the pulmonary arteries, lack of perfusion of the obstructed pulmonary vasculature, and overperfusion of the unobstructed pulmonary vasculature. Thrombosis was confirmed by nonselective angiocardiography in each case. In 1 case, selective angiocardiography showed marked reduction of the transit time of contrast medium from the right atrium to the aorta. Hypertension proximal to the site of thrombosis was confirmed in 2 cases by showing increases in the right ventricular systolic pressures (80 mm of Hg in one case and 54 mm of Hg in the other case). In 3 cases, there was moderate hypoxemia with hypocapnia, suggesting a ventilation-perfusion mismatch. Clinical findings other than respiratory distress included hepatomegaly, ventral edema, orthopnea, and a jugular pulse. Pulmonary artery thrombosis, as it occurred in these 3 cases, was compared with the disease in man. It was concluded that pulmonary artery thrombosis should be suspected in cases of intractable dyspnea, right-sided heart failure of unexplained origin, and acute unexplainable death.
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PMID:Pulmonary artery thrombosis in three dogs with hyperadrenocorticism. 723 99

Abnormal liver tests, right upper quadrant pain and hepatomegaly occurring in an obese or in a diabetic patient may point to the presence of fat or of glycogen accumulation in the liver parenchymal cells. Marked hepatomegaly due to cytoplasmic glycogen deposition is mainly found in poorly controlled insulin-dependent diabetic patients. If accompanied by cushingoid features, growth retardation and by delayed puberty, a diagnosis of Mauriac syndrome can be made. Hyperglycaemia, insulin administration and increased concentrations of the counterregulatory hormone cortisol may all play a role in the glycogen deposition by their concerted actions on the glycogen phosphorylase and synthase enzymes, promoting the accumulation of glycogen. Hypercortisolism may be responsible for growth retardation and delayed puberty in Mauriac patients. Regression of hepatomegaly and of the associated clinical characteristics may be obtained by a better metabolic control due to the administration of long-acting insulin and the change from single to twice daily injections. Fatty liver is rare in insulin-dependent diabetic patients and is indicative of a poor diabetic control. This process is quickly reversible by adequate insulin treatment. Steatosis is frequently found in maturity-onset diabetics and in obese patients. The pathogenetic mechanisms leading to the accumulation of triglycerides and of fatty acids in the hepatocytes can easily be understood from the normal cycling of fatty acids between the adiopose tissue and the liver. Histologic features of nonalcoholic steatohepatitis can also be found in obese and in diabetic patients. Steatohepatitis may rarely evolve into cirrhosis. In general, there is no correlation between the degree of the biochemical alterations and the severity of the histological findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver disturbances in obesity and diabetes mellitus. 858 Oct 74

The case records of six cats with hyperadrenocorticism presented to the Department of Clinical Veterinary Medicine, University of Cambridge, over an 11-year period were reviewed. Signalment and clinical signs were similar to previous reports but, in contrast to other reports, only three cats had diabetes mellitus on presentation. Abdominal radiographs revealed an adrenal mass in one case, obesity in all cases but no hepatomegaly. The adrenal glands were identified ultrasonographically in three out of six cases. Clinicopathological findings were non-specific. The diabetic cats had a significantly lower serum potassium concentration than the non-diabetic cats (P < 0.05). Results of adrenocorticotrophic hormone (ACTH) stimulation tests were supportive of a diagnosis of hyperadrenocorticism in the five cats in which they were performed. Five cats had pituitary-dependent hyperadrenocorticism (PDH) and one had an adrenal tumour. Differentiation between the two forms of hyperadrenocorticism was possible preoperatively in five out of six cats. Adrenal histopathology confirmed hyperplasia in four cats and adenocarcinoma in one cat. Three cats with PDH underwent bilateral adrenalectomy and two of these cats had low, flat ACTH stimulation tests postoperatively and survived for significant periods. The cat with an adrenal tumour underwent partial unilateral adrenalectomy, maintained a positive ACTH stimulation test postoperatively and was euthanased one week after surgery.
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PMID:Hyperadrenocorticism in six cats. 957 59

The specificity of conventional radiography in assessing canine hyperadrenocorticism was evaluated by comparing the Incidence of related radiographic findings in 24 hyperadrenocorticoid, 15 diabetic and 20 hypothyroid dogs. Hyperadrenocorticoid dogs showed significantly more perihilar bronchial mineralisation than other groups. There was no significant variation between the disease groups with respect to obesity, hepatomegaly, contour of the caudoventral hepatic margin, peripheral bronchial mineralisation or osteopenia. Adrenal mineralisation and calcinosis cutis were rare findings observed only in hyperadrenocorticoid dogs. The effect of obesity on the radiographic appearance of bone was studied using a dissected lumbar spine from a canine cadaver. An osteopenic effect could be demonstrated by superimposition of a 10 cm-thick fat block. The low specificity of almost all common signs in canine hyperadrenocorticism and the low incidence of characteristic findings demonstrate the limited potential of radiography in assessing this condition. Radiographic assessment of bone density is unreliable because of artefactual osteopenic effects of high kVp settings necessary in obese dogs.
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PMID:Osteopenia and other radiographic signs in canine hyperadrenocorticism. 1110 87

Laparoscopic adrenalectomy is gaining widespread acceptance. To evaluate this new approach, the authors evaluated 40 laparoscopic adrenalectomies. Between June 1995 and February 1999, 40 lateral transperitoneal laparoscopic adrenalectomies were performed in 38 patients. The clinical diagnoses were primary aldosteronism (20 patients), Cushing adenoma (2 patients), cortical hyperplasia with hypercortisolism (2 patients), pheochromocytoma (8 patients), and other conditions (6 patients). There were no deaths or subsequent procedures. The mean operative time was 121 minutes. One procedure performed for hypercortisolism was converted to open adrenalectomy because of hepatomegaly and postoperative adhesions. Seven patients had complications: one patient with small pulmonary embolus with transient dyspnea, one patient with pneumothorax, two patients with postoperative bleeding, two patients with prolonged pain at a trocar wound, and one patient with a urinary tract infection. Lateral transperitoneal laparoscopic adrenalectomy seems to be a safe and effective minimally invasive approach for adrenal surgery, and the authors consider it to be the standard surgical procedure for benign adrenal tumors.
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PMID:An institutional experience with 40 first lateral transperitoneal laparoscopic adrenalectomies. 1114 14

A 13-year-old, crossbreed dog presented with a history of recent onset polydipsia, progressive lethargy, weakness and reduced appetite. Blood tests showed raised concentrations of alkaline phosphatase and alanine aminotransferase with marginally low serum potassium. There was a leucocytosis with a mature neutrophilia and no eosinophils. Endocrine tests showed a normal aldosterone concentration and an exaggerated adrenocorticotropic hormone (ACTH) stimulation test, consistent with a diagnosis of hyperadrenocorticism (HAC). A diagnosis of adrenal-dependent HAC was made, based on the presence of a calcified mass involving the left adrenal gland, and hepatomegaly, on radiography and ultrasonography. The owners declined surgical adrenalectomy. Medical management with trilostane rapidly improved the clinical signs and normalised the serum chemistry. ACTH stimulation tests showed an improvement in post-ACTH cortisol concentrations and were used to make dose adjustments where necessary. At the time of writing, no adverse side effects had been seen and the dog remained well after 80 weeks of treatment.
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PMID:Trilostane treatment of a dog with functional adrenocortical neoplasia. 1265 28


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