Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dogs with portosystemic encephalopathy (PSE) are known to develop pituitary-dependent hyperadrenocorticism, but there have been no reports on the plasma protein binding of cortisol in these dogs. Since the liver is involved in the synthesis of corticosteroid-binding globulin (CBG) and other transport proteins for cortisol, the binding characteristics of these proteins and thus the biologically-active free fraction of cortisol might be altered in dogs with PSE. We investigated the total concentration of cortisol and the free fraction and the free cortisol concentration in plasma of thirty-two dogs with PSE due to inherited portosystemic shunts or chronic active hepatitis with cirrhosis. We found a significantly higher free fraction (14.7 +/- 5.8%, P < 0.0001) and free cortisol concentration (26.3 +/- 23.1 nM, P < 0.001) in these dogs than in healthy controls (8.2 +/- 2.3% and 9.2 +/- 7.2 nM, respectively). Moreover, basal concentrations of total cortisol in the dogs with PSE were higher than in the healthy controls (190 +/- 146 nM v. 107 +/- 65, P < 0.01). The per cent free cortisol in plasma was not significantly correlated with the concentration of albumin or the total cortisol in plasma. We conclude that there is decreased binding of cortisol in plasma of dogs with PSE due to decreased hepatic synthesis of cortisol binding proteins. The presence of increased concentrations of free cortisol in these dogs indicates that their basal pituitary-adrenocortical activity was increased, probably due to aberrant neurotransmission in brain centers associated with pituitary function, as a result of hepatic encephalopathy.
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PMID:Increased free cortisol in plasma of dogs with portosystemic encephalopathy (PSE). 782 25

The aim of this study was to investigate whether hypercortisolism in dogs with congenital portosystemic shunts disappeared after surgical closure of the shunts concomitantly with recovery from hepatic encephalopathy. We examined 22 dogs before and four weeks after partial surgical closure of a single, large congenital portosystemic shunt (PSS). Parameters measured to characterise the basal activity of the pituitary-adrenal axis were the cortisol:creatinine (c/c) ratio in home-sampled urine and total and free cortisol in plasma. The binding characteristics of cortisol binding globulin (CBG) in pooled pre- and postoperative plasma were also determined. Ammonia and bile acid concentrations were measured in plasma to characterise the liver perfusion and function. Clinical symptoms relevant to liver function, cortisol excess, and hepatic encephalopathy were recorded semiquantitatively using a standardized questionnaire. The dogs had hypercortisolism before surgery, which had normalized four weeks later. The pre- and postoperative concentrations (means +/- SEM) were, respectively, 238+/-45 nM and 126+/-19 nM for total cortisol, 15.5+/-2.6 nM and 8.4+/-1.3 nM for free cortisol in plasma, 13.4+/-4.3 x 10(-6) and 3.9+/-0.4 x 10(-6) for c/c in urine. The pre- and postoperative Bmax values of CBG were 41 and 79, and Kd values were 3.8 and 5.5. The concentrations of ammonia were 217+/-23 microM and 32+/-3.1 microM, and of bile acids 1 10+/-33 and 11.1+/-2.0 microM, respectively. We conclude that there is a close relation between portosystemic encephalopathy and hypercortisolism in dogs with PSS and that both deviations resolve completely within four weeks of closure of the shunt.
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PMID:Fast resolution of hypercortisolism in dogs with portosystemic encephalopathy after surgical shunt closure. 1008 14

Cushing syndrome (CS) occurs rarely in children. The clinical presentation of CS varies according to the extent and duration of glucocorticoid excess, and urolithiasis is one of the common complications of CS. We report the first case of a patient with CS associated with acute kidney injury (AKI) due to urolithiasis. A 6-year-old boy came to the emergency room with seizure. On physical examination, he had clinical features of CS and high blood pressure. Brain computerized tomography (CT) suggested posterior reversible encephalopathy syndrome due to hypertension. On the evaluation of hypertension, the laboratory tests suggested adrenocortical tumor, but the abdominal CT suggested pheochromocytoma. During further evaluation, his condition deteriorated with AKI due to bilateral ureteral stones, therefore he underwent continuous renal replacement therapy in the intensive care unit. After controlling hypercortisolism with etomidate and performing ureteral stent indwelling, resection of an adrenal mass was performed, and the mass was histologically confirmed as an adrenocortical adenoma. We review the clinical manifestations and diagnosis, and management of CS associated with urolithiasis and AKI. Early recognition and careful monitoring of urolithiasis in CS are important to avoid severe complications of urolithiasis.
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PMID:Cushing syndrome with acute kidney injury due to ureteral stones in a 6-year-old boy. 3287 46