Steroid hepatopathy pathogenesis

Idiopathic refers to a condition which has an unknown cause. the diagnosis is often seen in older dogs that are not on steroids or who are not suffering from  a disease related to chronic stress.  These conditions appear similar to liver disorders that are seen when a dog is on steroids. There is also an absence of lab tests which indicate a problem such as Cushing’s disease or other chronic disorder.  Dogs receiving this diagnosis usually have elevated levels of the liver enzyme ALP as well as abnormal concentrations of hormones such as progesterone, estradiol DHEAS-S or Hydroxy-progesterone.

There are several well-recognized forms of vascular injury to the liver, including Budd-Chiari syndrome, hepatic sinusoidal obstruction syndrome, passive congestion due to heart failure, hepatic infarction, and ischemic hepatitis. Congestive hepatopathy refers to hepatic manifestations attributable to passive hepatic congestion, as occurs in patients with right-sided heart failure. Passive congestion often coexists with reduced cardiac output, making their relative contributions to hepatic injury intertwined. (See "Pathogenesis of liver injury in circulatory failure" .)

Zycortal® (Dechra Veterinary Products) is indicated for replacement therapy for mineralocorticoid deficiency in dogs with primary hypoadrenocorticism.  Zycortal contains desoxycortone pivalate (DOCP) – an aldosterone analogue with purely mineralocorticoid effect.  Zycortal is available as a prolonged-release suspension for subcutaneous injection and the dosing interval is approximately 25 days.  The exact dose to be given and the interval between treatments depend on the dog’s clinical response as well as sodium and potassium levels.  A glucocorticoid (. prednisolone) is also needed daily to replace the missing cortisol.  To obtain a Monitoring and Dose Adjustment Flowchart, or for further advice, contact Dechra by e-mailing [email protected]

Reported are the clinical and pathologic features of glycogenic hepatopathy, a pathologic overloading of hepatocytes with glycogen that is associated with poorly controlled diabetes mellitus. Fourteen cases were studied by stains, including hematoxylin and eosin, trichrome, periodic acid-Schiff, and periodic acid-Schiff with diastase. Ultrastructural analysis was performed in 2 cases. Medical records were reviewed for clinical presentations, laboratory findings, and clinical outcomes. The individuals ranged from 8 to 25 years of age. All had type I diabetes mellitus with poor glycemic control. The clinical presentations included hepatomegaly, abdominal pain, and elevated transaminases (range, 50-1600 IU/L). The transaminases were dramatically elevated in 3 cases to greater than 10 times the upper limit of normal. All biopsies showed diffusely pale staining hepatocytes on hematoxylin and eosin stains, with excessive glycogen accumulation demonstrated by periodic acid-Schiff stains. Ultrastructural examination revealed marked glycogen accumulation in the cytoplasm and nuclei. Most cases showed no evidence for fatty liver disease: steatosis was absent in 12 of 14 cases, simple steatosis was seen in 1 of 14 cases, and mild steatohepatitis was present in 1 of 14 cases. Mallory hyaline was absent in all cases, acidophil bodies were only rarely seen, and inflammation was absent or minimally present. Fibrosis was typically absent, with only 2 cases demonstrating focal mild fibrosis. Three patients had adequate follow-up and demonstrated improvement of liver enzyme levels with control of blood glucose. We conclude that glycogenic hepatopathy can cause hepatomegaly and significant transaminase elevations in individuals with type I diabetes mellitus. The pathology is distinct from steatohepatitis.

Steroid hepatopathy pathogenesis

steroid hepatopathy pathogenesis

Reported are the clinical and pathologic features of glycogenic hepatopathy, a pathologic overloading of hepatocytes with glycogen that is associated with poorly controlled diabetes mellitus. Fourteen cases were studied by stains, including hematoxylin and eosin, trichrome, periodic acid-Schiff, and periodic acid-Schiff with diastase. Ultrastructural analysis was performed in 2 cases. Medical records were reviewed for clinical presentations, laboratory findings, and clinical outcomes. The individuals ranged from 8 to 25 years of age. All had type I diabetes mellitus with poor glycemic control. The clinical presentations included hepatomegaly, abdominal pain, and elevated transaminases (range, 50-1600 IU/L). The transaminases were dramatically elevated in 3 cases to greater than 10 times the upper limit of normal. All biopsies showed diffusely pale staining hepatocytes on hematoxylin and eosin stains, with excessive glycogen accumulation demonstrated by periodic acid-Schiff stains. Ultrastructural examination revealed marked glycogen accumulation in the cytoplasm and nuclei. Most cases showed no evidence for fatty liver disease: steatosis was absent in 12 of 14 cases, simple steatosis was seen in 1 of 14 cases, and mild steatohepatitis was present in 1 of 14 cases. Mallory hyaline was absent in all cases, acidophil bodies were only rarely seen, and inflammation was absent or minimally present. Fibrosis was typically absent, with only 2 cases demonstrating focal mild fibrosis. Three patients had adequate follow-up and demonstrated improvement of liver enzyme levels with control of blood glucose. We conclude that glycogenic hepatopathy can cause hepatomegaly and significant transaminase elevations in individuals with type I diabetes mellitus. The pathology is distinct from steatohepatitis.

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