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538    PART IV   Hepatobiliary and Exocrine Pancreatic Disorders


            of acute-phase proteins in electrophoresis indicates severe   Serum Glucose Concentration
            hepatic dysfunction with a poor prognosis, whereas hypoal-  Hypoglycemia is an unusual event associated with hepatobi-
  VetBooks.ir  buminemia combined with normal or elevated acute-phase   liary disease in dogs and especially in cats. There is a lost
                                                                 ability to maintain normal serum glucose concentrations in
            protein levels indicates a good prognosis. Hypoalbuminemia
            of any cause is unusual in cats, except in those with nephrotic
                                                                 disease  when  20%  of  the  functional  hepatic  mass  or  less
            syndrome. When interpreting serum protein concentrations,   animals with acquired chronic progressive hepatobiliary
            the clinician should remember that total protein values for   remains. This inability to maintain a normal serum glucose
            young cats and dogs are lower than those for adults, and   concentration is presumably caused by the loss of hepato-
            puppy serum albumin concentration is similar to that in   cytes with functioning gluconeogenic and glycolytic enzyme
            adults, whereas kitten serum albumin concentration is lower   systems and impaired hepatic degradation of insulin. Hepa-
            than that in adult cats.                             tocyte senescence may also play a role. Hypoglycemia is
                                                                 often a near-terminal event in dogs with chronic progressive
            Serum Urea Nitrogen Concentration                    hepatobiliary disease. In striking contrast is the frequent
            The formation of urea as a means of detoxifying ammonia   observation of hypoglycemia in dogs with congenital PSS,
            derived from intestinal sources takes place only in the liver.   particularly small-breed dogs. Hypoglycemia in patients
            Despite this apparent advantage as a specific measure of   with PSS has been suggested to be the result of an increase
            hepatic function, serum urea concentration is commonly   in circulating insulin concentration caused by reduced first-
            affected by several nonhepatic factors; the capability of the   pass metabolism in the liver, as observed in humans, but a
            liver to detoxify urea is so great that it is not noticeably   more recent study showed normal to low insulin concentra-
            reduced until severe, extensive end-stage liver disease has   tion  in  dogs  with  PSS  and  hypoglycemia,  which  did  not
            developed. Prolonged, restricted protein intake because of   support this hypothesis, so the cause remains unknown.
            complete anorexia or intentional reduction in protein intake   Hypoglycemia is also common as a paraneoplastic syndrome
            for therapeutic purposes (e.g., chronic kidney disease; urate,   in dogs with large hepatocellular carcinomas and can be
            cystine, or struvite urolithiasis) is the most common cause   associated with the production of insulin-like growth factor
            of low blood urea nitrogen (BUN) concentration. Prior fluid   by the tumor. In either case, if hypoglycemia is identified and
            therapy and/or marked polydipsia or polyuria of nonrenal   confirmed by repeating the test using sodium fluoride, if
            causes will also result in a decrease in the BUN level. As   necessary, and if nonhepatic causes (e.g., functional hypo-
            always, reference ranges should be considered for each   glycemia, sepsis, insulinoma or other neoplasm producing
            species when interpreting BUN values. For example, a BUN   an insulin-like substance, or Addison disease; see Chapter
            concentration of 12 mg/dL is well within normal limits for   50) are excluded, a primary hepatic tumor (e.g., hepatocel-
            dogs but is subnormal for cats. If low BUN levels are noted   lular carcinoma), PSS, or severe generalized hepatopathy is
            in a cat or dog with normal water intake and a good appetite   suspected.
            for a diet with the appropriate protein content for the species
            (on a dry matter basis, 22% for dogs and 35%-40% for cats),
            the possibility of hepatic inability to convert ammonia to   DIAGNOSTIC TESTS TO ASSESS
            urea or portosystemic shunting of ammonia away from the   PANCREATIC INFLAMMATION
            liver should be investigated.                        AND FUNCTION
                                                                 Specific Tests of Pancreatic Inflammation
            Serum Cholesterol Concentration                      The most specific tests for the pancreas are the catalytic
            Total cholesterol concentration is included in serum chem-  assays for amylase and lipase and the immunoassays for
            istry profiles by many commercial laboratories but affords   trypsin-like immunoreactivity (TLI) and pancreatic lipase
            useful information for only a limited number of hepatobili-  immunoreactivity (PLI). Catalytic assays rely on the ability
            ary diseases. High total cholesterol values are observed in   of the molecule to catalyze a reaction in vivo and thus rely
            cats and dogs with severe intrahepatic cholestasis involving   on the presence of active enzyme; however, they are not
            bile ducts or EBDO because of impaired excretion of free   species-specific. The sensitivity and specificity of the tradi-
            cholesterol into the bile and subsequent regurgitation into   tional catalytic assays in dogs are relatively poor, particularly
            the  blood. Hypocholesterolemia has  been  documented in   for amylase, and in cats, traditional amylase and lipase are
            dogs with chronic severe hepatocellular disease and fre-  of questionable diagnostic value. However, recently a new
            quently in cats and dogs with congenital PSS. It has been   lipase assay has been developed, which appears to be
            speculated that hypocholesterolemia is a sign of markedly   more sensitive and specific than the traditional lipase and
            altered intestinal absorption of (and increased use of) cho-  also shows very good agreement with PLI. This is the
            lesterol for bile acid synthesis when the enterohepatic recir-  1,2-o-dilauryl-rac-glycero glutaric acid-(6′-methylresorufin)
            culation of bile acids is disturbed, as occurs with PSS. In   ester (DGGR) lipase assay. The enzyme and substrate inter-
            other hepatobiliary diseases of cats and dogs, the total cho-  actions in this assay are more selective than with the
            lesterol values vary considerably. Normal values in 4-week-  traditional multistep colorimetric lipase assay that uses
            old kittens are higher than those for adults; 8-week-old   1,2-diglyceride (1,2-DiG) as the substrate. It is proposed
            puppy reference ranges are the same as those for adults.  that, with the new assay, hydrolysis with other lipases and
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