Mild increases in ALKP, GGT, and total bilirubin
indicate cholestasis. This is further supported by the 3+ bilirubinuria
evident on urinalysis. No evidence of hemolytic disease is apparent on
CBC data, making intrahepatic or posthepatic cholestasis most likely.
Two-fold increase in ALT and AST suggest
hepatocellular injury and leakage. Serum CPK concentration to rule out a
contribution from muscle tissue is not available. In hyperthyroidism,
increased circulating thyroid hormone concentrations are thought to
exert a toxic effect on hepatocytes, resulting in swelling and increased
leakage enzyme concentrations. Lipidosis (distention of hepatocytes with
lipid material) is also possible secondary to the increased mobilization
of body fat stores in catabolic hyperthyroid patients. Hepatocyte
swelling, via either mechanism, may contribute to the development of
intra-hepatic cholestasis via occlusion of canalicular structures.
Mild elevation in total protein is attributable to
mild increase in globulin concentration, and a low normal albumin
concentration. This pattern suggests inflammation/chronic antigenic
stimulation. Leukogram changes include only a slight mature neutrophilia,
which may be seen with chronic, mild, compensated inflammation, but are
far more commonly seen with physiologic stress. Dehydration should also
be considered and could be ruled out on physical examination. A
concentrated urine specific gravity would be compatible with
dehydration. In the face of dehydration, hypoalbuminemia may be a
problem (serum concentration will further decrease with rehydration).
Rule outs for hypoalbuminemia in this patient would have to include
renal loss, given the 3+ proteinuria seen on urinalysis. A urine protein
to creatinine ratio may be indicated to better quantitate urine protein
losses. Hypertension in hyperthyroid patients may result in proteinuria.
Slight hyponatremia and low normal chloride
concentration indicate that sodium and chloride are moving in parallel.
Increased renal losses are possible attributable to hypertension
secondary to hyperthyroidism (pressure diuresis).