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).