Complications to thyroid surgery are not uncommon. The high frequency of hypocalcaemia treated with vitamin D after 6 months is a cause of concern.

This investigation was undertaken to determine the possible role of growth hormone (GH) in the hormonal regulation of hepatic low density lipoprotein (LDL) receptor expression. Treatment of normal rats with estrogen (ethynylestradiol, 5 mg/kg per day) increased the number of hepatic LDL receptors, and the LDL receptor mRNA levels were increased 2.4-fold. However, when hypophysectomized rats were treated with estrogen, the hepatic LDL receptor number and the mRNA levels only increased slightly. Treatment with GH was important to restore the induction of hepatic LDL receptors in hypophysectomized estrogen-treated rats. Further, the hypocholesterolemic effect of estrogen was abolished in hypophysectomized rats, and GH reversed this effect. To assess the effect of GH in humans, hepatic LDL receptor binding activity was determined in liver biopsy specimens from gallstone pitients pretreated with GH (12 international units/day) prior to operation. GH administration induced hepatic LDL receptors -2-fold, and this was accompanied by a 25% decrease in serum cholesterol. The LDL receptor stimulation caused by GH treatment was of similar magnitude as that observed upon 3 weeks of treatment with an established hypolipidemic drug (pravastatin or simvastatin). The data show that GH has an important role in the regulation of hepatic LDL receptors and suggest that GH secretion may be important for the control of plasma LDL levels in humans.The activity of low density lipoprotein (LDL) receptors in the liver constitutes a major mechanism by which dietary and hormonal agents may regulate plasma cholesterol levels (1, 2). Thus, by controlling LDL catabolism, the number of hepatic LDL receptors has a direct influence on the plasma LDL level. The molecular regulation of LDL receptors by cholesterol through end-product inhibition has been elucidated in detail (3, 4). In contrast, our understanding of hormonal regulation of hepatic LDL receptors is fragmentary.A dramatic stimulation of the hepatic LDL receptor activity occurs during treatment with pharmacological doses of estrogen (5), and this is paralleled by a markedly increased clearance of plasma LDL concomitant with a profound decrease in plasma cholesterol (6-9). The physiological relevance of the estrogen-stimulated hepatic LDL receptor expression is unclear, but it has been shown to be coupled to an elevated LDL receptor mRNA level (10). The strong stimulatory effect of estrogens on LDL receptors in the liver in vivo has been difficult to reproduce in cell culture (11,12), indicating that the mechanism for stimulation may be partly indirect. An indirect action is also supported by the previous observation that estrogen failed to decrease plasma cholesterol when given to hypophysectomized (Hx) rats (13). The induction of hepatic LDL receptors by estrogen administration is probably the most efficient treatment available, and it is therefore of major importance to understand the mechanism(s) responsible for the stimulatory effect of this hormone on hepatic LDL receptors....

Inhibition of hepatic HMG-CoA reductase by pravastatin results in an increased expression of hepatic LDL receptors, which explains the lowered plasma levels of LDL cholesterol.

Circulating levels of 7cz-hydroxy-4-cholesten-3-one have been compared with activities of the rate-limiting enzyme in bile acid synthesis. microsomal cholesterol 7l-hydroxylase, measured in liver biopsies obtained from patients undergoing surgery for gallstone disease. Some patients were treated with cholcstyraminc or bile acids prior to operation in order to alter the feed-back inhibition of the enzyme. The levels of the sterol were similar in untreated patients and in patients treated with ursodeoxycholic acid (median concentration 17 and 13 nglml. respectively), and so were the activities of the enzyme (median activity 7.0 and 5.5 pmol/min/mg protein, respectively). The sterol levels and enzyme activities were significantly increased in patients treated with cholestyramine (91 ng/ml and 45 pmol/min/mg protein) and decreased in patients treated with chenodeoxycholic acid (< 2.0 ng/ml and 0.7 pmol/min/mg protein). There was a strong positive correlation (r=0.90, P