A randomized controlled trial comparing cholecystocholangiography with cystic duct cholangiography during laparoscopic cholecystectomy.

BACKGROUND: The rate of intraoperative cholangiography fell after the advent of laparoscopic cholecystectomy due to the perceived difficulty of cystic duct cannulation. It is suggested that cholecystocholangiography (CCC) is a valid and easier alternative. The present study compares cystic duct cholangiography (CDC) to CCC with evaluation of procedural time, success rate, image quality, cost and radiation exposure. METHODS: Patients undergoing laparoscopic cholecystectomy were randomized to CCC (n = 40) or CDC (n = 36). Details of operative times, radiation exposure, and use of disposable equipment were recorded prospectively. Cholangiograms were performed using image intensification and were scored from 0 to 6 according to adequacy of images. Data were analysed on an intention-to-treat basis with the chi-squared test, t-test or Fisher's exact test. RESULTS: The success rate for CDC was 100% and for CCC it was 72% (P = 0.0005). Patients with a failed CCC went on to have CDC for a success rate in the CCC arm of 92.5%. Comparing CDC to CCC, there was no significant difference in cost ($30.16 vs $33.36: P = 0.11), operative time (1 h 13 min vs 1 h 3 min; P = 0.19) or cholangiogram time (8 vs 9 min: P = 0.39). There was a significant difference in screening time (0:41 vs 1:33 min; P < 0.0001), adequate image quality (100 vs 72.5%, P = 0.0005) and procedure-related complications (0 vs 5; P = 0.03). CONCLUSIONS: A significant number of CCC fail. Successful CCC provides inferior image quality and greater radiation exposure. It provides no benefit in time or cost and cannot be recommended for operative cholangiography.

Growth hormone administration stimulates energy expenditure and extrathyroidal conversion of thyroxine to triiodothyronine in a dose-dependent manner and suppresses circadian thyrotrophin levels: studies in GH-deficient adults.

OBJECTIVE: The impact of exogenous GH on thyroid function remains controversial although most data add support to a stimulation of peripheral T4 to T3 conversion. For further elucidation we evaluated iodothyronine and circadian TSH levels in GH-deficient patients as part of a GH dose-response study. PATIENTS: Eight GH-deficient adults, who received stable T4 substitution due to central hypothyroidism; two patients, who were euthyroid without T4 supplementation were studied separately. DESIGN: All patients were initially studied after at least 4 weeks without GH followed by 3 consecutive 4-week periods in fixed order during which they received daily doses of 1, 2 and 4 IU of GH/m2 body surface area. The patients were hospitalized for 24 hours at the end of each period. MEASUREMENTS: Circulating total and free concentrations of T4 and T3, total rT3 and TSH were measured once at the end of each study period. Circadian TSH levels were recorded during the period without GH and during GH treatment with 2 IU GH. RESULTS: Highly significant GH dose-dependent increases in total and free T3 and a reduction in rT3 were observed. The T3/T4 ratio also increased with increasing GH dosages (P < 0.001). In seven patients subnormal T3 levels were recorded in the period off GH, despite T4 levels well within the normal range. Resting energy expenditure also increased and correlated with free T3 levels (r = 0.47, P < 0.05). The circadian TSH levels exhibited a significant nocturnal increase during the period without GH, whereas GH therapy significantly suppressed the TSH levels and blunted the circadian rhythm (mean TSH levels (mU/l) 0.546 +/- 0.246 (no GH) vs 0.066 +/- 0.031 (2 IU GH) (P < 0.05)). The two euthyroid non-T4 substituted patients exhibited qualitatively similar changes in all parameters. CONCLUSIONS: GH administration stimulated peripheral T4 to T3 conversion in a dose-dependent manner. Serum T3 levels were subnormal despite T4 substitution when the patients were off GH but normalized with GH therapy. Energy expenditure increased with GH and correlated with free T3 levels. GH caused a significant blunting of serum TSH. These findings suggest that GH plays a distinct role in the physiological regulation of thyroid function in general, and of peripheral T4 metabolism in particular.

Fuel metabolism, energy expenditure, and thyroid function in growth hormone-treated obese women: a double-blind placebo-controlled study.

Growth hormone (GH) promotes protein anabolism and lipolysis. Its effects on glucose metabolism include suppression of glucose oxidation and may be associated with insulin resistance. In addition, GH stimulates energy expenditure (EE) and peripheral thyroid hormone metabolism. GH secretion is reduced in obese patients, but whether this is of pathophysiological significance is incompletely understood. In a double-blind placebo-controlled crossover design, we studied the effects of GH administration (0.03 mg.kg ideal body weight [IBW]-1.d-1) on fuel metabolism, EE, and thyroid function in 10 obese women (age, 30.4 +/- 2.4 years; body mass index [BMI], 37.0 +/- 2.8 kg/m2, mean +/- SE) with a normal prestudy oral glucose tolerance test (OGTT). Each treatment period (GH or placebo) lasted 5 weeks, separated by a 5-week washout period. At the end of each treatment period, subjects were studied in the basal state (8:00 AM) and during a euglycemic glucose clamp including indirect calorimetry and isotopic measurement of glucose turnover. Lean body mass (LBM) was assessed at the end of each period by dual-energy x-ray absorptiometry. In the basal state, GH induced a significant increase in circulating levels of free fatty acids (FFA), glucose, insulin, and C-peptide. This was associated with a significant increase in resting EE (kcal/24 h, 1,934 +/- 92 placebo v 2,323 +/- 134 GH, P < .001), a decrease in the respiratory exchange ratio (RER), and increased rates of lipid oxidation (mg.kg LBM-1.min-1, 1.55 +/- 0.09 placebo v 2.20 +/- 0.13 GH, P < .01). GH increased the rate of total basal glucose turnover, whereas oxidative glucose disposal was significantly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Beneficial effects of GH replacement therapy in adults.

Growth hormone deficiency in adults is associated with psychosocial maladjustment, reduced muscle strength, and reduced exercise capacity. Body composition is significantly altered, with increased fat and decreased muscle volume as compared with healthy subjects. Kidney function is subnormal. Epidemiological data suggest premature mortality owing to cardiovascular disease in hypopituitary patients. Short-term GH treatment trials have shown improved psychosocial performance, normalization of body composition, increased muscle strength, improved exercise capacity, increased cardiac performance, and normalization of kidney function. Thus GH replacement therapy in GH-deficient adults exhibits potential long-term beneficial effects. A number of important questions have to be addressed before long-term GH replacement therapy in GH-deficient adults can be considered on a routine basis.