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Objectives: The sensitivities of the pituitary to thyroxine feedback, and the thyroid to thyrotropin stimulation determine the free thyroxine /thyrotropin feedback loop and can be described mathematically by two curves. It is not well understood how the two curves combine in a healthy population with normal thyroid function to express the individual balance points that are observed. This study was directed at this issue testing the possibilities of random combination and directed linkage between the two curves. Methods: We reverse-engineered two sets of population data, on the assumption of independent combinations of thyroid and pituitary sensitivities, to obtain estimates of the curve describing thyroid sensitivity. Sensitivity studies were performed. Results: No analysis resulted in a physiologically feasible estimate of the curve describing thyroid sensitivity. There was evidence of linkage of the two curves in terms of their combination throughout the normal range. Thyroid response curves reflecting a low free thyroxine response to thyrotropin tended to be combined in individuals with thyrotropin curves reflecting a high thyrotropin response to free thyroxine, and vice versa. Conclusions: Thyroid and pituitary sensitivities are linked, being combined in individuals in a non-random directed pattern. Direct mutual interaction may contribute to this linkage. This linkage precludes the derivation of the curves describing these sensitivities from population data of the free thyroxine and thyrotropin relationship and complicates their derivation by physiological experimentation. This linkage and probable interaction may also bestow evolutionary advantage by minimising inter-individual variation in free thyroxine levels and by augmenting homeostasis.

Purpose: The aim of this study was to determine early weight loss-associated changes in subcutaneous abdominal white adipose tissue (WAT) gene expression in obese men with lowered serum testosterone by RNA next-generation sequencing. Methods: Fourteen men, mean age (IQR) 51.6 years (43.4–54.5), BMI 38.3 kg/m2(34.6–40.8) and total testosterone 8.4 nmol/L (7.5–9.5) provided subcutaneous WAT samples at baseline and after 2 weeks of a very low energy diet. Results: Body weight loss was similar in participants receiving testosterone (n= 6), −5.27 kg [95% CI −6.17; −4.26], and placebo (n= 8), −4.57 kg [95% CI −6.10; −3.55], p= 0.86. In placebo-treated men, of the 14,410 genes expressed in subcutaneous WAT, four genes, Angiopoietin-like 4, Semaphorin 3 G, Neuropilin 2 and Angiopoietin 4, were upregulated (adjusted false discovery rate P< 0.05). In an exploratory analysis comparing men receiving testosterone and placebo, the most-upregulated gene in the testosterone group (exploratory p< 0.0005) was the neuropeptide y receptor 2. Conclusions: In obese men, dieting is associated with upregulation of WAT-expressed Angiopoietin-like 4, a secreted protein that regulates lipid metabolism, Semaphorin 3 G, a proposed adipocyte differentiation factor and secreted adipokine, and its receptor Neuropilin 2, as well as Angiopoietin 4, a vascular integrity factor. In an exploratory analysis, testosterone was associated with the upregulation of neuropeptide y receptor 2, a receptor involved in appetite regulation. Further studies are needed to confirm these observations and their potential biological implications. Trial registration: clinicaltrials.gov, Identifier NCT01616732, Registration date: June 8, 2012.

Androgen deprivation therapy (ADT) for prostate cancer (PCa) leads to a selective loss of leg muscle function during walking. Rodent models of ADT have demonstrated that the levator ani is exquisitely androgen sensitive.

Background: Patient responses to levothyroxine (LT4) monotherapy vary considerably. We sought to differentiate contributions of FT4 and FT3 in controlling pituitary thyroid stimulating hormone (TSH) secretion.Methods: We retrospectively assessed the relationships between TSH and thyroid hormones in 319 patients with thyroid carcinoma through 2914 visits on various LT4 doses during follow-up for 5.5 years (median, IQR 4.2, 6.9). We also associated patient complaints with the relationships.Results: Under varying dose requirements (median 1.84 µg/kg, IQR 1.62, 2.11), patients reached TSH targets below 0.4, 0.1 or 0.01 mIU/l at 73%, 54% and 27% of visits. While intercept, slope and fit of linearity of the relationships between lnTSH and FT4/FT3 varied between individuals, gender, age, LT4 dose and deiodinase activity influenced the relationships in the cohort (all p< 0.001). Deiodinase activity impaired by LT4 dose significantly affected the lnTSH–FT4 relationship. Dose increase and reduced conversion efficiency displaced FT3–TSH equilibria. In LT4-treated patients, FT4 and FT3 contributed on average 52% versus38%, and by interaction 10% towards TSH suppression. Symptomatic presentations (11%) accompanied reduced FT3 concentrations (–0.23 pmol/l, p= 0.001) adjusted for gender, age and BMI, their relationships being shifted towards higher TSH values at comparable FT3/FT4 levels.Conclusions: Variation in deiodinase activity and resulting FT3 levels shape the TSH–FT4 relationship in LT4-treated athyreotic patients, suggesting cascade control of pituitary TSH production by the two hormones. Consequently, measurement of FT3 and calculation of conversion efficiency may identify patients with impaired biochemistry and a resulting lack of symptomatic control.

Background: Thyroid hormones are controlled by the hypothalamic–pituitary–thyroid (HPT) axis through a complex network of regulatory loops, involving the hormones TRH, TSH, FT4, and FT3. The relationship between TSH and FT4 is widely used for diagnosing thyroid diseases. However, mechanisms of FT3 homeostasis are not well understood.Objective: We used mathematical modelling to further examine mechanisms that exist in the HPT axis regulation for protecting circulating FT3 levels.Methods: A mathematical model consisting of a system of four coupled first-order parameterized non-linear ordinary differential equations (ODEs) was developed, accounting for the interdependencies between the hormones in the HPT axis regulation. While TRH and TSH feed forward to the pituitary and thyroid, respectively, FT4 and FT3 feed backward to both the pituitary and hypothalamus. Stable equilibrium solutions of the ODE system express homeostasis for a particular variable, such as FT3, if this variable stays in a narrow range while certain other parameter(s) and system variable(s) may vary substantially.Results: The model predicts that (1) TSH-feedforward protects FT3 levels if the FT4 production rate declines and (2) combined negative feedback by FT4 and FT3 on both TSH and TRH production rates keeps FT3 levels insensitive to moderate changes in FT4 production rates and FT4 levels. The optimum FT4 and FT3 feedback and TRH and TSH-feedforward ranges that preserve FT3 homeostasis were found by numerical continuation analysis. Model predictions were in close agreement with clinical studies and individual patient examples of hypothyroidism and hyperthyroidism.Conclusions: These findings further extend the concept of HPT axis regulation beyond TSH and FT4 to integrate the more active sister hormone FT3 and mechanisms of FT3 homeostasis. Disruption of homeostatic mechanisms leads to disease. This provides a perspective for novel testable concepts in clinical studies to therapeutically target the disruptive mechanisms.

Background/Aim:Operating far from its equilibrium resting point, the thyroid gland requires stimulation via feedback-controlled pituitary thyrotropin (TSH) secretion to maintain adequate hormone supply. We explored and defined variations in the expression of control mechanisms and physiological responses across the euthyroid reference range. Methods:We analyzed the relational equilibria between thyroid parameters defining thyroid production and thyroid conversion in a group of 271 thyroid-healthy subjects and 86 untreated patients with thyroid autoimmune disease. Results:In the euthyroid controls, the FT3-FT4 (free triiodothyronine-free thyroxine) ratio was strongly associated with the FT4-TSH ratio (tau = -0.22, p < 0.001, even after correcting for spurious correlation), linking T4 to T3 conversion with TSH-standardized T4 production. Using a homeostatic model, we estimated both global deiodinase activity and maximum thyroid capacity. Both parameters were nonlinearly and inversely associated, trending in opposite directions across the euthyroid reference range. Within the panel of controls, the subgroup with a relatively lower thyroid capacity (<2.5 pmol/s) displayed lower FT4 levels, but maintained FT3 at the same concentrations as patients with higher functional and anatomical capacity. The relationships were preserved when extended to the subclinical range in the diseased sample. Conclusion:The euthyroid panel does not follow a homogeneous pattern to produce random variation among thyroid hormones and TSH, but forms a heterogeneous group that progressively displays distinctly different levels of homeostatic control across the euthyroid range. This suggests a concept of relational stability with implications for definition of euthyroidism and disease classification.

Background/Aim:Operating far from its equilibrium resting point, the thyroid gland requires stimulation via feedback-controlled pituitary thyrotropin (TSH) secretion to maintain adequate hormone supply. We explored and defined variations in the expression of control mechanisms and physiological responses across the euthyroid reference range. Methods:We analyzed the relational equilibria between thyroid parameters defining thyroid production and thyroid conversion in a group of 271 thyroid-healthy subjects and 86 untreated patients with thyroid autoimmune disease. Results:In the euthyroid controls, the FT3-FT4(free triiodothyronine-free thyroxine) ratio was strongly associated with the FT4-TSH ratio (tau = -0.22, p < 0.001, even after correcting for spurious correlation), linking T4to T3conversion with TSH-standardized T4production. Using a homeostatic model, we estimated both global deiodinase activity and maximum thyroid capacity. Both parameters were nonlinearly and inversely associated, trending in opposite directions across the euthyroid reference range. Within the panel of controls, the subgroup with a relatively lower thyroid capacity (<2.5 pmol/s) displayed lower FT4levels, but maintained FT3at the same concentrations as patients with higher functional and anatomical capacity. The relationships were preserved when extended to the subclinical range in the diseased sample. Conclusion:The euthyroid panel does not follow a homogeneous pattern to produce random variation among thyroid hormones and TSH, but forms a heterogeneous group that progressively displays distinctly different levels of homeostatic control across the euthyroid range. This suggests a concept of relational stability with implications for definition of euthyroidism and disease classification.

Several influences modulate biochemical responses to a weight-adjusted levothyroxine (l-T4) replacement dose. We conducted a secondary analysis of the relationship of l-T4dose to TSH and free T3(FT3), using a prospective observational study examining the interacting equilibria between thyroid parameters. We studied 353 patients on steady-state l-T4replacement for autoimmune thyroiditis or after surgery for malignant or benign thyroid disease. Peripheral deiodinase activity was calculated as a measure of T4–T3conversion efficiency. In euthyroid subjects, the median l-T4dose was 1.3 μg/kg per day (interquartile range (IQR) 0.94,1.60). The dose was independently associated with gender, age, aetiology and deiodinase activity (all P<0.001). Comparable FT3levels required higher l-T4doses in the carcinoma group (n=143), even after adjusting for different TSH levels. Euthyroid athyreotic thyroid carcinoma patients (n=50) received 1.57 μg/kg per day l-T4(IQR 1.40, 1.69), compared to 1.19 μg/kg per day (0.85,1.47) in autoimmune thyroiditis (P<0.01, n=76) and 1.08 μg/kg per day (0.82, 1.44) in patients operated on for benign disease (P< 0.01, n=80). Stratifying patients by deiodinase activity categories of <23, 23–29 and >29 nmol/s revealed an increasing FT3–FT4dissociation; the poorest converters showed the lowest FT3levels in spite of the highest dose and circulating FT4(P<0.001). An l-T4-related FT3–TSH disjoint was also apparent; some patients with fully suppressed TSH failed to raise FT3above the median level. These findings imply that thyroid hormone conversion efficiency is an important modulator of the biochemical response to l-T4; FT3measurement may be an additional treatment target; and l-T4dose escalation may have limited success to raise FT3appropriately in some cases.

Background: Animal studies suggest that undercarboxylated osteocalcin may improve insulin sensitivity viaits effect on testicular testosterone production. Human studies have been conflicting. Men undergoing androgen deprivation therapy (ADT) for prostate cancer experience profound hypogonadism resulting in increased insulin resistance. In a randomised controlled trial (RCT) of zoledronic acid versus placebo in men commencing extended-duration ADT, we aimed to examine the effects on fat mass and glucose metabolism. We hypothesised that zoledronic acid, which reduces osteocalcin concentrations, would worsen ADT-induced insulin resistance.Methods: This was a prespecified secondary analysis of an RCT designed to evaluate the effects of zoledronic acid on bone microarchitecture in 76 men with non-metastatic prostate cancer undergoing curative radiotherapy combined with adjuvant ADT (n= 39 randomised to a single dose of zoledronic acid 5 mg, n= 37 randomised to matching placebo). Oral glucose tolerance tests to determine Matsuda Index were performed at 0, 3, 12 and 24 months. Using a mixed model, mean adjusted differences [MAD (95% confidence interval)] between the groups over time are reported.Results: Over 24 months of ADT, fat mass increased and lean mass decreased for both groups, with no significant between group difference [MAD 401 g (−1307; 2103), p= 0.23 and −184 g (−1325; 955), p= 0.36 respectively]. Bone remodelling markers C-telopeptide [MAD −176 ng/l (−275; −76), p< 0.001 and P1NP −18 mg/l (−32; −5), p< 0.001] as a surrogate for osteocalcin, remained significantly lower in the zoledronic acid group, compared with placebo. There was no mean adjusted between-group difference for homeostatic model assessment 2 insulin resistance (HOMA2-IR) [−0.2 (−0.6; 0.2), p= 0.45], HbA1c [−0.1% (−0.3; 0.1), p= 0.64] or Matsuda Index [0.8 (−1.1; 2.7), p= 0.38]. The Matsuda Index decreased in both groups consistent with worsening insulin resistance with ADT.Conclusion: A single dose of zoledronic acid does not appear to influence glucose metabolism in men newly commencing ADT. Further study to evaluate the endocrine relationship between bisphosphonates, bone and glucose metabolism is required.Trial Registration Number: [ClinicalTrials.gov identifier: NCT01006395].

Objective:After primary successful antithyroid drug treatment (ATDT), Graves' disease has a relapse rate of 30% to 50%. Previous studies have evaluated age, gender, goiter volume, smoking habits, and the presence of thyrotropin-receptor antibodies (TRAb) as predictive markers to facilitate an individualized patient management. Despite higher sensitivity and specificity of the new second generation human TSH-receptor assay, the predictive value of TRAb for relapse of hyperthyroidism is still controversial. In a recent prospective multicenter study we have previously shown that suppressed or low TSH values predict both early (persistence) and late relapse of Graves' disease. We now present a more detailed analysis of the predictive value of TSH and TRAb for recurrent hyperthyroidism. Methods:Four weeks after withdrawal of ATDT, 96 patients were available for thyroid function tests, including a sensitive third-generation TSH assay and a second-generation recombinant TSH receptor assay. Relapse of Graves' disease was evaluated for a total follow-up of 2 years. Results:Within 2 years, 47 of 96 patients (49%) developed relapse of hyperthyroidism. Nine patients relapsed within the first 4 weeks after withdrawal of ATDT and were thus considered to have persistent Graves' disease. Ten of 15 other patients with TSH levels below 0.3 mU/L without overt hyperthyroidism relapsed within 2 years. Twenty-five of 65 patients with normal TSH (0.3–3.0 mU/L) and 3 of 4 patients with TSH values above 3 mU/L also had recurrent hyperthyroidism. After ATDT cessation, TSH had a positive predictive value of 70% and a negative predictive value of 62% (specificity 85%) for relapse of Graves 'disease. Mean TRAb levels in the group of patients with relapse were significantly higher (11.1 IU/L ± 0.17) than TRAb values in the remission group (4.5 IU/L ± 0.6), p< 0.001. Using a cutoff value of 1.5 IU/L, TRAb had low positive and negative predictive values of 49% and 54%, respectively (specificity, 14%), but with a cutoff level of 10 IU/L, predictive values improved to 83% and 62%, respectively (specificity, 92%). Combination of TSH and TRAb determinations did not further improve prediction of relapse. Other factors such as gender, age, goiter volume, smoking habits, presence of thyroid-associated ophthalmopathy, and urinary iodine excreation did not show a significant influence on relapse rate. Conclusion:Low TSH values 4 weeks after ATDT withdrawal predict relapse of Graves' disease, both early (persistence) and, to a lesser extend, within 2 years of follow-up. Also, TRAb above 10 IU/L found in a small subset of patients, correlated with a higher relapse rate.

Antithyroid drugs are effective in restoring euthyroidism in Graves' disease, but many patients experience relapse after withdrawal. Prevention of recurrence would therefore be a desirable goal. In a prospective study, patients with successful outcome of 12 to 15 months antithyroid drug therapy were stratified for risk factors and randomly assigned to receive levothyroxine in a variable thyrotropin (TSH)-suppressive dose for 2 years or no treatment. The levothyroxine group was randomized to continue or discontinue levothyroxine after 1 year. End points included relapse of overt hyperthyroidism. Of 346 patients with Graves' disease enrolled 225 were euthyroid 4 weeks after antithyroid drug withdrawal and were randomly assigned to receive levothyroxine (114 patients) or no treatment (controls, 111 patients). Of those not randomized, 39 patients showed early relapse within 4 weeks, 61 endogenous TSH suppression, 7 TSH elevation, and 14 had to be excluded. Dropout rate during the study were 13.3. Kaplan-Meier analyses showed relapse rates to be similar in the levothyroxine group (20 after 1 year, 32 after 2 years) and the randomized controls (18, 24), whereas relapses were significantly more frequent in the follow-up group of patients with endogenously suppressed TSH (33, 49). Levothyroxine therapy did not influence TSH-receptor antibody, nor did it reduce goiter size. The best prognostic marker available was basal TSH determined 4 weeks after withdrawal of antithyroid drugs (posttreatment TSH). The study demonstrates that levothyroxine does not prevent relapse of hyperthyroidism after successful restoration of euthyroid function by antithyroid drugs and characterizes posttreatment TSH as a main prognostic marker.

Posterior retroperitoneoscopic adrenalectomy is one of the new endoscopic methods in endocrine surgery. In a prospective clinical study 142 posterior retroperitoneoscopic adrenalectomies (72 right, 70 left) were performed in 130 patients (52 males, 78 females, age 49.1 ± 14.9 years). Indications were primary adrenal tumors (unilateral, n= 118; bilateral, n= 2), adrenal metastases (n= 2), and bilateral ACTH-dependent hyperplasias (n= 10). Tumor size ranged from 0.5 to 7.0 cm (mean 2.7 ± 1.4 cm). Partial adrenalectomies were performed in 39 patients. Conversion to open posterior adrenalectomy was necessary in five patients and seven procedures (5%). Intraoperative and postoperative complications were minor and occurred in 5% and 13%, respectively. Mortality was zero. Operating time was 101 ± 39 minutes (range 35–285 minutes) and depended on tumor type (pheochromocytoma versus others; p< 0.01), tumor size (< 3 vs. = 3 cm; p< 0.05), gender (p< 0.05), and extent of resection (partial versus complete, p< 0.05. Twenty-three adrenalectomies (17%) were performed within 1 hour or less. Blood loss was 54 ± 72 ml. Consumption of analgesics was low (mean 6 mg piritramide postoperatively). Median duration of hospitalization was 3 days. Posterior retroperitoneoscopic adrenalectomy is a safe method that has become a standard procedure in endocrine surgery.

Posterior retroperitoneoscopic adrenalectomy is one of the new endoscopic methods in endocrine surgery. In a prospective clinical study 142 posterior retroperitoneoscopic adrenalectomies (72 right, 70 left) were performed in 130 patients (52 males, 78 females, age 49.1 ± 14.9 years). Indications were primary adrenal tumors (unilateral, n= 118; bilateral, n= 2), adrenal metastases (n= 2), and bilateral ACTH-dependent hyperplasias (n= 10). Tumor size ranged from 0.5 to 7.0 cm (mean 2.7 ± 1.4 cm). Partial adrenalectomies were performed in 39 patients. Conversion to open posterior adrenalectomy was necessary in five patients and seven procedures (5%). Intraoperative and postoperative complications were minor and occurred in 5% and 13%, respectively. Mortality was zero. Operating time was 101 ± 39 minutes (range 35–285 minutes) and depended on tumor type (pheochromocytoma versus others; p< 0.01), tumor size (< 3 vs. ≥ 3 cm; p< 0.05), gender (p< 0.05), and extent of resection (partial versus complete, p< 0.05. Twenty-three adrenalectomies (17%) were performed within 1 hour or less. Blood loss was 54 ± 72 ml. Consumption of analgesics was low (mean 6 mg piritramide postoperatively). Median duration of hospitalization was 3 days. Posterior retroperitoneoscopic adrenalectomy is a safe method that has become a standard procedure in endocrine surgery.

AbstractWe present the results of a pre-evaluation of the thyroid function test free thyroxine, free triiodothyronine and third generation TSH using the Elecsys®electrochemiluminescence immunoassay system. A collaborative field study between the development center of the manufacturer and a clinical chemistry laboratory addressed the reliability and comparability of the new Elecsys®assays to established methods under clinical laboratory conditions using samples from routine in vitrothyroid testing. Preliminary (reference) formulations of the reagents and several electrochemiluminescent pilot models were used for assay measurements, either in the company's research center or in the clinical setting. The new thyroid assays were compared with the respective Enzymun-Test®assays, performed on the ES 300 automated immunoassay analyzer. A WHO standard was used for standardization of TSH, whereas an equilibrium dialysis method was applied for free triiodothyronine. The free thyroxine assay was standardized against the Enzymun-Test®free thyroxine assay, which had previously been calibrated against equilibrium dialysis.The aim of this field study was to support the optimization of the technology used for Elecsys®in an early stage of development and thereby prepare the ground for the adaptation of the immunoassays to the final Elecsys®2010 random access analyzer. A subsequent multicenter evaluation demonstrated that the requirements of routine thyroid testing in terms of reliability were fulfilled by the system.

Abstract. The insensitivity of Graves' thyroid to stimulation of cAMP formation by TSH as well as Graves' immunoglobulins in vitro is well known. The present study was performed to find out Graves' sera which may induce a final activation i.e. stimulation of T3release in Graves' thyroid slices despite this insensitivity of tissue and to characterize determinants responsible for the efficiency of those sera.Out of 20 sera from patients with active untreated Graves' disease 6 were found to stimulate T3release from Graves' thyroid in vitro. These 6 sera were effective in stimulating different Graves' glands, irrespective of pretreatment with propranolol, thiamazole (methimazole) or thiamazole plus iodine. In contrast, a significant response to bTSH was not observed in any Graves' gland. For comparison, 17/20 of the same sera were able to stimulate T3release when tested on human goitrous thyroid. Sera which stimulated Graves' slices revealed no higher stimulating activities in goitrous tissue than serum samples which did not. All sera were additionally assessed for TSH binding inhibiting immunoglobulins in a radioreceptor assay. Remarkably, Graves' thyroid stimulating sera had a low or absent TSH binding inhibiting activity.Thus, hormone release from Graves' thyroid in vitro – in contrast to that from goitrous tissue – could only be activated by a minority of Graves' sera. These Graves' thyroid stimulating sera could be characterized to contain a selected spectrum of biologically active antibodies with a high TSH agonistic potency stimulating in the presence of a negligible TSH binding inhibiting activity. We conclude the qualitative composition of the antibody spectrum in the individual sera, such as the occurrence of so-called 'TSH superagonists', rather than the height of antibody titre as determined by various methods seems to be relevant for their Graves' thyroid stimulating potency.

Posterior retroperitoneoscopic adrenalectomy is a new minimally invasive method. It represents an alternative to conventional open procedures and laparoscopic techniques. Between July 1994 and November 1995 a total of 30 retroperitoneoscopic adrenalectomies were performed on 27 patients. In 24 patients, unilateral tumors were seen (size 1–7 cm): seven Cushing adenomas, five Conn adenomas, seven pheochromocytomas, four hormonally inactive tumors, one cyst. Three patients suffered from Cushing syndrome with bilateral adrenal gland hyperplasias (two inoperable pituitary gland tumors, one bronchial carcinoid with ACTH secretion). The operations were carried out in prone position. After balloon dilatation of the retroperitoneum and creation of a pneumoperitoneum the preparation of the adrenal gland was performed via three trocar sites positioned below the 12th rib. Twenty-five adrenalectomies were completed endoscopically, and five times (among four patients) conversion to the conventional posterior technique was necessary. The average operating time of complete endoscopic adrenalectomies was 124 minutes (45–225 minutes); blood loss was 10 to 120 ml. With minimal need for postoperative analgesia (average dosage 7.9 mg of piritramide), mobilization and adequate food uptake were possible on the day of operation. The posterior retroperitoneoscopic adrenalectomy is a relatively fast, safe method, with the advantages of the posterior open approach and minimally invasive surgery. It therefore represents an important addition to adrenal gland surgery.

In the treatment of endemic goitre, the concept of giving levothyroxine in combination with iodine offers a promising therapeutic approach by influencing not only TSH secretion but also intrathyroidal iodine content. However, little is known about the doses of iodine necessary to correct intrathyroidal iodine deficiency. To get more information on this important issue, we conducted a prospective, double-blind study on the effect of a monotherapy with 500 μg iodide/day and a combined treatment with 100 μg levothyroxine and 100 μg iodide/day on thyroid iodine concentration as measured by fluorescence scintigraphy. In a group of 12 patients, a 4-month treatment with 100 μg levothyroxine and 100 μg iodide/day did not significantly affect thyroid iodine concentration (0.35±0.14 vs 0.37±0.11 mg/g). The application of 500 μg iodide/day in these patients during a second 4-month period resulted in a sharp increase in thyroid iodine concentration from 0.37±0.11 to 0.61±0.14 mg/g (p<0.01). Another group of 8 patients first treated with 500 μg iodide/day also showed a significant increase in iodine concentration from 0.35±0.14 to 0.65±0.20 mg/g (p<0.01). After switching to the combination regimen during a second 4-month period, thyroid iodine concentration slightly decreased, particularly in those patients with high iodine concentrations after monotherapy with iodide (0.65±0.20 vs 0.50±0.12 mg/g, p<0.05). In conclusion, treatment with 500 μg iodide/day could sharply increase thyroid iodine concentration in patients with endemic goitre. In contrast, a combination of 100 μg levothyroxine and 100 μg iodide/day had no significant effect on thyroid iodine concentration.

Abstract. Posterior retroperitoneoscopic adrenalectomy is a new minimally invasive method. It represents an alternative to conventional open procedures and laparoscopic techniques. Between July 1994 and November 1995 a total of 30 retroperitoneoscopic adrenalectomies were performed on 27 patients. In 24 patients, unilateral tumors were seen (size 1–7 cm): seven Cushing adenomas, five Conn adenomas, seven pheochromocytomas, four hormonally inactive tumors, one cyst. Three patients suffered from Cushing syndrome with bilateral adrenal gland hyperplasias (two inoperable pituitary gland tumors, one bronchial carcinoid with ACTH secretion). The operations were carried out in prone position. After balloon dilatation of the retroperitoneum and creation of a pneumoperitoneum the preparation of the adrenal gland was performed via three trocar sites positioned below the 12th rib. Twenty-five adrenalectomies were completed endoscopically, and five times (among four patients) conversion to the conventional posterior technique was necessary. The average operating time of complete endoscopic adrenalectomies was 124 minutes (45–225 minutes); blood loss was 10 to 120 ml. With minimal need for postoperative analgesia (average dosage 7.9 mg of piritramide), mobilization and adequate food uptake were possible on the day of operation. The posterior retroperitoneoscopic adrenalectomy is a relatively fast, safe method, with the advantages of the posterior open approach and minimally invasive surgery. It therefore represents an important addition to adrenal gland surgery.: