Nutrition, body composition and physical activity have differential impact on the determination of lipidemic blood profiles between young females with different blood cholesterol concentrations.

INTRODUCTION: This cross-sectional study explored whether nutrition, body composition, and physical activity energy expenditure (PAΕΝ) have a differential impact on lipidemic blood profiles among young females with different blood cholesterol concentrations. METHODS: One hundred thirty-five young female students (N = 135) were allocated into three groups according to their blood cholesterol concentrations (Chol): (A) Normal [NL; Chol: < 200 mg·dL-1; n = 56 Age: 21.4 ± 2.6 yrs, Body Mass Index (BMI): 22.1 ± 2.0 kg·m-2], (B) Borderline (BL; Chol: ≥200 mg·dL-1 and <240 mg·dL-1; n = 44 Age: 21.6 ± 2.5 yrs, BMI: 24.2 ± 3.1 kg·m-2) and (C) High level (HL; Chol: ≥240 mg·dL-1; n = 35 Age: 22.5 ± 2.4 yrs, BMI: 28.9 ± 2.1 kg·m-2). Body composition [bioelectrical impedance analysis including lean body mass (LBM) and body fat mass], nutritional intake (recall questionnaire), daily physical activity energy expenditure through activity trackers and resting blood lipids concentrations were evaluated. RESULTS: Multiple linear regression analyses revealed that in the NL group, lean mass, daily PAΕΝ and daily energy balance were the determinant parameters of blood lipidemic profiles (B: -0.815 to 0.700). In the BL group, nutrition, body composition and daily physical activity energy expenditure exhibited similar impacts (B: -0.440 to 0.478). In the HL group, nutritional intake and body fat mass determined blood lipidemic profile (B: -0.740 to 0.725). CONCLUSION: Nutrition, body composition and daily PAΕΝ impact on blood lipids concentration is not universal among young females. In NL females, PAEN, energy expenditure and LBM are the strongest determinants of blood lipids, while in HL females, nutritional intake and body fat mass are. As PAΕΝ increases, the importance of nutrition and body fat decreases, and vice versa.

Body Composition, Fasting Blood Glucose and Lipidemic Indices Are Not Primarily Determined by the Nutritional Intake of Middle-Aged Endurance Trained Men-Another "Athletes' Paradox"?

Systematic, regular high-volume endurance training induces significant metabolic adaptations in glucose and lipids metabolism, which seems to affect the negative impact of unhealthy nutrition, at least in animal models. The present study aimed to investigate the main determinants of body composition, blood glucose and lipids concentrations between middle-aged sedentary individuals (Sed) and well-trained endurance athletes (Run), both following an unhealthy high-fat diet. In thirty-five Sed (Age: 54.0 ± 6.6 yrs, Body Mass: 77.1 ± 10.5 kg, BMI: 31.3 ± 6.0 kg·m-2) and thirty-six Run (Age: 51.6 ± 5.2 yrs, Body Mass: 85.8 ± 3.4 kg, BMI: 23.2 ± 1.8 kg·m-2), body composition, nutritional intake, energy expenditure, resting metabolic rate (RMR), respiratory exchange ratio (RER), and blood glucose and lipids concentrations were evaluated. Multiple linear regression analyses revealed that body composition, blood glucose and lipids' concentrations in the Run group were primarily determined by the energy expenditure (B: -0.879 to -1.254), while in the Sed group, by their energy intake (B:-0.754 to 0.724). In conclusion, it seems that in well-trained endurance middle-aged athletes, body composition, blood glucose, and lipids concentrations seem to be determined by their training-induced daily energy expenditure and not by their nutritional intake per se. At the same time, nutrition is the primary determinant in aged-matched sedentary individuals, even if they both follow high-fat diets.

Comparison of short-term hypocaloric high-protein diets with a hypocaloric Mediterranean diet: Effect on body composition and health-related blood markers in overweight and sedentary young participants.

OBJECTIVES: The aim of the present study was to compare the short-term effects of a hypocaloric Mediterranean diet and two high protein diets, with and without whey protein supplementation, on body composition, lipidemic profile, and inflammation and muscle-damage blood indices in overweight, sedentary, young participants. METHODS: Thirty-three young, overweight, male and female participants (mean ± SD age: 22.8 ± 4.8 y; body mass: 85.5 ± 10.2 kg; body fat percentage: 34.3% ± 8.1%) were randomly allocated to three different hypocaloric (-700 kcal/d) diets: a Mediterranean diet (MD; n = 10), a high-protein diet (HP; n = 10) diet, and a high-protein diet with whey supplementation (n = 10). The intervention lasted 6 wk. Body composition and biochemical indices were evaluated 1 wk before and after the nutritional interventions. RESULTS: Body and fat mass were decreased in the MD and HP groups (-3.5% ± 1.1% and -5.9% ± 4.2% for body and fat mass respectively in MD, and -1.7% ± 1.2% and -2.0% ± 1.8% for body and fat mass respectively in HP;P < 0.05), with no significant decline of fat-free mass observed in the MD group. The MD group's diet beneficially altered the lipid profile (P < 0.05), but the HP and HPW groups' diets did not induce significant changes. Subclinical inflammation and muscle-damage indices significantly increased in the HP and HPW groups (7.4% ± 3.5% and 66.6% ± 40.1% for neutrophils and CRP respectively in HP, and 14.3% ± 6.4% and 266.6% ± 55.1% for neutrophils and CRP respectively in HPW; P < 0.05) but decreased in the MD group (1.8% ± 1.2% and -33.3% ± 10.1% for neutrophils and CRP respectivelyc; P < 0.05). Energy intake of carbohydrates and proteins were significantly related to the changes in body composition and biochemical blood markers (r = -0.389 and -0.889; P < 0.05). CONCLUSIONS: Among the three hypocaloric diets, only the Mediterranean diet induced positive changes in body composition and metabolic profile in overweight, sedentary individuals.

The importance of protein intake in master marathon runners.

OBJECTIVES: The aim of this study was to investigate the relationships between protein intake (during the tapering period and the race), marathon performance, body composition, acute race-induced changes, and selected metabolic- and muscle damage-related blood biomarkers in recreational master runners. METHODS: In 58 experienced master runners (58.28 y ± 1.07 y, 174.06 cm ± 0.72 cm, 78.51 kg ± 0.76 kg body mass, 21.38% ± 0.52% body fat, mean ± SEM), nutritional intake was evaluated 1 wk before the race and during the marathon. Body composition was evaluated before and 2 h after the race. Blood samples were collected at the same time points. RESULTS: Body fat and lean body mass (LBM) were significantly reduced after the marathon (P < 0.01; η2: 0.311-0.888). Significant negative correlations were observed between energy intake from carbohydrates and proteins (expressed per LBM), marathon performance, and race-induced changes of blood metabolic-muscle damage indices (P < 0.05; r: -0.522 to -0.789). Positive correlations were observed between energy from carbohydrates and proteins per LBM, and body mass and LBM changes (P < 0.05; r: 0.485-0.814). The specific contribution of protein intakes per LBM (beta coefficient: -0.789 to 0.615) on race-induced changes of body composition and blood markers was the same as that of carbohydrate intakes per LBM (beta coefficient: -0.777 to 0.559). CONCLUSIONS: Marathon-induced changes in body composition and metabolic blood indices are highly related to protein intake, either during the tapering period or during the race, with runners experiencing the lowest changes when consuming higher protein intakes.

The hypothalamus-pituitary-gonad axis: Tales of mice and men.

Reproduction is controlled by the hypothalamic-pituitary-gonadal (HPG) axis. Gonadotropin-releasing hormone (GnRH) neurons play a central role in this axis through production of GnRH, which binds to a membrane receptor on pituitary gonadotrophs and stimulates the biosynthesis and secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Multiple factors affect GnRH neuron migration, GnRH gene expression, GnRH pulse generator, GnRH secretion, GnRH receptor expression, and gonadotropin synthesis and release. Among them anosmin is involved in the guidance of the GnRH neuron migration, and a loss-of-function mutation in its gene leads to a failure of their migration from the olfactory placode to the hypothalamus, with consequent anosmic hypogonadotropic hypogonadism (Kallmann syndrome). There are also cases of hypogonadotropic hypogonadim with normal sense of smell, due to mutations of other genes. Another protein, kisspeptin plays a crucial role in the regulation of GnRH pulse generator and the pubertal development. GnRH is the main hypothalamic regulator of the release of gonadotropins. Finally, FSH and LH are the essential hormonal regulators of testicular functions, acting through their receptors in Sertoli and Leydig cells, respectively. The main features of the male HPG axis will be described in this review.

The Sertoli cell: Novel clinical potentiality.

The Sertoli cell is important for endocrine and paracrine control of spermatogenesis. Functions attributed to Sertoli cells are: (1) supportive and trophic functions for the cells of the seminiferous epithelium, (2) transport of mature spermatids towards the lumen of seminiferous tubules, (3) secretion of androgen binding protein, (4) production of substances with endocrine or paracrine action for spermatogenesis control and (5) interaction with intertubular endocrine Leydig cells. Inhibin B and anti-Müllerian hormone (AMH) are glycoproteins belonging to the transforming growth factor ß (TGF-ß) superfamily; they are produced almost exclusively by the Sertoli cells and have been proposed as direct markers of their function and indirect markers of spermatogenesis. Serum inhibin B and AMH concentrations seem to constitute additional diagnostic parameters in male subfertility as they reflect Sertoli cell function. Stimulated concentrations of serum inhibin B and AMH do not add clinically relevant information in subfertile men compared to basal concentrations of these hormones. Serum inhibin B and AMH concentrations correlate with testicular histology/cytology but are not superior to FSH as predictors of the presence of sperm in testicular sperm extraction (TESE)/fine needle aspiration (FNA) biopsy in men with azoospermia.

Genetic basis of familial isolated hyperparathyroidism: a case series and a narrative review of the literature.

Primary hyperparathyroidism is a heterogeneous clinical entity. In the clinical setting, the diagnosis and management of familial isolated hyperparathyroidism (FIHP) and other familial hyperparathyroidism (FHPT) forms continue to rely on clinical, laboratory, and histological findings, with careful examination of the family. In this article, we report a case series of FIHP in a four-generation Greek family, with no identifiable gene mutations. Clinical approach and long-term follow-up are discussed and a narrative review of the genetic basis of this entity has been performed.

Recombinant human thyrotropin-aided radioiodine therapy in tracheal obstruction by an invading well-differentiated thyroid carcinoma.

Papillary thyroid carcinomas (PTCs) usually extend to lymph nodes in the neck and mediastinum. Rarely, they invade the neighboring upper airway anatomical structures. We report a 56-year-old woman who presented with symptoms of upper airway obstruction. Imaging studies revealed a lesion derived from the thyroid which invaded and obstructed the trachea, which appeared to be a highly differentiated PTC. Total thyroidectomy was performed, with removal of the endotracheal part of the mass along with the corresponding anterior tracheal rings. Two months later, a whole body I(131) scan after recombinant human thyroid-stimulating hormone (rh-TSH) administration was performed and revealed a residual mass in upper left thyroid lobe. Subsequently, 150 mCi I(131) were given following rh-TSH administration. Nine months later, there was no sign of residual tumor. This case is the first one reported in the literature regarding rh-TSH administration prior to RAI ablation in a PTC obstructing the trachea.

Gonadotropin-releasing hormone neuropeptides and receptor in human breast cancer: correlation to poor prognosis parameters.

Expression of the two gonadotropin-releasing hormone homologue peptides GnRHI and GnRHII and their receptor GnRHR has been demonstrated in a number of malignancies. In hormone-dependent breast cancer, GnRH analogs are used for therapy in premenopausal women. Gene expression of GnRHI, II and R was studied in breast biopsies from primary breast adenocarcinoma obtained from the tumor and the adjacent benign tissue. Levels were evaluated by a multiplex real-time RT-PCR. GnRHI transcripts were detected in 14.7% of the benign and 29.4% malignant biopsies and GnRHII in 21.2% benign and 44.1% malignant biopsies. GnRHR was also more frequent in the malignant (54.2%) than in the benign (24.0%) biopsies, at similar expression levels. No transcripts were detected in biopsies from healthy individuals. There was a strong correlation between the presence of GnRHI and GnRHII transcripts and their receptor in the benign and the malignant biopsies. GnRHI, II and R expression correlated significantly with poor prognosis pathological parameters. Immunohistochemistry for GnRHR revealed expression in malignant cells and in epithelial cells of mammary ducts of the adjacent area with pre-cancerous features. In contrast, GnRH I and II peptides were rarely expressed at low levels in breast cancer cells. In conclusion GnRH peptides and receptor are expressed more frequently in breast tumors than in the adjacent mammary tissue, representing a malignant feature. Their expression correlated to tumor characteristics of poor prognosis and was therefore related to more aggressive malignancies. Concomitant expression of peptides and receptor supports an autocrine/paracrine regulating role.

The complex interaction between obesity, metabolic syndrome and reproductive axis: a narrative review.

The aim of this narrative review is to provide current evidence for the interaction between obesity, metabolic syndrome (MS) and reproductive axis. Gonadotropin-releasing hormone (GnRH) pulses and, consequently, normal function of reproductive (hypothalamus-pituitary-gonadal) axis depend on normal energy balance, which presupposes sufficient food intake, reasonable energy consumption and average thermoregulatory costs. In case of an energy imbalance, reproductive dysfunction may occur. In young women, excessive leanness is accompanied by puberty delay, whereas premature puberty might be a manifestation of obesity. In a similar way, obesity in men affects fertility. Excess adipose tissue results in increased conversion of testosterone to estradiol, which may lead to secondary hypogonadism through reproductive axis suppression. Moreover, oxidative stress at the level of the testicular micro-environment may result in decreased spermatogenesis and sperm damage. Products of the adipocyte, such as leptin, adiponectin and resistin, and gut peptides, such as ghrelin, are considered to be crucial in the interaction between energy balance and reproduction. Finally, an indirect evidence for the interplay between MS and reproductive axis is the fact that when treating components of one, parameters of the other can be improved as well. These therapeutic interventions include lifestyle modifications, pharmacological agents, such as sex hormone replacement therapy, and surgical procedures. Although many issues remain unclear, the elucidation of the complex interaction between MS and reproductive axis will have obvious clinical implications in the therapeutic approach of both entities.

Diagnostic and therapeutic review of cystic parathyroid lesions.

BACKGROUND: Parathyroid cysts (PC) are uncommon entities in routine clinical practice. The vast majority are nonfunctioning and are commonly present as asymptomatic nodular cervical lesions. PC should be considered in the differential diagnosis of an asymptomatic neck mass. Large PC can manifest with compressive symptoms of the surrounding tissues. OBJECTIVE: The aim of this study is to describe nine new cases of PC and review the current literature regarding the clinical presentation, the aetiopathology, the diagnostic procedures, as well as the therapeutic approaches for this relatively rare clinical entity. METHODS-PATIENTS: We present nine new patients (7 females and 2 males) diagnosed with PC, which in three were ectopic. The diagnosis of PC was based on the elevated levels of PTH in the cysts fluid. Six of the patients had nonfunctioning parathyroid lesions, while the other three had functioning ones. Patients with functioning PC had elevated serum calcium and PTH levels. Five out of nine of the cases had no symptoms, while two patients had compressive symptoms and the other two had signs and symptoms of hypercalcaemia. Needle aspiration (NA) was performed in five out of six patients with nonfunctioning PC. Surgery was the treatment in all three patients with functioning PC. RESULTS: Remission after NA was achieved in four out of five patients with non-functioning PC (follow-up time: 17.7±2.3 months). In two of them, two and three aspirations were needed. One patient with nonfunctioning PC submitted to surgery with no previous NA. Patients with functioning PC maintained remission after surgery (mean follow-up time: 22.1±2.9 months). In one of them, a second surgery was performed due to the co-existence of an ectopic parathyroid adenoma. CONCLUSIONS: The diagnosis of a PC can be established by finding high levels of PTH in the fluid collected by the aspiration of the cyst. PTH and Ca levels in the serum can differentiate functioning from nonfunctioning PC. The treatment of choice in nonfunctioning cysts is aspiration. Surgical removal of the cyst is indicated in hyperfunctioning cysts in cases of relapse after NA in nonfunctioning cysts and when compressive symptoms are present. Based on our series, which appears to be one of the largest reported, we propose a diagnostic algorithm to guide the diagnostic and therapeutic approach to PC.

The corticotropin releasing factor system in cancer: expression and pathophysiological implications.

Malignant tumors express multiple factors that have some role in the regulating networks supporting their ectopic growth. Recently, increased interest has been developing in the expression and biological role of the neuropeptides and receptors of the corticotropin releasing factor (CRF) system, the principal neuroendocrine mediator of the stress response, especially in the light of several R&D programs for small molecule antagonists that could present some anticancer therapeutic benefit. In the present article, we review the literature suggesting that the CRF system could be involved in the regulation of human cancer development. Potential implication in growth, metastasis, angiogenesis, or immune parameters via activation of locally expressed receptors could be clinically exploited by presenting targets of new therapeutic approaches.

Thyroid autoimmunity and miscarriage.

The relation of thyroid autoimmunity to miscarriage is an important issue that has attracted the interest of many investigators. A number of papers have been published so far, which include healthy women, women with recurrent miscarriage and those undergoing assisted reproductive techniques. Most studies have shown a significant positive association between the presence of thyroid autoantibodies and miscarriage rate. It is of interest that women with high titers do not show a higher miscarriage rate when compared with women having low titers, although, there is no general agreement on this issue. There are three possible explanations for the assumed association of thyroid autoimmunity with miscarriage: 1) pregnancy loss is an epiphenomenon and not a direct effect of the thyroid autoantibodies, the presence of thyroid autoantibodies reflecting a generalized activation of the immune system; 2) delayed conception from the presence of thyroid autoantibodies; hence, when women with thyroid autoimmunity become pregnant, face a higher risk of miscarriage because of older age; and 3) the pregnancy loss is secondary to a subtle deficiency in thyroid hormone concentrations or a lower capacity of the thyroid to adequately adapt to the demands of pregnancy.

Thyroid autoimmunity, infertility and miscarriage.

Thyroid autoimmunity (TAI), infertility and miscarriage are currently issues of extreme interest that have attracted the attention of many investigators. Several papers have been published, focusing on women of childbearing age that include healthy women, women with recurrent miscarriage and those undergoing assisted conception. Most of these studies show a significant association between the presence of thyroid autoantibodies, infertility and a higher miscarriage rate. The underlying pathogenetic mechanisms, which might explain the association between TAI and infertility, remain speculative given the scarce information from animal models and from in vitro data addressing the potential effects of TAI on fertility. Adequate levels of circulating thyroid hormones are of primary importance for normal reproductive function and inadequate delivery of triiodothyronine to granulosa and stromal cells may disrupt normal female reproductive function. With regards to the association between TAI and miscarriage, a close relationship has been largely confirmed in recent studies. The aim of this review is to present the relevant information published so far in the literature regarding TAI and miscarriage in euthyroid female individuals.

Growth hormone-binding protein is directly and IGFBP-3 is inversely associated with risk of female breast cancer.

OBJECTIVE: Several components of the GH and IGF systems have been implicated in the development of malignancies. All components of these hormonal systems have never been jointly evaluated in female breast cancer, and previous studies have not examined the role of IGF-binding proteins (IGFBP-4, IGFBP-6) or GH-binding protein (GHBP). DESIGN: Hospital-based case-control study. METHODS: In this sample of primarily postmenopausal women, we obtained serum measures of IGF-I, IGF-II, and binding proteins IGFBP-1, IGFBP-3, IGFBP-4, IGFBP-6, as well as GHBP, insulin, and leptin from 74 breast cancer cases and 76 control subjects. RESULTS: In crude analyses, we found lower age-standardized mean IGF-I, IGFBP-3, IGFBP-4, IGFBP-6, and higher IGFBP-1 and GHBP in breast cancer cases when compared with controls. Multivariate models mutually adjusted for other GH-IGF system components and classical breast cancer risk factors demonstrated an inverse association between IGFBP-3 and risk of breast cancer (odds ratio (OR) = 0.2, P < 0.01) and a direct association between GHBP and disease risk (OR = 3.3, P < 0.01). No significant associations were detected in multivariate analyses among IGF-I, IGF-II or IGFBP-1, IGFBP-4, IGFBP-6 with risk of breast cancer, indicating that these factors may not have effects independent of and/or comparable with IGFBP-3 and GHBP. CONCLUSIONS: These results support a protective role of IGFBP-3 and demonstrate for the first time an increased risk of breast cancer with higher GHBP, after accounting for variation in IGFs, IGFBPs, and classical breast cancer risk factors.

Total and high-molecular-weight adiponectin in breast cancer: in vitro and in vivo studies.

BACKGROUND: Obesity is a major risk factor for breast cancer. We hypothesized that obesity-induced decreases in total and/or high-molecular-weight (HMW) adiponectin levels may underlie this association. METHODS: We measured serum total and HMW adiponectin in a hospital-based case-control study of 74 female breast cancer patients and 76 controls. In parallel, expression of adiponectin and its receptors AdipoR1/R2 were measured in tissue samples using RT-PCR, and protein expression of AdipoR1/R2 was localized and quantified using immunohistochemistry. Finally, we documented AdipoR1/R2 expression in several breast cancer cell lines and studied adiponectin signaling and the effect of adiponectin on proliferation in the T47D breast cancer cell line in vitro. RESULTS: Women with the highest adiponectin levels had a 65% reduced risk of breast cancer (P = 0.04). This association became stronger after adjustment for age, body mass index, and hormonal and reproductive factors (P = 0.02). Modeling HMW instead of total adiponectin produced similar results and did not offer any additional predictive value. Breast cancer cells expressed AdipoR1/R2 but not adiponectin. Expression of AdipoR1, but not AdipoR2, was higher in tumor tissue than both adjacent and control tissues. Exposure of T47D cells to adiponectin significantly inhibited the percentage of viable cells to 86% and proliferation to 66% but had no effect on apoptosis. These effects were associated with activation of ERK1/2 but not AMP-activated protein kinase or p38MAPK. CONCLUSION: These studies suggest that adiponectin may act as a biomarker of carcinogenesis and may constitute a molecular link between obesity and breast cancer.

Efficient testing of the RET gene by DHPLC analysis for MEN 2 syndrome in a cohort of patients.

BACKGROUND: Multiple Endocrine Neoplasia type 2 (MEN 2) is an autosomal dominant inherited syndrome characterized by a strong predisposition for developing endocrine tumors. MEN 2 is caused by germline mutations in the ret proto-oncogene. We investigated the feasibility of using the DHPLC technique in mutation detection of the ret gene in members of MTC families. We compared DHPLC analysis with direct sequencing with regard to sensitivity, reliability, cost and time. MATERIALS AND METHODS: Exons 10 and 11 were amplified with PCR from forty-three samples in seventeen unrelated Greek families and were analyzed for mutations by DHPLC and DNA sequencing. RESULTS: Eight PCR amplicons showed a distinct non-wild-type DHPLC profile. Sequence analysis confirmed different nucleotide variations: six of them were localized in exon 10 and two in exon 11. Mutations were detected in five out of seventeen families tested (29%). CONCLUSION: None of the alterations detected by direct sequencing was missed by DHPLC. We conclude that DHPLC is a fast, sensitive, cost-efficient and reliable method for the scanning of ret germline mutations.

The therapeutic value of SST-A octreotide alone or with adjuvant treatment in patients with advanced medullary thyroid carcinoma and positive (111)In-octreotide scan.

Medullary thyroid carcinoma (MTC) as a neuroendocrine tumour arising from C cells of the thyroid gland secrets hormonal peptides; among them, calcitonine (CT) and carcino-embryonic antigen (CEA). These two peptides are used for the diagnosis and treatment response of MTC cases. In patients with advanced MTC, scintigraphy by [(111)In-DTPA-d-phe1]-octreotide is able to detect somatostatin receptors (SSTR) and thus identify regional lymph nodes and/or distal metastases. In this article, we have studied the use of [(111)In-DTPA-d-phe1]-octreotide in the treatment of patients with advanced MTC, and a positive octreotide scan. Twenty-two patients were studied, 16 with persistent MTC and six with relapsed MTC. All patients' tumours were detected by [(111)In-DTPA-d-phe1]-octreotide-scan to be SSTR positive. All patients were treated with the somatostatin analog (SST-A) octreotide, for 3-21 months. Nine patients were treated only with SST-A (Group A). The remaining 13 patients (Group B) received adjuvant treatment as follows: six patients received chemotherapy (Ch), five patients received both Ch and external radiotherapy (eRT) and two patients received only eRT. Results were as follows: Group B patients as compared to Group A patients had about the same objective and biological response. Patients of Group B had relatively better subjective response (less diarrheas and abdominal cramps) versus Group A patients, although this finding was not significant. Group B patients had a longer mean survival time after treatment as compared to Group A patients: 39 months (with a range of 4-72 months) versus 20 months (with a range of 3-60 months) respectively, (P<0.05). Also Group B patients had longer than Group A patients mean total survival time - measured from the start of the disease: 138 (18-270) versus 97 (13-235) months respectively (P<0.05). Based on the above findings, it is the opinion of the authors that patients with advanced MTC and SSTR tumor expression in vivo as indicated by [(111)In-DTPA-d-phe1]-octreotide scanning, when submitted to treatment with SST-A octreotide and adjuvant Ch and/or eRT treatment may have a better treatment response than if submitted to treatment with SST-A octreotide alone. More cases are being studied by us at the present.

Thyroid carcinoma in children and adolescents: presentation, clinical course, and outcome of therapy in 23 children and adolescents in Northern Greece.

OBJECTIVE: To define clinical presentation, surgical complications, follow-up characteristics, and survival of 23 children and adolescents with thyroid carcinoma. DESIGN: Retrospective analysis of data of 23 children and adolescents with thyroid carcinoma cared for in the Theagenion Cancer Hospital, Thessaloniki. RESULTS: At the time of diagnosis cervical lymph node metastases were present in 18 (78.2%), mediastinal in 2 (8.69%), and pulmonary in 3 patients (13%). Total thyroidectomy was performed in 21 patients, with lymph node dissection in 18 and subtotal thyroidectomy in 2. No significant post-operative complications were observed. Histological examination revealed differentiated thyroid carcinoma (DTC). Tumor was multifocal in 11 (47.8%) and bilateral in 7 subjects (63.6%). Thyroid capsule invasion, vascular invasion, soft tissue involvement, and parathyroid gland invasion was observed in 12 out of 23 patients (52.1%). All patients received thyroxine suppressive therapy and 21 of them additional therapy with radioactive iodine (131I). During follow-up (5.5 years), 6 out of the 23 patients presented new metastases in the cervical and mediastinal lymph nodes, lungs, and bones. At last follow-up, 11 patients (47.8%) had residual disease but all were alive. CONCLUSIONS: Thyroid carcinoma in children and adolescents can be quite aggressive. When a young patient presents thyroid nodule or multinodular goiter or palpable lymph nodes, the existence of thyroid carcinoma must be seriously considered.

Cerebellar metastasis as first metastasis from papillary thyroid carcinoma.

Brain metastasis is an uncommon complication of differentiated thyroid carcinoma. Even more, cerebellar metastases from papillary thyroid carcinoma (PTC) are exceptional. We report a 69-year-old male patient with infiltrative PTC who developed high levels of thyroglobulin (Tg) and deteriorated neurological symptoms four years after the initial diagnosis. Computerized tomography (CT) of the brain demonstrated a cerebellar mass and the patient underwent surgery. Pathology revealed metastasis from PTC. Immunochemistry was positive for Tg. The patient had no other sites of distant metastases. Although PTC has generally a good prognosis, metastases to the cerebellum can occur, even as the first metastatic site, despite the fact that appropriate therapy (surgery, radioactive iodine therapy, TSH suppression therapy, chemotherapy and external radiotherapy) had been given for the primary tumour.