A note on a core catcher of a cooperative game

In Driessen (1986) it is shown that for games satisfying a certain condition the core of the game is included in the convex hull of the set of certain marginal worth vectors of the game, while it is conjectured that the inclusion holds without any condition on the game. In this note it is proved that the inclusion holds for all games

Thyroid-hormone therapy and thyroid cancer: a reassessment.

Experimental studies and clinical data have demonstrated that thyroid-cell proliferation is dependent on thyroid-stimulating hormone (TSH), thereby providing the rationale for TSH suppression as a treatment for differentiated thyroid cancer. Several reports have shown that hormone-suppressive treatment with the L-enantiomer of tetraiodothyronine (L-T(4)) benefits high-risk thyroid cancer patients by decreasing progression and recurrence rates, and cancer-related mortality. Evidence suggests, however, that complex regulatory mechanisms (including both TSH-dependent and TSH-independent pathways) are involved in thyroid-cell regulation. Indeed, no significant improvement has been obtained by suppressing TSH in patients with low-risk thyroid cancer. Moreover, TSH suppression implies a state of subclinical thyrotoxicosis. In low-risk patients, the goal of L-T(4) treatment is therefore to obtain a TSH level in the normal range (0.5-2.5 mU/l). Only selected patients with high-risk papillary and follicular thyroid cancer require long-term TSH-suppressive doses of L-T(4). In these patients, careful monitoring is necessary to avoid undesirable effects on bone and heart

Thyroid stimulating hormone (TSH) ≥2.5mU/l in early pregnancy: prevalence and subsequent outcomes

Objective: There remains controversy over how women with abnormal thyroid function tests in pregnancy should be classified. In this study we assessed the proportion of women with thyroid stimulating hormone (TSH) ≥ 2.5 mU/l in a large obstetric cohort, and examined how many have gone on to develop thyroid disease in the years since their pregnancy. Study design: 4643 women were recruited and samples taken in early pregnancy between 2007 and 2010. Thyroid function tests were analysed in 2014; in women with raised TSH computerised health records and prescription databases were used to identify thyroid disease detected since pregnancy. Results: 58 women (1.5%) had a TSH over 5 mU/l and 396 women (10.3%) had TSH between 2.5 and 5 mU/l. Women with TSH > 5mU/l delivered infants of lower birthweight than those with TSH < 2.5 mU/l; there were no other differences in obstetric outcomes between the groups. Of those who have had thyroid tests since their pregnancy, 78% of those with TSH > 5 mU/l and 19% of those with TSH between 2.5 and 5 mU/l have gone on to be diagnosed with thyroid disease. Conclusions: Using a TSH cut-off of 2.5 mU/l in keeping with European and US guidelines means that over 12% of women in this cohort would be classified as having subclinical hypothyroidism. Treatment and monitoring of these women would have major implications for planning of obstetric services

Thyroxine treatment with softgel capsule formulation. Usefulness in hypothyroid patients without malabsorption

Background: Levothyroxine sodium (LT4) is the therapy of choice for hypothyroidism. In the last decade, new LT4 formulations, such as liquid and softgel capsules, became available. Even if some evidence has been reached in the efficacy of liquid LT4 in patients with suboptimal TSH on tablet LT4, the usefulness of softgel LT4 has been rarely studied. This study aimed at evaluating the effect of switching from tablet to softgel LT4 patients without increased need for LT4. TSH was used as proxy of LT4 bioavailability and effectiveness. Methods: During the period from April to August 2017, 19 patients on tablet LT4 treatment for hypothyroidism, mostly due to autoimmune thyroiditis, were enrolled. Subjects with causes of malabsorption or increased requirement of LT4 were previously excluded. Patients finally included were asked to switch from tablet to softgel LT4 formulation at unchanged dose and ingestion fashion (30 min before breakfast). TSH was measured with chemiluminescence immunoassays. results: According to exclusion and inclusion criteria, 19 patients were finally selected. One of these had headache 4 days later and come back to tablet LT4, and 18 of them (16W/2M; mean age = 55 years; BMI 22.7 kg/m2) completed the study. They were treated with a median LT4 dose of 88 μg/day and showed a median TSH value of 3.33 mIU/L. The rate of cases with TSH ≤ 4.0 mIU/L was 61.1% (11/18 cases). When patients were re-evaluated after 3 months of softgel LT4, we observed that TSH reached levels under 4.0 mIU/L in 16/18 (88.9%) patients, TSH was lower in 11 cases, and in 6 out of 7 patients with pre-switch TSH values over the normal range. Overall, TSH values on softgel LT4 (median 1.90 mIU/L) was significantly lower from that observed during tablet LT4 (p = 0.0039). conclusion: These data show that hypothyroid patients with no proven malabsorption may have an improved TSH following 3 months from the switch from tablet to softgel LT4 preparation at unchanged dose

TRH: Pathophysiologic and clinical implications

Thyrotropin releasing hormone is thought to be a tonic stimulator of the pituitary TSH secretion regulating the setpoint of the thyrotrophs to the suppressive effect of thyroid hormones. The peptide stimulates the release of normal and elevated prolactin. ACTH and GH may increase in response to exogenous TRH in pituitary ACTH and GH hypersecretion syndromes and in some extrapituitary diseases. The pathophysiological implications of extrahypothalamic TRH in humans are essentially unknown. The TSH response to TRH is nowadays widely used as a diganostic amplifier in thyroid diseases being suppressed in borderline and overt hyperthyroid states and increased in primary thyroid failure. In hypothyroid states of hypothalamic origin, TSH increases in response to exogenous TRH often with a delayed and/or exaggerated time course. But in patients with pituitary tumors and suprasellar extension TSH may also respond to TRH despite secondary hypothyroidism. This TSH increase may indicate a suprasellar cause for the secondary hypothyroidism, probably due to portal vessel occlusion. The TSH released in these cases is shown to be biologically inactive

TSH-CHECK-1 test: diagnostic accuracy and potential application to initiating treatment for hypothyroidism in patients on anti-tuberculosis drugs.

Thyroid-stimulating hormone (TSH) promotes expression of thyroid hormones which are essential for metabolism, growth, and development. Second-line drugs to treat tuberculosis (TB) can cause hypothyroidism by suppressing thyroid hormone synthesis. Therefore, TSH levels are routinely measured in TB patients receiving second-line drugs, and thyroxin treatment is initiated where indicated. However, standard TSH tests are technically demanding for many low-resource settings where TB is prevalent; a simple and inexpensive test is urgently needed

Evaluation of the ADVIA (R) Centaur (TM) TSH-3 assay

An analytical evaluation of the thyroid stimulating hormone (TSH-3) assay on the Sayer ADVIA(R) Centaur(TM) immunoassay system was performed. General analytical requirements (linearity, resistance to typical interferences, absence of a carry-over effect) were fulfilled and reproducibility was satisfactory. Inter-assay coefficient of variation (CV) of a human serum pool with a concentration of 0.014 mU/l was 22.3%; at concentrations between 0.26 and 83 mU/l CV was below 6%. Method comparison study demonstrated close agreement of TSH results compared to those obtained with the Roche Elecsys(R) 2010 TSH assay (ADVIA Centaur = 1.08 x Elecsys - 0.18 mU/l; r = 0.987; n = 324). Handling and practicability of the ADVIA Centaur system proved to be convenient with a very high sample throughput. We conclude that the ADVIA Centaur TSH-3 assay meets requirements for clinical use

Intrauterine Zn deficiency favors thyrotropin-releasing hormone-increasing effects on thyrotropin serum levels and induces subclinical hypothyroidism in weaned rats

Individuals who consume a diet deficient in zinc (Zn-deficient) develop alterations in hypothalamic-pituitary-thyroid axis function, i.e., a low metabolic rate and cold insensitivity. Although those disturbances are related to primary hypothyroidism, intrauterine or postnatal Zn-deficient adults have an increased thyrotropin (TSH) concentration, but unchanged thyroid hormone (TH) levels and decreased body weight. This does not support the view that the hypothyroidism develops due to a low Zn intake. In addition, intrauterine or postnatal Zn-deficiency in weaned and adult rats reduces the activity of pyroglutamyl aminopeptidase II (PPII) in the medial-basal hypothalamus (MBH). PPII is an enzyme that degrades thyrotropin-releasing hormone (TRH). This hypothalamic peptide stimulates its receptor in adenohypophysis, thereby increasing TSH release. We analyzed whether earlier low TH is responsible for the high TSH levels reported in adults, or if TRH release is enhanced by Zn deficiency at weaning. Dams were fed a 2 ppm Zn-deficient diet in the period from one week prior to gestation and up to three weeks after delivery. We found a high release of hypothalamic TRH, which along with reduced MBH PPII activity, increased TSH levels in Zn-deficient pups independently of changes in TH concentration. We found that primary hypothyroidism did not develop in intrauterine Zn-deficient weaned rats and we confirmed that metal deficiency enhances TSH levels since early-life, favoring subclinical hypothyroidism development which remains into adulthood

Longitudinal evidence of the impact of normal thyroid stimulating hormone variations on cognitive functioning in very old age

The purpose of this study was to examine longitudinal associations among thyroid stimulating hormone (TSH) levels and cognitive performance. Data collected at the first three assessment times, approximately 3 years apart, are reported for the survivors (n=45) from a previously published cross-sectional study. Participants were aged 75–93 years at baseline, and data reported were collected in the Kungsholmen Project, a longitudinal project investigating aging and dementia. Analyses revealed that although declining verbal fluency and visuospatial abilities were accompanied by simultaneously declining TSH levels, the pattern of cross-sectional and longitudinal results are interpreted such that declining TSH levels may have caused episodic memory deficits later on. These results were obtained in the examination of 6-year but not 3-year change, and after removal of the cognitive variation associated with depressive mood symptoms