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Träfflista för sökning "L773:0300 0664 srt2:(2010-2014)"

Sökning: L773:0300 0664 > (2010-2014)

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1.
  • Alvehus, Malin, et al. (författare)
  • Adipose tissue IL-8 is increased in normal weight women after menopause and reduced after gastric bypass surgery in obese women
  • 2012
  • Ingår i: Clinical Endocrinology. - : Wiley-Blackwell. - 0300-0664 .- 1365-2265. ; 77:5, s. 684-690
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective:  The menopausal transition is characterized by increased body fat accumulation, including redistribution from peripheral to central fat depots. This distribution is associated with an increased risk of type 2 diabetes and cardiovascular disease which are linked to low-grade inflammation. We determined whether postmenopausal women have higher levels of inflammatory markers, compared to premenopausal women. We also wanted to determine if these markers are reduced by stable weight loss in obese women. Design and methods:  Anthropometric data, blood samples, and subcutaneous adipose tissue biopsies were collected from normal weight premenopausal and postmenopausal women and obese women before and 2 years after gastric bypass surgery. Serum protein levels and adipose tissue gene expression of inflammatory markers were investigated. Results:  IL-8 expression in adipose tissue and circulating levels were higher in postmenopausal versus premenopausal women. IL-8 expression was associated with waist circumference, independent of menopausal status. IL-6 expression and serum levels of monocyte chemoattractant protein (MCP)-1 were higher in postmenopausal versus premenopausal women. Two years after gastric bypass surgery, adipose expression of IL-8, tumor necrosis factor-α, and MCP-1 decreased significantly. Serum insulin levels were associated with inflammation-related gene expression before gastric bypass surgery, but these associations disappeared after surgery. Conclusion:  Postmenopausal women have an increased inflammatory response in the subcutaneous fat and circulation. Inflammatory markers in adipose tissue decreased significantly after surgery-induced weight loss. This effect may be beneficial for metabolic control and reduced cardiovascular risk after weight loss. © 2011 Blackwell Publishing Ltd.
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  • Bang, Peter, et al. (författare)
  • Identification and management of poor response to growth-promoting therapy in children with short stature
  • 2012
  • Ingår i: Clinical Endocrinology. - : Blackwell Publishing / Society for Endocrinology. - 0300-0664 .- 1365-2265. ; 77:2, s. 169-181
  • Forskningsöversikt (refereegranskat)abstract
    • Growth hormone (GH) is widely prescribed for children with short stature across a range of growth disorders. Recombinant human (rh) insulin-like growth factor-1 (rhIGF-1) therapy is approved for severe primary IGF-I deficiency a state of severe GH resistance. Evidence is increasing for an unacceptably high rate of poor or unsatisfactory response to growth-promoting therapy (i.e. not leading to significant catch up growth) in terms of change in height standard deviation score (SDS) and height velocity (HV) in many approved indications. Consequently, there is a need to define poor response and to prevent or correct it by optimizing treatment regimens within accepted guidelines. Recognition of a poor response is an indication for action by the treating physician, either to modify the therapy or to review the primary diagnosis leading either to discontinuation or change of therapy. This review discusses the optimal investigation of the child who is a candidate for GH or IGF-1 therapy so that a diagnosis-based choice of therapy and dosage can be made. The relevant parameters in the evaluation of growth response are described together with the definitions of poor response. Prevention of poor response is addressed by discussion of strategy for first-year management with GH and IGF-1. Adherence to therapy is reviewed as is the recommended action following the identification of the poorly responding patient. The awareness, recognition and management of poor response to growth-promoting therapy will lead to better patient care, greater cost-effectiveness and increased opportunities for clinical benefit.
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  • Birgander, Mats, et al. (författare)
  • Adrenergic and cardiac dysfunction in primary hyperparathyroidism.
  • 2012
  • Ingår i: Clinical Endocrinology. - : Wiley. - 1365-2265 .- 0300-0664. ; 76, s. 189-195
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Primary hyperparathyroidism (PHPT) is associated with cardiovascular morbidity and premature death but the underlying mechanisms are incompletely understood. The aim of this study was to investigate if adrenergic dysfunction may be a contributing factor. Patients and methods: Forty-nine patients with mild PHPT (serum calcium 2.7 ± 0.1 mmol/L) and 48 control subjects, matched for age and sex, were examined; patients within 1 month before parathyroidectomy (PTX) and 6 months postoperatively; control subjects at inclusion. Heart rate variability (HRV) was analyzed in 24-hour electrocardiograms, and plasma concentrations of epinephrine and norepinephrine were measured at rest and immediately after standardized physical tests. Results: At baseline, the patients showed, compared to the controls, reduced stress-related increase of circulating epinephrine (P < 0.05) and norepinephrine (P < 0.05). No significant change was observed 6 months after PTX. At baseline, there were no significant differences between patients and controls in HRV or heart rate but 6 months after curative PTX, the patients showed significantly reduced HRV in both frequency and time domain, and their maximum and average heart rate had decreased (P = 0.011 and P = 0.018, respectively). The patients with the highest preoperative levels of circulating parathyroid hormone showed the greatest changes in heart rate and HRV postoperatively. Conclusions: This study demonstrates a previously unknown impairment of catecholamine response to physical stress in PHPT along with changes of HRV, also indicating adrenergic dysfunction. These factors should be considered in the ongoing controversy regarding the management of patients with mild "asymptomatic" PHPT.
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5.
  • Brorsson, Camilla, et al. (författare)
  • Saliva stimulation with glycerine and citric acid does not affect salivary cortisol levels
  • 2014
  • Ingår i: Clinical Endocrinology. - : Wiley. - 0300-0664 .- 1365-2265. ; 81:2, s. 244-248
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE:In critically ill patients with hypotension, who respond poorly to fluids and vasoactive drugs, cortisol insufficiency may be suspected. In serum over 90% of cortisol is protein-bound, thus routine measures of total serum cortisol may yield 'false lows' due to hypoproteinaemia. Thus, the occurrence of cortisol insufficiency could be overestimated in critically ill patients. Salivary cortisol can be used as a surrogate for free serum cortisol, but in critically ill patients saliva production is decreased, and insufficient volume of saliva for analysis is a common problem. The aim of this study was to investigate if a cotton-tipped applicator with glycerine and citric acid could be used for saliva stimulation without affecting salivary cortisol levels.DESIGN:Prospective, observational study.PARTICIPANTS:Thirty-six volunteers (six males, 30 females), age 49 ± 9 years, without known oral mucus membrane rupture in the mouth.MEASUREMENTS:Forty-two pairs of saliva samples (22 paired morning samples, 20 paired evening samples) were obtained before and after saliva stimulation with glycerine and citric acid. Salivary cortisol was analysed using Spectria Cortisol RIA (Orion Diagnostica, Finland).RESULTS:The paired samples correlated significantly (P < 0·0001) and there was no significant difference between un-stimulated and stimulated salivary cortisol levels.CONCLUSIONS:Saliva stimulation with a cotton-tipped applicator containing glycerine and citric acid did not significantly influence salivary cortisol levels in healthy volunteers. This indicates that salivary cortisol measurement after saliva stimulation may be a useful complement when evaluating cortisol status in critically ill patients.
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8.
  • Cervato, Sara, et al. (författare)
  • AIRE gene mutations and autoantibodies to interferon omega in patients with chronic hypoparathyroidism without APECED
  • 2010
  • Ingår i: Clinical Endocrinology. - : Wiley. - 0300-0664 .- 1365-2265. ; 73:5, s. 630-636
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective To assess autoimmune regulator (AIRE) gene mutations, class II HLA haplotypes, and organ- or non-organ-specific autoantibodies in patients with chronic hypoparathyroidism (CH) without associated Addison's disease (AD) or chronic candidiasis (CC). Patients and Measurements Twenty-four patients who had CH without AD or CC were included in the study. AIRE gene mutations in all 14 exons were studied using PCR in 24 patients, 105 healthy controls and 15 first-degree relatives of CH patients with AIRE mutations. Human leucocyte antigens (HLA) were determined for all 24 patients and 105 healthy controls. Autoantibodies to a range of antigens including NACHT leucine-rich-repeat protein-5 (NALP5) and interferon omega (IFN omega) were tested in all 24 patients. Results AIRE gene mutations were found in 6 of 24 (25%) patients, all females, and this was significantly higher (P < 0.001) compared with AIRE mutations found in healthy controls (2/105). Three patients (12.5%) had homozygous AIRE mutations characteristic of Autoimmune-Poly-Endocrinopathy-Candidiasis-Ectodermal-Dystrophy and all three were also positive for IFN omega-autoantibodies. Three patients (12.5%) had heterozygous AIRE mutations; two of these were novel mutations. One of the patients with heterozygous AIRE mutations was positive for both NACHT leucine-rich-repeat protein 5 and IFN omega autoantibodies. Heterozygous AIRE mutations were found in 10 of 15 first-degree relatives of CH patients with AIRE mutations, although none was affected by CH. Class II HLA haplotypes were not statistically different in patients with CH compared to healthy controls. Conclusions Analysis of AIRE gene mutations together with serum autoantibody profile should be helpful in the assessment of patients with CH, in particular young women with associated autoimmune diseases.
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9.
  • Crump, Casey, et al. (författare)
  • PRETERM BIRTH AND RISK OF MEDICALLY TREATED HYPOTHYROIDISM IN YOUNG ADULTHOOD.
  • 2011
  • Ingår i: Clinical Endocrinology. - : Wiley. - 1365-2265 .- 0300-0664. ; 75, s. 255-260
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Previous studies suggest that low birth weight is associated with thyroid autoimmunity and hypothyroidism in later life, but the potential effect of preterm birth, independent of fetal growth, is unknown. Our objective was to determine whether preterm birth is independently associated with medically treated hypothyroidism in young adulthood. Design/Participants: National cohort study of 629,806 individuals born in Sweden from 1973 through 1979, including 27,935 born preterm (<37 weeks). Measurements: Thyroid hormone prescription during 2005-2009 (ages 25.5-37.0 years), obtained from all outpatient and inpatient pharmacies throughout Sweden. Results: Preterm birth was associated with increased relative odds of thyroid hormone prescription in young adulthood, after adjusting for fetal growth and other potential confounders. This association appeared stronger among twins than singletons (P=0.04 for the interaction). Twins had increased relative odds across the full range of preterm gestational ages, whereas singletons had increased relative odds only if born very preterm (23-31 weeks). Among twins and singletons, respectively, adjusted odds ratios for individuals born preterm (<37 weeks) were 1.54 (95% CI, 1.11-2.14) and 1.08 (95% CI, 0.98-1.19), and for individuals born very preterm (23-31 weeks) were 2.62 (95% CI, 1.30-5.27) and 1.59 (95% CI, 1.18-2.14), relative to full-term births. Conclusions: This national cohort study suggests that preterm birth is associated with an increased risk of medically treated hypothyroidism in young adulthood. This association was independent of fetal growth and appeared stronger among twins than singletons. Additional studies are needed to confirm these new findings in other populations and to elucidate the mechanisms.
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10.
  • Decker, Ralph, 1968, et al. (författare)
  • Decreased GH dose after the catch-up growth period maintains metabolic outcome in short prepubertal children with and without classic GH deficiency
  • 2012
  • Ingår i: Clinical endocrinology. - : Wiley. - 0300-0664 .- 1365-2265. ; 77:3, s. 407-15
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Few studies have evaluated metabolic outcomes following growth hormone (GH) treatment in short prepubertal children during different periods of growth. Previously, we found that individualized GH dosing in the catch-up period reduced the variation in fasting insulin levels by 34% compared with those receiving a standard GH dose. We hypothesized that the GH dose required to maintain beneficial metabolic effects is lower during the prepubertal growth phase after an earlier catch-up growth period. DESIGN: Short prepubertal children with isolated GH deficiency or idiopathic short stature were randomized to individualized GH treatment (range, 17-100 mug/kg/day) or a standard dose in a preceding 2-year study. After achieving near mid-parental height(SDS) (,) children receiving an individualized dose were randomized to either a 50% reduced individualized dose (RID, n=28) or an unchanged individualized dose (UID, n=37) for 2 years. The dose remained unchanged in 33 children initially randomized to receive a standard dose (FIX, 43 mug/kg/day).We evaluated whether the variations in metabolic parameters measured during maintenance growth diminished in RID compared with UID or FIX. RESULTS: We observed less variation in fasting insulin levels (-50%), insulin sensitivity as assessed by homeostasis model assessment (-55.1%), lean soft tissue (-27.8%) and bone mineral content (-31.3%) in RID compared with UID (all p<0.05), but no differences compared with FIX. CONCLUSIONS: Continued individualized GH treatment after the catch-up growth period is safe and reduces hyperinsulinism. Individualized GH dose can be reduced once the desired height(SDS) is achieved to avoid overtreatment in terms of metabolic outcome.
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