Clinical Endocrinology (CLIN ENDOCRINOL )

Publisher: Blackwell Publishing

Description

Clinical Endocrinology publishes papers and reviews which focus on the practical aspects of clinical endocrinology, such as protocols for investigation of endocrine disorders, imaging in endocrinology and the clinical application of molecular endocrinology. It also features reviews, current therapy papers and cases of the month. Clinical Endocrinology is essential reading not only for those engaged in endocrinological research but also for those involved primarily in clinical practice.

Impact factor 3.35

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    Impact factor
  • 5-year impact
    3.26
  • Cited half-life
    7.40
  • Immediacy index
    0.87
  • Eigenfactor
    0.02
  • Article influence
    0.99
  • Website
    Clinical Endocrinology website
  • Other titles
    Clinical endocrinology (Oxford, England: Online)
  • ISSN
    0300-0664
  • OCLC
    46569692
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Blackwell Publishing

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
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    • Some journals impose embargoes typically of 6 or 12 months, occasionally of 24 months
    • no listing of affected journals available as yet
  • Conditions
    • See Wiley-Blackwell entry for articles after February 2007
    • Publisher's version/PDF cannot be used
    • On author's server, institutional server or subject-based server
    • Server must be non-commercial
    • Publisher copyright and source must be acknowledged with set statement ("The definitive version is available at www.blackwell-synergy.com")
    • Articles in some journals can be made Open Access on payment of additional charge
    • 'Blackwell Publishing' is an imprint of 'Wiley'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: We are aware of no study examining the effects of selenium supplementation on metabolic profiles of patients with polycystic ovary syndrome (PCOS). This study was conducted to evaluate the effects of selenium supplementation on glucose homeostasis parameters and lipid concentrations in women with PCOS. This randomized, double-blind, placebo-controlled trial was conducted among 70 women diagnosed with PCOS and aged 18-40 years old. Participants were randomly divided into two groups to receive 200 μg per day selenium supplements (N=35) or placebo (N=35) for 8 weeks. Fasting blood samples were taken at baseline and after 8 weeks' intervention to quantify glucose, insulin and lipid concentrations. After 8 weeks of intervention, subjects who received selenium supplements had significantly decreased serum insulin levels (-29.83±47.29 vs. +9.07±77.12 pmol/L, P=0.013), homeostasis model of assessment-insulin resistance (HOMA-IR) (-1.15±1.81 vs. +0.42±3.09, P=0.011), homeostatic model assessment-Beta cell function (HOMA-B) (-19.06±30.95 vs. +4.55±47.99, P=0.017) and increased quantitative insulin sensitivity check index (QUICKI) (+0.03±0.04 vs. +0.0009±0.05, P=0.032) compared with placebo. In addition, supplementation with selenium resulted in a significant reduction in serum triglycerides (-0.14±0.55 vs. +0.11±0.30 mmol/L, P=0.025) and VLDL-C concentrations (-0.03±0.11 vs. +0.02±0.06 mmol/L, P=0.025) compared with placebo. In conclusion, 200 microgram per day selenium supplementation for 8 weeks among PCOS women had beneficial effects on insulin metabolism parameters, triglycerides and VLDL-C levels; however, it did not affect FPG and other lipid profiles. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 12/2014;
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    ABSTRACT: Medullary thyroid carcinoma (MTC) is a rare disease that can be inherited or sporadic; its pathogenesis is related to activating mutations in the RET gene. This study describes our 20 year experience regarding RET genetic screening in MTC. We performed RET genetic screening in 1556 subjects, 1007 with an apparently sporadic MTC, 95 with a familial form and 454 relatives of RET positive MTC patients. A germline RET mutation was found in 68/1007 (6.7%) sporadic MTC patients while 939 MTC patients were negative for germline RET mutations. We then identified a total of 137 gene carriers (GC). These subjects initiated a clinical evaluation for the diagnosis of MEN 2. A total of 139 MEN 2 families have been followed: 94 FMTC, 33 MEN 2A, 12 MEN 2B. Thirty-three different germline RET mutations were identified. Codon 804 was the most frequently altered codon particularly in FMTC (32/94, 34%) while codon 634 was the most frequently altered codon in MEN 2A (31/33, 94%); MEN 2B cases were exclusively associated with an M918T mutation at exon 16. Our 20 year study demonstrated that RET genetic screening is highly specific and sensitive, it allows the reclassification as hereditary of apparently sporadic cases and the identification of GC who require an adequate follow-up. We confirmed that FMTC is the most prevalent MEN 2 syndrome and that it is strongly correlated with non-cysteine RET mutations. According to these findings, a new paradigm of follow up of hereditary MTC cases might be considered in the next future. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 12/2014;
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    ABSTRACT: hyperparathyroidism is a frequent cause of hypercalcaemia. Primary hyperparathyroidism, induced by a solitary parathyroid adenoma (PTA) and less frequently multiple PTA's, has an estimated prevalence of 3 in 1000 patients (1). The diagnosis is usually based on an elevated serum calcium concentration and a raised or inappropriately normal parathyroid hormone (PTH) concentration. If treatment is indicated, surgery is the treatment modality of choice for most patients. Recently, minimally invasive approaches have been introduced which have less complications compared to a classic open surgical procedure. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 11/2014;
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    ABSTRACT: We thank Agilli et al.(1) for their comments and the opportunity to clarify a number of points from our work entitled 'Biomarkers and insulin sensitivity in women with PCOS: Characteristics and predictive capacity'.(2) Agilli et al., raised concerns regarding potential confounding factors for leptin(1) . We noted in our study by Cassar et al., and made reference to other papers outlining this cohort, that participants underwent a screening process to assess eligibility.(2, 3) This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 11/2014;
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    ABSTRACT: Centripetal obesity is associated with systemic low-grade inflammation and an increased cardiovascular risk. Patients in long-term remission of Cushing's syndrome (CS) report persisting abdominal fat accumulation. However, this has previously not been adequately objectified. Therefore we investigated the adipose tissue distribution and adipocytokine profiles of patients in long-term remission of CS.
    Clinical Endocrinology 10/2014;
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    ABSTRACT: The tumour spectrum associated with multiple endocrine neoplasia type 1 (MEN1) has been known for many years. New data suggest that females with MEN1 may face an additional, hitherto unrecognised, risk of early-onset breast cancer. The menin protein is certainly known to have to have a role in regulating estrogen receptor activity; but how robust are the data linking MEN1 to breast cancer? This article examines the published data from the viewpoint of a cancer geneticist and considers whether there really is a justifiable indication for enhanced breast surveillance in women with MEN1. This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 10/2014;
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    ABSTRACT: Objective Augmented brown adipose tissue (BAT) mass and activity leads to higher basic metabolic rate which is beneficial against obesity. Our aim was to investigate whether habitual (i.e., usual weekly participation) physical activity is linked with BAT activity and mass in humans, in a group of patients undergoing 18F-fluorodeoxyglucose positron emission tomography/computed tomography (PET/CT) scanning.DesignCross-sectional study.PatientsForty cancer patients [26 male; 14 female; age 52.7±17.5; body mass index (BMI) 26.4±4.5].MeasurementsPatients completed the “usual week” form of the International Physical Activity Questionnaire and underwent assessment of BAT activity/mass via 18F-fluorodeoxyglucose PET/CT.ResultsWe detected a significant association between habitual physical activity (METs-minute/week) and BAT activity [normalized by BW (τ=0.28, p=0.02), BSA (τ=0.29, p=0.02), and LBM (τ=0.38, p=0.002)]. We also found a significant negative relationship between BMI and BAT activity [normalized by BW (τ=-0.30, p=0.006), BSA (τ=-0.31, p=0.004), and LBM (τ=-0.45, p=0.001)] as well as a significant negative relationship between age and BAT activity [normalized by LBM (τ=-0.28, p=0.01)]. The results also indicate significant differences between low/moderate/high levels of habitual physical activity and BAT activity (P<0.05). Moreover, BAT activity was different across the BMI categories (normal/overweight/obese) in both sexes (P<0.05). Finally, BAT activity was greater in women than in men (P<0.05).Conclusions Increased participation in habitual physical activity is associated with higher BAT activity. Moreover, individuals with normal BMI demonstrate higher BAT activity compared to overweight and obese individuals. Finally, age is inversely linked with BAT activity, while women demonstrate higher BAT activity than men.This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 09/2014; in press.
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    ABSTRACT: Adrenal insufficiency has been reported as cause of severe hypoglycaemia in patients with type 1 diabetes in several case reports [1]. The pathophysiological mechanisms include altered glucose metabolism and impaired hormonal counter-regulatory response to hypoglycaemia. Thus, lack of cortisol results in increased insulin sensitivity due to reduced hepatic glucose production and enhanced glucose uptake and utilization by peripheral tissues. This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 07/2014;
  • Clinical Endocrinology 03/2014; 80(3).
  • Clinical Endocrinology 12/2013; 79(6).
  • Clinical Endocrinology 04/2013;
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    ABSTRACT: Background Insulin‐like growth factor 1 insensitivity caused by IGF1R mutations has been previously identified as one of the causes of growth impairment in children born small for gestational age (SGA). Objective To analyse the IGF1R in children born SGA. SubjectsFrom an initial cohort of 54 sequential children born SGA, without catch‐up growth, 25 children were selected for this IGF1R study due to the presence of serum IGF‐1 values above the mean for their age and sex. Methods The proximal IGF1R promoter region, the entire coding region and the exon–intron boundaries were directly sequenced, and multiplex ligation‐dependent probe amplification analysis was performed. Fibroblast cultures were developed from one patient with a mutation for the in vitro characterization of IGF‐1 insensitivity. ResultsThe copy number variation analysis did not identify deletions involving the IGF1R gene. We identified two children carrying heterozygous nucleotide substitutions in IGF1R : c.16G>A/p.Gly6Arg and c.1531C>T/p.Arg511Trp. The first variant (p.Gly6Arg) was identified in control subjects (0·3%) and in a relative with normal growth; thus, it was considered to be a rare benign allelic variation. The second variant (p.Arg511Trp) was not found in 306 alleles from control subjects, and it segregated with the growth impairment phenotype in the patient's family. Fibroblasts obtained from this patient had a significantly reduced proliferative response and AKT phosphorylation after IGF‐1 stimulation compared with control fibroblasts. Conclusion The identification of an inactivating IGF1R mutation in the present cohort should encourage further studies of larger series to establish the precise frequency of this molecular defect in children with growth impairment of a prenatal onset.
    Clinical Endocrinology 04/2013; 78(4).
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    ABSTRACT: Sex hormone binding globulin (SHBG) is a glycoprotein composed of two 373‐amino‐acid subunits. The SHBG gene and a promotor region have been identified. The SHBG receptor has yet to be cloned but is known to act through a G‐protein‐linked second‐messenger system following plasma membrane binding. The principal function of SHBG has traditionally been considered to be that of a transport protein for sex steroids, regulating circulating concentrations of free (unbound) hormones and their transport to target tissues. Recent research suggests that SHBG has functions in addition to the binding and transport of sex steroids. Observational studies have associated a low SHBG concentration with an increased incidence of type 2 diabetes mellitus (DM) independent of sex hormone levels in men and women. Genetic studies using Mendelian randomization analysis linking three single nucleotide polymorphisms of the SHBG gene to risk of developing type 2 DM suggest SHBG may have a role in the pathogenesis of type 2 DM. The correlation between SHBG and insulin resistance that is evident in a number of cross‐sectional studies is in keeping with the suggestion that the association between SHBG and incidence of type 2 DM is explained by insulin resistance. Several potential mechanisms may account for this association, including the identification of dietary factors that influence SHBG gene transcription. Further research to characterize the SHBG‐receptor and the SHBG second messenger system is required. An interventional study examining the effects on insulin resistance of altering SHBG concentrations may help in determining whether this association is causal.
    Clinical Endocrinology 03/2013; 78(3).
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    ABSTRACT: Infertility with azoospermia requires a diligent search for reversible factors and treatment to restore natural fertility, even though most cases are due to untreatable primary spermatogenic failure and are destined to require consideration of assisted reproductive treatment (ART) options. Complete clinical and diagnostic evaluation is essential for avoiding both unnecessary ART and overlooking important co‐morbidities. Gonadotrophin deficiency is the most treatable cause, resulting from drug effects or congenital or acquired disease, and medical therapy is highly efficacious. A range of uncommon endocrinocrinopathies may also result in reversible azoospermia. Finally, obstructive azoospermia may be surgically remediable in selected cases.
    Clinical Endocrinology 02/2013; 78(2).
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    ABSTRACT: Objective The insulin tolerance test (ITT) is contraindicated in a proportion of patients with suspected ACTH deficiency. The aim of this study was to investigate the diagnostic accuracy of the glucagon stress test (GST) compared with the overnight metyrapone test (OMT) in patients with contraindications to ITT. DesignThis was a prospective comparison of the GST to the OMT in patients with suspected ACTH deficiency and contraindications to the ITT. The OMT was used as the standard for comparison. The study was conducted at two tertiary referral centres for pituitary disease. PatientsSeventy‐eight patients underwent contemporaneous OMT and GST of whom 61 had sufficient suppression of cortisol during the OMT to be included in the comparison. Forty had suffered traumatic brain injury, 36 had organic pituitary disorders and two were classified as ‘other’. MeasurementsACTH sufficiency was defined as 0800h 11‐deoxycortisol ≥ 200 nmol/l on OMT and peak cortisol ≥ 440 nmol/l on GST, as per local reference ranges. ResultsThere was significant discrepancy between the proportion of patients diagnosed with ACTH deficiency using the OMT (39%) and GST (89%). From our data, a GST peak cortisol cut‐off of ≥350 nm provides the combination of optimal sensitivity (71%) and specificity (57%), compared with a higher sensitivity (88%) but poor specificity (11%) using a cut‐off of ≥440 nm. Conclusions The GST should be used with caution as a diagnostic test of ACTH reserve. The OMT should be used in preference to the GST to assess the hypothalamic pituitary adrenal axis where ITT is contraindicated.
    Clinical Endocrinology 01/2013; 78(5).
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    ABSTRACT: Abstract CONTEXT: It has been suggested that patients with papillary thyroid cancer (PTC) harbouring the BRAF(V600E) mutation have a worse prognosis. We showed in PTC that high levels of urokinase plasminogen activator (uPA) and its cognate receptor (uPAR) inversely correlate with disease-free interval (DFI). OBJECTIVES: To investigate the effects of BRAF(V600E) on the expression of uPA and uPAR and to evaluate the prognostic relevance of BRAF(V600E) alone or in combination with uPA and uPAR. DESIGN/SETTING/PATIENTS/INTERVENTION: The case study included 91 patients with PTC. All patients underwent thyroidectomy and radioiodine therapy. Follow-up was available for 75 patients. MAIN OUTCOME MEASURES: The BRAF(V600E) mutation was analysed by sequencing and mutant allele-specific PCR amplification; uPA and uPAR expression by quantitative RT-PCR. RESULTS: BRAF(V600E) was found in 44 of the 91 patients and associated with older age, but not with high-risk clinicopathological features. Urokinase PA and uPAR mRNA levels were higher in tumour tissues by 9·51 ± 1·30 and 4·64 ± 0·44 fold, respectively, compared to normal matched tissues, being significantly higher in BRAF(V600E) -positive patients. In vitro induction of BRAF(V600E) in PCCL3 cells caused a significant increase in both uPA and uPAR mRNAs. Higher levels of uPA and uPAR correlated with lymph node metastases, TNM stage and disease recurrences. Kaplan-Meier and multivariate analyses demonstrated that uPA and uPAR were associated with shorter DFI, while the BRAF(V600E) was not. CONCLUSION: In PTC, BRAF(V600E) induces uPA and uPAR expression. The latter, but not BRAF(V600E) , associates with advanced stages and shorter DFI. If confirmed in larger case studies, they may represent reliable prognostic markers for more accurate risk stratification and postoperative decision-making in patients with PTC.
    Clinical Endocrinology 11/2012; 77(5):780.