Clinical Endocrinology (CLIN ENDOCRINOL)

Publisher: Wiley

Journal 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.

Current impact factor: 3.35

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 3.353
2012 Impact Factor 3.396
2011 Impact Factor 3.168
2010 Impact Factor 3.323
2009 Impact Factor 3.201
2008 Impact Factor 3.398
2007 Impact Factor 3.37
2006 Impact Factor 3.358
2005 Impact Factor 3.412
2004 Impact Factor 3.023
2003 Impact Factor 2.767
2002 Impact Factor 2.674
2001 Impact Factor 2.465
2000 Impact Factor 2.922
1999 Impact Factor 2.833
1998 Impact Factor 3.101
1997 Impact Factor 2.447
1996 Impact Factor 2.414
1995 Impact Factor 2.279
1994 Impact Factor 2.657
1993 Impact Factor 2.642
1992 Impact Factor 2.211

Impact factor over time

Impact factor
Year

Additional details

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

Wiley

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Some journals have separate policies, please check with each journal directly
    • On author's personal website, institutional repositories, arXiv, AgEcon, PhilPapers, PubMed Central, RePEc or Social Science Research Network
    • Author's pre-print may not be updated with Publisher's Version/PDF
    • Author's pre-print must acknowledge acceptance for publication
    • On a non-profit server
    • Publisher's version/PDF cannot be used
    • Publisher source must be acknowledged with citation
    • Must link to publisher version with set statement (see policy)
    • If OnlineOpen is available, BBSRC, EPSRC, MRC, NERC and STFC authors, may self-archive after 12 months
    • If OnlineOpen is available, AHRC and ESRC authors, may self-archive after 24 months
    • Publisher last contacted on 07/08/2014
    • This policy is an exception to the default policies of 'Wiley'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Follicle-stimulating hormone plays a crucial role in spermatogenesis. The aim of this study was to evaluate the efficacy of treatment with FSH in Chinese infertility population. Prospective, randomized double-blind, placebo-controlled clinical study. 354 men affected by idiopathic oligozoospermia from three medical centers. This study contained three parts: (1) Treatment with different doses of rhFSH (50IU, 100IU, 200IU and 300IU); (2) The efficacy of rhFSH at different periods (2, 3, 4, 5 months); (3) FSH treatment in patients with different levels of inhibin B (normal level group, low level group and high level group). Semen parameters were evaluated in all subjects. The patients who had not reached spontaneous pregnancy underwent assisted reproductive techniques. Sperm number was significantly increased after treatment with FSH at doses of at least 200 IU, and the improvement was observed beginning at the third month. The significant improvement in both morphology and forward motility were observed beginning at the fifth month. Moreover, 300IU rhFSH administration for 5 months could significantly improve the spontaneous pregnancy rate (12/40) and ART pregnancy rate (14/28), while the rates for placebo group were 2/29 and 5/27, respectively. The seminal parameters (total sperm count, sperm concentration, forward motility and morphology) were significantly improved in the normal and low level inhibin B groups, but no significant variation was observed in the high level group at the end of the study. The efficacy of FSH treatment was associated with the dose of FSH and duration of treatment, and FSH therapy was more effective in patients with normal and low level of inhibin B. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 03/2015; DOI:10.1111/cen.12770
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    ABSTRACT: Acromegaly is a chronic disorder usually diagnosed late in the disease evolution. Such delayed diagnosis may result in substantial morbidity and mortality as well as the inability to achieve the treatment goals of normalizing biochemical disease markers and controlling tumour mass without harming normal pituitary function. Somatostatin analogues (SSA) are accepted as first-line medical therapy or as second-line therapy in patients undergoing unsuccessful surgery and are considered a cornerstone in the treatment of acromegaly. However, because a high percentage of patients experience SSA treatment failure, the identification of biomarkers associated with a successful or unsuccessful response to all classes of medical therapy would help in the choice of treatment and potentially allow for a quicker normalization of biochemical parameters. The current treatment algorithms for acromegaly are based upon a "trial and error" approach with additional treatment options provided when disease is not controlled. In many other diseases, therapeutic algorithms have been evolving towards personalized treatment with medication that best matches individual disease characteristics, using biomarkers that identify therapeutic response. Additionally, a personalized approach to complementary treatment of comorbidities present in the acromegalic patient is also required. This paper will discuss the development of a potential treatment algorithm for acromegaly addressing the biochemical control of the disease as well of its associated comorbidities, under a personalized approach based upon markers of prognostic and predictive significance, such as tumour size, MRI adenoma signal, GH value after acute octreotide test, granular adenoma pattern, Ki-67, somatostatin receptor phenotype, AIP expression, gsp mutations, RAF kinase activity, E-cadherin and beta arrestin-1. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 02/2015; DOI:10.1111/cen.12731
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    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; DOI:10.1111/cen.12699
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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; DOI:10.1111/cen.12686
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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; DOI:10.1111/cen.12681
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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; DOI:10.1111/cen.12678
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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; 82(2). DOI:10.1111/cen.12639
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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; 82(3). DOI:10.1111/cen.12614
  • Clinical Endocrinology 03/2014; 80(3). DOI:10.1111/cen.12244
  • Clinical Endocrinology 12/2013; 79(6). DOI:10.1111/cen.12273
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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 05/2013; 78(5). DOI:10.1111/cen.12043
  • 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). DOI:10.1111/cen.12048
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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). DOI:10.1111/cen.12086
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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). DOI:10.1111/cen.12026
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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.