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
    3.40
    Show impact factor history
     
    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
  • Restrictions
    • 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 version cannot be used
    • On author or institutional 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-Blackwell'
  • Classification
    ​ yellow

Publications in this journal

  • Clinical Endocrinology 01/2014; 80(3).
  • Clinical Endocrinology 04/2013;
  • Source
    [Show abstract] [Hide abstract]
    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 01/2013; 78(2).
  • Clinical Endocrinology 01/2013; 79(6).
  • [Show abstract] [Hide abstract]
    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 01/2013; 78(3).
  • [Show abstract] [Hide abstract]
    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 01/2013; 78(4).
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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.
  • Clinical Endocrinology 01/2011; 75(4).
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    ABSTRACT: Objective To determine the frequency distribution of LMNA 1908C>T SNP and its association with generalized obesity, abdominal obesity and coexistent metabolic disorders in nondiabetic Asian Indians living in a metropolitan city of north India.Design A cross‐sectional population‐based study of LMNA 1908C>T polymorphism with obesity and insulin resistance as outcome.Patients Five hundred and fifty‐one Asian Indians, with 240 obese and 289 nonobese subjects.Measurements Allelic and genotypic frequency of LMNA 1908C>T were determined by PCR‐RFLP. Association of LMNA alleles and genotypes was analysed with various measures of obesity [BMI ≥25 kg/m2, percentage body fat (by DEXA); subcutaneous and intra‐abdominal fat at L2–3 level by single slice MRI in a subsample and surrogate marker of insulin resistance (fasting serum insulin levels >10 μU/ml in men and >11 μU/ml in women).Results Forty‐six per cent of the subjects had generalized obesity while 54% had abdominal obesity. Frequency of C and T alleles was 0·71 and 0·29, respectively. Higher frequency of variant allele (T) was observed in obese than nonobese individuals (P = 0·001). On multivariate analysis adjusting for age, gender and serum insulin levels, subjects with LMNA1908T/T genotype were at 5·6 times higher risk [OR (95% CI): 5·6 (2·5–12·2), P = 0·001], while individuals with genotypes with at least one T allele, i.e. 1908C/T and T/T genotypes, were at 2·7 times higher odds to develop generalized obesity [OR (95% CI): 2·7 (1·8–4·1), P = 0·001].Conclusion LMNA 1908T/T and C/T genotypes emerged as independent genetic risk factors for generalized obesity in Asian north Indians.
    Clinical Endocrinology 01/2011; 75(5).
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    ABSTRACT: Objective The percentage of patients with thyroid cancer incidentally diagnosed during a 18F‐fluorodeoxyglucose Positron Emission Tomography with computed tomography (CT) (FDG‐PET/CT) for nonthyroid diseases ranges between 26% and 50%.Design Retrospective assessment of the clinical and pathological features of thyroid incidentalomas at FDG‐PET/CT, aiming to identify potential predictors of malignancy.Patients Fifty‐two patients with incidental thyroid uptake at FDG‐PET/CT were retrospectively included [38 W, age 64·1 ± 12·5 years (mean ± SD)]. An arbitrary cut‐off level of 5·0 for the ‘maximum standardized uptake value’ (SUV max) was chosen to differentiate benign from malignant tumours. Complete thyroid function, neck ultrasonography (US) features, and cyto‐histological results were reported for all cases.Results In our institution, the prevalence of incidental thyroid 18F‐fluorodeoxyglucose (18F‐FDG) uptake was nearly 1·76%. The prevalence of focal uptake correlated with greater risk of malignancy (P P 5·0 (P Conclusions The presence of focal uptake with high SUV max and euthyroidism correlate with high likelihood of malignancy. Performing a neck US would have to be recommended in all patients with euthyroidism and an incidental FDG‐PET/CT focal thyroid uptake. We do not suggest to use FDG‐PET/CT as a screening tool for thyroid cancer in the general population, because of both its high cost and low incidence of thyroid incidentaloma at FDG‐PET/CT.
    Clinical Endocrinology 01/2011; 75(4).
  • Clinical Endocrinology 01/2009; 72(1):32-7.
  • Clinical Endocrinology 02/2008; 68(1):153-4.
  • Clinical Endocrinology 02/2008; 68(1):1.

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