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: 3.46

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 3.457
2013 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 3.41
Cited half-life 8.00
Immediacy index 0.92
Eigenfactor 0.02
Article influence 1.07
Website Clinical Endocrinology website
Other titles Clinical endocrinology (Oxford, England: Online)
ISSN 1365-2265
OCLC 46569692
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Wiley

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    • Non-Commercial
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    • 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: Objective: To evaluate the use and interpretation of growth hormone (GH) stimulation tests used across the UK for diagnosing GH deficiency. Background: Previous studies show poor consensus on the use of GH stimulation tests. Sex steroid priming and retesting in the transition period are areas not previously surveyed. Design: Data were collected from tertiary paediatric endocrinologists, paediatricians with a specialist interest in endocrinology, and biochemists across the UK over six months through distributing electronic surveys. Results: At least three different GH stimulation tests were used by 33% of departments. Glucagon and insulin doses varied most, and sampling frequency varied most using insulin. All laboratories use a recommended chemiluminescence immunoassay with an acceptable coefficient of variability. The GH peak for diagnosing GH deficiency varied from 6μg/L to 8μg/L. A wide range of clinical scenarios prompted retesting in the transition period, suggesting non-standardised current practice. Seventy-five percent of departments use sex steroid priming, but follow criteria variously combining bone age, chronological age and pubertal stage, together with variations in steroid type and dose. Conclusions: Although a contentious diagnostic test, GH stimulation tests remain the gold standard for diagnosing GH deficiency. Our data suggest that together with variation in indication, protocol and interpretation, there is considerable variation in current practices pertaining to priming and retesting in transition. Given the current financial climate and the need for careful resource management, this study emphasises the considerable need for consensus in the investigation, diagnosis and long-term follow-up of these children, at least nationally if not internationally. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · Clinical Endocrinology
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    ABSTRACT: Many authors recommend total thyroidectomy for patients with papillary thyroid carcinoma (PTC) > 1 cm, even if the tumor is sporadic, unilateral, ≤ 4 cm, and apparently restricted to the thyroid. In the last edition of the guidelines of the British Thyroid Association (BTA), lobectomy is as accepted for the treatment of patients with PTC as total thyroidectomy if nodular disease is unilateral and the tumor is sporadic, measures ≤ 4 cm, and exhibits no extrathyroid extension (ETE) or apparent lymph node (LN) metastases (cN0). This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · Clinical Endocrinology
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    ABSTRACT: Bariatric surgery is a highly effective treatment for severe obesity, resulting in substantial weight loss and normalizing obesity-related comorbidities. However, long-term consequences can occur, such as post-bariatric surgery hypoglycemia. This is a challenging medical problem, and the number of patients presenting with it has been increasing. Roux-en-Y gastric bypass (RYGB) is the most popular bariatric procedure, and it is the surgery most commonly associated with the development of post-bariatric surgery hypoglycemia. To date, the pathogenesis of this condition has not been completely established. However, various factors-particularly increased post-prandial glucagon-like peptide (GLP)-1 secretion-have been considered as crucial mediator. The mechanisms responsible for diabetic remission after bariatric surgery may be responsible for the development of hypoglycemia, which typically occurs 1-3 hours after a meal and is concurrent with inappropriate hyperinsulinemia. Carbohydrate-rich foods usually provoke hypoglycemic symptoms, which can typically be alleviated by strict dietary modifications, including carbohydrate restriction and avoidance of high-glycemic-index foods and simple sugars. Few patients require further medical intervention, such as medications, but some patients have required a pancreatectomy. Because this option is not always successful, it is no longer routinely recommended. Clinical trials are needed to further determine the pathophysiology of this condition as well as the best diagnostic and treatment approaches for these patients. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · Clinical Endocrinology
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    ABSTRACT: Objective: We investigated the value of the stimulated thyroglobulin (Tg) level at the time of recombinant human thyrotropin (rhTSH)-aided remnant ablation for predicting disease status 1 year later in DTC patients who underwent total thyroidectomy with central neck dissection (CND). Design, setting, and participant: This was a prospective observational study of 253 consecutive DTC patients who underwent rhTSH-aided RAI ablation after total thyroidectomy and prophylactic CND. Patients with evidence of initial distant metastasis or positive Tg antibodies were excluded. Major outcome measure: We compared rhTSH-stimulated Tg level at RAI ablation according to disease status at 1 year and evaluated optimal cutoff value of rhTSH-stimulated Tg. Binary logistic regression analysis was performed to investigate the independent predictive factors for disease status 1 year after ablation RESULTS: Among study participants, 228 (90.1%) were considered disease free at 1 year after remnant ablation. Patients with persistent or recurrent disease were more likely to be aged ≥45 years, and to have N1b stage, TNM stage III or IV, and higher rhTSH-stimulated Tg level at RAI ablation. The optimal cutoff of rhTSH-stimulated Tg for predicting persistent or recurrent disease was 1.79 ng/mL, with a negative predictive value of 99.5%. A serum rhTSH-stimulated Tg level ≥1.79 at the time of ablation was independently associated with persistent or recurrent disease 1 year later. N1b stage tended to be associated with persistent or recurrent disease. Conclusion: A low stimulated serum Tg level at rhTSH-aided RAI ablation may be a favorable prognostic marker in the setting of prophylactic CND. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · Clinical Endocrinology
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    ABSTRACT: Objective: To clarify which factors may influence the serum Tg level in an adult population and how this may affect Tg as a biomarker of iodine deficiency (ID). Design and methods: Two identical cross-sectional studies were performed before (C1a: 1997-98, n=4649) and after (C2: 2004-05, n=3570) the Danish mandatory iodine fortification (IF) of salt (2000). Additionally, a follow-up study of C1a was performed after IF (C1b: 2008-10, n=2465). The studies took place in two regions with mild (Copenhagen) and moderate (Aalborg) ID before IF. Serum Tg was measured by immunoradiometric method and investigated as outcome variable in multivariate models. Results: Multiple factors were associated with serum Tg. Some were directly related to iodine intake (cohort, urinary iodine concentration (UIC) level and region), and some were likely mediators of iodine intake effects on Tg (thyroid nodularity, thyroid size and autonomy with low TSH). Others were caused by Tg assay interference (Tg-Ab positivity), aggravation of ID (childbirths and smoking) or TSH stimulation of the thyroid. Estimated 24-hour urinary iodine excretion was a more sensitive predictor of Tg than UIC. Iodine supplement users had low median Tg values compared with non-users both before and after IF. Conclusions: Multiple factors should be taken into consideration when evaluating Tg as a marker of ID in adult populations, and the Tg results may depend on the assay used. Still, Tg is a sensitive marker of ID. We suggest including a reference population with known sufficient iodine intake when Tg is used to evaluate ID. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · Clinical Endocrinology
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    ABSTRACT: Objective: We aimed to determine outcome predictors of papillary thyroid cancer (PTC) persistence and recurrence, separately. Context: The factors contributing to either persistence or recurrence of PTC are poorly defined, since both outcomes are usually evaluated together. Design and patients: In this 10-year follow-up cohort study, 190 PTC patients were evaluated (18-85 years old; registered from 01/01/1990 to 12/31/1999 at a Brazilian Cancer Care referral Hospital). After initial surgery, we examined persistence (disease detected up to 1 year), recurrence (disease detected after 1 year) and PTC-free status (disease absence during follow-up). Measurements: Outcome predictors were modeled using multinomial logit regression analysis. Results: The univariate analysis showed that persistence and recurrence were significantly associated with lymph node metastasis (OR=12.33; OR=2.84, respectively), local aggressiveness (OR=5.22; OR=3.35), and extrathyroidal extension (OR=5.07; OR=7.11). Persistence was associated with male sex (OR=3.49), age above 45 years old at diagnosis (OR=1.03), macroscopic lymph node metastasis (OR=5.85), local aggressiveness (OR=5.22), each 1-cm tumor size increase (OR=1.34), a cancer care referral hospital as the place of initial surgery (OR=2.3), thyroidectomy or near total-thyroidectomy) OR=3.03) and neck dissection (OR=3.19). Recurrence was associated with the time of radioactive iodine ((131) I) therapy (OR=3.71). After data modeling, persistence was associated with macroscopic lymph node metastasis (OR=6.17), 1-cm increases in tumor size (OR=1.30), and thyroidectomy or near total-thyroidectomy (OR=3.82); while recurrence was associated with surgery at referral hospital (OR=3.79). Conclusions: The best predictors of persistence were tumor size and macroscopic lymph node metastasis; when the initial surgery is of quality, the recurrence depends more on tumor's biology aspects. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · Clinical Endocrinology
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    ABSTRACT: Prader-Willi syndrome (PWS) is characterized by hyperphagia with impaired satiety. PWS patients have very high acylated ghrelin (AG) with normal unacylated ghrelin (UAG) levels, resulting in an elevated AG/UAG ratio, suggesting an intrinsic defect in the ghrelin regulation. Normally, food intake induces satiety and a drop in AG and UAG levels, but it is unknown if these levels also decline in PWS. To evaluate whether the high AG levels in PWS decline in response to glucose intake during an oral glucose tolerance test (OGTT), and to investigate the effects of growth hormone (GH) treatment on this response. Method: Serum levels of AG, UAG and AG/UAG ratio during an OGTT were determined in 24 GH-treated patients with PWS (median age 19.0, range 14.2-25.9 years) and in 10 GH-stop patients (of whom 5 were in GH-treated group; 18.5, 14.5-20.3 years). In GH-treated and GH-stop young adults with PWS, there was a sharp decline of AG levels and a decrease of UAG levels in the first 30 minutes after the glucose load, which resulted in a lower AG/UAG ratio. GH-treated patients had significantly lower AG levels than GH-stop patients at baseline and during the OGTT. All UAG levels and AG/UAG ratios were lower in the GH-treated patients, although not significantly. In young adults with PWS, an oral glucose load significantly reduces AG and UAG levels, suggesting normal regulation of the ghrelin axis by food intake. GH treatment results in lower AG levels at baseline and during OGTT, suggesting a more favorable metabolic profile. Our findings might suggest that the impaired satiety is not the result of an abnormal response of the orexigenic ghrelin to food intake. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · Clinical Endocrinology
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    ABSTRACT: Much has been written about maintaining the safety of patients on glucocorticoid replacement during illness and the sometimes inadequate response of non endocrine colleagues providing inpatient care and the need for increased awareness. Another group of patients that merit urgent attention in the inpatient setting are those with diabetes insipidus [1]. In the UK there has been one case reported in the press nationally and other cases (including two locally) across the UK where patients with diabetes insipidus have not received the care that they require at best resulting in a near miss, at worst contributing to their death [2,3]. Knowledge of how to manage diabetes insipidus in health is limited to endocrine outpatient settings, where as inpatient care will expose these patients to a range of medical staff with no expertise in this area. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · Clinical Endocrinology
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    ABSTRACT: Serum amino-terminal propeptide of C-type natriuretic peptide (NT-proCNP) levels have been proposed as a biomarker of linear growth in healthy children. The usefulness of NT-proCNP in patients with achondroplasia (ACH)/hypochondroplasia (HCH) remains to be elucidated. The objective was to study whether serum NT-proCNP level is a good biomarker for growth in ACH/HCH and other patients of short stature. This was a longitudinal cohort study. Sixteen children with ACH (aged 0∙4–4∙3 years), 6 children with HCH (2∙7–6∙3 years), 23 children with idiopathic short stature (ISS) (2∙2–9∙0 years), 8 short children with GH deficiency (GHD) (2∙9–6∙8 years), and 5 short children born small for gestational age (SGA) (2∙0–6∙6 years). ACH/HCH patients received GH treatment for 1 year. Serum NT-proCNP levels and height were measured. NT-proCNP levels positively correlated with height velocity in these short children (P < 0∙05, r = 0∙27). NT-proCNP levels inversely correlated with age in children with ISS alone (P < 0∙01, r = −0∙55). Serum NT-proCNP levels in ACH/HCH patients were increased 3 months following the initiation of GH treatment (P < 0∙05). Height SDS gain during GH treatment for 1 year was positively correlated with the changes in NT-proCNP levels after the initiation of GH (P < 0∙01, r = 0∙72). Serum NT-proCNP levels may be a good biomarker to indicate the effect of GH treatment on growth in ACH/HCH patients at least in the first year and height velocity in short stature patients. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · Clinical Endocrinology
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    ABSTRACT: Context: End-stage renal disease has been associated with derangement of the HPA function. The dynamics of this axis in early stages of renal disease (CKD) has not been assessed. Objectives: To evaluate in patients with CKD at stages 1-4 (KDOQI): the diurnal variation of salivary cortisol; the suppressibility of cortisol in saliva and serum after an overnight oral 1 mg dexamethasone suppression test (1 mg DST) with simultaneous measurement of circulating dexamethasone. Design and methods: 80 CKD outpatients and 40 healthy subjects were included. All CKD collected whole saliva at 08.00 and 23.00 h (SAF23 ) on two non-consecutive days. Thereafter at 08.00h, following 1 mg DST, saliva and blood were obtained. Salivary and serum cortisol as well as CBG were assessed by RIA, dexamethasone by ELISA and serum free cortisol was calculated. Results: SAF23 correlated negatively with glomerular filtration rate (GFR). The fraction of free cortisol in serum and saliva after 1 mg DST, correlated positively and significantly in both patients with CKD and healthy subjects (r:0.86 and r:0.85, respectively; p<0.0001 for both). Ten percent of CKD with GFR< 90 ml/min/1.73 m(2) had false positive results unrelated to dexamethasone and CBG concentrations. Conclusions: False positive responses to 1 mg DST were associated with GFR < 90 ml/min/1.73 m(2) . This could not be ascribed to either defects in dexamethasone absorption or CBG concentrations. Higher dexamethasone doses were necessary to achieve adequate HPA suppression. Salivary cortisol was useful to assess circadian cortisol levels and feed-back regulation in CKD. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · Clinical Endocrinology
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    ABSTRACT: Objective: Glucocorticoid substitution is essential in patients with chronic primary adrenocortical insufficiency (Addison's disease) and both over-treatment and inadequate dosage have deleterious effects. Individual sensitivity to glucocorticoids is partly genetically determined. Context: To test the hypothesis whether the well-characterized SNPs of the GR and HSD11B1 genes may modulate the individual sensitivity to exogenous glucocorticoids and may influence clinical and/or laboratory parameters and the glucocorticoid substitution dosage in patients with Addison's disease. Patients and methods: 68 patients with primary adrenocortical insufficiency were involved. Clinical and laboratory data, as well as the dosage of the hormone replacement therapy were collected. Peripheral blood DNA was isolated, and the GR and HSD11B1 SNPs were examined using allele-specific PCR or Taqman assay on Real Time PCR. Results: The allele frequency of the GR N363S polymorphism was higher in patients compared to the control group and the disease appeared significantly earlier in patients harbouring the GR A3669G compared to non-carriers. These patients had higher ACTH level measured at the time of diagnosis. Homozygous BclI carriers had higher body mass index (BMI) and lower total hydrocortisone equivalent supplementation dose needed than heterozygous or non-carriers. The BMI and weight gain during hormone replacement therapy were also higher in carriers of the HSD11B1 rs4844880 treated with glucocorticoids other than dexamethasone. Conclusion: The BclI polymorphism of the GR gene and the rs4844880 of the HSD11B1 gene may contribute to weight gain and may affect the individual need of glucocorticoid substitution dose in these patients. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · Clinical Endocrinology
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    ABSTRACT: Objective: Mutations of the genes encoding Succinate Dehyrdrogenase B and D (SDHB, SDHD) are associated with highly penetrant phenotypes, including paragangliomas and phaeochromocytomas. Patients with these mutations require lifelong surveillance, however there is currently ambiguity regarding the optimal screening regimen. We sought to determine the utility of Fluorodeoxyglucose (18F) positron emission tomography (18F-FDG PET) imaging, compared to other modalities for detecting SDHB and SDHD mutation-related lesions . Design: A retrospective audit of patients with SDHB or SDHD mutation. Patients: All adult patients with confirmed SDHB and SDHD mutations who underwent 18F-FDG PET/CT at our institution between 1/7/2011 and 30/5/2015. Measurements: 18F-FDG PET/computed tomography (CT) performed during surveillance of patients with SDHB and SDHD mutations. Lesion numbers and locations detected by 18F-FDG PET were compared to those identified on the CT component, as well as other imaging modalities and histology when available. Results: Thirty-one 18F-FDG PET/CT studies were completed on twenty two patients. For SDHB (twenty patients), there were 5 positive and 21 negative studies. There were no false-negative 18F-FDG PET studies. Positive 18F-FDG PET findings correlated with magnetic resonance imaging (MRI), CT and [68Ga]-DOTA(0)-Tyr(3)-octreotate (68Ga DOTATATE PET/CT imaging with no missed lesions; the only potential false-positive result relating to nonspecific post-operative changes (sensitivity 100.0%, specificity 95.5%). For SDHD (two patients), lesions were detected on 18F-FDG PET and correlated with other imaging in three of five studies. Metastatic lesions were incompletely visualised on 18F-FDG PET but were detected on the non-contrast fusion CT. Conclusions: 18F-FDG PET/CT is suitable for detecting SDHB and SDHD mutation-related lesions and may be considered effective for periodic surveillance of patients with these mutations. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · Clinical Endocrinology
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    ABSTRACT: Objective: There are currently no good histological or molecular markers to differentiate benign from malignant phaeochromocytomas and paraganglinomas (PPGLs). Our previous cross-sectional study observed that ERBB-2 overexpression was associated with malignant PPGLs. The present study aimed to evaluate the predictive value of ERBB-2 overexpression for metastasis in PPGLs in a large population. Methods: A total of 262 patients diagnosed as PPGLs in our institution between 2002 and 2012 were included. We analysed ERBB-2 protein expression in the primary PPGL tumours by immunohistochemistry (IHC) and ERBB-2 amplification by fluorescence in situ hybridisation (FISH). Direct Sanger sequencing was performed to examine ERBB-2 exon 20 mutations. The occurrence of malignant PPGLs was documented in the follow-up period. Kaplan-Meier analysis and Cox proportional hazard models were used to evaluate the association between ERBB-2 overexpression and metastasis of PPGLs. Results: Twenty-six (9.9%) patients had ERBB-2-overexpression in their primary PPGL tumours, which was significantly associated with ERBB-2 amplification (17/25, 68%). No ERBB-2 mutation was found. At a median follow-up of 4.5 years, a total of 23 malignant PPGLs were documented, including eight (30.8%) patients in the ERBB-2 overexpression group and 15 (6.4%) patients in the ERBB-2 negative group. The incidence rate of metastasis was 5.3 per 100 person-years versus 1.4 per 100 person-years in the ERBB-2 overexpression and ERBB-2 negative groups (P<0.001) respectively. Kaplan-Meier analysis showed that ERBB-2 overexpression was associated with decreased metastasis-free survival (P=0.001, log-rank test). After adjusting for primary tumour size and location, Cox regression analysis revealed that ERBB-2 overexpression was independently associated with risk of malignant PPGLs (HR=2.78; 95%CI, 1.12 to 6.90; P=0.028). Conclusion: Patients harbouring tumours with ERBB-2 overexpression have a significantly higher risk of developing malignant PPGLs. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · Clinical Endocrinology
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    ABSTRACT: Hypogonadotrophic hypogonadism (HH) is commonly associated with ageing, obesity and type 2 diabetes. The indications for pituitary imaging are controversial and current guidelines are based on small case series. Retrospective case series from a secondary/tertiary Endocrinology referral centre. All men presenting to the Edinburgh Centre for Endocrinology and Diabetes with hypogonadotrophic hypogonadism (testosterone < 10 nmol/L and normal prolactin) from 2006 – 2013 in whom pituitary MRI was performed (n = 281). All HH patients referred in 2011 (n=86) were reviewed to assess differences between those selected for pituitary MRI and those who were not scanned. Pituitary MRI was normal in 235 men (83.6%), with 24 microadenomas (8.5%), 5 macroadenomas (1.8%) and 1 craniopharyngioma (0.4%) identified. The remaining 16 (5.7%) comprised a range of minor pituitary abnormalities including small cysts and empty sella. All men with abnormal imaging studies had otherwise normal pituitary function. Imaging abnormalities were associated with a significantly lower age at presentation (50 vs. 54 years, p = 0.02) but no differences in testosterone or gonadotrophin levels were observed. Current Endocrine Society guidelines would have prompted imaging in only 3 of 6 patients with significant pituitary pathology. Structural pituitary disease is more common in isolated HH than in the general population and current guidelines do not accurately identify ‘at risk’ individuals. Full anterior pituitary function testing has a low yield in patients presenting with hypogonadism. The optimal strategy for determining the need for pituitary imaging remains uncertain. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · Clinical Endocrinology
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    ABSTRACT: We report the case of secondary adrenal insufficiency in a 56-year-old woman with a history of post-Roux-en-Y gastric bypass hyperinsulinemic hypoglycemia, undergoing experimental treatment with pasireotide. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · Clinical Endocrinology
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    ABSTRACT: Background: The prognostic value of the telomerase reverse transcriptase (TERT) promoter mutation, resulting in poor clinical outcomes of papillary thyroid carcinoma (PTC), has been generally confirmed. To data, there is no high-level evidence approving the association of TERT promoter mutation and aggressive clinical behaviors in PTC. To systematically evaluate it, a systematic review and meta-analysis of the published literatures were carried out METHODS: We conducted a systematic search in PubMed, EMBASE, OVID and web of science databases for relevant studies. We selected all the studies that reported clinicopathological features of PTC patients with information available on TERT promoter mutation status. Individual study-specific odds ratios (ORs) and 95% confidence intervals (CIs) were calculated, as were Mantel-Haenszel pooled odds ratios for the combined studies. Results: Eight eligible trials involved 2035 patients were included in the analysis. The average prevalence of the TERT promoter mutation was 10.32%. Compared with the wild-type TERT promoter gene, the TERT promoter mutation was associated with male gender, lymph node metastasis, extrathyroidal extension, distant metastasis, advanced TNM stage III/IV, poor clinical outcome(persistence or recurrence) and mortality. The associations were generally consistent across the different study populations. Conclusions: Thus, our findings from this large meta-analysis definitively demonstrate that TERT promoter mutation-positive PTC is more likely to manifest with aggressive clinicopathological characteristics. In appropriate clinical settings, testing for the TERT promoter mutation is likely to be useful in assisting the risk stratification and management of PTC. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · Clinical Endocrinology