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Shih-Rong Lin Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan

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Shih-Fen Chen Department of Obstetrics and Gynecology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan

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Yu-Cih Yang Management Office for Health Data, China Medical University Hospital, Taichung, Taiwan

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Chung-Y Hsu Graduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan

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Yu-Chih Shen Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan
Department of Psychiatry, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan
School of Medicine, Tzu Chi University, Hualien, Taiwan

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Hyperthyroidism contributes to many other disease conditions, including neurodegenerative diseases. Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. The purpose of this study was to investigate the risk of PD in patients with hyperthyroidism. A total of 8788 patients with hyperthyroidism and 8788 controls (without hyperthyroidism) matched by age, gender, index year, and Charlson Comorbidity Index (CCI) score were enrolled between 2000 and 2012. Patients were then followed until the end of 2013 using Taiwan’s National Health Insurance Research Database, at which time participants who developed PD were identified. Cox regression analysis was used to calculate the hazard ratio (HR) with a 95% CI of PD incidence rate between patients with hyperthyroidism and unaffected controls. Patients with hyperthyroidism had a significantly increased risk of PD compared with unaffected controls (1.21 vs 0.45 per 1000 person-years, HR: 2.69, 95% CI: 1.08–6.66) after adjusting for age, gender, CCI score, comorbidities, and antithyroid therapy. Hyperthyroidism and PD may share common manifestations. After excluding the first year of observation, a similar result is obtained (HR: 2.57, 95% CI: 1.61–4.01). Also, this study found that older age (HR: 3.74–8.53), more comorbidities (HR: 1.58–1.63), and specific comorbidities (brain injury (HR: 1.57) and cerebrovascular disease (HR: 3.44)) were associated with an increased risk of developing PD. Patients with hyperthyroidism have an increased risk of developing PD. Additional prospective clinical studies are warranted to examine the relationship between hyperthyroidism and PD and determine if there is an intervention that could reduce PD risk.

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Natércia Neves Marques de Queiroz University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Franciane Trindade Cunha de Melo University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Fabrício de Souza Resende University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Luísa Corrêa Janaú University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Norberto Jorge Kzan de Souza Neto University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Manuela Nascimento de Lemos University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Ana Carolina Lobato Virgolino University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Maria Clara Neres Iunes de Oliveira University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Angélica Leite de Alcântara University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Lorena Vilhena de Moraes University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Tiago Franco David University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Wanderson Maia da Silva University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Scarlatt Souza Reis University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Márcia Costa dos Santos University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Ana Carolina Contente Braga de Souza University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Pedro Paulo Freire Piani University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Neyla Arroyo Lara Mourão University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Karem Mileo Felício University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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João Felício Abrahão Neto University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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João Soares Felício University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Objective:

Investigate the prevalence of vitamin D deficiency in an equatorial population through a large-sample study.

Methods:

Cross-sectional study with 30,224 healthy individuals from the North Region, in Brazil (Amazônia – state of Pará), who had 25-hydroxy-vitamin D (25(OH)D) and intact parathyroid hormone (PTH) serum levels measured by immunoassay method. Those with history of acute or chronic diseases were excluded. Abnormal levels of calcium, creatinine, glycemia and albumin were also exclusion criteria.

Results:

25(OH)D levels were 29.1 ± 8.2 ng/mL and values <12.7 ng/mL were equal to < −2 s.d. below average. Hypovitaminosis D was present in 10% of subjects according to the Institute of Medicine (values <20 ng/mL) and in 59%, in consonance with Endocrine Society (values 20–30 ng/mL as insufficiency and <20 ng/mL as deficiency) criteria. Individuals were divided according to four age brackets: children, adolescents, adults and elderly, and their 25(OH)D levels were: 33 ± 9; 28.5 ± 7.4; 28.3 ± 7.7; 29.3 ± 8.5 ng/mL, respectively. All groups differed in 25(OH)D, except adolescents vs adults. Regression model showed BMI, sex, living zone (urban or rural) and age as independent variables to 25(OH)D levels. Comparing subjects with vitamin D deficiency (<20 ng/mL) to those with vitamin D insufficiency (20–30 ng/mL), a difference between PTH levels in these two groups was observed (95.9 ± 24.7 pg/mL vs 44.2 ± 64.5 pg/mL; P < 0.01). Additionally, the most accurate predictive vitamin D level for subclinical hyperparathyroidism in ROC curve was 26 ng/mL.

Conclusion:

Our equatorial population showed low prevalence of vitamin D hypovitaminosis ranging with age bracket. The insufficient category by Endocrine Society was corroborated by our PTH data.

Open access
Anastasia Ibba SSD Endocrinologia Pediatrica e Centro Screening Neonatale, Ospedale Pediatrico Microcitemico, ‘A. Cao’, AO Brotzu, Cagliari, Italy

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Francesca Corrias SSD Endocrinologia Pediatrica e Centro Screening Neonatale, Ospedale Pediatrico Microcitemico, ‘A. Cao’, AO Brotzu, Cagliari, Italy

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Chiara Guzzetti SSD Endocrinologia Pediatrica e Centro Screening Neonatale, Ospedale Pediatrico Microcitemico, ‘A. Cao’, AO Brotzu, Cagliari, Italy

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Letizia Casula SSD Endocrinologia Pediatrica e Centro Screening Neonatale, Ospedale Pediatrico Microcitemico, ‘A. Cao’, AO Brotzu, Cagliari, Italy

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Mariacarolina Salerno Dipartimento di Pediatria, Università Federico II, Napoli, Italy

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Natascia di Iorgi Dipartimento di Pediatria, IRCCS Istituto Giannina Gaslini, Università di Genova, Genova, Italy
Dipartimento di Neuroscienze, Riabilitazione, Oftalmologia, Genetica e Scienze Materno-infantili, Università di Genova, Genova, Italy

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Gianluca Tornese SSD Endocrinologia Pediatrica, Clinica Pediatrica, IRCCS Materno-infantile Burlo Garofolo, Trieste, Italy

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Giuseppa Patti Dipartimento di Pediatria, IRCCS Istituto Giannina Gaslini, Università di Genova, Genova, Italy
Dipartimento di Neuroscienze, Riabilitazione, Oftalmologia, Genetica e Scienze Materno-infantili, Università di Genova, Genova, Italy

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Giorgio Radetti Dipartimento di Pediatria, Ospedale Generale Regionale, Bolzano, Italy

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Mohamad Maghnie Dipartimento di Pediatria, IRCCS Istituto Giannina Gaslini, Università di Genova, Genova, Italy
Dipartimento di Neuroscienze, Riabilitazione, Oftalmologia, Genetica e Scienze Materno-infantili, Università di Genova, Genova, Italy

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Marco Cappa UOC di Endocrinologia, Dipartimento Universitario Ospedaliero, Ospedale Pediatrico Bambino Gesù IRCCS, Roma, Italy

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Sandro Loche SSD Endocrinologia Pediatrica e Centro Screening Neonatale, Ospedale Pediatrico Microcitemico, ‘A. Cao’, AO Brotzu, Cagliari, Italy

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A number of studies have evaluated the role of IGF1 measurement in the diagnosis of growth hormone deficiency (GHD). This study aimed to evaluate the accuracy and the best cut-off of IGF1 SDS in the diagnosis of GHD in a large cohort of short children and adolescents. One-hundred and forty-two children and adolescents with GHD ((63 organic/genetic (OGHD), 79 idiopathic (IGHD)) and 658 short non-GHD children (median age 10.4 years) were included in the analysis. The two groups were subdivided according to age (G1 <6, G2 6 <9, G3 9 <12, G4 ≥12) and to pubertal status. Serum IGFI was measured by the same chemiluminescence assay in all samples and expressed as age- and sex-based SDS. Receiver operating characteristic (ROC) analysis was used to evaluate the optimal IGF1 SDS cut-off and the diagnostic accuracy. Median IGF1 SDS was significantly lower in the GHD than in non-GHD patients. The area under the curve (AUC) was 0.69, with the best IGF1 cut-off of −1.5 SDS (sensitivity 67.61%, specificity 62.62%). The AUC was 0.75 for OGHD and 0.63 for IGHD. The accuracy was better in the pubertal (AUC = 0.81) than the prepubertal group (AUC = 0.64). In our cohort, IGF1 measurement has poor accuracy in discriminating GHD from non-GHD. Our findings confirm and reinforce the belief that IGF1 values should not be used alone in the diagnosis of GHD but should be interpreted in combination with other clinical and biochemical parameters.

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María L Bacigalupo Departamento de Química Biológica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química y Fisicoquímica Biológicas, Buenos Aires, Argentina

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Verónica G Piazza Departamento de Química Biológica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química y Fisicoquímica Biológicas, Buenos Aires, Argentina

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Nadia S Cicconi Departamento de Química Biológica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química y Fisicoquímica Biológicas, Buenos Aires, Argentina

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Pablo Carabias Departamento de Química Biológica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química y Fisicoquímica Biológicas, Buenos Aires, Argentina

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Andrzej Bartke Department of Internal Medicine, Geriatrics Research, Southern Illinois University School of Medicine, Springfield, Illinois, USA

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Yimin Fang Department of Internal Medicine, Geriatrics Research, Southern Illinois University School of Medicine, Springfield, Illinois, USA

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Ana I Sotelo Departamento de Química Biológica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química y Fisicoquímica Biológicas, Buenos Aires, Argentina

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Gabriel A Rabinovich Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas, and Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina

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María F Troncoso Departamento de Química Biológica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química y Fisicoquímica Biológicas, Buenos Aires, Argentina

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Johanna G Miquet Departamento de Química Biológica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química y Fisicoquímica Biológicas, Buenos Aires, Argentina

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Transgenic mice overexpressing growth hormone (GH) spontaneously develop liver tumors, including hepatocellular carcinoma (HCC), within a year. The preneoplastic liver pathology in these mice recapitulates that observed in humans at high risk of developing hepatic cancer. Although increased expression of galectin 1 (GAL1) in liver tissue is associated with HCC aggressiveness, a link between this glycan-binding protein and hormone-related tumor development has not yet been explored. In this study, we investigated GAL1 expression during liver tumor progression in mice continuously exposed to high levels of GH. GAL1 expression was determined by Western blotting, RT-qPCR and immunohistochemistry in the liver of transgenic mice overexpressing GH. Animals of representative ages at different stages of liver pathology were studied. GAL1 expression was upregulated in the liver of GH-transgenic mice. This effect was observed at early ages, when animals displayed no signs of liver disease or minimal histopathological alterations and was also detected in young adults with preneoplastic liver pathology. Remarkably, GAL1 upregulation was sustained during aging and its expression was particularly enhanced in liver tumors. GH also induced hepatic GAL1 expression in mice that were treated with this hormone for a short period. Moreover, GH triggered a rapid increment in GAL1 protein expression in human HCC cells, denoting a direct effect of the hormone on hepatocytes. Therefore, our results indicate that GH upregulates GAL1 expression in mouse liver, which may have critical implications in tumorigenesis. These findings suggest that this lectin could be implicated in hormone-driven liver carcinogenesis.

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Nikolina Zdraveska University Children’s Hospital Skopje, Faculty of Medicine, Skopje, Republic of Macedonia

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Maja Zdravkovska Institute of Patophysiology and Nuclear Medicine, Faculty of Medicine, Skopje, Republic of Macedonia

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Violeta Anastasovska University Children’s Hospital Skopje, Faculty of Medicine, Skopje, Republic of Macedonia

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Elena Sukarova-Angelovska University Children’s Hospital Skopje, Faculty of Medicine, Skopje, Republic of Macedonia

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Mirjana Kocova University Children’s Hospital Skopje, Faculty of Medicine, Skopje, Republic of Macedonia

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Background

Diagnostic re-evaluation is important for all patients with congenital hypothyroidism (CH) for determining the etiology and identifying transient CH cases. Our study is a first thyroxine therapy withdrawal study conducted in Macedonian CH patients for a diagnostic re-evaluation. We aimed to evaluate the etiology of CH, the prevalence of transient CH and identify predictive factors for distinguishing between permanent (PCH) and transient CH (TCH).

Materials and methods

Patients with CH aged >3 years underwent a trial of treatment withdrawal for 4 weeks period. Thyroid function testing (TFT), ultrasound and Technetium-99m pertechnetate thyroid scan were performed thereafter. TCH was defined when TFT remained within normal limits for at least 6-month follow-up. PCH was diagnosed when TFT was abnormal and classified according the imaging findings.

Results

42 (55%) patients had PCH and 34 (45.0%) patients had TCH. Thyroid agenesia was the most prevalent form in the PCH group. Patients with TCH had lower initial thyroid-stimulating hormone (TSH) values (P < 0.0001); higher serum thyroxine levels (P = 0.0023) and lower mean doses of levothyroxine during treatment period (P < 0.0001) than patients with PCH. Initial TSH level <30.5 IU/mL and levothyroxine dose at 3 years of age <2.6 mg/kg/day were a significant predictive factors for TCH; sensitivity 92% and 100%, specificity 75.6% and 76%, respectively.

Conclusion

TCH presents a significant portion of patients with CH. Initial TSH value and levothyroxine dose during treatment period has a predictive role in differentiating TCH from PCH. Earlier re-evaluation, between 2 and 3 years age might be considered in some patients requiring low doses of levothyroxine.

Open access
Ying Hua Department of Administrative Office, The First People's Hospital of Xiaoshan District, Xiaoshan Affiliated Hospital of Wenzhou Medical University, Hangzhou, Zhejiang, China

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Jinqiong Fang Department of Administrative Office, The First People's Hospital of Xiaoshan District, Xiaoshan Affiliated Hospital of Wenzhou Medical University, Hangzhou, Zhejiang, China

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Xiaocong Yao Department of Osteoporosis Care and Control, The First People's Hospital of Xiaoshan District, Xiaoshan Affiliated Hospital of Wenzhou Medical University, Hangzhou, Zhejiang, China

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Zhongxin Zhu Department of Osteoporosis Care and Control, The First People's Hospital of Xiaoshan District, Xiaoshan Affiliated Hospital of Wenzhou Medical University, Hangzhou, Zhejiang, China
Department of Clinical Research Center, The First People's Hospital of Xiaoshan District, Xiaoshan Affiliated Hospital of Wenzhou Medical University, Hangzhou, Zhejiang, China

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Background

Obesity and osteoporosis are major public health issues globally. The prevalence of these two diseases prompts the need to better understand the relationship between them. Previous studies, however, have yielded controversial findings on this issue. Therefore, our aim in this study was to evaluate the independent association between waist circumference (WC), as a marker of obesity, and the bone mineral density (BMD) of the lumbar spine among middle-aged adults using data from the National Health and Nutrition Examination Survey (NHANES).

Methods

Our analysis was based on NHANES data from 2011 to 2018, including 5084 adults, 40–59 years of age. A weighted multiple linear regression analysis was used to evaluate the association between WC and lumbar BMD, with smooth curve fitting performed for non-linearities.

Results

After adjusting for BMI and other potential confounders, WC was negatively associated with lumbar BMD in men (β = −2.8, 95% CI: −4.0 to −1.6) and premenopausal women (β = −2.6, 95% CI: −4.1 to −1.1). On subgroup analysis stratified by BMI, this negative association was more significant in men with a BMI ≥30 kg/m2 (β = −4.1, 95% CI: −6.3 to −2.0) and in pre- and postmenopausal women with a BMI <25 kg/m2 (premenopausal women: β= −5.7, 95% CI: −9.4 to−2.0; postmenopausal women: β=−5.6, 95% CI: −9.7 to −1.6). We further identified an inverted U-shaped relationship among premenopausal women, with a point of inflection at WC of 80 cm.

Conclusions

Our study found an inverse relationship between WC and lumbar BMD in middle-aged men with BMI ≥30 kg/m2, and women with BMI <25 kg/m2.

Open access
Sanna Mustaniemi Public Health Promotion Unit, National Institute for Health and Welfare, Helsinki, Finland
PEDEGO Research Unit, MRC Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland

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Marja Vääräsmäki Public Health Promotion Unit, National Institute for Health and Welfare, Helsinki, Finland
PEDEGO Research Unit, MRC Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland

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Johan G Eriksson Department of General Practice and Primary Health Care, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
Folkhälsan Research Centre, Helsinki, Finland

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Mika Gissler Information Services Department, National Institute for Health and Welfare, Helsinki, Finland
Division of Family Medicine, Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Stockholm, Sweden

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Hannele Laivuori Medical and Clinical Genetics, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
Department of Obstetrics and Gynaecology, Tampere University Hospital, Tampere, Finland
Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland
Institute for Molecular Medicine Finland, Helsinki Institute of Life Science, University of Helsinki, Helsinki, Finland

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Hilkka Ijäs Public Health Promotion Unit, National Institute for Health and Welfare, Helsinki, Finland
PEDEGO Research Unit, MRC Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland

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Aini Bloigu PEDEGO Research Unit, MRC Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland

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Eero Kajantie Public Health Promotion Unit, National Institute for Health and Welfare, Helsinki, Finland
PEDEGO Research Unit, MRC Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland
Children’s Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland

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Laure Morin-Papunen PEDEGO Research Unit, MRC Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland

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Objective

To study the roles of self-reported symptoms and/or prior diagnosis of polycystic ovary syndrome (PCOS) and other potential risk factors for gestational diabetes mellitus (GDM) and to clarify whether the screening of GDM in early pregnancy is beneficial for all women with PCOS.

Design

The FinnGeDi multicentre case-control study including 1146 women with singleton pregnancies diagnosed with GDM and 1066 non-diabetic pregnant women. There were 174 women with PCOS (symptoms and/or diagnosis self-reported by a questionnaire) and 1767 women without PCOS (data missing for 271).

Methods

The study population (N = 1941) was divided into four subgroups: GDM + PCOS (N = 105), GDM + non-PCOS (N = 909), non-GDM + PCOS (N = 69), and controls (N = 858). The participants’ characteristics and their parents’ medical histories were compared.

Results

The prevalence of PCOS was 10.4% among GDM women and 7.4% among non-diabetics (odds ratios (OR) 1.44, 95% CI: 1.05–1.97), but PCOS was not an independent risk for GDM after adjustments for participants’ age and pre-pregnancy BMI (OR 1.07, 95% CI: 0.74–1.54). In a multivariate logistic regression analysis, the most significant parameters associated with GDM were overweight, obesity, age ≥35 years, participant’s mother’s history of GDM, either parent’s history of type 2 diabetes (T2D) and participant’s own preterm birth.

Conclusions

The increased risk of GDM in women with PCOS was related to obesity and increased maternal age rather than to PCOS itself, suggesting that routine early screening of GDM in PCOS women without other risk factors should be reconsidered. Instead, family history of GDM/T2D and own preterm birth were independent risk factors for GDM.

Open access
Stavroula A Paschou Department of Endocrinology and Diabetes, Hellenic Red Cross Hospital, Athens, Greece

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Eleni Palioura Department of Endocrinology and Diabetes, Hellenic Red Cross Hospital, Athens, Greece

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Dimitrios Ioannidis Department of Endocrinology and Diabetes, Sismanoglio-Amalia Fleming Hospital, Athens, Greece

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Panagiotis Anagnostis Unit of Reproductive Endocrinology, First Department of Obstetrics and Gynecology, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece

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Argyro Panagiotakou Department of Endocrinology and Diabetes, Sismanoglio-Amalia Fleming Hospital, Athens, Greece

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Vasiliki Loi Department of Endocrinology and Diabetes, Hellenic Red Cross Hospital, Athens, Greece

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Georgios Karageorgos Department of Endocrinology and Diabetes, Sismanoglio-Amalia Fleming Hospital, Athens, Greece

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Dimitrios G Goulis Unit of Reproductive Endocrinology, First Department of Obstetrics and Gynecology, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece

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Andromachi Vryonidou Department of Endocrinology and Diabetes, Hellenic Red Cross Hospital, Athens, Greece

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Objective

The aim of this study was to investigate the impact of adrenal hyperandrogenism on insulin resistance and lipid profile in women with polycystic ovary syndrome (PCOS).

Patients and methods

We studied 372 women with PCOS according to the NIH criteria. 232 age- and BMI-matched women served as controls in order to define adrenal hyperandrogenism (DHEA-S >95th percentile). Then, patients with PCOS were classified into two groups: with adrenal hyperandrogenism (PCOS-AH, n = 108) and without adrenal hyperandrogenism (PCOS-NAH, n = 264). Anthropometric measurements were recorded. Fasting plasma glucose, insulin, lipid profile, sex hormone-binding globulin (SHBG) and androgen (TT, Δ4A, DHEA-S) concentrations were assessed. Free androgen index (FAI) and homeostatic model assessment-insulin resistance (HOMA-IR) index were calculated.

Results

Women with PCOS-AH were younger than PCOS-NAH (P < 0.001), but did not differ in the degree and type of obesity. No differences were found in HOMA-IR, total cholesterol, HDL-c, LDL-c and triglyceride concentrations (in all comparisons, P > 0.05). These metabolic parameters did not differ between the two groups even after correction for age. Women with PCOS-AH had lower SHBG (29.2 ± 13.8 vs 32.4 ± 11.8 nmol/L, P = 0.025) and higher TT (1.0 ± 0.2 vs 0.8 ± 0.4 ng/mL, P = 0.05) and Δ4A (3.9 ± 1.2 vs 3.4 ± 1.0 ng/mL, P = 0.007) concentrations, as well as FAI (14.1 ± 8.0 vs 10.2 ± 5.0, P < 0.001). These results were confirmed by a multiple regression analysis model in which adrenal hyperandrogenism was negatively associated with age (P < 0.001) and SHBG concentrations (P = 0.02), but not with any metabolic parameter.

Conclusions

Women with PCOS and adrenal hyperandrogenism do not exhibit any deterioration in insulin resistance and lipid profile despite the higher degree of total androgens.

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Hiren Patt Department of Endocrinology, Seth G.S. Medical College & KEM Hospital, Mumbai, Maharashtra, India

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Katrin Koehler Department of Paediatrics, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany

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Sailesh Lodha Eternal Hospital, Jaipur, Rajasthan, India

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Swati Jadhav Department of Endocrinology, Seth G.S. Medical College & KEM Hospital, Mumbai, Maharashtra, India

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Chaitanya Yerawar Department of Endocrinology, Seth G.S. Medical College & KEM Hospital, Mumbai, Maharashtra, India

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Angela Huebner Department of Paediatrics, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany

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Kunal Thakkar Department of Endocrinology, Seth G.S. Medical College & KEM Hospital, Mumbai, Maharashtra, India

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Sneha Arya Department of Endocrinology, Seth G.S. Medical College & KEM Hospital, Mumbai, Maharashtra, India

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Sandhya Nair Department of Endocrinology, Seth G.S. Medical College & KEM Hospital, Mumbai, Maharashtra, India

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Manjunath Goroshi Department of Endocrinology, Seth G.S. Medical College & KEM Hospital, Mumbai, Maharashtra, India

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Hosahithlu Ganesh Department of Endocrinology, AJ Institute of Medical sciences, Mangalore, India

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Vijaya Sarathi Department of Endocrinology, Vydehi Institute of Medical Sciences and Research Center, Bengaluru, India

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Anurag Lila Department of Endocrinology, Seth G.S. Medical College & KEM Hospital, Mumbai, Maharashtra, India

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Tushar Bandgar Department of Endocrinology, Seth G.S. Medical College & KEM Hospital, Mumbai, Maharashtra, India

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Nalini Shah Department of Endocrinology, Seth G.S. Medical College & KEM Hospital, Mumbai, Maharashtra, India

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Objective

To study genotype–phenotype spectrum of triple A syndrome (TAS).

Methods

Retrospective chart analysis of Indian TAS patients (cohort 1, n = 8) and review of genotyped TAS cases reported in world literature (cohort 2, n = 133, 68 publications).

Results

Median age at presentation was 4.75 years (range: 4–10) and 5 years (range: 1–42) for cohorts 1 and 2, respectively. Alacrima, adrenal insufficiency (AI), achalasia and neurological dysfunction (ND) were seen in 8/8, 8/8, 7/8 and 4/8 patients in cohort 1, and in 99, 91, 93 and 79% patients in cohort 2, respectively. In both cohorts, alacrima was present since birth while AI and achalasia manifested before ND. Mineralocorticoid deficiency (MC) was uncommon (absent in cohort 1, 12.5% in cohort 2). In cohort 1, splice-site mutation in exon 1 (p.G14Vfs*45) was commonest, followed by a deletion in exon 8 (p.S255Vfs*36). Out of 65 mutations in cohort 2, 14 were recurrent and five exhibited regional clustering. AI was more prevalent, more often a presenting feature, and was diagnosed at younger age in T group (those with truncating mutations) as compared to NT (non-truncating mutations) group. ND was more prevalent, more common a presenting feature, with later age at onset in NT as compared to T group.

Conclusion

Clinical profile of our patients is similar to that of patients worldwide. Alacrima is the earliest and most consistent finding. MC deficiency is uncommon. Some recurrent mutations show regional clustering. p.G14Vfs*45 and p.S255Vfs*36 account for majority of AAAS mutations in our cohort. Phenotype of T group differs from that of NT group and merits future research.

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Jiaxi Li Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China

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Pu Huang Department of Health Management Center, Changsha Central Hospital, University of South China, Changsha, Hunan, China

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Jing Xiong Department of Endocrinology, Xiangya Third Hospital, Central South University, Changsha, Hunan, China

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Xinyue Liang Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China

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Mei Li Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China

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Hao Ke Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China

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Chunli Chen Department of Dermatology, Xiangya Third Hospital, Central South University, Changsha, Hunan, China

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Yang Han Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China

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Yanhong Huang Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China

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Yan Zhou Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China

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Ziqiang Luo Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China
Hunan Key Laboratory of Organ Fibrosis, Central South University, Changsha, Hunan, China

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Dandan Feng Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China
Hunan Key Laboratory of Organ Fibrosis, Central South University, Changsha, Hunan, China

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Chen Chen School of Biomedical Sciences, University of Queensland, St Lucia, Brisbane, Queensland, Australia

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Objective

Ghrelin regulates body weight, food intake, and blood glucose. It also regulates insulin secretion from pancreatic islet cells. LEAP2 is a newly discovered endogenous ligand of the growth hormone secretagogue’s receptor (GHSR). It not only antagonizes the stimulation of GHSR by ghrelin but also inhibits the constitutive activation of GHSR as an inverse agonist. Type 2 diabetes (T2D) patients have endocrine disorders with metabolic imbalance. Plasma levels of ghrelin and LEAP2 may be changed in obese and T2D patients. However, there is no report yet on circulating LEAP2 levels or ghrelin/LEAP2 ratio in T2D patients. In this study, fasting serum ghrelin and LEAP2 levels in healthy adults and T2D patients were assessed to clarify the association of two hormones with different clinical anthropometric and metabolic parameters.

Design

A total of 16 females and 40 males, ages 23–68 years old normal (n  = 27), and T2D patients (n  = 29) were enrolled as a cross-sectional cohort.

Results

Serum levels of ghrelin were lower but serum levels of LEAP2 were higher in T2D patients. Ghrelin levels were positively correlated with fasting serum insulin levels and HOMA-IR in healthy adults. LEAP2 levels were positively correlated with age and hemoglobin A1c (HbA1c) in all tested samples. Ghrelin/LEAP2 ratio was negatively correlated with age, fasting blood glucose, and HbA1c.

Conclusions

This study demonstrated a decrease in serum ghrelin levels and an increase in serum LEAP2 levels in T2D patients. LEAP2 levels were positively correlated with HbA1c, suggesting that LEAP2 was associated with T2D development. The ghrelin/LEAP2 ratio was closely associated with glycemic control in T2D patients showing a negative correlation with glucose and HbA1c.

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