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Paal Methlie Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway
Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Steinar Hustad Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Ralf Kellman Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Bjørg Almås Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Martina M Erichsen Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Eystein S Husebye Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway
Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Kristian Løvås Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway
Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Objective

Liquid chromatography–tandem mass spectrometry (LC–MS/MS) offers superior analytical specificity compared with immunoassays, but it is not available in many regions and hospitals due to expensive instrumentation and tedious sample preparation. Thus, we developed an automated, high-throughput LC–MS/MS assay for simultaneous quantification of ten endogenous and synthetic steroids targeting diseases of the hypothalamic–pituitary–adrenal axis and gonads.

Methods

Deuterated internal standards were added to 85 μl serum and processed by liquid–liquid extraction. Cortisol, cortisone, prednisolone, prednisone, 11-deoxycortisol, dexamethasone, testosterone, androstenedione and progesterone were resolved by ultra-high-pressure chromatography on a reversed-phase column in 6.1 min and detected by triple-quadrupole mass spectrometry. The method was used to assess steroid profiles in women with Addison's disease (AD, n=156) and blood donors (BDs, n=102).

Results

Precisions ranged from 4.5 to 10.1% relative standard deviations (RSD), accuracies from 95 to 108% and extraction recoveries from 60 to 84%. The method was practically free of matrix effects and robust to individual differences in serum composition. Most postmenopausal AD women had extremely low androstenedione concentrations, below 0.14 nmol/l, and median testosterone concentrations of 0.15 nmol/l (interquartile range 0.00–0.41), considerably lower than those of postmenopausal BDs (1.28 nmol/l (0.96–1.64) and 0.65 nmol/l (0.56–1.10) respectively). AD women in fertile years had androstenedione concentrations of 1.18 nmol/l (0.71–1.76) and testosterone concentrations of 0.44 nmol/l (0.22–0.63), approximately half of those found in BDs of corresponding age.

Conclusion

This LC–MS/MS assay provides highly sensitive and specific assessments of glucocorticoids and androgens with low sample volumes and is suitable for endocrine laboratories and research. Its utility has been demonstrated in a large cohort of women with AD, and the data suggest that women with AD are particularly androgen deficient after menopause.

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Emanuelle Nunes-Souza Pelé Pequeno Príncipe Research Institute, Água Verde, Curitiba, Parana, Brazil
Faculdades Pequeno Príncipe, Rebouças, Curitiba, Parana, Brazil
Centro de Genética Molecular e Pesquisa do Câncer em Crianças (CEGEMPAC) at Universidade Federal do Paraná, Agostinho Leão Jr., Glória, Curitiba, Parana, Brazil

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Mônica Evelise Silveira Laboratório Central de Análises Clínicas, Hospital de Clínicas, Universidade Federal do Paraná, Centro, Curitiba, Paraná, Brazil

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Monalisa Castilho Mendes Pelé Pequeno Príncipe Research Institute, Água Verde, Curitiba, Parana, Brazil
Faculdades Pequeno Príncipe, Rebouças, Curitiba, Parana, Brazil
Centro de Genética Molecular e Pesquisa do Câncer em Crianças (CEGEMPAC) at Universidade Federal do Paraná, Agostinho Leão Jr., Glória, Curitiba, Parana, Brazil

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Seigo Nagashima Serviço de Anatomia Patológica, Hospital de Clínicas, Universidade Federal do Paraná, General Carneiro, Alto da Glória, Curitiba, Parana, Brazil
Departamento de Medicina, PUC-PR, Prado Velho, Curitiba, Parana, Brazil

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Caroline Busatta Vaz de Paula Serviço de Anatomia Patológica, Hospital de Clínicas, Universidade Federal do Paraná, General Carneiro, Alto da Glória, Curitiba, Parana, Brazil
Departamento de Medicina, PUC-PR, Prado Velho, Curitiba, Parana, Brazil

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Guilherme Guilherme Vieira Cavalcante da Silva Serviço de Anatomia Patológica, Hospital de Clínicas, Universidade Federal do Paraná, General Carneiro, Alto da Glória, Curitiba, Parana, Brazil
Departamento de Medicina, PUC-PR, Prado Velho, Curitiba, Parana, Brazil

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Giovanna Silva Barbosa Serviço de Anatomia Patológica, Hospital de Clínicas, Universidade Federal do Paraná, General Carneiro, Alto da Glória, Curitiba, Parana, Brazil
Departamento de Medicina, PUC-PR, Prado Velho, Curitiba, Parana, Brazil

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Julia Belgrowicz Martins Pelé Pequeno Príncipe Research Institute, Água Verde, Curitiba, Parana, Brazil
Faculdades Pequeno Príncipe, Rebouças, Curitiba, Parana, Brazil

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Lúcia de Noronha Serviço de Anatomia Patológica, Hospital de Clínicas, Universidade Federal do Paraná, General Carneiro, Alto da Glória, Curitiba, Parana, Brazil
Departamento de Medicina, PUC-PR, Prado Velho, Curitiba, Parana, Brazil

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Luana Lenzi Departamento de Análises Clínicas, Universidade Federal do Paraná, Curitiba, Paraná, Brazil

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José Renato Sales Barbosa Pelé Pequeno Príncipe Research Institute, Água Verde, Curitiba, Parana, Brazil
Centro de Genética Molecular e Pesquisa do Câncer em Crianças (CEGEMPAC) at Universidade Federal do Paraná, Agostinho Leão Jr., Glória, Curitiba, Parana, Brazil

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Rayssa Danilow Fachin Donin Centro de Genética Molecular e Pesquisa do Câncer em Crianças (CEGEMPAC) at Universidade Federal do Paraná, Agostinho Leão Jr., Glória, Curitiba, Parana, Brazil

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Juliana Ferreira de Moura Pós Graduação em Microbiologia, Parasitologia e Patologia, Departamento de Patologia Básica – UFPR, Curitiba, Brazil

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Gislaine Custódio Faculdades Pequeno Príncipe, Rebouças, Curitiba, Parana, Brazil
Laboratório Central de Análises Clínicas, Hospital de Clínicas, Universidade Federal do Paraná, Centro, Curitiba, Paraná, Brazil

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Cleber Machado-Souza Pelé Pequeno Príncipe Research Institute, Água Verde, Curitiba, Parana, Brazil
Faculdades Pequeno Príncipe, Rebouças, Curitiba, Parana, Brazil
Centro de Genética Molecular e Pesquisa do Câncer em Crianças (CEGEMPAC) at Universidade Federal do Paraná, Agostinho Leão Jr., Glória, Curitiba, Parana, Brazil

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Enzo Lalli Institut de Pharmacologie Moléculaire et Cellulaire CNRS, Sophia Antipolis, Valbonne, France

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Bonald Cavalcante de Figueiredo Pelé Pequeno Príncipe Research Institute, Água Verde, Curitiba, Parana, Brazil
Faculdades Pequeno Príncipe, Rebouças, Curitiba, Parana, Brazil
Centro de Genética Molecular e Pesquisa do Câncer em Crianças (CEGEMPAC) at Universidade Federal do Paraná, Agostinho Leão Jr., Glória, Curitiba, Parana, Brazil
Departamento de Saúde Coletiva, Universidade Federal do Paraná, Curitiba, Paraná, Brazil

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Objective

Adaptive changes in DHEA and sulfated-DHEA (DHEAS) production from adrenal zona reticularis (ZR) have been observed in normal and pathological conditions. Here we used three different cohorts to assess timing differences in DHEAS blood level changes and characterize the relationship between early blood DHEAS reduction and cell number changes in women ZR.

Materials and methods

DHEAS plasma samples (n = 463) were analyzed in 166 healthy prepubertal girls before pubarche (<9 years) and 324 serum samples from 268 adult females (31.9–83.8 years) without conditions affecting steroidogenesis. Guided by DHEAS blood levels reduction rate, we selected the age range for ZR cell counting using DHEA/DHEAS and phosphatase and tensin homolog (PTEN), tumor suppressor and cell stress marker, immunostaining, and hematoxylin stained nuclei of 14 post-mortem adrenal glands.

Results

We confirmed that overweight girls exhibited higher and earlier DHEAS levels and no difference was found compared with the average European and South American girls with a similar body mass index (BMI). Adrenopause onset threshold (AOT) defined as DHEAS blood levels <2040 nmol/L was identified in >35% of the females >40 years old and associated with significantly reduced ZR cell number (based on PTEN and hematoxylin signals). ZR cell loss may in part account for lower DHEA/DHEAS expression, but most cells remain alive with lower DHEA/DHEAS biosynthesis.

Conclusion

The timely relation between significant reduction of blood DHEAS levels and decreased ZR cell number at the beginning of the 40s suggests that adrenopause is an additional burden for a significant number of middle-aged women, and may become an emergent problem associated with further sex steroids reduction during the menopausal transition.

Open access
Enrique Pedernera Universidad Nacional Autónoma de México, Facultad de Medicina, Departamento de Embriología y Genética, Ciudad de México, México

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Flavia Morales-Vásquez Instituto Nacional de Cancerología, Ciudad de México, México

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María J Gómora Universidad Nacional Autónoma de México, Facultad de Medicina, Departamento de Embriología y Genética, Ciudad de México, México

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Miguel A Almaraz Universidad Nacional Autónoma de México, Facultad de Medicina, Departamento de Embriología y Genética, Ciudad de México, México

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Esteban Mena Universidad Nacional Autónoma de México, Facultad de Medicina, Secretaría General, Ciudad de México, México
Universidad La Salle, Posgrado de la Facultad de Ciencias Químicas, Ciudad de México, México

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Delia Pérez-Montiel Instituto Nacional de Cancerología, Ciudad de México, México

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Elizabeth Rendon Hospital Militar de Especialidades de la Mujer y Neonatología. Ciudad de México, México

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Horacio López-Basave Instituto Nacional de Cancerología, Ciudad de México, México

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Juan Maldonado-Cubas Universidad La Salle, Posgrado de la Facultad de Ciencias Químicas, Ciudad de México, México

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Carmen Méndez Universidad Nacional Autónoma de México, Facultad de Medicina, Departamento de Embriología y Genética, Ciudad de México, México

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The incidence of ovarian cancer has been epidemiologically related to female reproductive events and hormone replacement therapy after menopause. This highlights the importance of evaluating the role of sexual steroid hormones in ovarian cancer by the expression of enzymes related to steroid hormone biosynthesis in the tumor cells. This study was aimed to evaluate the presence of 17β-hydroxysteroid dehydrogenase type 1 (17β-HSD1), aromatase and estrogen receptor alpha (ERα) in the tumor cells and their association with the overall survival in 111 patients diagnosed with primary ovarian tumors. Positive immunoreactivity for 17β-HSD1 was observed in 74% of the tumors. In the same samples, aromatase and ERα revealed 66% and 47% positivity, respectively. No association was observed of 17β-HSD1 expression with the histological subtypes and clinical stages of the tumor. The overall survival of patients was improved in 17β-HSD1-positive group in Kaplan–Meier analysis (P = 0.028), and 17β-HSD1 expression had a protective effect from multivariate proportional regression evaluation (HR = 0.44; 95% CI 0.24–0.9; P = 0.040). The improved survival was observed in serous epithelial tumors but not in nonserous ovarian tumors. The expression of 17β-HSD1 in the cells of the serous epithelial ovarian tumors was associated with an improved overall survival, whereas aromatase and ERα were not related to a better survival. The evaluation of hazard risk factors demonstrated that age and clinical stage showed worse prognosis, and 17β-HSD1 expression displayed a protective effect with a better survival outcome in patients of epithelial ovarian tumors.

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Anouar Aznou Department of Internal Medicine, Amsterdam University Medical Centers, MB Amsterdam, the Netherlands

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Rick Meijer Department of Internal Medicine, Amsterdam University Medical Centers, MB Amsterdam, the Netherlands

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Daniel van Raalte Department of Internal Medicine, Amsterdam University Medical Centers, MB Amsterdam, the Netherlands

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Martin den Heijer Department of Internal Medicine, Amsterdam University Medical Centers, MB Amsterdam, the Netherlands

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Annemieke Heijboer Endocrine Laboratory, Department of Clinical Chemistry, Amsterdam University Medical Centers, MB Amsterdam, the Netherlands

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Renate de Jongh Department of Internal Medicine, Amsterdam University Medical Centers, MB Amsterdam, the Netherlands

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Objective

The mechanisms underlying the development of peripheral insulin resistance are complex. Several studies have linked sclerostin, an osteocyte-derived inhibitor of the Wnt/β-catenin pathway, to obesity and insulin resistance. The aim of this study was to investigate (1) whether serum sclerostin is associated with insulin sensitivity in lean and/or obese women; and (2) whether hyperinsulinaemia affects serum sclerostin concentrations.

Design

A cross-sectional study.

Methods

Insulin sensitivity was measured in lean (BMI < 25 kg/m2) and obese (BMI > 30 kg/m2) women using a hyperinsulinaemic–euglycaemic clamp. Serum sclerostin was measured at baseline and during the clamp procedure.

Results

We studied 21 lean and 22 obese women with a median age of 40 and 43 years and a median BMI of 22.4 and 33.5 kg/m2, respectively. Obese women had higher serum sclerostin than lean women (122 ± 33 vs 93 ± 33 nmol/L, P < 0.01). Higher serum sclerostin was associated with lower insulin sensitivity in obese, but not in lean individuals (difference in M-value between highest and lowest quartile: −7.02 mg/kg/min, P = 0.03 and 1.59 mg/kg/min, P = 0.50, respectively). Hyperinsulinaemia did not affect serum sclerostin in lean nor obese women (P > 0.5).

Conclusion

Serum sclerostin is negatively associated with insulin sensitivity as measured with the hyperinsulinaemic–euglycaemic clamp in obese, but not lean women. This indicates a potential role of the Wnt/β-catenin pathway in regulating insulin sensitivity particularly in obese individuals. Our findings remain hypothesis-generating and should be confirmed by additional studies.

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Franca Genest Clinical Trial Unit, Orthopedic Department, University of Wuerzburg, Wuerzburg, Germany

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Michael Schneider Clinical Trial Unit, Orthopedic Department, University of Wuerzburg, Wuerzburg, Germany

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Andreas Zehnder Clinical Trial Unit, Orthopedic Department, University of Wuerzburg, Wuerzburg, Germany

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Dominik Lieberoth-Leden Clinical Trial Unit, Orthopedic Department, University of Wuerzburg, Wuerzburg, Germany

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Lothar Seefried Clinical Trial Unit, Orthopedic Department, University of Wuerzburg, Wuerzburg, Germany

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Purpose

Aging and concurrent constitutional changes as sarcopenia, osteoporosis and obesity are associated with progressive functional decline. Coincidence and mutual interference of this risk factors require further evaluation.

Methods

Cross-sectional evaluation of musculoskeletal health in a community-dwelling cohort of men aged 65–90 years. Objectives included descriptive analysis of age-related decline in physical performance, prevalence of osteoporosis (FRAX-Score), sarcopenia (EWGSOP criteria) and obesity (BMI > 30 kg/m2) and their coincidence/interference.

Results

Based on 507 participants assessed, aging was associated with progressive functional deterioration, regarding power (chair rise test −1.54% per year), performance (usual gait speed −1.38% per year) and muscle force (grip strength −1.52% per year) while muscle mass declined only marginally (skeletal muscle index −0.29% per year). Prevalence of osteoporosis was 41.8% (n = 212) while only 22.9% (n = 116) of the participants met the criteria for sarcopenia and 23.7% (n = 120) were obese. Osteosarcopenia was found in n = 79 (15.6%), sarcopenic obesity was present in 14 men (2.8%). A combination of all three conditions could be confirmed in n = 8 (1.6%). There was an inverse correlation of BMI with physical performance whereas osteoporosis and sarcopenia did not interfere with functional outcomes.

Conclusion

Based on current definitions, there is considerable overlap in the prevalence of osteoporosis and sarcopenia, while obesity appears to be a distinct problem. Functional decline appears to be associated with obesity rather than osteoporosis or sarcopenia. It remains to be determined to what extend obesity itself causes performance deficits or if obesity is merely an indicator of insufficient activity eventually predisposing to functional decline.

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Haojie Zhang Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China

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Yuke Cui Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China

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Ruihua Dong Key Laboratory of Public Health Safety of Ministry of Education, Collaborative Innovation Center of Social Risks Governance in Health, School of Public Health, Fudan University, Shanghai, China

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Wen Zhang Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China

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Shihan Chen Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China

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Heng Wan Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China

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Chi Chen Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China

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Yi Chen Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China

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Yuying Wang Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China

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Chunfang Zhu Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China

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Bo Chen Key Laboratory of Public Health Safety of Ministry of Education, Collaborative Innovation Center of Social Risks Governance in Health, School of Public Health, Fudan University, Shanghai, China

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Ningjian Wang Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China

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Yingli Lu Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China

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Background

Bone is thought to be the reservoir of the human lead burden, and vitamin D is associated with bone turnover. We aimed to explore whether exposure to lower 25-hydroxy vitamin D (25(OH)D) levels was associated with higher blood lead levels (BLLs) by increasing the bone turnover rate in individuals with type 2 diabetes.

Methods

A total of 4103 type 2 diabetic men and postmenopausal women in Shanghai, China, were enrolled in 2018. Their 25(OH)D, β-C-terminal telopeptide (β-CTX), N-MID osteocalcin and procollagen type 1 N-peptide (P1NP) levels were detected. Their BLLs were determined by atomic absorption spectrometry. Mediation analyses were performed to identify the possible role that bone turnover played in the underlying mechanisms.

Results

In both the men and postmenopausal women, all three bone turnover markers were inversely associated with 25(OH)D and positively associated with the BLL (all P < 0.01) after adjusting for age, current smoking habits, metabolic parameters, duration of diabetes, vitamin D intake, and use of anti-osteoporosis medication. In the mediation analyses, none of the direct associations between 25(OH)D and BLL was significant for the three bone turnover markers, but all three bone turnover markers were found to be significant mediators of the indirect associations between 25(OH)D and BLL.

Conclusion

The association between vitamin D and BLL was fully mediated by bone turnover markers in type 2 diabetic patients (mediation effect). This finding suggested that vitamin D may protect against blood lead exposure from the bone reservoir by decreasing bone turnover in individuals with type 2 diabetes.

Open access
Tingting Jia Department of Implantology, School of Stomatology, Shandong University, Jinan, People’s Republic of China
Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan, People’s Republic of China

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Ya-nan Wang Department of Implantology, School of Stomatology, Shandong University, Jinan, People’s Republic of China
Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan, People’s Republic of China

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Dongjiao Zhang Department of Implantology, School of Stomatology, Shandong University, Jinan, People’s Republic of China
Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan, People’s Republic of China

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Xin Xu Department of Implantology, School of Stomatology, Shandong University, Jinan, People’s Republic of China
Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan, People’s Republic of China

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Diabetes-induced advanced glycation end products (AGEs) overproduction would result in compromised osseointegration of titanium implant and high rate of implantation failure. 1α,25-dihydroxyvitamin D3 (1,25VD3) plays a vital role in osteogenesis, whereas its effects on the osseointegration and the underlying mechanism are unclear. The purpose of this study was to investigate that 1,25VD3 might promote the defensive ability of osseointegration through suppressing AGEs/RAGE in type 2 diabetes mellitus. In animal study, streptozotocin-induced diabetic rats accepted implant surgery, with or without 1,25VD3 intervention for 12 weeks. After killing, the serum AGEs level, bone microarchitecture and biomechanical index of rats were measured systematically. In vitro study, osteoblasts differentiation capacity was analyzed by alizarin red staining, alkaline phosphatase assay and Western blotting, after treatment with BSA, AGEs, AGEs with RAGE inhibitor and AGEs with 1,25VD3. And the expression of RAGE protein was detected to explore the mechanism. Results showed that 1,25VD3 could reverse the impaired osseointegration and mechanical strength, which possibly resulted from the increased AGEs. Moreover, 1,25VD3 could ameliorate AGEs-induced damage of cell osteogenic differentiation, as well as downregulating the RAGE expression. These data may provide a theoretical basis that 1,25VD3 could work as an adjuvant treatment against poor osseointegration in patients with type 2 diabetes mellitus.

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Lijuan Yuan Department of Biochemistry and Molecular Biology, Center for DNA Typing, Air Force Medical University, Xi’an, Shaanxi, People’s Republic of China
Department of General Surgery, Tangdu Hospital, Air Force Medical University, Xi’an, Shaanxi, People’s Republic of China

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Xihui Chen Department of Biochemistry and Molecular Biology, Center for DNA Typing, Air Force Medical University, Xi’an, Shaanxi, People’s Republic of China

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Ziyu Liu Department of Microbiology, Air Force Medical University, Xi’an, Shaanxi, People’s Republic of China

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Dan Wu Department of Biochemistry and Molecular Biology, Center for DNA Typing, Air Force Medical University, Xi’an, Shaanxi, People’s Republic of China

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Jianguo Lu Department of General Surgery, Tangdu Hospital, Air Force Medical University, Xi’an, Shaanxi, People’s Republic of China

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Guoqiang Bao Department of General Surgery, Tangdu Hospital, Air Force Medical University, Xi’an, Shaanxi, People’s Republic of China

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Sijia Zhang Department of Biochemistry and Molecular Biology, Center for DNA Typing, Air Force Medical University, Xi’an, Shaanxi, People’s Republic of China

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Lifeng Wang Department of Biochemistry and Molecular Biology, Air Force Medical University, Xi’an, Shaanxi, People’s Republic of China

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Yuanming Wu Department of Biochemistry and Molecular Biology, Center for DNA Typing, Air Force Medical University, Xi’an, Shaanxi, People’s Republic of China

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Primary hypertrophic osteoarthropathy (PHO) is a rare familial disorder with reduced penetrance for females. The genetic mutations associated with PHO have been identified in HPGD and SLCO2A1, which involved in prostaglandin E2 metabolism. Here, we report 5 PHO patients from four non-consanguineous families. Two heterozygous mutations in solute carrier organic anion transporter family member 2A1 (SLCO2A1) were identified in two brothers by whole-exome sequencing. Three heterozygous mutations and one homozygous mutation were identified in other three PHO families by Sanger sequencing. However, there was no mutation in HPGD. These findings confirmed that homozygous or compound heterozygous mutations of SLCO2A1 were the pathogenic cause of PHO. A female individual shared the same mutations in SLCO2A1 with her PHO brother but did not have any typical PHO symptoms. The influence of sex hormones on the pathogenesis of PHO and its implication were discussed.

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Elena Valassi Endocrinology/Medicine Department, Hospital Sant Pau, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER, Unidad 747), IIB-Sant Pau, ISCIII and Universitat Autònoma de Barcelona (UAB), Barcelona, Spain

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Natalia García-Giralt URFOA, IMIM (Institut Hospital del Mar d’Investigacions Mèdiques), Universitat Autònoma de Barcelona, Barcelona, Spain

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Jorge Malouf Mineral Metabolism Unit, Medicine Department, Hospital Sant Pau, Barcelona, Spain

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Iris Crespo Endocrinology/Medicine Department, Hospital Sant Pau, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER, Unidad 747), IIB-Sant Pau, ISCIII and Universitat Autònoma de Barcelona (UAB), Barcelona, Spain

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Jaume Llauger Radiology Department, Hospital Sant Pau, Barcelona, Spain

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Adolfo Díez-Pérez URFOA, IMIM (Institut Hospital del Mar d’Investigacions Mèdiques), Universitat Autònoma de Barcelona, Barcelona, Spain

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Susan M Webb Endocrinology/Medicine Department, Hospital Sant Pau, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER, Unidad 747), IIB-Sant Pau, ISCIII and Universitat Autònoma de Barcelona (UAB), Barcelona, Spain

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Background

Biochemical control of GH/IGF-I excess in acromegaly (ACRO) is associated with persistent impairment of trabecular microstructure leading to increased risk of vertebral fractures. Circulating miRNAs modulate the activity of osteoblasts and osteoclasts, and may be potential biomarkers of osteoporosis.

Aims

Identify differentially expressed miRNAs in the serum of patients with controlled ACRO vs controls and correlate miRNA levels with both biochemical and structural bone parameters.

Patients and methods

Twenty-seven patients with controlled ACRO (11 males, 16 females; mean age, 48 ± 5 years; BMI, 28 ± 4 kg/m2) and 27 age-, gender- and BMI-matched controls were recruited. Areal BMD at lumbar spine and femur, and trabecular bone score were assessed; volumetric BMD was measured by quantitative computed tomography QCT-Pro (Mindways). Twenty miRNAs, chosen by their putative role in bone, were quantified in serum using real-time qPCR.

Results

In ACRO patients, miR-103a-3p and miR-191-5p were found overexpressed, whereas miR-660-5p was underexpressed (P < 0.001). miR-103a-3p levels were negatively associated with both trabecular vBMD at trochanter and serum osteoprotegerin concentrations (P < 0.05) and positively with vitamin D concentrations (P < 0.01) and total cross-sectional area of the femoral neck (P < 0.05). miR-660-5p levels were correlated with both trabecular vBMD at trochanter and OPG concentrations (P < 0.05), but were negatively associated with vitamin D levels (P < 0.05). A negative correlation between miR-103-a-3p and miR-660-5p was found in both groups (P < 0.001).

Conclusions

Circulating miR-103a-3p and miR-660-5p are differentially expressed in controlled ACRO patients and associated with bone structural parameters. miRNAs may be one of the mechanisms involved in the pathogenesis of bone disease and could be used as biomarkers in ACRO patients.

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Kaisu Luiro Department of Obstetrics and Gynecology, Reproductive Medicine Unit, Helsinki University Hospital and University of Helsinki, Helsinki, Finland

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Kristiina Aittomäki Department of Medical Genetics, Helsinki University Hospital, Helsinki, Finland

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Pekka Jousilahti Department of Public Health Solutions, National Institute for Health and Welfare, Helsinki, Finland

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Juha S Tapanainen Department of Obstetrics and Gynecology, Reproductive Medicine Unit, Helsinki University Hospital and University of Helsinki, Helsinki, Finland
Department of Obstetrics and Gynecology, University of Oulu and Oulu University Hospital, Medical Research Center, PEDEGO Research Unit, Oulu, Finland

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Objective

To study the use of hormone therapy (HT), morbidity and reproductive outcomes of women with primary ovarian insufficiency (POI) due to FSH-resistant ovaries (FSHRO).

Design

A prospective follow-up study in a university-based tertiary clinic setting.

Methods

Twenty-six women with an inactivating A189V FSH receptor mutation were investigated by means of a health questionnaire and clinical examination. Twenty-two returned the health questionnaire and 14 were clinically examined. Main outcome measures in the health questionnaire were reported as HT, morbidity, medication and infertility treatment outcomes. In the clinical study, risk factors for cardiovascular disease (CVD) and metabolic syndrome (MetS) were compared to age-matched controls from a national population survey (FINRISK). Average number of controls was 326 per FSHRO subject (range 178–430). Bone mineral density and whole-body composition were analyzed with DXA. Psychological and sexual well-being was assessed with Beck Depression Inventory (BDI21), Generalized Anxiety Disorder 7 (GAD-7) and Female Sexual Function Index (FSFI) questionnaires.

Results

HT was initiated late (median 18 years of age) compared with normal puberty and the median time of use was shorter (20–22 years) than the normal fertile period. Osteopenia was detected in 9/14 of the FSHRO women despite HT. No major risk factors for CVD or diabetes were found.

Conclusions

HT of 20 years seems to be associated with a similar cardiovascular and metabolic risk factor profile as in the population control group. However, optimal bone health may require an early-onset and longer period of HT, which would better correspond to the natural fertile period.

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