existing uncertain evidence regarding this issue using the systematic review and meta-analysis of all published literature. Methods Literature search We performed the meta-analysis following the Preferred Reporting Items for Systematic Reviews
Yongli Fu, Yaowu Sun, Jiankun Zhang and Yu Cheng
Agnès Linglart, Martin Biosse-Duplan, Karine Briot, Catherine Chaussain, Laure Esterle, Séverine Guillaume-Czitrom, Peter Kamenicky, Jerome Nevoux, Dominique Prié, Anya Rothenbuhler, Philippe Wicart and Pol Harvengt
adolescence. Causes of phosphate wasting are mostly due to genetic defects in factors necessary for phosphate handling; for a review read (1) . They have been summarized in Table 1 . In this review, we will consider two different types of phosphate wasting
Jes Sloth Mathiesen, Jens Peter Kroustrup, Peter Vestergaard, Kirstine Stochholm, Per Løgstrup Poulsen, Åse Krogh Rasmussen, Ulla Feldt-Rasmussen, Sten Schytte, Stefano Christian Londero, Henrik Baymler Pedersen, Christoffer Holst Hahn, Bjarki Ditlev Djurhuus, Jens Bentzen, Sören Möller, Mette Gaustadnes, Maria Rossing, Finn Cilius Nielsen, Kim Brixen, Anja Lisbeth Frederiksen, Christian Godballe and the Danish Thyroid Cancer Group (DATHYRCA)
One patient RET tested subsequent to the end date of the RET cohort in December 31, 2014. To classify the 207 molecularly unclassified MTC patients, several sources were used. First, a review of available medical records ( n = 149) was
Satoshi Higuchi, Hideki Ota, Takuya Ueda, Yuta Tezuka, Kei Omata, Yoshikiyo Ono, Ryo Morimoto, Masataka Kudo, Fumitoshi Satoh and Kei Takase
. Cardiovascular manifestations of pheochromocytoma . Cardiology in Review 2017 25 215 – 222 . ( https://doi.org/10.1097/CRD.0000000000000141 ) 10.1097/CRD.0000000000000141 28786897 4 Yu R Nissen NN Bannykh SI . Cardiac complications as initial
K G Samsom, L M van Veenendaal, G D Valk, M R Vriens, M E T Tesselaar and J G van den Berg
genomic landscape of SI-NETs remains poorly elucidated and biomarkers have not yet been identified. Moreover, the genetic constitution of SI-NETs has been shown to differ compared to pancreatic NETs ( 11 ). With this review we aim to provide the clinician
Zeming Liu, Di Hu, Yihui Huang, Sichao Chen, Wen Zeng, Ling Zhou, Wei Zhou, Min Wang, Haifeng Feng, Wei Wei, Chao Zhang, Danyang Chen and Liang Guo
undertook the research, Y H H, S C C and W Z performed the analyses, Z M L and D H wrote the main manuscript text and prepared figures. All authors reviewed the manuscript. References 1 Pacini F Schlumberger M Dralle H Elisei R Smit JW Wiersinga W
Benjamin G Challis, Andrew S Powlson, Ruth T Casey, Carla Pearson, Brian Y Lam, Marcella Ma, Deborah Pitfield, Giles S H Yeo, Edmund Godfrey, Heok K Cheow, V Krishna Chatterjee, Nicholas R Carroll, Ashley Shaw, John R Buscombe and Helen L Simpson
involved in tumour development and autonomous insulin secretion. Patients and methods Study population We retrospectively reviewed medical records of patients presenting to our institution between 2003 and 2016 with a diagnosis of
Nese Cinar and Alper Gurlek
Adipose tissue secretes a variety of active biological substances, called adipocytokines, that act in an autocrine, paracrine, and endocrine manner. They have roles in appetite control, thermogenesis, and thyroid and reproductive functions. All these molecules may lead to local and generalized inflammation, mediating obesity-associated vascular disorders including hypertension, diabetes, atherosclerosis, and insulin resistance. Thyroid dysfunction is associated with changes in body weight, thermogenesis, and energy expenditure. The connections between cardiovascular risk factors such as dyslipidemia, impaired glucose tolerance, insulin resistance, atherosclerosis, and thyroid dysfunction have been reported in several studies. The adipocytokines serve as causative or protective factors in the development of these disorders in the states of thyroid dysfunction. Abnormal levels of adipocytokines (adiponectin (ADP), leptin, resistin, vaspin, and visfatin) in hypo- and hyperthyroidism have been reported with controversial results. This review aims to update the implication of novel adipokines ADP, vaspin, and visfatin in thyroid dysfunction.
David Koeckerling, Jeremy W Tomlinson and Jeremy Cobbold
Non-alcoholic fatty liver disease is a chronic liver disease which is closely associated with components of the metabolic syndrome. Its high clinical burden results from the growing prevalence, inherent cardiometabolic risk and potential of progressing to cirrhosis. Patients with non-alcoholic fatty liver disease show variable rates of disease progression through a histological spectrum ranging from steatosis to steatohepatitis with or without fibrosis. The presence and severity of fibrosis are the most important prognostic factors in non-alcoholic fatty liver disease. This necessitates risk stratification of patients by fibrosis stage using combinations of non-invasive methods such as composite scoring systems and/or transient elastography. A multidisciplinary approach to treatment is advised, centred on amelioration of cardiometabolic risk through lifestyle and pharmacological interventions. Despite the current lack of licensed, liver-targeted pharmacotherapy, several promising agents are undergoing late-phase clinical trials to complement standard management in patients with advanced disease. This review summarises the current concepts in diagnosis and disease progression of non-alcoholic liver disease, focusing on pragmatic approaches to risk assessment and management in both primary and secondary care settings.
Chunliang Yang, Junyi Li, Fei Sun, Haifeng Zhou, Jia Yang and Chao Yang
Hyperglycemia is the consequence of blood glucose dysregulation and a driving force of diabetic complications including retinopathy, nephropathy and cardiovascular diseases. The serum and glucocorticoid inducible kinase-1 (SGK1) has been suggested in the modulation of various pathophysiological activities. However, the role of SGK1 in blood glucose homeostasis remains less appreciated. In this review, we intend to summarize the function of SGK1 in glucose level regulation and to examine the evidence supporting the therapeutic potential of SGK1 inhibitors in hyperglycemia. Ample evidence points to the controversial roles of SGK1 in pancreatic insulin secretion and peripheral insulin sensitivity, which reflects the complex interplay between SGK1 activation and blood glucose fluctuation. Furthermore, SGK1 is engaged in glucose absorption and excretion in intestine and kidney, and participates in the progression of hyperglycemia induced secondary organ damage. As a net effect, blockage of SGK1 activation via either pharmacological inhibition or genetic manipulation seems to be helpful in glucose control at varying diabetic stages.