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Jingya Zhou, Meng Zhang, Lin Lu, Xiaopeng Guo, Lu Gao, Weigang Yan, Haiyu Pang, Yi Wang and Bing Xing

(ACTH)-dependent and ACTH-independent etiologies. The former includes Cushing’s disease (CD) and ectopic ACTH syndrome (EAS), and the latter includes adrenocortical adenoma (ACA), adrenocortical carcinoma (ACC), primary bilateral macronodular adrenal

Open access

Nikolina Zdraveska, Maja Zdravkovska, Violeta Anastasovska, Elena Sukarova-Angelovska and Mirjana Kocova

dyshormonogenesis due to defects of thyroid hormone biosynthesis. The etiologic evaluation of CH is possible through several examinations, such as ultrasonography, scintigraphy, thyroglobulin measurement and perchlorate discharge test. There are also cases where the

Open access

Luigi Laino, Silvia Majore, Nicoletta Preziosi, Barbara Grammatico, Carmelilia De Bernardo, Salvatore Scommegna, Anna Maria Rapone, Giacinto Marrocco, Irene Bottillo and Paola Grammatico

category of DSD was found to be related to a large number of different DNA alterations, thus requiring multiple genetic studies to possibly achieve a precise etiological diagnosis in every patient. Subjects and methods Patients A cohort of 88 individuals

Open access

Lia Ferreira, João Silva, Susana Garrido, Carlos Bello, Diana Oliveira, Hélder Simões, Isabel Paiva, Joana Guimarães, Marta Ferreira, Teresa Pereira, Rita Bettencourt-Silva, Ana Filipa Martins, Tiago Silva, Vera Fernandes, Maria Lopes Pereira and Adrenal Tumors Study Group of the Portuguese Society of Endocrinology

for 69 (24.8%) patients. Data regarding etiological investigation were available in 246 patients. The most common causes were autoimmune adrenalitis (61.0%), genetic-related AD (14.2%) and infectious adrenalitis (7.3%). Thirty-eight cases (15

Open access

Dirk Weismann, Andreas Schneider and Charlotte Höybye

regarding the maximum rate of correction, which can safely be applied, and a gradual decrease in recommended upper limits over time can be observed ( 10 , 12 ). HN is a complicated condition with a large number of etiologies and treatment options. From a

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H A Booij, W D C Gaykema, K A J Kuijpers, M J M Pouwels and H M den Hertog

of the etiology and effect of PD in these acute acquired brain injuries may assist in developing rational interventions and improve outcome. Methodology MEDLINE and EMBASE were searched for potentially relevant articles for the period January

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N Bergmann, F Gyntelberg and J Faber

etiology seems multifactorial, which calls for new areas of prevention and intervention. One potential risk factor for the development of MES is chronic psychosocial stress, in the following referred to as stress. In general it is accepted to divide the

Open access

Rossella Cannarella, Teresa Mattina, Rosita A Condorelli, Laura M Mongioì, Giuseppe Pandini, Sandro La Vignera and Aldo E Calogero

be involved in the etiology of neurological symptoms of these patients. In fact, IGF1 protein has been reported to pass through the blood–brain barrier, and it is involved in normal central nervous system (CNS) development by promoting neuronal cell

Open access

Jordyn Silverstein, Wesley Kidder, Susan Fisher, Thomas A Hope, Samantha Maisel, Dianna Ng, Jessica Van Ziffle, Chloe E Atreya and Katherine Van Loon

. Expanding upon the existing literature which only described the clinical features of CRC during pregnancy, our study sought to improve our understanding of etiologic factors that might contribute to the development of CRC in pregnant women. It is notable

Open access

Athanasios D Anastasilakis, Marina Tsoli, Gregory Kaltsas and Polyzois Makras

Langerhans cell histiocytosis (LCH) is a rare disease of not well-defined etiology that involves immune cell activation and frequently affects the skeleton. Bone involvement in LCH usually presents in the form of osteolytic lesions along with low bone mineral density. Various molecules involved in bone metabolism are implicated in the pathogenesis of LCH or may be affected during the course of the disease, including interleukins (ILs), tumor necrosis factor α, receptor activator of NF-κB (RANK) and its soluble ligand RANKL, osteoprotegerin (OPG), periostin and sclerostin. Among them IL-17A, periostin and RANKL have been proposed as potential serum biomarkers for LCH, particularly as the interaction between RANK, RANKL and OPG not only regulates bone homeostasis through its effects on the osteoclasts but also affects the activation and survival of immune cells. Significant changes in circulating and lesional RANKL levels have been observed in LCH patients irrespective of bone involvement. Standard LCH management includes local or systematic administration of corticosteroids and chemotherapy. Given the implication of RANK, RANKL and OPG in the pathogenesis of the disease and the osteolytic nature of bone lesions, agents aiming at inhibiting the RANKL pathway and/or osteoclastic activation, such as bisphosphonates and denosumab, may have a role in the therapeutic approach of LCH although further clinical investigation is warranted.