Searchable abstracts of presentations at key conferences in endocrinology

ea0065mte4.1 | Fighting liver fat | SFEBES2019

Fighting liver fat

Cobbold Jeremy , Tomlinson Jeremy

Non-alcoholic fatty liver disease (NAFLD) is the most highly prevalent chronic liver condition and is associated with significant adverse outcomes, both through liver-specific morbidity and mortality, but perhaps more importantly, through adverse cardiovascular and metabolic outcomes. NAFLD is a spectrum of disease, extending from simple steatosis, through to inflammation and fibrosis and risk of cirrhosis. The mechanisms that govern hepatic lipid accumulation and the predispo...

ea0094p265 | Reproductive Endocrinology | SFEBES2023

Non-invasive assessment of liver abnormalities in turner syndrome: A Follow-up Study

Calanchini Matilde , Shipley Alexandra , Cobbold Jeremy , Tomlinson Jeremy , Turner Helen

Background: We have previously reported abnormal liver function tests (LFTs), FIB-4 scores and liver stiffness measurements (LSM, Fibroscan) in patients with Turner syndrome (TS), but longitudinal data defining the impact of TS on liver phenotype are limited.Methods: We undertook a retrospective longitudinal follow-up audit (OUH; 8348) of 24 women with TS who had abnormal LFTs and underwent at least 2 assessments (median...

ea0044p113 | Diabetes and Cardiovascular | SFEBES2016

High risk populations: Attitudes to NAFLD among diabetologists

Marjot Thomas , Sbardella Emilia , Hazlehurst Jonathan , Moolla Ahmad , Cobbold Jeremy , Tomlinson Jeremy

Introduction: Non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2DM) are common conditions that regularly coexist and can act synergistically to drive adverse outcomes. The prevalence of NAFLD in T2DM is 70%, with 16% having evidence of advanced hepatic fibrosis.Aims: Our study therefore had two aims: Firstly, to define the attitudes and current clinical practice of diabetes specialists towards NAFLD across the UK and secondly, to implement...

ea0041gp65 | Clinical Case Reports | ECE2016

Turner syndrome and liver involvement: is there a place for treatment with ursodeoxycholic acid?

Calanchini Matilde , Moolla Ahmad , Cobbold Jeremy , Tomlinson Jeremy W , Fabbri Andrea , Grossman Ashley , Turner Helen

Introduction: Abnormalities in liver biochemistry are frequent in Turner’s syndrome (TS) with a reported prevalence between 20 and 80%. While their aetiology remains unclear, metabolic factors and intrahepatic biliary disease have been postulated. Moreover, some TS patients have a predominantly cholestatic biochemical abnormality and others a hepatitic picture. Ursodeoxycholic acid (UDCA) has been shown to be a useful treatment of cholestatic disease.<p class="abstext...

ea0077pl9 | Society for Endocrinology Medal Lecture | SFEBES2021

Revisiting Cushing’s: The power of pre-receptor metabolism

Tomlinson Jeremy

Glucocorticoids have potent effects on almost every tissue in the body and this is exemplified in patients with Cushing’s disease. Whilst Cushing’s disease is rare, glucocorticoids are commonly prescribed for their anti-inflammatory actions, but their use is associated with a series of undesirable adverse effects, including obesity, insulin resistance, hypertension, myopathy and osteoporosis. Within tissues, glucocorticoids (both endogenous and exogenous) are metabol...

ea0086sk1.1 | Radiology for the endocrinologist | SFEBES2022

Trials and tribulations of targeting 11β-HSD1

Tomlinson Jeremy

Within tissues, glucocorticoids (both endogenous and exogenous) are metabolised by a series of enzymes that have the ability to tightly control local hormone availability and thus regulate binding to, and activation of, the glucocorticoid receptor. The 11β-hydroxysteroid dehydrogenases (type 1 [11β-HSD1] and type 2 11β-HSD2]) interconvert active (cortisol, prednisolone and corticosterone) and inactive glucocorticoids (cortisone, prednisone and 11-dehydrocorticos...

ea0049s25.3 | HPA axis regulation during a woman's life: impact on metabolic outcomes | ECE2017

11β-hydroxysteroid dehydrogenase activity, androgen excess, and metabolic outcomes in woman

Tomlinson Jeremy

Steroid hormones have potent metabolic effects. Glucocorticoid excess is characterized by central adiposity, insulin resistance, type 2 diabetes and increased cardiovascular risk. Whilst endogenous glucocorticoid excess is rare, local tissue-specific availability of glucocorticoid is controlled by a series of enzymes that are, at a pre-receptor level, able to regulate cortisol’s ability to bind and activate the glucocorticoid receptor. 11β-hydroxysteroid dehydrogenas...

ea0044cmw3.6 | Workshop 3: How do I… | SFEBES2016

How do I determine Cortisol deficiency in the critically ill patient?

Tomlinson Jeremy

Critical illness is associated with significant morbidity and mortality. The changes in the hypothalamo-pituitary-adrenal (HPA) axis that occur during critical illness are complex and whilst early studies had suggested improved outcome in patients with septic shock treated with parenteral glucocorticoids, this was not endorsed in subsequent studies and it remains a highly controversial area.In patients with underlying pituitary or adrenal disease where c...

ea0038cmw1.4 | Workshop 1: How do I do it? (Supported by <emphasis role="italic">Clinical Endocrinology</emphasis> and <emphasis role="italic">Endocrinology, Diabetes &amp; Metabolism Case Reports</emphasis>) | SFEBES2015

How do I manage adrenal suppression?

Tomlinson Jeremy

Two to three percent of the UK population are prescribed glucocorticoid (GC) therapy and their adverse effects are associated with significant morbidity and mortality. Suppression of the hypothalamo-pituitary–adrenal (HPA) axis with the potential risk of adrenal crisis is a recognised complication of therapy. There are significant clinical challenges, not only recognition and diagnosis of the condition, but also in terms of management. There is no doubt that the prevalenc...

ea0034s2.1 | The upside of glucocorticoids in metabolism (Supported by <emphasis role="italic">Journal of Endocrinology</emphasis>) | SFEBES2014

Insulin sensitization of adipose tissue by glucocorticoids

Tomlinson Jeremy

Current dogma suggests that glucocorticoids (GCs) cause insulin resistance in all tissues. Whilst it is clear that they cause global, whole body insulin resistance, we have challenged the concept that the actions of GCs are the same in all tissues. Using a variety of human cell-based models, we have shown that in contrast to their actions in skeletal muscle and liver, GCs cause insulin sensitization in human adipose tissue, enhancing insulin-stimulated PKB/akt phosphorylation,...