Searchable abstracts of presentations at key conferences in endocrinology

ea0086hdi2.5 | How do I...? 2 | SFEBES2022

How do I investigate hypophosphataemia?

Turner Jeremy

Hypophosphataemia is a common mineral metabolic abnormality affecting 2-3% of all hospital in patients and up to 34% of ICU patients. The causes are numerous. Over the last two decades following the identification of Fibroblast growth factor-23 (FGF-23) as the phosphaturic hormone responsible for Autosomal Dominant Hypophosphataemic Rickets (ADHR) in 2000 there has been an explosion in the understanding of phosphate homeostatic physiology and disorders of phosphate homeostasis...

ea0065ns2.3 | Management of Hyper and Hypocalcaemia | SFEBES2019

Patient management of hypocalcaemia & the patient perspective

Turner Jeremy

Acute hypocalcaemia can be a serious and potentially fatal medical emergency while chronic hypocalcaemia may be debilitating and is often associated with reduced quality of life. The usual aetiology of hypocalcaemia is hypoparathyroidism which is sufficiently rare to be officially recognised as an ‘orphan’ condition. Other causes of hypocalcaemia include vitamin D deficiency and hypomagnesaemia secondary to proton pump inhibitor therapy. The relative rarity of hypopa...

ea0044cmw3.4 | Workshop 3: How do I… | SFEBES2016

How do I manage refractory hypercalcaemia?

Turner Jeremy

Hypercalcaemia is a moderately common condition accounting for approximately 1% of all acute general medical presentations. Guidance on emergency management of the hypercalcaemic patient, aimed primarily at the generalist and at guiding initial stages of management has recently been developed by the society (

ea0086p40 | Bone and Calcium | SFEBES2022

Yet another case of hypercalcaemia!

Gaur Smriti , Gunda Rohini , Turner Jeremy

We present an interesting case of immobilisation hypercalcaemia. Case: A 22-year-old female with no significant past medical history was admitted following a road traffic accident (RTA). She suffered severe abdominal injury, skull and multiple limb fractures and underwent left below-knee amputation, bowel resection and nephrostomy. The admission to ITU was prolonged, and seven weeks into the admission, she developed hypercalcaemia (adjusted calcium: 3.8, N: 2.2 – 2.6 mmol...

ea0028p45 | Clinical practice/governance and case reports | SFEBES2012

A protocol for avoidance of post-thryoidectomy hypocalcaemia, results of first 12 months’ audit

Alexandre Leo , Pain Simon , Turner Jeremy

Background: Total and completion thyroidectomy are commonly performed operations for the treatment of thyroid disease. Post-operative hypocalcaemia is a frequent complication of this surgery, and is associated with morbidity and prolonged length of stay (LOS).Methods: In January 2010 we introduced a protocol for the avoidance and management of post-operative of hypocalcaemia based on risk-stratification by post-operative PTH levels in patients undergoing...

ea0094p191 | Bone and Calcium | SFEBES2023

Spontaneous remission of hypercalcaemia in PHPT due to necrosis of parathyroid adenoma

Wahid Alam , Turner Jeremy , Pain Simon

Primary hyperparathyroidism (PHPT) affects approximately 0.3% of the UK population. The most frequent cause is solitary parathyroid adenoma, less commonly parathyroid hyperplasia, multiple adenomas, and parathyroid carcinoma. Cinacalcet is a calcimimetic which may be used in treatment of PHPT in certain circumstances. We report here a case of PHPT, treated by Cinacalcet, wherein apparently spontaneous necrosis of a parathyroid adenoma and resolution of hypercalcaemia occurred....

ea0086op5.3 | Bone and Calcium | SFEBES2022

Lower bone mineral density is associated with primary hyperparathyroidism patients with abnormal vitamin D metabolite ratio (VMR): A case-control study

Tang Jonathan , Malik Mohammad , Turner Jeremy , Fraser William

Introduction: The role of vitamin D and calcium metabolism has long been implicated in the clinical manifestation of primary hyperparathyroidism (PHPT). The skeletal response to the overproduction of PTH is less predictable, and the effect on bone loss can be greater in some patients. In this study, we established associations between vitamin D metabolism, vitamin D metabolite ratio (VMR) 1,25OH2D:24,25OH2D with rates of bone loss in PHPT patients who did not undergo surgery.<...

ea0028p164 | Obesity, diabetes, metabolism and cardiovascular | SFEBES2012

The role of metalloproteinases and their inhibitors in adipose tissue inflammation and the development of type 2 diabetes

Fenech Matthew , Swingler Tracey , Gavrilovic Jelena , Sampson Mike , Turner Jeremy

The development of insulin resistance and type 2 diabetes mellitus (T2DM) in obesity involves (a) adipose inflammation, and (b) restricted adipose expansion with ectopic lipid deposition. Metalloproteinases (MPs) and tissue inhibitors of metalloproteinases (TIMPs) constitute a key regulatory system in inflammation and tissue remodelling. Evidence of MP and TIMP involvement in adipose tissue inflammation and modulation of adipose expansion is currently restricted to work in adi...

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...

ea0077oc5.3 | Bone and Calcium | SFEBES2021

Role of Intact and C-Terminal FGF-23 Assays in the Investigation of Metabolic Bone Disease.

Jethwa Kishan , Bhatti Sumbal , Chipchase Allison , Piec Isabelle , Fraser William , Turner Jeremy

Fibroblast growth factor 23 (FGF-23) is a phosphatonin produced by osteocytes in response to serum phosphate concentration. Immunoassays are widely employed to detect C-terminal fragments of FGF-23 (cFGF-23). Quantitative assays for intact FGF-23 (iFGF-23) measurement are also available. Causes of increased FGF-23 include Tumour Induced Osteomalacia (TIO), X-linked hypophosphataemic rickets (XLH) and end stage renal disease (ESRD). We observed that some individuals, with no id...