Searchable abstracts of presentations at key conferences in endocrinology

ea0038p481 | Thyroid | SFEBES2015

Recurrent Hashimoto’s encephalopathy: a case report of reversible coma and status epilepticus

Agha Adnan , Htun Htwe , Ahmed Adeeba

Background: Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT) also known as Hashimoto’s encephalopathy (HE), is a rare immune-mediated complication independent of functional status of thyroid, which leads to either stroke-like symptoms, or presents as diffuse progressive symptoms of altered mental status, seizures, and cognitive dysfunction. Here we present a case of SREAT in a female with recurrent episodes.Case histo...

ea0065p390 | Reproductive Endocrinology and Biology | SFEBES2019

A rare case of hyperprolactinaemia

Musharraf Adeel , Ahmed Adeeba , Saraf Sanjay , Jones Sharon

44 years old lady was referred to Endocrinology Clinic with history of secondary amenorrhea and hyperprolactinaemia (7800), that responded to Cabergolin treatment, which was discontinued after 2 months due to side effects (headaches). There was no galactorrhea or visual field defects. MRI Pituitary initially reported as Empty Sella. Her prolactin levels rose further along with headach after she discontinued Cabergoline (and refused alternatives). She eventually agreed for nigh...

ea0038p88 | Clinical practice/governance and case reports | SFEBES2015

Haemofiltration as a treatment option in refractory life-threatening diabetic ketoacidosis

Agha Adnan , Nawaz Sarfraz , Saleem Mazhar , Jones Sharon , Ahmed Adeeba

Background: Treating life-threatening diabetic ketoacidosis (DKA) with a pH of <6.9 is extremely challenging and often refractory to treatment using standard fixed dose insulin DKA management protocols which may not work effectively at this low pH because of increased insulin resistance. I.v. bicarbonate (HCO3) use in this situation can be considered but remains controversial due to the risk of significant side effects as well as limited evidence in literature. ...

ea0025p311 | Steroids | SFEBES2011

Hepatic 11β-hydroxysteroid dehydrogenase type 1 expression is dynamically related across the liver lobule and is linked to metabolic status

Ahmed Adeeba , Semjonous Nina , Rabbitt Elizabeth , Stewart Paul

Nearly all the functions of the liver display zonation in distribution within each the lobule. Hepatic cortisol availability is controlled by enzymes that regenerate cortisol from inactive cortisone (11β-hydroxysteroid dehydrogenase type 1, 11β-HSD1). Dysregulation of hepatic 11β-HSD1 activity has been implicated in insulin resistance. Key processes such as gluconeogenesis are located in the periportal hepatocytes, although current dogma describes hepatic 11&#94...

ea0013p288 | Steroids | SFEBES2007

Glucose-6-phosphate disposal and regulation of 11β-hydroxysteroid Dehydrogenase type 1: A new link between cellular glucose metabolism and the HPA axis

Ahmed Adeeba , Lavery Gareth , Tomlinson Jeremy , Cooper Mark , Chou Janice , McKiernan Patrick , Elias Elwyn , Walker Elizabeth , Stewart Paul

Microsomal glucose-6-phosphatase (G6Pase) and glucose-6-phosphate transporter (G6PT) are key enzymes in regulation of blood glucose concentration. Deficiency of G6Pase gives rise to glycogen storage disease type Ia (GSDIa) whilst mutations in G6PT cause GSDIb. Both are characterized by growth retardation, hypoglycemia, hepatomegaly, nephromegaly. G6Pase shares its substrate (G6P) with hexose-6-phosphate-dehydrogenase (H6PDH), an ER enzyme functionally coupled with, and which c...

ea0021oc1.8 | Diabetes and metabolism | SFEBES2009

Cortisol metabolism and hepatic expression of 11β-hydroxysteroid dehydrogenase type 1 in patients with non-alcoholic fatty liver disease

Ahmed Adeeba , Brady Theresa , Bailey Claire , Guest Phillip , Wagenmakers Anton , Newsome Phillip , Hubscher Stephan , Elias Elwyn , Adams David , Tomlinson Jeremy , Stewart Paul

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. The role of glucocorticoids (GC) in its pathogenesis, is highlighted in patients with GC excess, Cushing’s syndrome, who develop central adiposity, insulin resistance and in 20% of cases, NAFLD. Although circulating cortisol levels are normal in patients with NAFLD, hepatic cortisol availability is controlled by enzymes that regenerate cortisol from inactive cortisone (11&#94...