Endocrine Abstracts

A 43-year-old Bangladeshi lady was seen in the endocrinology clinic after recent admission to hospital with vomiting and headaches. Her past medical history included Type 2 diabetes, hypertension, ischaemic heart disease and goitre. During admission, a diagnosis of euglycaemic diabetic ketoacidosis (DKA) was made (pH 7.31, bicarbonate 18.3, glucose 7.8 and ketones 6.1) secondary to SGLT-2 inhibitor. This was managed with a fixed rate insulin infusion, intravenous fluid hydration and cessation of SGLT-2 inhibitor. Brain imaging was arranged for further assessment of her persistent headaches and vomiting. An incidental left sided pituitary macroadenoma, measuring 17 x 11 x 8 mm, with grade II cavernous involvement, was confirmed on MRI imaging. On resolution of DKA, the patient was discharged home on a basal bolus insulin regime. In clinic, review of the history revealed a 5-year history of worsening intermittent headaches associated with visual blurring, increasing nose, jaw and hand size, splayed teeth and two-year history neck swelling with hoarse voice. On systems enquiry, there was a one-year history of oligomenorrhoea, significant hair loss and polyarthralgia with no change in bowel habit. On examination, features of acromegaly were noted including coarse features, spade-like hands, splayed teeth and macroglossia. She was hypertensive with a BP of 150/98 mmHg. Cardiovascular, respiratory, and abdominal examinations were unremarkable. Visual fields were intact to red pin with no focal neurology. Further investigations showed: HbA1c 70mmol/mol, C-peptide 574, Triple Ab negative, elevated IGF-1 411 mg/l(65.6 -249.2), Free T4 13.8 pmol/l, TSH 1.05mU/l, ACTH 4ng/l, Cortisol 348nmol/l, prolactin 125mU/l, oestradiol< 19 pmol/l, LH 42unit/l, FSH 68unit/land Testosterone <0.5nmol/l. A new diagnosis of acromegaly was made after she failed to suppress her GH levels on an oral glucose tolerance test and she has been referred to tertiary endocrinology services. DKA as the presenting feature of acromegaly is a rare occurrence but nonetheless an important diagnosis to not overlook as can be life-threatening if left untreated. Proposed mechanisms for the development of DKA in patients with acromegaly include increased insulin resistance, inhibition of fatty acid metabolism and increasing lipolysis leading to ketosis, due to GH and IGF-1 excess. Glucagon has also been considered as a possible contributing factor to DKA development and may be increased in acromegaly. Excessive glucagon reduces hepatic fructose 2,6 biphosphate, a metabolite that inhibits gluconeogenesis in the liver and induces hepatic ketogenesis.