Summary Objective Radioiodine (RAI) is an effective treatment for Graves’ thyrotoxicosis but is associated with a failure rate of 15% and may be a risk factor for thyroid eye disease (TED) and weight gain. We sought to examine predictors of RAI failure, weight gain, TED and patient satisfaction. Design Retrospective cohort study. Patients A total of 655 episodes of RAI in Graves’ thyrotoxicosis patients (2006‐2015). Measurements Biochemical assessment, including TFTs and thyrotropin receptor antibodies (TRAb), clinical features (eg, TED, weight and thionamide use) and patient questionnaire. Results The treatment failure rate was 17%. Failure was greater with higher fT4 (P = 0.002) and higher TRAb (P = 0.004). Failure rate was 42.2% when TRAb >40 U/L. Median weight gain was 3.2 kg in those with normal fT4 prior to RAI and 5.8 kg when fT4 was elevated (P < 0.001). New TED developed in 7.6% but was not associated with post‐RAI dysthyroidism. Treatment satisfaction was generally high (median response 8/10). Conclusions Treatment failure after RAI occurs in predictable groups and this should be reflected in the information provided to patients. Weight gain is common and may not entirely be explained by a return to pre‐thyrotoxic baseline. We were unable to detect any significant impact of post‐RAI dysthyroidism on weight gain, TED or thyroid symptoms in this large cohort.

Abdominal pain and vomiting are common presentations to the emergency medical ward. Management of recurrent abdominal pain and vomiting can be difficult, especially in patients who have diabetes. People with diabetes can present with vomiting and abdominal pain that can cause a diagnostic dilemma. Are the symptoms due to an acute or chronic complication of their diabetes or to other causes? In patients with diabetes who also use cannabis, further diagnostic challenges can arise as recurrent vomiting and abdominal pain due to diabetic gastroparesis and cannabinoid hyperemesis syndrome (CHS) can present in similar ways. We present a case series of four patients with type 1 diabetes who had multiple admissions with abdominal pain and vomiting mimicking diabetic gastroparesis, all of whom were eventually diagnosed with CHS.

Pituitary incidentalomas are common findings with increasing use of modern neuroradiological imaging undertaken for symptoms unrelated to pituitary disease. The prevalence of these lesions is ~10% in autopsy studies and the incidence varies from 10% to 38% on magnetic resonance imaging in the published literature. They are almost always benign in nature and most are non-functioning (non-secreting) adenomas. Although many individuals are asymptomatic at diagnosis, some with functioning (secreting) pituitary adenomas or larger non-functioning adenomas have symptoms. All identified cases should have a thorough clinical and endocrinological evaluation to help with precise management, which depends on the size of the lesion, hormonal status (functioning versus non-functioning adenoma) and the presence of visual deficits resulting from optic nerve compression by the pituitary adenoma. Here, we provide an overview of the initial assessment and management of pituitary incidentalomas for clinicians not routinely involved in the management of pituitary disease.

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Introduction Giant invasive prolactinomas are rare pituitary tumours and have a male preponderance of 9: 1. In majority of cases, dopamine agonists (DA) are the treatment of choice in lowering prolactin and tumour shrinkage. Surgery may be opted in those with acute compressive symptoms or visual loss. Prolactinomas are known to invade the sellar floor, sphenoid sinus and clivus. Spontaneous CSF leak is rare in untreated patients with invasive prolactinomas compared to those on DA who respond with rapid tumour shrinkage that causes unplugging of the conduits resulting in CSF rhinorrhoea. We present 5 male patients with untreated giant invasive prolactinomas with skull base destruction where close surveillance was opted over DA treatment. Results Five male patients with median age of 73±10 years were studied. 1 patient presented with headache, vomiting and 6th nerve palsy which spontaneously resolved over weeks. 2 patients were diagnosed during work up of other hormonal deficiencies and in 2 patients giant tumours were incidentally found on imaging for head injury. Prolactin values ranged from 55,641 to 835,800 mIU/L. Hormonal deficiency was present in 3/5; anterior hypopituitarism (1) and symptomatic secondary hypogonadism (2). MRI imaging in all patients showed extensive skull base bony erosion, with tumour invasion into sphenoid sinus and clivus. Additionally, the patient with largest tumour had invasion into right orbital roof and floor of right anterior cranial fossa. In other patients, tumour had also invaded occipital condyles (1), bilateral cavernous sinus (1). All patients were discussed in tertiary neurosurgical MDT. As the risk of CSF leakage due to tumour shrinkage outweighed the benefits of tumour reduction, a decision not for medical treatment was agreed with patients and planned for active surveillance with MRI scans and regular clinical and visual fields assessments. The mean follow-up period was 4±1 years. One patient was very frail and decided not for radiological surveillance. DA treatment is being considered for the patient with the largest tumour which has grown further causing frontal lobe invasion. There was no significant tumour size increase in other 4 patients and none had spontaneous CSF leak. Discussion Risk stratification for CSF leak with DA treatment is difficult as it depends on the invasion, tumour response to DAs and the extent of underlying bony destruction. This may cause a dilemma on whether or not to treat some patients with DAs. The risk of CSF leak, bacterial meningitis and the subsequent need for urgent surgical repair may outweigh the benefits of tumour reduction with DAs particularly in some patients with low symptom burden. In our experience, patient counselling, active radiological surveillance and considering treatment with change in symptoms (visual deterioration, compressive pathology) could be an appropriate management option in such patients. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.