Context and objective Thyroid autoimmunity has been reported to be associated with SARS-CoV-2 and the SARS-CoV-2 vaccination recently. We report a series of patients who presented with new onset or relapse of Graves’ disease related hyperthyroidism shortly after receiving the SARS-CoV-2 mRNA vaccine at a single tertiary institution in Singapore. Methods and results We describe 12 patients who developed hyperthyroidism within a relatively short interval (median onset of 17 (range: 5 - 63) days) after receiving the SARS-CoV-2 mRNA vaccine. The majority were females (11/12) with median age of 35.5 (range: 22-74) years. Six patients had new onset hyperthyroidism, while the other six had relapse of previously well-controlled Graves’ disease. TSH Receptor antibody concentrations ranged from 2.4-32 IU/L. Majority of the patients were able to go for the second dose of the vaccine without any further exacerbations. Literature review revealed 21 other similar cases reported from across the world. Conclusion Our case series provide insight into the characteristics of individuals in whom Graves’ disease was triggered by the SARS-CoV-2 vaccination. Clinicians need to be vigilant of precipitation or exacerbation of autoimmune thyroid disorders in predisposed individuals after exposure to the SARS-CoV-2 vaccination. Further epidemiological and mechanistic studies are required to elucidate the possible associations between the SARS-CoV-2 vaccines and the development of thyroid autoimmunity.

Patients with intra-cerebral metastases often receive glucocorticoids, particularly in the presence of peri-lesional vasogenic cerebral oedema. We present a case of presumptive lung carcinoma with cerebral metastases where central diabetes insipidus was unmasked after glucocorticoid administration and correction of undiagnosed central hypocortisolism.

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Objective: Brown adipose tissue (BAT) controls metabolic rate through thermogenesis. As its regulatory factors during the transition from hyperthyroidism to euthyroidism are not well established, our study investigated the relationships between supraclavicular brown adipose tissue (sBAT) activity and physiological/metabolic changes with changes in thyroid status. Design: Participants with newly diagnosed Graves’ disease were recruited. A thionamide anti-thyroid drug (ATD) such as carbimazole (CMZ) or thiamazole (TMZ) was prescribed in every case. All underwent energy expenditure (EE) measurement and supraclavicular infrared thermography (IRT) within a chamber calorimeter, as well as 18F-fluorodeoxyglucose (18F-FDG) positron-emission tomography/magnetic resonance (PET/MR) imaging scanning, with clinical and biochemical parameters measured during hyperthyroidism and repeated in early euthyroidism. PET sBAT mean/maximum standardized uptake value (SUV mean/max), MR supraclavicular fat fraction (sFF) and mean temperature (Tscv) quantified sBAT activity. Results: Twenty-one (16 female/5 male) participants aged 39.5 ± 2.5 years completed the study. The average duration to attain euthyroidism was 28.6 ± 2.3 weeks. 8 participants were BAT-positive while 13 were BAT-negative. sFF increased with euthyroidism (72.3 ± 1.4% to 76.8 ± 1.4%; P<0.01), but no changes were observed in PET SUV mean and Tscv. Significant changes in serum free triiodothyronine (FT3) levels was related to BAT-status (interaction P value= 0.04). FT3 concentration at hyperthyroid state was positively associated with sBAT PET SUV mean (r=0.58, P=0.01) and resting metabolic rate (RMR) (P<0.01). Conclusion: Hyperthyroidism does not consistently lead to detectable increase in BAT activity. FT3 reduction during transition to euthyroidism correlated with BAT activity.

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The sensitivity of HbA1c as a screening test for DM in this study was significantly higher than that reported previously. This work provides additional evidence supporting the inclusion of HbA1c as one of the screening tests for DM.

A 56 year old man, previously well, presented to our Emergency Department with a 5-day history of abdominal distension, vomiting, breathlessness, and haemoptysis. He had a preceding history of hypertension, which had been diagnosed one year ago, and for which he was not on treatment. The gastrointestinal effects of phaeochromocytoma may range from mild and non-specific abdominal pain and vomiting 1 to more severe refractory constipation, ileus, and enterocolitis 3-8. Catecholamines suppress intestinal motility via direct effects on alpha-and beta-adrenergic receptors in the gut, resulting in reduced intestinal tone and peristalsis, and contraction of intestinal sphincters 4,6. Furthermore, catecholamine-mediated contraction of smooth muscle in the mesenteric vasculature, in combination with increased intestinal metabolic demand, result in bowel ischaemia, which in itself may contribute to dysmotility 4,6-8. Cases of paralytic ileus associated with phaeochromocytoma have been occasionally reported since the mid-1900s 3-8 , with ileus usually resolving after tumour resection and/or alpha-blockade 3-4,8. The recognition of ileus as a complication of phaeochromocytoma is important, as there is a possibility of progression to bowel infarction and perforation if diagnosis and treatment are delayed 4,6-7. Paralytic ileus and venous thromboembolism are two relatively uncommon manifestations of phaeochromocytoma. It is rarer still for both to occur simultaneously, as in our patient.

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