Thyroid artery embolization (TAE) is a minimally invasive technique that induces selective ischemic necrosis of the thyroid parenchyma, thereby reducing thyroid hormone synthesis with few associated complications. Successful cases of TAE as a bridge therapy before total thyroidectomy in patients with refractory thyrotoxicosis are rare. We present the case of a 36‐year‐old man with a history of Graves’ disease and poor adherence to medical therapy who presented with clinical features of thyrotoxicosis. On physical examination, he exhibited active moderate‐to‐severe orbitopathy (EUGOGO classification; clinical activity score 5/7) and a grade III goiter, reflecting advanced and poorly controlled disease. Paraclinical findings revealed markedly elevated free T4 levels and suppressed TSH. The diagnosis of uncontrolled hyperthyroidism was made, with a Burch–Wartofsky score of 40 points, indicating an impending thyroid storm. Medical therapy at maximally tolerated doses did not result in a complete clinical response; therefore, a total thyroidectomy was planned, preceded by therapeutic plasma exchange (TPE). Due to intolerance to TPE, TAE was performed as a bridge therapy, followed by total thyroidectomy without complications. The patient was discharged with a resolution of symptoms and progressive normalization of thyroid hormone levels. TAE may represent a valuable bridging therapy before total thyroidectomy in selected patients with severe thyrotoxicosis due to Graves’ disease who are refractory to or unsuitable for conventional therapies.
Capivasertib is a serine/threonine kinase AKT (AKT1–3) inhibitor, disrupting phosphorylation of AKT substrates. When combined with fulvestrant, it is approved for hormone receptor-positive advanced breast cancer. Capivasertib therapy frequently causes hyperglycemia, including diabetic ketoacidosis (DKA). Ensure glycemic control before initiation and maintain ongoing blood glucose monitoring to reduce the risk of this potentially fatal complication. We present a case of metastatic breast cancer with initially controlled blood glucose who developed ketoacidosis and myocardial infarction during capivasertib therapy.
Background Localization of recurrent or residual insulinoma may be particularly challenging in postoperative setting, especially in the presence of postoperative anatomical distortion and inconclusive conventional imaging. Case Presentation A 71‐year‐old man developed recurrent endogenous hyperinsulinemic hypoglycemia following apparently curative surgical enucleation of a pancreatic insulinoma. The postoperative course was complicated by intra‐abdominal hemorrhage and pseudocyst formation, resulting in marked anatomical distortion. Despite persistent biochemical evidence of insulinoma recurrence, serial contrast–enhanced computed tomography (CT) and 68 Ga‐DOTATOC PET/CT failed to identify residual disease. Subsequent glucagon‐like peptide‐1 receptor (GLP‐1R) imaging with 68 Ga‐NODAGA‐Exendin‐4 PET/CT demonstrated focal tracer uptake in the pancreatic head, highly suggestive of recurrent or residual insulinoma. Endoscopic ultrasound (EUS) subsequently confirmed a small lesion in the uncinate process, which was successfully treated with EUS–guided radiofrequency ablation (EUS‐RFA). Following the procedure, hypoglycemic episodes resolved, with normalization of glucose, insulin, and C‐peptide levels and no signs of recurrence at follow‐up. Conclusion This case highlights the clinical value of GLP‐1 receptor PET/CT for localizing insulinoma in the context of negative conventional or somatostatin receptor (SSTR)–based imaging. Accurate functional localization may directly guide minimally invasive therapeutic interventions and help avoid high‐risk reoperative pancreatic surgery.
Background:Hypertriglyceridaemia (HTG) is a common condition resulting from genetic and environmental factors. Second-generation antipsychotic (SGA) medications are classically associated with the development of metabolic syndrome, of which HTG is a hallmark feature. Severe HTG is the third most common cause of acute pancreatitis, which has significant associated morbidity and mortality risk. It is therefore vital to rapidly and sustainably reduce triglyceride levels in patients presenting with severe HTG. Clinical Case:A 35-year-old gentleman with a history of psychiatric illness taking SGA medications (quetiapine and risperidone) presented to our hospital with apparent hyponatraemia. With associated hyperosmolality (302 mOsm/kg), a diagnosis of pseudohyponatraemia was made. Upon further investigation, pseudohyponatraemia was identified to be due to severe HTG (72.8 mmol/L) and hyperglycaemia (26.0 mmol/L). There were no clinical or biochemical features of pancreatitis. A variable-rate infusion of intravenous insulin was commenced. Over the 10-day admission a fall in triglycerides to 10.5 mmol/L was observed without any adverse events. Acute pancreatitis did not develop during the inpatient admission or during outpatient follow-up, and triglyceride levels have fallen substantially (3.2 mmol/L at 5 months) having been switched from quetiapine and risperidone to aripiprazole, an SGA associated with less metabolic disturbance. Conclusion:This case demonstrates the safe and effective management of SGA-associated severe HTG with intravenous insulin infusion to prevent acute pancreatitis. It also highlights the utility of pseudohyponatraemia as a useful way of detecting severe HTG and the impact of SGA medications in the aetiology of severe HTG.
Ectopic Cushing's syndrome (ECS) is a rare but important cause of ACTH-dependent Cushing's syndrome. Metyrapone, a steroidogenesis inhibitor targeting 11-β hydroxylase, has shown effectiveness in controlling hypercortisolism. However, little is known about the practical aspects of its initiation, use, and effectiveness in ECS. We present three cases of severe hypercortisolism secondary to ECS managed with metyrapone and report our experience. Case 1: a 56-year-old male with high-grade neuroendocrine carcinoma. Case 2: a 67-year-old man with a history of stage IIB non-small cell lung cancer (NSCLC) with metastatic neuroendocrine carcinoma. Case 3: a 64-year-old man with metastatic prostate cancer. Biochemical control was achieved with rapid titration of low doses of daily metyrapone in all three cases. Based on our experience, we recommend an initial dose of 1000-1500 mg of metyrapone daily, in divided doses, with physiologic glucocorticoid replacement to mitigate the risk of adrenal insufficiency. Despite improvements in cortisol levels and stabilization of metabolic derangements, all three patients ultimately transitioned to comfort-focused care. Given the rarity, heterogeneity, and aggressiveness of this condition, rapid diagnosis and standardized pharmacologic approach are difficult to achieve. More data are needed to guide optimal therapy selection, dosing, and titration in ECS.
