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.
Hypercalcaemia is a recognised complication of thyrotoxicosis usually related to increased bone resorption. However, coexistent hyperphosphataemia is uncommon and may create diagnostic uncertainty. It is postulated that serum calcium and phosphate levels rise due to high bone turnover and increased renal reabsorption of phosphate in response to excess thyroxine. Hypercalcaemia may also alter the clinical presentation of thyrotoxicosis, making both diagnosis and management challenging. We report two patients with this unusual biochemical presentation. The first patient was a 69-year-old woman who presented with body aches, lethargy, low mood, constipation, polyuria, and proximal muscle weakness for 2 months. The second was a 56-year-old woman who presented with palpitations, anxiety, tremulousness, dyspnoea, dysphagia, and headache for 4 months. Both had multinodular goitres (MNGs) without eye disease. Their TSH levels were undetectably low with extremely high free T4 levels. Serum calcium and phosphate levels were high in both patients. ALP levels were mildly elevated, vitamin D levels were deficient or insufficient, and parathyroid hormone (PTH) levels were low-normal. DXA scans revealed severe osteoporosis. Both patients improved clinically and biochemically with adequate intravenous hydration, frusemide, carbimazole, propranolol, and bisphosphonates. The second patient underwent a successful left thyroid lobectomy, while the first patient remained well on medical treatment. Unexplained hypercalcaemia and hyperphosphataemia should alert the clinicians to the possibility of underlying thyrotoxicosis. Prompt recognition and management is essential to prevent bone loss, correct metabolic abnormalities, and avoid complications. Clinicians should also consider the possibility of hypercalcaemia associated with thyroid dysfunction in patients presenting with nonspecific symptoms such as fatigue, constipation, proximal weakness, polyuria, or mood changes.
