Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2020) 70 EP40 | DOI: 10.1530/endoabs.70.EP40

ECE2020 ePoster Presentations Adrenal and Cardiovascular Endocrinology (58 abstracts)

Persistent hypokalaemia leading to a diagnosis carcinoid lung cancer. A case study

Benjamin Woolner 1 , Batool Rizvi 2 , Jaysankar Mattappillil 2 & Ali Naqvi 2


1Stroke Unit, St Mary’s Hospital, Newport, United Kingdom; 2St Mary’s Hospital, Medical Assessment Unit, Newport, United Kingdom


Background: An 81-year-old gentleman presented to his GP with a 2 week history of reduced appetite, lethargy and 2–3 kg weight loss over the last month. On routine bloods, his potassium was noted to be 2.2 mmol/l. He was being treated in the community with indapamide, losartan and amlodipine for hypertension. He was admitted to hospital for IV replacement. However, he had persistent hypokalaemia (<2.9 mmol/l) for 3 days despite appropriate replacement and suspension of potential medications driving his hypokalaemia. An initial VBG on admission showed a hypokalaemic metabolic alkalosis, and a routine chest X-ray showed a suspicious looking lesion. The follow up CT chest revealed a left lower lobe lesion, consistent with a new malignancy (T2b/N3/M0), with evidence of idiopathic pulmonary fibrosis, bilateral pleural effusions and calcifications. These CT findings raised suspicions of an ACTH secreting small cell lung cancer, despite the patient not having any cushingoid features. His serum cortisol was 398 nmol/l. He had a partial response following an overnight dexamethasone test (cortisol 99 nmol/l). Cortisol levels throughout the day were 342, 357, 301, and 345 nmol/l at 0600 h. Cortisol was suppressed to 76 nmol/l following low dose dexamethasone suppression which was indicative of Cushing’s Syndrome. His ACTH was not very high at 9 ng/l. He was referred to the lung malignancy MDT. A PET scan revealed significantly increased uptake of FDG in the 4 cm left lower lobe lung mass, typical of a carcinoid tumour. Tumour histology was positive for ACTH, synaptophysin, chromograffin and CD56 secretion. Proliferation index assessed with Ki67, was <1%. Further blood tests revealed an elevated chromograffin A (76 pmol/l) suggestive of a neuroendocrine tumour. Urine 5-HIAA testing which was positive with a reading of 113, suggestive of carcinoid syndrome. Repeat test was 26. Normal range (5–35). 24 h free cortisol excretion was elevated at 213 mmol/l. He has no other symptoms or signs of carcinoid syndrome: facial flushing, diarrhoea, wheezing, heart failure or Cushing’s syndrome. His potassium levels remained stable following medication adjustment, and intervention with steroid synthesis inhibitors was not necessary. He was referred for surgery but unfortunately he was not a surgical candidate due to cardiac issues and anaesthetic risk. In the meantime, he has functionally deteriorated and referred to palliative team.

Volume 70

22nd European Congress of Endocrinology

Online
05 Sep 2020 - 09 Sep 2020

European Society of Endocrinology 

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