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CASE REPORT
Hypokalaemic metabolic alkalosis, hypertension and diabetes: what is the link
  1. Marius Vögelin1,
  2. Richard Cathomas2,
  3. Niklaus Kamber3 and
  4. Thomas Fehr1
  1. 1 Department of Internal Medicine, Kantonsspital Graubunden, Chur, Switzerland
  2. 2 Department of Internal Medicine, Division of Oncology, Kantonsspital Graubunden, Chur, Switzerland
  3. 3 Department of Internal Medicine, Division of Endocrinology, Kantonsspital Graubunden, Chur, Switzerland
  1. Correspondence to Professor Thomas Fehr, Thomas.fehr{at}ksgr.ch

Abstract

Two years after diagnosis of a metastatic neuroendocrine gastrin-secreting tumour and after several cycles of chemotherapy and peptide receptor radionuclide therapy, a 56-year-old woman presented with hypokalaemic metabolic alkalosis, hypertension, leg oedema and new-onset diabetes mellitus. Further investigations revealed renal potassium loss confirmed by a transtubular potassium gradient of 16, fully suppressed serum aldosterone, but instead highly elevated blood levels of morning cortisol and adrenocorticotropic hormone as well as increased urinary excretion of glucocorticoid and mineralocorticoid metabolites. Ruling out other causes, paraneoplastic hypercortisolism was diagnosed. Pharmacological inhibition of the steroid 11β-hydroxylase with metyrapone resulted in complete resolution of metabolic alkalosis, hypokalaemia, hypertension, hyperglycaemia and leg oedema within 1 week.

  • fluid electrolyte and acid-base disturbances
  • endocrine cancer
  • drugs: endocrine system
  • diabetes
  • hypertension
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Footnotes

  • Contributors MV, TF, RC and NK were involved in acquisition of data and patient care. MV, TF and RC wrote the article. All authors were involved in the interpretation of data and revising it critically for its content. All authors gave their final approval of the version to be submitted.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent Parental/guardian consent obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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