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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 11\u03b2-hydroxylase with metyrapone resulted in complete resolution of metabolic alkalosis, hypokalaemia, hypertension, hyperglycaemia and leg oedema within 1\u2009week.<\/jats:p>","DOI":"10.1136\/bcr-2018-227068","type":"journal-article","created":{"date-parts":[[2019,1,19]],"date-time":"2019-01-19T04:45:12Z","timestamp":1547873112000},"page":"bcr-2018-227068","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":2,"title":["Hypokalaemic metabolic alkalosis, hypertension and diabetes: what is the link"],"prefix":"10.1136","volume":"12","author":[{"given":"Marius","family":"V\u00f6gelin","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Kantonsspital Graubunden, Chur, Switzerland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard","family":"Cathomas","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of 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