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Charlotte Boughton, David Taylor, Lea Ghataore, Norman Taylor and Benjamin C Whitelaw

Background This case demonstrates hypertension and hypokalaemia due to a mineralocorticoid effect induced by posaconazole. Two distinct mechanisms have been identified: inhibition of 11β hydroxylase leading to the accumulation of the

Open access

A Chinoy, N B Wright, M Bone and R Padidela

, secondary hyperaldosteronism and emesis in DKA all cause net depletion of body stores of potassium ( 1 ). Despite this, hypokalaemia is not commonly encountered at presentation in DKA because insulin deficiency and metabolic acidosis shifts potassium from

Open access

A Tabasum, C Shute, D Datta and L George

Background Hereditary tubulopathies can present in adults with symptoms of recurrent hypokalaemia. They can present later in life due to a missed diagnosis at a younger age or patients being asymptomatic. Herein, we present a case of Gitelman

Open access

Pedro Marques, Nicola Tufton, Satya Bhattacharya, Mark Caulfield and Scott A Akker

(twice daily). She was taking oral potassium supplements due to long-standing hypokalaemia and denied any exogenous glucocorticoid administration or chronic ingestion of liquorice. Physical examination revealed a gravid uterus but was otherwise

Open access

F Serra, S Duarte, S Abreu, C Marques, J Cassis and M Saraiva

cushingoid, with hyperpigmentation and facial rounding, purple striae on the abdomen, scattered bruises and central obesity. Laboratory results revealed glycaemia >200 mg/dl, high white blood cell count with high neutrophils and severe hypokalaemia (1.9 mmol

Open access

Benjamin G Challis, Chung Thong Lim, Alison Cluroe, Ewen Cameron and Stephen O’Rahilly

MWS commonly present with diarrhoea, dehydration and symptoms associated with severe electrolyte depletion, particularly those related to hypokalaemia. Symptomatic hyperglycaemia and new-onset diabetes are very rare manifestations of MWS. Herein we

Open access

S Hussain, E Panteliou, D M Berney, R Carpenter, M Matson, A Sahdev, M Bell, E O'Sullivan and W M Drake

normotensive without medication, hypokalaemia persisted and hypertension had subsequently recurred. Outcome and follow-up Histological examination revealed multi-nodular proliferation of neoplastic cells with capsular invasion and extension beyond the

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G Leksic, A M Alduk, V Molnar, A Haxhiu, A Haxhiu, A Balasko, N Knezevic, T Dusek and D Kastelan

/115 mmHg. He had no renal bruits and no signs of the Cushing’s syndrome. A laboratory analysis showed marked hypokalaemia of 2.4 mmol/L. Investigation Ambulatory 24-h BP monitoring revealed >82% of readings above normal. A hormonal workup, performed

Open access

Stephanie Wei Ping Wong, Yew Wen Yap, Ram Prakash Narayanan, Mohammad Al-Jubouri, Ashley Grossman, Christina Daousi and Yahya Mahgoub

Background Patients with Cushing’s syndrome may require admission to hospital with a variety of medical emergencies including hypokalaemia, diabetic emergencies, venous thromboembolic events, sepsis, congestive cardiac failure, strokes or

Open access

Snezana Burmazovic, Christoph Henzen, Lukas Brander and Luca Cioccari

the first 24 h after admission, her urine output was 3880 mL. Investigation Initial laboratory analysis revealed severe hypernatraemia (serum sodium concentration 161 mmol/L), moderate hypokalaemia (3.2 mmol/L), hyperglycaemia (BGL: 35.4 mmol