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Endocrine Abstracts (2024) 104 P39 | DOI: 10.1530/endoabs.104.P39

SFEIES24 Poster Presentations Adrenal & Cardiovascular (40 abstracts)

Diuretic induced flaccid paralysis as first presentations of primary aldosteronism

Liam O’Murchadha 1 , Ian M. Brennan 2 , Claire L. Donohoe 3 , Sabah Abdelfadil 4 , Vivion Crowley 4 & Agnieszka Pazderska 1


1Department of Endocrinology, St. James’s Hospital, Dublin, Ireland; 2Department of Interventional Radiology, St. James’s Hospital, Dublin, Ireland; 3Trinity St. James’s Cancer Institute, Dublin, Ireland; 4Department of Biochemistry, St. James’s Hospital, Dublin, Ireland


Introduction: Hypokalaemia related flaccid paralysis is a rare condition of transient, severe muscle weakness caused by temporary muscle excitability loss due to low plasma potassium concentrations. We present two patients who were diagnosed with primary aldosteronism after developing profound muscle weakness, following initiation of diuretics.

Case 1: A 35-year-old European male presented to the Emergency Department with severe limb pains, weakness and evidence of leg oedema. He had commenced thiazide diuretics six weeks previously. Serum potassium was low; 2.1 mmol/l (3.5-5.2 mmol/l) with elevated creatine kinase; 9067 U/l (<308U/l). Despite five antihypertensive agents, blood pressure was 173/112mmHg. Primary aldosteronism was suspected and then confirmed with elevated aldosterone concentration of 1331 pmol/l following saline suppression testing. Imaging demonstrated a unilateral 21mm adrenal lesion consistent with an adenoma. The patient underwent adrenalectomy, achieving biochemical and clinical cures.

Case 2: A 55-year-old Irish male with a 28-year history of hypertension was suspected to have a secondary aetiology. To complete biochemical assessment, his usual aldosterone antagonist was discontinued and substituted for indapamide. Four weeks later, he had developed profound lethargy and progressive muscle fatigue. He was unable to walk due to lower limb weakness. Blood results revealed potassium of 1.6 mmol/l, resultant myositis and ECG features consistent with severe hypokalaemia. He required prolonged management in Intensive Care. After medication substitution and an appropriate time interval, primary aldosteronism was suggested by direct renin of 8mU/l and elevated plasma aldosterone of 1730 pmol/l. Adrenal Vein Sampling demonstrated lateralisation of aldosterone production correlating with CT imaging. The patient underwent adrenalectomy with complete biochemical and partial clinical response.

Discussion: Primary hyperaldosteronism rarely presents with hypokalaemic paralysis, particularly in the context of thiazide treatment. Given these medications form part of hypertension management guidelines, it is crucial to be cognisant of this risk, especially when aldosteronism is suspected.

Volume 104

Joint Irish-UK Endocrine Meeting 2024

Belfast, Northern Ireland
14 Oct 2024 - 15 Oct 2024

Society for Endocrinology 

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