Endocrine Abstracts

Case history: 73-year-old woman recently commenced on oral diuretics for peripheral oedema was admitted with severe hypokalaemia and refractory hypertension. Conn’s syndrome was initially considered but admission of regular liquorice consumption made a diagnosis of hypokalaemic hypertension (pseudoaldosteronism) secondary to liquorice over-indulgence more likely. She went on to develop cardiomyopathy and had haematemesis from a bleeding duodenal ulcer (DU). Endocrine tests as an outpatient excluded Conn’s syndrome.

Investigations: Following intravenous replacement for hypokalaemia (K+ 2.1) and hypomagnesaemia (Mg2+ 0.50) on admission, Ms X became hyperkalaemic (K+ 6.1). An electrocardiogram (ECG) showed new widespread T-wave inversion and serial raised troponins (122, 101, 90). She developed fast AF and an echocardiogram showed reduced left ventricular (LV) function and regional akinesis which had spontaneously improved on a subsequent echocardiogram, consistent with Takutsubo cardiomyopathy (TC). Ms X had an episode of coffee ground vomiting. Bloods showed haemoglobin had dropped to 6.7 and urea had risen to 30.2 (Glasgow-Blatchford score 14). Urgent oesophagogastroduodenoscopy (OGD) showed a DU with adherent clot over it; a repeat 5 days later showed no active bleeding. Endocrine tests as an outpatient excluded Conn’s syndrome (aldosterone 131, renin 35.7).

Results and treatment: Ms X was provisionally treated as a NSTEMI with dual antiplatelets (aspirin & clopidogrel) given her raised troponins and ischaemic ECG at the time of her rebound hyperkalaemia. A repeat ECG showed fast AF, treated with bisoprolol and anticoagulation (apixaban). Antiplatetlets were discontinued after TC confirmed on echocardiography due to their inefficacy in TC. Following her episode of haematemesis, Ms X was transfused and culprit blood-thinning medications were withheld. OGD showed DU with adherent clot. She was commenced on high-dose intravenous omeprazole before switching to oral. Anticoagulation was not reinstituted given Ms X’s excessive alcohol intake and high re-bleeding risk.

Conclusions and points for discussion: Liquorice-induced pseudoaldoateronism with cardiac muscle failure resembling dilated cardiomyopathy has been previously reported. The pattern of spontaneous improvement in LV function over time described was mirrored by Ms X but it is difficult to determine whether her TC reflected the cumulative effect of chronic liquorice use or was secondary to its withdrawal. The liquorice herb (Glycyrrhizin glabra) confers gastroprotective effects and has been used as an anti-ulcer drug. The withdrawal of liquorice from Ms X may have precipitated the development of a DU. However, bleeding from it was likely potentiated by concurrent use of anti-platelets/anticoagulants without acid suppression.