A 31-year-old woman presented with a one-week history of headache, generalised lethargy, weakness and poor appetite. Clinical examination showed that her blood pressure was 200/120 mmHg. On an earlier occasion, her blood pressure was found to be normal by a general practitioner whom she last visited three months earlier when she had an upper respiratory tract infection. Investigations showed hypokalaemia, suppressed serum renin and aldosterone. Further history was taken and revealed that she had been craving for guava fruits which she ate with flavoured "asam boi" (containing glycyrrhizic acid) at least three spoonfuls twice a day for the past six weeks. The hypertension and hypokalaemia resolved after two weeks of stopping the "asam boi". Her clinical picture was compatible with exogenously-induced hypermineralocortoidism.
Recent discoveries of somatic mutations permit the recognition of subtypes of aldosterone-producing adenomas with distinct clinical presentations and pathological features. Here we describe three women with hyperaldosteronism, two who presented in pregnancy and one who presented after menopause. Their aldosterone-producing adenomas harbored activating mutations of CTNNB1, encoding β-catenin in the Wnt cell-differentiation pathway, and expressed LHCGR and GNRHR, encoding gonadal receptors, at levels that were more than 100 times as high as the levels in other aldosterone-producing adenomas. The mutations stimulate Wnt activation and cause adrenocortical cells to de-differentiate toward their common adrenal-gonadal precursor cell type. (Funded by grants from the National Institute for Health Research Cambridge Biomedical Research Centre and others.).