Pseudobartter Syndrome induced by starvation.

V Bravis, S Hewett, A Mohd Afandi, S Qureshi, M S Yee

Introduction: PseudoBartter syndrome, a complex pattern of seemingly unrelated metabolic abnormalities, is frequently seen in patients with eating disorders, particularly those who indulge in purging behaviours. We present a case that, despite divergent background history and clinical presentation, possesses the unifying pathophysiology that ultimately leads to this syndrome.

Case: A 35-year old Latvian man, with a diagnosis of schizophrenia, was referred to the medical team with severe hypokalaemia. His psychiatric illness involved delusions around food intake and fasting as a means of religious cleansing.  He had a 7-year history of religion-based desire to “clense himself” of previous sins and the damage he had done to his body through alcohol and smoking. He initially became a vegetarian and for the 3 years preceding this presentation he began abstaining from breakfast on Sundays prior to Church in order to make the Eucharist more sacred. This progressed to fasting for longer periods with no purging incidents. He had no concerns regarding body image. At the time of his presentation he had starved himself for 4 weeks. He was on treatment with Risperidone. Clinically, he was cachectic with BMI of 15 and dehydrated but haemodynamically stable with BP 105/70mmHg. Apart from critical hypokalemia (K 2.4mmol/L), his metabolic screen was significant for hyponatraemia (121 mmol/L), hypochloraemia (72 mmol/L) and an elevated bicarbonate level of 52 mmol/L. Magnesium was normal (1.0 mmol/L). ECG revealed flattened T waves, ST depression and U waves. Short synachthen test was normal (peak cortisol 967nmol/L). Urine electrolytes were: Na<20, K 93.7, Cl<20, Mg 3.9. Plasma renin activity was elevated (39 nmol/L/h), as was aldosterone (3800 pmol/L). Renal tract ultrasound, however, showed no nephrocalcinosis. Despite refusing food, the patient accepted medical therapy with iv electrolyte replacement and supplementation with oral Slow-K and Amiloride. Risperidone was changed to Olanzapine. He was safely discharged.

Discussion: This case shares the metabolic abnormalities of Bartter syndrome. Our patient had hypokalaemia, hyponatraemia, hypochloraemia, metabolic alkalosis, hyperreninaemia, hyperaldosteronism and an inappropriately elevated urinary K. However, urinary Na and Cl were preserved and serum Mg was also normal. It is important to appreciate that the complex self-perpetuating pathophysiology of prolonged starvation with low chloride diet led to the hypokalaemic metabolic alkalosis characteristic of PseudoBartter syndrome.