A 71-year-old male patient with no significant past medical history was admitted to hospital with acute hepatitis in July 2014 with bilirubin 98 μmol/l, ALT 1703 IU/l, and ALP 223 IU/l. Liver ultrasound showed a normal sized liver with normal echotexture. Liver screen including hepatitis A, B, C, E, and autoantibody screen was negative. Liver biopsy revealed acute hepatitis with patchy necrosis and inflammatory infiltrate consistent with inflammation, drugs, or autoimmune hepatitis.
Whilst an inpatient, he was noted to be hypercalcaemic at 3.51 mmol/l with a hypophosphatemia of 0.50 mmol/l. As he was symptomatic, further investigations as an inpatient showed an elevated parathormone of 35.3 pmol/l and elevated 24 h urinary calcium of 18.1 mmol/24 h. Bisphosphonates and i.v. fluids failed to lower his calcium levels. Imaging revealed a left inferior parathyroid adenoma and he was referred for an inpatient parathyroidectomy. Whilst awaiting this, he was commenced on cinacalcet. Post operatively, his parathormone, calcium, and liver functions tests improved.
A literature search showed that simultaneous development of acute primary hyperparathyroidism and hepatitis is very rare and has been described only once before. It has previously been postulated that antibodies to hepatitis B virus may alter the calcium set point allowing uncontrolled synthesis of parathormone. It is also possible that our patient may have had mild primary hyperparathyroidism previously unknown to us which was then triggered by the hepatitis episode. However, what remains unusual is, his hyperparathyroidism was resistant to regular calcium lowering treatment and therefore, needed inpatient cinacalcet and parathyroidectomy.