Dr Henry Guo1, Dr Anojian Koneshamoorthy2, Dr I-Lynn Lee2, Dr Nicole Lioufas1
1Department of Nephrology, Western Health, Melbourne, Australia, 2Department of Endocrinology, Western Health, Melbourne, Australia
Background:
Hyperprolactinaemia is common in patients with end stage renal disease, occurring in about 37-70%, with levels not affected by haemodialysis. However, significant elevation of prolactin should raise suspicion of pituitary abnormalities, which may impact on metabolic bone health.
Case Report:
A 30-year-old man with severe tertiary hyperparathyroidism, presents with an atraumatic subacute right neck of femur fracture (NOF) after haemodialysis. Previous fractures include atraumatic contralateral subcapital NOF, multilevel vertebral crush fractures, and bilateral rib fractures. Initial investigations demonstrated a serum corrected calcium of 2.40 mmol/L, phosphate of 1.18 mmol/L and an alkaline phosphatase of 2740 units/L (reference value 30-110 units/L). 25-dihydroxy Vitamin D level was 30 nmol/L, and a parathyroid hormone level was unrecordably high at > 212.0 pmol/L. He was managed on 120mg of cinacalcet prior with intermittent non-compliance.
A secondary osteoporosis screen was performed, which revealed hypogonadotropic hypogonadism caused by hyperprolactinaemia of 5719 mIU/L and 4412 mIU/L pre- and post-dialysis, with undetectable macroprolactin. A pituitary MRI revealed a 4.6 x 5mm pituitary microadenoma with no chiasmal compression. He commenced cabergoline 0.5 mg weekly.
Subtotal parathyroidectomy was performed. To minimise hungry bone syndrome, he received calcitriol 0.75 mcg three times a day for three days prior, 2 mg of intravenous zoledronic acid, and 100,000 IU of intramuscular cholecalciferol. Nonetheless, he had protracted hypocalcaemia requiring six days of intravenous calcium infusion. He was discharged with calcitriol and calcium supplementation, and cabergoline weekly.
Conclusion:
Profound hypogonadism should prompt further investigations of the pituitary-gonadal axis which can be suppressed by prolactin-producing pituitary adenomas in patients with end stage renal failure. Hyperprolactinaemia can potentially compound already deleterious effects on bone health.
Biography:
Henry is a current second-year registrar at Monash Health. He is interested in general nephrology, including dialysis, vascular access, CKD-MBD and Renal Supportive Care.