Session: MON 199-237-Disorders of Parathyroid Hormone & Calcium Homeostasis
Poster Board MON-217
Clinical Case: We present a 48 year old man with history of chronic pancreatitis with pseudocyst formation, diabetes mellitus secondary to his chronic pancreatitis, hypertension and alcoholic liver cirrhosis (MELD 28 and Child-Pugh C) complicated by portal hypertension with gastric and esophageal varices and hepatic encephalopathy who was admitted after having a witnessed grand mal seizure. On our exam, he had typical stigmata of advanced liver disease. Hypercalemia with peak corrected calcium of 12.1 ng/dL (8.9-10.3) was noted. Liver function testing demonstrated an AST of 83 U/L (15-40), ALT of 39 IU/L (14-63), ALP of 88 IU/L (38-126), alb of 2.3 mg/dl (3.4-5), t. bili. of 7.5 mg/dL (6.5-8.2), t. bili. of 1.8 mg/dL (0-0.3), and INR of 2.
The usual etiologies of hypercalcemia were unrevealing with iPTH of 2.9 pg/mL (12-88), PTH-rP of <0.74 pmol/L (<2), TSH of 1.24 mcIU/mL (0.34-5.6), Vit. D 25-OH of 26.1 ng/ml (15-60), Vit. D 1,25-OH of 14.6 pg/mL (10-75), 24hr urine calcium of 318 mg/24hr (100-300), ionized calcium of 1.48 mmol/L (1.15-1.29), negative hepatitis B/C serologies, and a negative HIV screen. Protein electrophoresis demonstrated a broad increase in the g region without an M-spike indicating cirrhosis with urine electrophoresis showing only albuminuria.
The patient's medications included Lisinopril, Propranolol, Lactulose, Spironolactone, Lasix, Insulin, and Rifaxamin.
Initially, the hypercalcemia was believed to be secondary to immobility but the hypercalcemia persisted after full ambulation. Further evaluation revealed an ACE level of 62 U/L (12-68), Vit. A of 3 ug/dL (19-83), and AFP of 5.3 ng/mL (0-9). Bone scan showed no osteoblastic process but a slight linear increased activity in the skull reported as a normal variant versus early Paget's. Subsequent skull x-rays were negative for Paget's. PET-CT did not reveal any abnormal FDG activity or evidence of sarcoidosis.
Conclusion: There have been reports of hypercalcemia in advanced liver disease without hepatocellular carcinoma and we believe this to be the cause in our patient. Though incompletely understood, the etiology is postulated to be secondary to hyperbilirubinemia via an unknown mechanism, which was present in our case. (3) This case demonstrates that our knowledge of calcium metabolism is not complete and there may be humoral and cellular processes in advanced liver disease leading to hypercalcemia.
Nothing to Disclose: VMP, KM, SLR, JDM, SKA
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