Endocrine Abstracts

Introduction: Serum calcium (Ca) is a major regulator of PTH secretion, but serum magnesium (Mg)also can modulate PTH secretion. Intracellular Mg depletion impairs the ability of the parathyroid to secrete PTH,which subsequently cause fall in the serum Ca concentration.

Case report: A 67 year old male patient was admitted to intensive care unit because of disturbance of consciousness, due to suspected hepatic encephalopathy. In his previous history, he had only symptoms suspected on alcoholic polyneuropathy. His Glasgow coma scale was 5, with laboratory findings that indicated liver cirrhosis: hemoglobin 99 g/L, mean corpuscular volume 108 fL, platelets 78 ×10⁹, glycemia 6.9 mmol/L, urea 24 mmol/L, creatinine 111 μmol/L, AST 99 IU/L, ALT 54 IU/L, GGT 267 IU/L, AP 212 IU/L, bilirubin 26 umol/l, LDH 312 IU/l, PV 20.6 s, APTT 44 s, fibrinogen 1.9 g/L, sodium 129 mmol/l, potassium 4.6 mmol/l and albumin 26 g/L. His total serum Ca was 1.12 mmol/L, and ionized Ca was 0.52 mmol/L. Ammonium was normal. Hepato-protective therapy was started with calcium replacement, but without improving the state of consciousness. Further evaluation revealed low PTH values with high phosphorus concentration, which confirmed hypoparathyroidism. By measuring magnesium, we realized hypomagnesemia (Mg 0.27 mmol/L) and add Mg supplementation. Two days after, a gradual increase in Ca, Mg and PTH concentrations lead to improved consciousness, and four days after he recovered completely. The patient developed alcoholic cirrhosis, still without elements of liver decompensation.

Conclusion: Usually hypocalcemic crisis presents with the classical symptomatology of tetany with extrapyramidal symptoms, accompanying with disturbance of consciousness leading to coma. In our patient, hypocalcemia appeared to result from transient hypoparathyroidism induced by magnesium deficiency due of prolonged alcohol abuse.