Serum magnesium levels in patients with alcoholic and non-alcoholic fatty liver.

BACKGROUND

Magnesium is currently a subject of major interest in biology and medicine. Magnesium is intimately involved in over 300 enzymatic reactions. particularly in processes involving the formation and utilization of ATP. It is known that alcoholism is connected with hypomagnesemia. There are also several studies describing the disorders of magnesium balance in patients with liver diseases.

OBJECTIVE

was to investigate the serum magnesium levels in patients with liver steatosis. We compared the magnesium levels in patients with non-alcoholic and alcoholic fatty liver to estimate if alcoholism is the only cause of magnesium disorders or if also liver function disorders play any role in the development of magnesium dysbalance in patients with liver steatosis.

METHODS

The studied group consisted of 44 patients with hepatic steatosis (25 non-alcoholic and 19 alcoholic). The control group consisted of 57 healthy subjects. Magnesium levels were assayed by atomic absorption spectrometry.

RESULTS

Serum magnesium levels were significantly decreased in patients with alcoholic (0.67 +/- 0.10 vs 1.02 +/- 0.11 mmol.l(-1)) and also in patients with non-alcoholic liver steatosis (0.65 +/- 0.14 vs 1.02 +/- 0.11 mmol.l(-1)). There were also moderately increased activities of aminotransferases and gamma-glutamyltransferase. Plasma triacylglycerols were increased in both studied groups. Albumin and prealbumin levels were not changed in comparison to the control group. There was a slight increase in plasma levels of immunoglobulin A and immunoglobulin G.

CONCLUSIONS

The results of our study showed hypomagnesemia in both studied groups. Decreased magnesium levels found also in patients with non-alcoholic fatty liver suggest that alcoholism cannot be the only cause of hypomagnesemia in patients with fatty liver. Hypomagnesemia is not only a laboratory symptom of fatty liver but due to its connection with increased oxidative stress it might be a risk factor in the progression of fatty liver to steatohepatitis (Tab. 3, Ref: 19).