Abstract
Transient increases in SGOT are seen in patients receiving parenteral nutrition. We found the magnitude of the increase in SGOT to correlate significantly (r = 0.69, p < 0.001) and inversely with the serum phosphate level measured at the same time as when the SGOT level was at its peak. Although the presence of the correlation does not implicate an etiological role for hypophosphatemia in the pathogenesis of hepatocellular injury, hypophosphatemia could possibly worsen the degree of fatty infiltration which is responsible for this increase in SGOT.

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