Pentoxifylline and thalidomide fail to reduce hepatic steatosis during total parenteral nutrition and bowel rest in the rat.
BACKGROUND
We suggested that the continuous translocation of endotoxin from Gram-negative bacterial overgrowth during bowel rest and total parenteral nutrition (TPN) causes the release of tumor necrosis factor (TNF), resulting in liver damage and hepatic dysfunction. Because TPN-induced hepatic steatosis was significantly reduced by the monoclonal antibodies against TNF, we attempted a more clinically applicable approach using pentoxifylline and thalidomide.


METHODS
A control group (group I) fed rat chow and four groups of rats receiving TPN were studied. Group II received TPN only; group III, TPN and 100 mg/kg/d pentoxifylline; group IV, TPN and 200 mg/kg/d pentoxifylline; and group V, TPN and 5 mg/kg/d thalidomide. On day 7, total liver fat was determined.


RESULTS
Bowel rest and TPN resulted in a significant (p < .0005) increase in liver fat content that was unaltered by either pentoxifylline or thalidomide.


CONCLUSIONS
Our results show no role for pentoxifylline or thalidomide in reducing TPN-associated hepatic steatosis.
Vromen
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Department of Surgery, Hebrew University Hadassak Medical School, Jerusalem, Israel.
Spira
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Bercovier
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Berry
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Freund
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D000818:Animals; D005234:Fatty Liver / Q000209:etiology / Q000517:prevention & control*; D008297:Male; D010289:Parenteral Nutrition, Total / Q000009:adverse effects*; D010431:Pentoxifylline / Q000627:therapeutic use*; D051381:Rats; D013792:Thalidomide / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
D014409:Tumor Necrosis Factor-alpha; D013792:Thalidomide; D010431:Pentoxifylline