Total parenteral nutrition therapy and liver injury: a histopathologic study with clinical correlation

• Published in: Human pathology Vol. 43; no. 6; pp. 826 - 833
• Main Authors: Naini, Bita V., MD, Lassman, Charles R., MD, PhD
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.06.2012; Elsevier; Elsevier Limited
• Subjects: Adolescent; Adult; Aged; Biological and medical sciences; Child; Child, Preschool; Cholestasis; Ductopenia; Enzymes; Excretory system; Female; Gallbladder diseases; Gastroenterology. Liver. Pancreas. Abdomen; Histology; Humans; Infant; Investigative techniques, diagnostic techniques (general aspects); Liver - pathology; Liver cirrhosis; Liver diseases; Liver Diseases - etiology; Liver Diseases - pathology; Liver injury; Liver. Biliary tract. Portal circulation. Exocrine pancreas; Male; Medical sciences; Middle Aged; Mortality; Nutrition; Other diseases. Semiology; Parenteral nutrition; Parenteral Nutrition, Total - adverse effects; Pathology; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques; Perivenular fibrosis; Retrospective Studies; Rodents; Studies; Total parenteral nutrition; TPN; Young Adult; TPN; Total parenteral nutrition; Cholestasis; Ductopenia; Perivenular fibrosis; Liver injury; Correlation; Digestive system; Liver; Biliary tract disease; Parenteral administration; Anatomic pathology; Histopathology; Treatment; Cholostasis; Fibrosis; Digestive diseases; Lesion
• ISSN: 0046-8177; 1532-8392
• DOI: 10.1016/j.humpath.2011.07.008

Summary Total parenteral nutrition (TPN) therapy is a well-recognized cause of liver injury. The histologic changes attributed to TPN in the literature vary widely. In this study, we describe the histopathologic changes associated with TPN therapy and relate these changes to various clinical parameters. We conducted a retrospective study of 89 patients who underwent biopsy or liver transplantation while on TPN. We report that (1) ductopenia, a previously unreported finding, is seen in a significant number of patients on TPN. It is more frequently seen in patients with low stage of fibrosis and may have an inverse relationship with the length of therapy; (2) Perivenular fibrosis is a feature frequently seen in patients with high-stage portal fibrosis. In fact, we find the combination of portal and perivenular fibrosis to be a characteristic of TPN injury; (3) Infants are more susceptible to TPN–related hepatocellular injury, are more likely to develop fibrosis, and progress to high-stage fibrosis more rapidly than older children and adults; (4) Cholestasis, although more common in infants, is the most common pathologic finding in all age groups; (5) Steatosis is more commonly seen in older children and adults than in infants; (6) Progression to fibrosis in infants may be dependent on the length of therapy and the underlying disease for which TPN is administered; and (7) Clinical markers of liver injury (eg, elevated liver enzymes) do not predict the degree of hepatocellular injury or fibrosis, and therefore, serial biopsies may be indicated for patients on TPN therapy.