Intrahepatic cholestasis with parenteral alimentation

Rodgers, Bryan; Hollenbeck, John I.; Donnelly, William H.; Talbert, James L.

doi:10.1016/0002-9610(76)90088-x

Cited by 90 publications

(32 citation statements)

References 7 publications

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“…1 Previous reports of PN-associated ChJ have advocated serial measurements of direct bilirubin, SGPT, SGOT, and alkaline phosphatase in patients receiving PN. [2][3][4][5] Although elevated serum bile salt concentrations may now, in fact,. be the most sensitive indicator of ChJ, this determination is unfortunately not routinely available.…”

mentioning

confidence: 99%

Laboratory Monitoring of Parenteral Nutrition‐Associated Hepatic Dysfunction in Infants

Vileisis¹,

Inwood²,

Hunt³

1981

J Parenter Enteral Nutr

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Hepatic dysfunction associated with parenteral nutrition (PN) is a well recognized occurrence. In order to define the temporal inter-relationships of direct bilirubin to other laboratory parameters, total and direct bilirubin, serum glutamic-pyruvic transaminase (SGPT), serum glutamic-oxaloacetic transaminase (SGOT), and alkaline phosphatase were measured prior to beginning PN and then weekly throughout the duration of PN in 60 consecutive neonates. Cholestatic jaundice (ChJ), defined as a direct bilirubin greater than or equal to 2.0 mg/dl, developed in 11 (33%) of 33 infants receiving PN for at least 2 weeks. Direct bilirubin was the most sensitive and earliest indicator of ChJ. SGOT and SGPT values in the ChJ group were not statistically different from the non-ChJ group until 2 weeks after the onset of cholestasis. Although there was a progressive increase in alkaline phosphatase during the course of PN, the increase was not greater in the ChJ group. In summary, direct bilirubin is the only laboratory indicator of hepatic status that need be determined serially in parenterally alimented infants. Although SGPT and SGOT may be helpful in characterizing hepatic dysfunction once ChJ has occurred, alkaline phosphatase levels do not reliably assess PN-associated liver injury.

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mentioning

confidence: 99%

Laboratory Monitoring of Parenteral Nutrition‐Associated Hepatic Dysfunction in Infants

Vileisis¹,

Inwood²,

Hunt³

1981

J Parenter Enteral Nutr

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“…The increase in alkaline phosphatase in patients with parenteral nutrition-associated cholestasis is well established [1][2][3][4][5][6][7]. How ever, in our study, 5 patients did not exhibit an increase in alkaline phosphatase.…”

Section: Discussionmentioning

confidence: 38%

“…Since then, a number of reports have reported similar abnormalities [2][3][4][5]. The basic histopathologic abnormality associated with abnormal hepatic function is that of cholestasis [6,7].…”

mentioning

confidence: 93%

Absence of Increase of Serum Alkaline Phosphatase Activity with Parenteral Nutrition-Associated Cholestasis: Possible Consequence of Hypozincemia and Hypomagnesemia

Nanji¹

1985

Enzyme

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We reviewed charts of 38 Patients who developed cholestasis whilst receiving total parenteral nutrition (TPN). A standard protocol was followed for administration of TPN and included crystalline amino acid solution with lipid emulsion and dextrose as calorie sources. 5 of the 38 patients did not exhibit an increase in alkaline phosphatase. This may be related to the concomitant low levels of either serum zinc or magnesium or both. We also obtained a positive correlation between serum levels of zinc and magnesium and the peak activity of alkaline phosphatase (r = 0.49, p < 0.01, r-0.55, p < 0.01, respectively) associated with cholestasis. We hypothesize that the reason for this association is related to both zinc and magnesium being activators of alkaline phosphatase activity.

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“…One consequence is increased difficulty in weaning such patients from ventilators. Atout the same time other workers described, in a similar patient popu lation, the development of fatty livers and subsequent liver dysfunction secondary to excess parenteral gluco.se [10][11][12][13]. The two phenomena are related.…”

Section: Introductionmentioning

confidence: 66%