Total Serum Bilirubin Predicts Fat‐Soluble Vitamin Deficiency Better Than Serum Bile Acids in Infants With Biliary Atresia
ABSTRACT Objective: Fat‐soluble vitamin (FSV) deficiency is a well‐recognized consequence of cholestatic liver disease and reduced intestinal intraluminal bile acid. We hypothesized that serum bile acid (SBA) would predict biochemical FSV deficiency better than serum total bilirubin (TB) level in in...
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| Published in | Journal of pediatric gastroenterology and nutrition Vol. 59; no. 6; pp. 702 - 707 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology
01.12.2014
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| Subjects | |
| Online Access | Get full text |
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| Abstract | ABSTRACT
Objective:
Fat‐soluble vitamin (FSV) deficiency is a well‐recognized consequence of cholestatic liver disease and reduced intestinal intraluminal bile acid. We hypothesized that serum bile acid (SBA) would predict biochemical FSV deficiency better than serum total bilirubin (TB) level in infants with biliary atresia.
Methods:
Infants enrolled in the Trial of Corticosteroid Therapy in Infants with Biliary Atresia after hepatoportoenterostomy were the subjects of this investigation. Infants received standardized FSV supplementation and monitoring of TB, SBA, and vitamin levels at 1, 3, and 6 months. A logistic regression model was used with the binary indicator variable insufficient/sufficient as the outcome variable. Linear and nonparametric correlations were made between specific vitamin measurement levels and either TB or SBA.
Results:
The degree of correlation for any particular vitamin at a specific time point was higher with TB than with SBA (higher for TB in 31 circumstances vs 3 circumstances for SBA). Receiver operating characteristic curve shows that TB performed better than SBA (area under the curve 0.998 vs 0.821). Including both TB and SBA did not perform better than TB alone (area under the curve 0.998).
Conclusions:
We found that TB was a better predictor of FSV deficiency than SBA in infants with biliary atresia. The role of SBA as a surrogate marker of FSV deficiency in other cholestatic liver diseases, such as progressive familial intrahepatic cholestasis, α‐1‐antitrypsin deficiency, and Alagille syndrome in which the pathophysiology is dominated by intrahepatic cholestasis, warrants further study. |
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| AbstractList | OBJECTIVEFat-soluble vitamin (FSV) deficiency is a well-recognized consequence of cholestatic liver disease and reduced intestinal intraluminal bile acid. We hypothesized that serum bile acid (SBA) would predict biochemical FSV deficiency better than serum total bilirubin (TB) level in infants with biliary atresia.METHODSInfants enrolled in the Trial of Corticosteroid Therapy in Infants with Biliary Atresia after hepatoportoenterostomy were the subjects of this investigation. Infants received standardized FSV supplementation and monitoring of TB, SBA, and vitamin levels at 1, 3, and 6 months. A logistic regression model was used with the binary indicator variable insufficient/sufficient as the outcome variable. Linear and nonparametric correlations were made between specific vitamin measurement levels and either TB or SBA.RESULTSThe degree of correlation for any particular vitamin at a specific time point was higher with TB than with SBA (higher for TB in 31 circumstances vs 3 circumstances for SBA). Receiver operating characteristic curve shows that TB performed better than SBA (area under the curve 0.998 vs 0.821). Including both TB and SBA did not perform better than TB alone (area under the curve 0.998).CONCLUSIONSWe found that TB was a better predictor of FSV deficiency than SBA in infants with biliary atresia. The role of SBA as a surrogate marker of FSV deficiency in other cholestatic liver diseases, such as progressive familial intrahepatic cholestasis, α-1-antitrypsin deficiency, and Alagille syndrome in which the pathophysiology is dominated by intrahepatic cholestasis, warrants further study. Fat-soluble vitamin (FSV) deficiency is a well-recognized consequence of cholestatic liver disease and reduced intestinal intraluminal bile acid. We hypothesized that serum bile acid (SBA) would predict biochemical FSV deficiency better than serum total bilirubin (TB) level in infants with biliary atresia. Infants enrolled in the Trial of Corticosteroid Therapy in Infants with Biliary Atresia after hepatoportoenterostomy were the subjects of this investigation. Infants received standardized FSV supplementation and monitoring of TB, SBA, and vitamin levels at 1, 3, and 6 months. A logistic regression model was used with the binary indicator variable insufficient/sufficient as the outcome variable. Linear and nonparametric correlations were made between specific vitamin measurement levels and either TB or SBA. The degree of correlation for any particular vitamin at a specific time point was higher with TB than with SBA (higher for TB in 31 circumstances vs 3 circumstances for SBA). Receiver operating characteristic curve shows that TB performed better than SBA (area under the curve 0.998 vs 0.821). Including both TB and SBA did not perform better than TB alone (area under the curve 0.998). We found that TB was a better predictor of FSV deficiency than SBA in infants with biliary atresia. The role of SBA as a surrogate marker of FSV deficiency in other cholestatic liver diseases, such as progressive familial intrahepatic cholestasis, α-1-antitrypsin deficiency, and Alagille syndrome in which the pathophysiology is dominated by intrahepatic cholestasis, warrants further study. OBJECTIVE:Fat-soluble vitamin (FSV) deficiency is a well-recognized consequence of cholestatic liver disease and reduced intestinal intraluminal bile acid. We hypothesized that serum bile acid (SBA) would predict biochemical FSV deficiency better than serum total bilirubin (TB) level in infants with biliary atresia. METHODS:Infants enrolled in the Trial of Corticosteroid Therapy in Infants with Biliary Atresia after hepatoportoenterostomy were the subjects of this investigation. Infants received standardized FSV supplementation and monitoring of TB, SBA, and vitamin levels at 1, 3, and 6 months. A logistic regression model was used with the binary indicator variable insufficient/sufficient as the outcome variable. Linear and nonparametric correlations were made between specific vitamin measurement levels and either TB or SBA. RESULTS:The degree of correlation for any particular vitamin at a specific time point was higher with TB than with SBA (higher for TB in 31 circumstances vs 3 circumstances for SBA). Receiver operating characteristic curve shows that TB performed better than SBA (area under the curve 0.998 vs 0.821). Including both TB and SBA did not perform better than TB alone (area under the curve 0.998). CONCLUSIONS:We found that TB was a better predictor of FSV deficiency than SBA in infants with biliary atresia. The role of SBA as a surrogate marker of FSV deficiency in other cholestatic liver diseases, such as progressive familial intrahepatic cholestasis, α-1-antitrypsin deficiency, and Alagille syndrome in which the pathophysiology is dominated by intrahepatic cholestasis, warrants further study. ABSTRACT Objective: Fat‐soluble vitamin (FSV) deficiency is a well‐recognized consequence of cholestatic liver disease and reduced intestinal intraluminal bile acid. We hypothesized that serum bile acid (SBA) would predict biochemical FSV deficiency better than serum total bilirubin (TB) level in infants with biliary atresia. Methods: Infants enrolled in the Trial of Corticosteroid Therapy in Infants with Biliary Atresia after hepatoportoenterostomy were the subjects of this investigation. Infants received standardized FSV supplementation and monitoring of TB, SBA, and vitamin levels at 1, 3, and 6 months. A logistic regression model was used with the binary indicator variable insufficient/sufficient as the outcome variable. Linear and nonparametric correlations were made between specific vitamin measurement levels and either TB or SBA. Results: The degree of correlation for any particular vitamin at a specific time point was higher with TB than with SBA (higher for TB in 31 circumstances vs 3 circumstances for SBA). Receiver operating characteristic curve shows that TB performed better than SBA (area under the curve 0.998 vs 0.821). Including both TB and SBA did not perform better than TB alone (area under the curve 0.998). Conclusions: We found that TB was a better predictor of FSV deficiency than SBA in infants with biliary atresia. The role of SBA as a surrogate marker of FSV deficiency in other cholestatic liver diseases, such as progressive familial intrahepatic cholestasis, α‐1‐antitrypsin deficiency, and Alagille syndrome in which the pathophysiology is dominated by intrahepatic cholestasis, warrants further study. |
| Author | Loomes, Kathleen M. Ng, Vicky L. Venkat, Veena L. Whitington, Peter F. Raghunathan, Trivellore Schwartz, Kathleen Turmelle, Yumirle Karpen, Saul J. Magee, John C. Murray, Karen F. Shneider, Benjamin L. Heubi, James E. Bezerra, Jorge A. Wang, Kasper Molleston, Jean Arnon, Ronen Teckman, Jeffrey Hertel, Paula M. Kerkar, Nanda Sokol, Ronald J. Rosenthal, Philip Sherker, Averell H. |
| AuthorAffiliation | Department of Pediatrics, Childrenʼs Hospital of Pittsburgh of UPMC, Pittsburgh, PA †Department of Surgery and Department of Biostatistics, University of Michigan, Ann Arbor, MI ‡Department of Pediatrics, Washington University, St Louis, MO §Department of Pediatrics, Mount Sinai Medical Center, New York, NY ||Department of Pediatrics, Cincinnati Childrenʼs Hospital Medical Center, Cincinnati, OH ¶Department of Pediatrics, Texas Childrenʼs Hospital, Houston #Department of Pediatrics, Childrenʼs Health Care of Atlanta, Atlanta, GA Department of Gastroenterology, Childrenʼs Hospital Los Angeles, Los Angeles, CA ††Department of Pediatrics, Childrenʼs Hospital of Philadelphia, Philadelphia, PA ‡‡Department of Pediatrics, Riley Childrenʼs Hospital, Indianapolis, IN §§Department of Pediatrics, Seattle Childrenʼs Hospital, Seattle, WA ||||Department of Pediatrics, Hospital for Sick Children, Toronto, Ontario, Canada ¶¶School of Public Health, University of Michigan, Ann Arbor ##Department of P |
| AuthorAffiliation_xml | – name: Department of Pediatrics, Childrenʼs Hospital of Pittsburgh of UPMC, Pittsburgh, PA †Department of Surgery and Department of Biostatistics, University of Michigan, Ann Arbor, MI ‡Department of Pediatrics, Washington University, St Louis, MO §Department of Pediatrics, Mount Sinai Medical Center, New York, NY ||Department of Pediatrics, Cincinnati Childrenʼs Hospital Medical Center, Cincinnati, OH ¶Department of Pediatrics, Texas Childrenʼs Hospital, Houston #Department of Pediatrics, Childrenʼs Health Care of Atlanta, Atlanta, GA Department of Gastroenterology, Childrenʼs Hospital Los Angeles, Los Angeles, CA ††Department of Pediatrics, Childrenʼs Hospital of Philadelphia, Philadelphia, PA ‡‡Department of Pediatrics, Riley Childrenʼs Hospital, Indianapolis, IN §§Department of Pediatrics, Seattle Childrenʼs Hospital, Seattle, WA ||||Department of Pediatrics, Hospital for Sick Children, Toronto, Ontario, Canada ¶¶School of Public Health, University of Michigan, Ann Arbor ##Department of Pediatrics, University of California San Francisco, San Francisco Department of Pediatrics, Johns Hopkins University, Baltimore †††National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD ‡‡‡Department of Pediatrics, University of Colorado School of Medicine and Childrenʼs Hospital Colorado, Aurora §§§Department of Pediatrics, Saint Louis University School of Medicine, St Louis, MO ||||||Department of Pediatric Surgery, Childrenʼs Hospital Los Angeles, Los Angeles, CA ¶¶¶Department of Pediatrics, Childrenʼs Memorial Hospital, Chicago, IL – name: 11 Department of Pediatrics, Seattle Children’s Hospital, Seattle, WA – name: 14 Department of Pediatrics, University of California San Francisco, San Francisco, California – name: 15 Department of Pediatrics, Johns Hopkins University, Baltimore, Maryland – name: 1 Department of Pediatrics, Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, PA – name: 10 Department of Pediatrics, Riley Children’s Hospital, Indianapolis, IN – name: 8 Department of Gastroenterology, Children’s Hospital Los Angeles, Los Angeles, CA – name: 7 Department of Pediatrics, Children’s Health Care of Atlanta, Atlanta, GA – name: 6 Department of Pediatrics, Texas Children’s Hospital, Atlanta, GA – name: 2 Department of Surgery and Department of Biostatistics, University of Michigan, Ann Arbor, MI – name: 4 Department of Pediatrics, Mount Sinai Medical Center, Cincinnati, OH – name: 9 Department of Pediatrics, Children’s Hospital of Philadelphia, Philadelphia, PA – name: 12 Department of Pediatrics, The Hospital for Sick Children, Toronto, Ontario, Canada – name: 13 School of Public Health, University of Michigan, Ann Arbor, MI – name: 18 Department of Pediatrics, Saint Louis University School of Medicine, Los Angeles, CA – name: 17 Department of Pediatrics, University of Colorado School of Medicine and Children’s Hospital Colorado, Aurora, CO – name: 3 Department of Pediatrics, Washington University, St. Louis, MO – name: 19 Department of Pediatric Surgery, Children’s Hospital Los Angeles, Los Angeles, CA – name: 20 Department of Pediatrics, Children’s Memorial Hospital, Chicago, IL – name: 5 Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH – name: 16 National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland |
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| Copyright | 2014 by European Society for European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition 2014 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology |
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| Notes | registration number: NCT00294684 This work was supported by U01 grants from the National Institute of Diabetes, Digestive and Kidney Disease (DK62453 [R.J.S.], DK84538 [K.W.], DK62500 [P.R.], DK62470 [S.J.K.], DK62436 [P.F.W.], DK84536 [J.M.], DK62503 [K.S.], DK62452 [Y.M.], DK62445 [R.A.], DK62497 [J.A.B.], DK62481 [K.M.L.], DK62466 [B.L.S.], DK84575 [K.F.M.], DK62470 [P.M.H.]) and CTSA grants from the National Center for Advancing Translational Sciences (UL1TR000154 [Colorado], UL1TR000130 [Los Angeles], UL1TR000004 [San Francisco], UL1TR000454 [Atlanta], UL1TR000150 [Chicago], UL1TR000006 [Indianapolis], Ul1TR000424 [Baltimore], UL1TR000448 [St Louis], UL1TR000077 [Cincinnati], UL1TR000003 [Philadelphia], UL1TR000005 [Pittsburgh], UL1TR000423 [Seattle]. This study was also funded by the National Institutes of Health. R.J.S. is a consultant for and on the scientific advisory board of YASOO Health, Inc, which is the distributor for AquADEKs and ADEKs. The company had no involvement in designing the research, interpreting the data, or writing the article. The other authors report no conflicts of interest. childrennetwork.org www.clinicaltrials.gov . ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-News-1 ObjectType-Feature-3 content type line 23 |
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Objective:
Fat‐soluble vitamin (FSV) deficiency is a well‐recognized consequence of cholestatic liver disease and reduced intestinal intraluminal bile... OBJECTIVE:Fat-soluble vitamin (FSV) deficiency is a well-recognized consequence of cholestatic liver disease and reduced intestinal intraluminal bile acid. We... Fat-soluble vitamin (FSV) deficiency is a well-recognized consequence of cholestatic liver disease and reduced intestinal intraluminal bile acid. We... OBJECTIVEFat-soluble vitamin (FSV) deficiency is a well-recognized consequence of cholestatic liver disease and reduced intestinal intraluminal bile acid. We... |
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| SubjectTerms | Avitaminosis - blood Avitaminosis - etiology Bile Acids and Salts - blood biliary atresia Biliary Atresia - blood Biliary Atresia - complications bilirubin Bilirubin - blood cholestasis Dietary Supplements Double-Blind Method fat‐soluble vitamin Female Humans Infant Infant, Newborn Male National Institute of Diabetes and Digestive and Kidney Diseases (U.S.) Placebos Prospective Studies serum bile acid United States Vitamin A - administration & dosage Vitamin A - blood Vitamin D - administration & dosage Vitamin D - blood Vitamin E - administration & dosage Vitamin E - blood Vitamin K - administration & dosage Vitamin K - blood Vitamins - administration & dosage |
| Title | Total Serum Bilirubin Predicts Fat‐Soluble Vitamin Deficiency Better Than Serum Bile Acids in Infants With Biliary Atresia |
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