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C M Y CM MY CY CMY K

NUTRITION Mullin • Matarese • GASTROINTESTINAL AND DISEASE Palmer NUTRITION DESK REFERENCE

While the gastrointestinal tract ingests, digests, and absorbs nutrients, the liver transforms nutrients, synthesizes plasma proteins, and detoxifies bacteria and toxins absorbed from the gut. It is therefore not surprising that

gastrointestinal and hepatic diseases have a major impact on the nutritional state of the individual. Integrating DISEASE LIVER AND GASTROINTESTINAL nutrition and the gastrointestinal system, the Gastrointestinal and Nutrition Desk Reference brings together experts in the field of nutrition, , and to offer dietary, nutritional, and natural therapies for gastrointestinal and hepatic ailments in order to improve overall health. NUTRITIONDESK REFERENCE

Providing a review of the digestive tract, liver, and core concepts, this important reference presents the nutritional consequences and considerations of digestive and liver disorders. Contributors examine the role of nutrition in gastrointestinal and liver disease, including alcoholic and nonalcoholic liver disease, viral , , malabsorption, colorectal disease, transplantation, pancreatitis, and inflammatory bowel disease.

Of special interest to the practitioner are chapters on food allergy and intolerance, the effects of medicinal plants, and the role of fiber in the gastrointestinal tract. The reference also addresses the challenges of managing nutritional issues for hospitalized patients, and covers eating disorders and ethical issues.

Other key topics include • Obesity • Clinical applications of probiotics • The impact of micronutrient deficiencies • Genomic applications for gastrointestinal care • Drug–drug and drug–nutrient interactions • Guidelines for performing a nutrition assessment

This comprehensive reference offers a toolbox of key concepts, charts, tables, algorithms, and practical therapeutic strategies for practitioners involved in gastrointestinal and hepatic nutrition care.

K10642

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Composite GASTROINTESTINAL AND LIVER DISEASE NUTRITION DESK REFERENCE

GASTROINTESTINAL AND LIVER DISEASE NUTRITION DESK REFERENCE

Edited by Gerard E. Mullin Laura E. Matarese Melissa Palmer

Boca Raton London New York

CRC Press is an imprint of the Taylor & Francis Group, an informa business Cover designed by Melissa Palmer, M.D.

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Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identifica- tion and explanation without intent to infringe. Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com Contents

Preface...... ix Editors ...... xi Contributors ...... xiii

Chapter 1 Major Components of the Gastrointestinal System and Their Role in Digestion ...... 1 Monica van Dongen and Gerard E. Mullin

Chapter 2 Malabsorption ...... 9 Babatunde Adeyefa and Carla W. Brady

Chapter 3 The Role of the Gut Microbiota and Probiotics in Gastrointestinal Disease Prevention and Management ...... 21 Gerard E. Mullin

Chapter 4 Short Bowel Syndrome ...... 35 Laura E. Matarese

Chapter 5 Celiac Disease ...... 51 S. Devi Rampertab

Chapter 6 Food Allergy and Food Intolerance ...... 65 John Leung and Sheila E. Crowe

Chapter 7 Anatomy and Physiology of the Liver ...... 81 Melissa Palmer

Chapter 8 Nutrition and Alcoholic Liver Disease ...... 91 Melissa Palmer

Chapter 9 Nutrition and Nonalcoholic and Viral Liver Diseases ...... 109 Melissa Palmer

Chapter 10 General Nutritional Guidelines for Liver Disease, Cirrhosis, and Its Complications ...... 139 Melissa Palmer

vii viii Contents

Chapter 11 Nutrition and Liver Transplantation ...... 159 Melissa Palmer

Chapter 12 Nutritional Considerations in Acute and Chronic Pancreatitis ...... 171 Deepa Gosine, Mohammed R. Kaleel, and Vikesh K. Singh

Chapter 13 Nutrition in Irritable Bowel Syndrome ...... 185 Ashley Koff and Gerard E. Mullin

Chapter 14 InŽammatory Bowel Disease ...... 197 S. Devi Rampertab, Amy Brown, and Gerard E. Mullin

Chapter 15 Nutrition and Colorectal Disease ...... 209 Myles R. Joyce and Victor W. Fazio

Chapter 16 Nutrition and Colorectal Cancer ...... 221 Mitra Rangarajan and Gerard E. Mullin

Chapter 17 The InŽuence of Bitter, Aromatic, and Pungent Medicinal Plants on Gut Function ...... 237 James Snow and Kevin Spelman

Chapter 18 Obesity and Nutrition ...... 251 Katrina B. Seidman and Lawrence J. Cheskin

Chapter 19 Micronutrients ...... 265 Omar S. Khokhar and Timothy O. Lipman

Chapter 20 Role of Fiber, Prebiotics, and Probiotics in Gastrointestinal Health and Disease ...283 Martin H. Floch and Violeta B. Popov

Chapter 21 Overview of Genomics and Gastrointestinal Health and Disease ...... 303 Ruth DeBusk

Chapter 22 Enteral Access and Enteral Nutrition ...... 317 Amy Berry and Mark H. DeLegge

Chapter 23 Parenteral Nutrition ...... 343 Mandy Corrigan, Bijo K. John, and Ezra Steiger Contents ix

Chapter 24 Pediatric Enteral and Parenteral Nutrition ...... 359 Jenifer Hampsey and Tiffani Hays

Chapter 25 Drug–Drug and Drug–Nutrient Interactions in Gastrointestinal Disease ...... 375 Mark G. Klang

Chapter 26 Nutrition Assessment ...... 387 Tina Colaizzo-Anas

Chapter 27 Critical Care Nutrition ...... 415 Tara Nealon and Jonathan Waitman

Chapter 28 Perioperative Nutrition Support ...... 423 Jill Schuman and Kishore R. Iyer

Chapter 29 Bariatric Surgery ...... 437 Scott A. Shikora, Kerri Anne Hawkins, and Meghan Ariagno

Chapter 30 Home Parenteral Nutrition (HPN) ...... 447 Alice Illian, Carol Ireton-Jones, and Kevin M. McNamara

Chapter 31 An Integrative Nutrition Approach to Eating Disorders ...... 457 Carolyn Coker Ross and Gerard E. Mullin

Chapter 32 Ethical and Medical–Legal Considerations ...... 471 Julie O’Sullivan Maillet

Preface

The gastrointestinal tract is concerned with ingesting, digesting, and absorbing nutrients and the liver is a metabolic engine that transforms nutrients, synthesizes plasma proteins, and detoxi˜es bacteria and toxins absorbed from the gut. It is therefore not surprising that gastrointestinal and hepatic diseases have a major impact on the nutritional state of the individual. This text is easily referred to, integrating the gastrointestinal tract and nutrition, and is a valuable addition to the literature of the practicing gastroenterologist. The desk reference is edited by Dr. Gerard Mullin, who directs the integration of nutrition and gastrointestinal disease at Johns Hopkins Medical Center; Dr. Laura Matarese, who specializes in the nutritional care of persons with gastrointestinal failure at East Carolina University; and Dr. Melissa Palmer, the medical director of hepatology at New York University in Plainview. They have track records and current interests suited to such a reference. The book has a total of 32 chapters covering a range of topics relevant to being a reference integrating nutrition with gastrointestinal disease. Three chapters, entitled “Major Components of the Gastrointestinal System and Their Role in Digestion,” “The Role of the Gut Microbiota and Probiotics in Gastrointestinal Disease Prevention,” and “Anatomy and Physiology of the Liver,” give the reader an understanding of the normal state. Other sections cover the role of nutrition in gastrointestinal and liver disease, including alcoholic and nonalcoholic liver disease, malabsorption, colorectal disease, transplantation, pancreatitis, and inŽammatory bowel disease. Of special interest to the practicing gastroenterologist are areas such as food allergy, food intolerances, effects of medicinal plants, and the role of ˜ber in the gastrointestinal tract. These areas are rarely covered in standard texts. The remaining chapters cover the standard areas of nutrition, namely, nutritional assessment, enteral and parenteral nutrition, home parenteral nutrition, obesity, critical care nutrition, and surgi- cal nutrition. Finally, there are two chapters that cover eating disorders and ethical issues. This text is a valuable practical reference for practicing gastroenterologists as it covers the impor- tant aspects of nutrition in gastrointestinal and liver disease.

Khursheed N. Jeejeebhoy University of Toronto St. Michael’s, Toronto

xi

Editors

GERARD E. MULLIN, MD Dr. Gerard Mullin is an associate professor in the Department of Medicine as well as director of Integrative Gastroenterology Nutrition Services at the Johns Hopkins Hospital. He is an internist, gastroenterologist, and nutritionist and the only physician in the United States who is board certi˜ed by the American Board of Internal Medicine for Gastroenterology, American Society of Enteral and Parenteral Nutrition, American College of Nutrition, and the American Board of Nutrition Physician Specialists. Nationally and internationally renowned for his work in integrative gastroenterology and nutrition, Mullin has accumulated over 15 years of clinical experi- ence in the ˜eld of integrative gastroenterology and earned his master’s degree in nutrition while in practice. He is an associate editor of several nutrition and integrative medicine journals. Dr. Mullin was selected by Dr. Andrew Weil to serve as a senior editor for the ˜rst book for physicians on integra- tive gastroenterology by Oxford Press released in December of 2010 and has contracts for three other books on nutrition and digestive health. He is also the former president of the Maryland and Long Island Societies of Parenteral and Enteral Nutrition and the cofounder of M&Mvites LLC, a ˜rm for designing digestive health nutraceuticals. In 2009, he was named the American Dietetic Association’s honorary member of the year. Dr. Mullin’s writing and communications skills are well known in both the medical and lay communities. He has been interviewed on radio and television and has contributed to stories in The New York Times, the Associated Press, ABC News, Good Morning America, Newsday, Martha Stewart Living, Rodale Press, Consumers Digest, Reader’s Digest, Prevention, Natural Health magazine, Body & Soul, Cooking Light, Women’s World, Men’s Health, Good Housekeeping, Glamour, and more. Dr. Mullin’s biography has been included in Marquis Who’s Who in the World and in Marquis Who’s Who in America numerous times. His contributions and discoveries have led to multiple awards and his continued selection as one of America’s Top Physicians by the Consumers’ Research Council of America since 2004. He received his medical degree from the University of Medicine and Dentistry of New Jersey and came to the Johns Hopkins Hospital in 1988 as a gastroenterology fellow.

LAURA E. MATARESE, PhD, RD, LDN, FADA, CNSC Dr. Laura Matarese is an associate professor of medicine in the Division of Gastroenterology, Hepatology, and Nutrition, Department of Internal Medicine, Brody School of Medicine, East Carolina University. She is responsible for the nutritional care of patients with intestinal failure. She is the author of over 150 books, chapters, manuscripts, abstracts, and videos and currently serves on the editorial boards of several ­journals. She has lectured extensively, both nationally and internation- ally, and has held numerous positions within the American Dietetic Association and the American Society for Parenteral and Enteral Nutrition. Dr. Matarese currently serves on the board of trustees of the

xiii xiv Editors

Oley Foundation and is president of the National Board of Nutrition Support Certi˜cation. She is the recipient of numerous awards including the American Dietetic Association Medallion Award, the American Dietetic Association Foundation Award for Excellence in the Practice of Clinical Nutrition, the American Society for Parenteral and Enteral Nutrition Award for Distinguished Achievement in Nutrition Support Dietetics, Excellence in Nutrition Support Education, and the ˜rst recipient of the Advanced Clinical Practice Award as well as the Dietitians in Nutrition Support Distinguished Service Award.

MELISSA PALMER, MD Dr. Melissa Palmer is medical director of hepatology at New York University Hepatology Associates, Plainview and is clinical professor of medicine at New York University. She graduated from Columbia University and was trained in hepatology at the Mount Sinai School of Medicine in New York City. Dr. Palmer is the author of the best-selling book Dr. Melissa Palmer’s Guide to Hepatitis and Liver Disease, which has been translated into multiple languages for worldwide use. She has authored numerous medical and lay-public book chapters and contributed to three encyclopedias on various liver-related topics. Her scienti˜c publications in the ˜eld of hepatology have appeared in such peer-reviewed journals as Hepatology, Gastroenterology, Seminars of Liver Disease, Transplantation, and Archives of Internal Medicine, and she is a contributing editor of numerous peer-reviewed journals. Dr. Palmer has been selected multiple times for inclusion in Castle Connolly’s Best Doctor in the New York Metro Area, for Consumer’s Research Council Top Physicians in America, and for the Patients’ Choice Award for Best Doctor in New York. Dr. Palmer runs the popular liver website www.liverdisease.com, which has been the top-ranked website for liver disease on Yahoo since 1996. She is frequently called upon by the media for her opinion on various topics related to liver disease. Dr. Palmer has appeared many times on television as a liver disease expert and has been cited for her expertise in such publications as the Wall Street Journal, TIME magazine, Cosmopolitan magazine, Women’s World, Money magazine, Prevention magazine, the Los Angeles Times, and Newsday. She has also appeared in numerous videos and CD-ROMs aimed at educating doctors and the public about hepatitis C and other liver diseases, such as primary biliary cirrhosis—some of which can be viewed on Youtube, www.youtube.com/users/ melissapalmermd. Dr. Palmer lectures to the medical and general public on liver disease–related topics on a regular basis. Since 1991, Dr. Palmer has sat on the medical advisory board of the New York chapter of the American Liver Foundation and been a member of the American Association for the Study of Liver Disease (AASLD), where she currently serves on both the Finance Committee and Development Committee, and has previously served on the Practice Guidelines Committee, the Enduring Educational Materials Committee, and the Program Evaluation Committee. Dr. Palmer has performed trials of various experimental medication for the treatment of hepatitis and other liver diseases since 1983 and is currently conducting research on new therapies for liver disease, speci˜cally in the area of hepatitis C and nonalcoholic fatty liver disease. Contributors

Babatunde Adeyefa, MD Sheila E. Crowe, MD, FRCPC, FACP, Resident, Department of Medicine FACG, AGAF Duke University Medical Center Professor of Medicine Durham, North Carolina Division of Gastroenterology & Hepatology Digestive Health Center of Excellence Meghan Ariagno, RD, LDN Charlottesville, Virginia Weight and Wellness Center Tufts Medical Center Ruth DeBusk, PhD, RD Boston, Massachusetts Private practice and Amy Berry, MS, RD, CNSD Adjunct Associate Professor at the University Surgical Nutrition Support Team of Medicine and Dentistry of New Jersey University of Virginia Health System Tallahassee, Florida Charlottesville, Virginia Mark H. DeLegge, MD Carla W. Brady, MD, MHS Division of Gastroenterology and Hepatology Assistant Professor Medical University of South Carolina Division of Gastroenterology Charleston, South Carolina Duke University Medical Center Durham, North Carolina Victor W. Fazio, MB, MS, MD (Hon), FRACS, FRACS (Hon), FACS, FRCS, Amy Brown, PhD, RD FRCS (Ed) Associate Professor of Medicine Cleveland Clinic Department of Complementary & Alternative Cleveland, Ohio Medicine John A. Burns School of Medicine Amy K. Fischer, BA University of Hawaii Master’s Candidate in Clinical Nutrition Honolulu, Hawaii The Steinhardt School New York University Lawrence J. Cheskin, MD, FACP New York, New York Associate Professor, Health Behavior & Society and Martin H. Floch, MD Director, Johns Hopkins Weight Management Clinical Professor of Medicine Center Yale University School of Medicine Baltimore, Maryland Section of Digestive Diseases Yale Medical Group Tina Colaizzo-Anas, PhD, RD, CDN New Haven, Connecticut Dietetics and Nutrition Buffalo, New York Deepa Gosine, MSc Pancreatitis Center Mandy Corrigan, MPH, RD, CNSC Division of Gastroenterology Cleveland Clinic The Johns Hopkins Hospital Cleveland, Ohio Baltimore, Maryland

xv xvi Contributors

Jenifer Hampsey, MS, RD, CSP, LDN Omar S. Khokhar, MD Pediatric Nutrition Practitioner Clinical Assistant Professor of Medicine Division of Pediatric GI and Nutrition University of Illinois College of Johns Hopkins Children’s Center Medicine-Peoria Baltimore, Maryland Peoria, Illinois

Kerri Anne Hawkins, MS, RD, LDN Mark G. Klang, PhD Supervisor of Clinical Dietitians Core Head, Research Pharmacy Weight and Wellness Center Sloan-Kettering Institute Tufts Medical Center New York, New York Boston, Massachusetts Ashley Koff, RD Tiffani Hays, MS, RD, CDE, LDN Registered Dietitian Assistant Director of Pediatric Nutrition Venice, California Division of Pediatric GI and Nutrition Johns Hopkins Children’s Center Baltimore, Maryland John Leung, MD Clinical Instructor Division of Gastroenterology Alice Illian, MSN, CRNI Tufts Medical Center Clinical Services, Coram Specialty Infusion Boston, Massachusetts Humble, Texas

Carol Ireton-Jones, PhD, RD, LD, CNSD, Timothy O. Lipman, MD FACN GI–Hepatology–Nutrition Section Nutrition Therapy Specialist/Consultant Washington DC Veterans Affairs Medical Carrollton, Texas Center Washington, DC Kishore R. Iyer, MBBS, FRCS, FACS Associate Professor of Surgery and Pediatrics Julie O’Sullivan Maillet, PhD, RD, FADA Director, Intestinal Rehabilitation and Interim Dean and Professor of Nutritional Transplantation Program Sciences Mount Sinai Medical Center School of Health Related Professions New York, New York University of Medicine and Dentistry of New Jersey Bijo K. John, MD Newark, New Jersey Cleveland Clinic Cleveland, Ohio Laura E. Matarese, PhD, RD, LDN, FADA, CNSC Myles R. Joyce, MB, Bch, BAO, MD, Associate Professor of Medicine MmedSci, FRSCI Division of Gastroenterology, Hepatology, and Digestive Disease Institute Nutrition The Cleveland Clinic Foundation Department of Internal Medicine Cleveland, Ohio Brody School of Medicine East Carolina University Greenville, North Carolina Mohammed R. Kaleel, MSc Pancreatitis Center Division of Gastroenterology Kevin M. McNamara, Pharm D The Johns Hopkins Hospital Clinical Pharmacist Baltimore, Maryland Tampa, Florida Contributors xvii

Gerard E. Mullin, MD, CNSP, FACN, AGAF Katrina B. Seidman, MS, RD, LDN Director of Integrative Gastroenterology Johns Hopkins University School of Public Nutrition Services Health and Johns Hopkins Center for Weight Management Associate Professor of Medicine Baltimore, Maryland Johns Hopkins School of Medicine The Johns Hopkins Hospital Scott A. Shikora, MD, FACS Baltimore, Maryland Director, Weight and Wellness Center Chief, Bariatric Surgery Tara Nealon, RD, CNSC Tufts Medical Center Nutrition Support Dietitian and Philadelphia, Pennsylvania Professor of Surgery Melissa Palmer, MD Tufts University School of Medicine Clinical Professor of Medicine Boston, Massachusetts New York University and Vikesh K. Singh, MD, MSc Director Hepatology Assistant Professor of Medicine NYU Hepatology Associates Plainview and Plainview, New York Director, Pancreatitis Center Medical Director, Pancreatic Islet Cell Violeta B. Popov, MD Autotransplantation Program Senior Gastroenterology Fellow Division of Gastroenterology Yale Digestive Diseases (Gastroenterology) The Johns Hopkins Hospital Sterling Hall of Medicine Baltimore, Maryland Yale University School of Medicine New Haven, Connecticut James Snow, RH (AHG) S. Devi Rampertab, MD Director Assistant Professor of Medicine Master of Science in Herbal Medicine Program Milton S. Hershey Medical Center Tai Sophia Institute Penn State University College of Medicine Laurel, Maryland Hershey, Pennsylvania Kevin Spelman, PhD, RH(AHG), MCPP Mitra Rangarajan, MSN, ANP-BC, MPH, Tai Sophia Institute CDE, MS, RD Laurel, Maryland Nurse Practitioner–GI Motility/Advanced Therapeutic Endoscopy/Pancreatic Disorders Ezra Steiger, MD, FACS Department of Gastroenterology and Hepatology Consultant in General Surgery and Johns Hopkins University School of Medicine Gastroenterology Baltimore, Maryland Digestive Disease Institute Carolyn Coker Ross, MD, MPH Cleveland Clinic Consultant Cleveland, Ohio Clinical Assistant Professor Monica van Dongen, MSN, CRNP Center for Integrative Medicine Division of Gastroenterology University of Arizona School of Medicine Denver, Colorado The Johns Hopkins Hospital Baltimore, Maryland Jill Schuman, RD, CNSD, CSP, CDN Clinical Nutrition Coordinator Jonathan Waitman, MD Intestinal Rehabilitation and Transplantation Medical Director of Nutrition Support Service Program Weil Cornell Medical Center Mount Sinai Medical Center New York Presbyterian Hospital New York, New York New York, New York

Major Components of the 1 Gastrointestinal System and Their Role in Digestion

Monica van Dongen and Gerard E. Mullin

The gastrointestinal (GI) system includes the GI tract and accessory organs that aid digestion. All components play a key role in the process of digestion, in order to provide the nutrients necessary to maintain normal body function. The entire digestive tract extends from mouth to anus in a continu- ous manner, which includes the esophagus, stomach, small intestine and large intestine (Figure 1.1). Accessory organs located outside of the GI tract include salivary glands, the pancreas, and the bili- ary system, which includes the liver, gallbladder, and bile ducts (Figure 1.1). The process of digestion begins with the mouth, which serves as an entryway into the GI tract. It contains the teeth, tongue, and salivary glands that aid digestion at this juncture. The teeth and tongue assist in the physical break down of food through mastication, while the salivary glands assist in the chemical breakdown through the production of saliva. Salivary glands serve to produce and release saliva into the mouth (Figure 1.2). Saliva helps to moisten food for easier swallowing and also contains amylase, an enzyme responsible for the breakdown of starch and lipids into sim- pler substances. Swallowing, which is accomplished through the use of the tongue and muscles in the Žoor of the mouth, moves food into the pharynx, which then diverts food into the esophagus. The esophagus is a muscular tube that lies behind the trachea, connecting the mouth to the stomach. It contains two sphincters, one at its upper end and one at the lower end. The upper sphincter serves to prevent air from entering the esophagus during respiration and the lower sphincter acts to prevent gastric reŽux into the esophagus. Food is passed through the esophagus and into the stomach via a series of peristaltic contractions (Figure 1.3). Once in the stomach, food is further broken down through mechanical and chemical digestion. The stomach is a pouch-like structure that acts to store and break down food received from the esophagus. Its strong muscular walls act like a churn, breaking food down into chyme, which is a thick liquid consistency. The glands within the stomach walls also secrete gastric acids and diges- tive enzymes that aid in the breakdown of nutrients, including hydrochloric acid and pepsinogen, the precursor of pepsin. Pepsin is an enzyme that digests proteins. Hydrochloric acid provides the acidic environment needed for the reaction of pepsin to denature proteins, and also to kill microor- ganisms that are often ingested with foods. Mucus is also secreted in the stomach; it acts to coat the cells of the stomach lining, protecting them from being damaged by the gastric acids and enzymes. The stomach also has a high capacity for storing food until it is passed into the small intestine. Under normal circumstances, the stomach expands to hold about 1000 mL of food at a time, but is capable of storing up to 2000–3000 mL. Anatomically, the stomach is divided into four major sections: the cardia, the fundus, the body, and the pylorus (Figure 1.4). The cardiac ori˜ce is the ˜rst portion of the stomach, directly below the lower esophageal sphincter (LES), where contents from the esophagus empty into the stomach. The fundus includes the upper curvature of the stomach, followed by the body, which is the cen- tral region of the stomach. The pylorus is the most distal section of the stomach, which connects

1 2 Gastrointestinal and Liver Disease Nutrition Desk Reference

Parotid gland

Sublingual gland

Submandibular gland

Esophagus

Liver Stomach

Spleen Splenic Gallbladder flexura of Duodenum transverse colon Pancreas Hepatic Transverse flexure colon Acending Jejunum colon Decending Ileum colon Cecum Sigmoid Appendix colon Sigmoid flexure Rectum Anus

FIGURE 1.1 The digestive tract, including accessory organs. (From http://www.biologycorner.com/anatomy/ digestive/notes_digestive.html)

Salivary glands

Parotid gland

Submandibular gland Sublingual gland

FIGURE 1.2 Salivary glands assist digestion by producing saliva. Saliva facilitates the movement of food through the digestive tract through moistening ingested contents. Salivary enzymes also assist through chemical breakdown of starch and lipids. (From http://www.biologycorner.com/anatomy/digestive/notes_ digestive.html) Major Components of the Gastrointestinal System and Their Role in Digestion 3

Peristalsis

Food Esophagus Circular muscles contract Previous mouthful of food swallowed Circular muscles relax Sphincters Stomach

FIGURE 1.3 Peristalsis is a contraction of smooth muscles that facilitates the movement of food from the mouth to the stomach. (From Purves, W. K., D. Sadava, G. H. Orians, and H. C. Heller. 1998. Life: The sci- ence of biology (4th ed.). Sinauer Associates [www.sinauer.com] and W.H. Freeman [www.whfreeman.com], http://www.cartage.org.lb/en/themes/sciences/LifeScience/GeneralBiology/Physiology/DigestiveSystem/ ComponentsDigestive/ComponentsDigestive.html, Gordonsville, VA.) to the small intestine and controls gastric emptying. The pylorus is further divided into two parts: the pyloric antrum, which is located directly below the body of the stomach, and the pyloric canal, which is the narrowest area of the stomach that connects to the small intestine. Once in the stomach, food is churned through muscular contractions of the stomach wall, reducing the food into partially digested food called chyme. Chyme remains in the pyloric canal until it is broken down to the right consistency to pass into the small intestine via the pyloric sphincter. After being processed in the stomach, food is passed into the small intestine where the majority of digestion and absorption occurs. The small intestine is the longest portion of the digestive tract, typically about 6 meters (20 feet) in length in the average adult, and is made up of three sections including the duodenum, jejunum, and ileum (Figure 1.5), which all serve distinct functions in the

Fundus Esophagus

Cardia

Longitudinal layer (outer) Pyloric Circular orifice Pyloric Lesser layer ree layers Duodenum sphincter curvature (middle) of smooth Oblique muscle layer (inner) Body

Greater curvature

Pylorus

Gastric folds

FIGURE 1.4 The stomach is divided into four major sections: the cardia, fundus, body, and pylorus. The stom- ach breaks food down into chyme before it is passed through to the small intestine. (From http://www.m111m. com/4images/data/media/126/stomach_anatomy.jpg. McGraw-Hill Companies, Inc., New York, NY.) 4 Gastrointestinal and Liver Disease Nutrition Desk Reference

Duodenum

Jejunum

Ileum

FIGURE 1.5 The small intestine is divided into three sections: the duodenum, the jejunum, and the ileum. (From http://www.carenewengland.org/healthGate/images/si55551448.jpg. Nucleus Medical Art, Inc., Kennesaw, GA.) digestion process. The majority of chemical digestion occurs in the duodenum. Once chyme enters the duodenum, intestinal hormones are released that signal the gallbladder and pancreas to release digestive enzymes to facilitate the degradation process. Bile is released from the gallbladder, which emulsi˜es fats to allow for absorption. Pancreatic juices, containing digestive enzymes, help in breaking down carbohydrates, proteins, and fats into their basic forms. Carbohydrates are broken down into monosaccharides, proteins are broken down into amino acids, and fats are broken down into glycerol and fatty acid chains. The second portion of the small intestine is the jejunum, where the majority of absorption occurs after nutrients are broken down into their basic forms by the duodenum. The ˜nal section of the small intestine is the ileum, where the remainder of absorption occurs. Speci˜cally, the ileum is selective in the absorption of vitamin B12 and bile salts, but also absorbs vitamins, electrolytes, and other nutrients that were not absorbed in the jejunum. In order to maximize absorption, the entire small intestine contains myriads of microscopic folds which increase the surface area available for absorption. The intestinal wall is marked by two types of folds: plicae circulares and rugae. The rugae allow extra tissue for the small intestine to extend and contract when needed, while plicae circulares are ˜xed ridges located on the intestinal wall. The entire lining of the small intestine contains millions of villi which are critical for absorption. Furthermore, each villus contains microscopic projections called microvilli, which house brush border cells that contain many digestive enzymes (Figure 1.6). Together, the intestinal folds, villi, and microvilli dramatically increase the surface area of the small intestine for maximal digestion and absorption of nutrients. Villi also contain capillary beds, where absorbed nutrients pass through to the bloodstream where they are carried to the liver, via the hepatic portal vein, for ˜ltering, pro- cessing, and distribution to the rest of the body (Figure 1.6). After food has been passed through the small intestine, the remaining undigested food is passed into the large intestine via the ileocecal valve. The large intestine, also known as the colon, is a mus- cular tube that is typically about 1.5 meters (5 feet) long in the average adult. It borders around the small intestine and consists of three main parts: the cecum, the colon, and the rectum. The cecum is a small pouch where food is ˜rst received from the small intestine that serves as a passageway to the colon. The colon is further divided into four sections: the ascending colon, transverse colon, descending colon, and sigmoid colon (Figure 1.7). The ascending colon extends from the cecum straight up to the lower border of the liver. The transverse colon then extends from the lower border of the liver across to the border of the spleen. The descending colon then turns downward until it meets the S-shaped sigmoid colon, which connects to the rectum. The two main functions of the colon are absorption of remaining water and electrolytes from the material passing through, and compression of the remaining food contents into a bolus for easier Major Components of the Gastrointestinal System and Their Role in Digestion 5

Villi

Microvilli

Blood vessels in folds of intestines

Brush border cells Capillaries

FIGURE 1.6 The small intestine is comprised of intestinal folds, villi, and microvilli, which allow for a large surface area to facilitate digestion and absorption. Capillaries assist in absorbing nutrients into the bloodstream to be distributed throughout the body. (From Purves, W. K., D. Sadava, G. H. Orians, H. C. Heller. 1998. Life: The science of biology (4th ed.). Sinauer Associates [www.sinauer.com] and W.H. Freeman [www.whfreeman. com], http://www.emc.maricopa.edu/faculty/farabee/biobk/biobookdigest.html, Gordonsville, VA.) excretion from the body. The rectum is where stool are stored until they are excreted from the body through the anus. The excretion of stool is regulated by the anal sphincter, which includes the inter- nal sphincter and external sphincter. The internal sphincter is an involuntary smooth muscle, which relaxes when it senses pressure in the rectum to allow for the passage of stool, and the external sphincter is a voluntary skeletal muscle that allows for voluntary contraction and relaxation of the anus in order to have conscious control of the excretion of waste from the body (Figure 1.8). Though not directly part of the digestive tract, accessory organs including the pancreas, liver, and gallbladder are important components of the GI system that assist in the process of digestion (Figure 1.9). The pancreas is an elongated gland, located behind the stomach, which directly con- nects to the duodenum via the pancreatic duct. The pancreas has both endocrine and exocrine func- tion. The endocrine function aids in the regulation of blood sugar through the production of insulin, but is not involved in digestion. The exocrine function, on the other hand, includes the synthesis of digestive juices that are secreted through the pancreatic duct into the small intestine. Speci˜cally,

Transverse colon

Descending colon

Ascending colon Appendix Sigmoid colon Rectum

FIGURE 1.7 The colon is divided into four main sections: the ascending colon, transverse colon, descending colon, and sigmoid colon. The colon acts to absorb water and electrolytes, and compresses digestive content into stool before being excreted from the body. (From MedlinePlus: http://medlineplus.gov/, http://www.nlm. nih.gov/medlineplus/ency/images/ency/fullsize/19220.jpg) 6 Gastrointestinal and Liver Disease Nutrition Desk Reference

Rectum

Internal anal sphincter

External anal sphincter

Anus

FIGURE 1.8 The rectum is a storage area for stool until it is excreted from the body through regulation by the internal and external anal sphincters. (From http://scienceblogs.com/neurotopia/anal%20sphincters.png) these juices contain sodium bicarbonate, amylase, lipase, and two major proteases: trypsin and chy- motrypsin. Sodium bicarbonate serves to neutralize acidic material from the stomach to keep the intestinal environment at a neutral pH. The other digestive enzymes break down food into simpler compounds so that they can be absorbed. Amylase breaks down carbohydrates, lipase breaks down fats, and proteases break down proteins. The liver is the largest gland in the body, located in the right upper quadrant of the abdomen just below the diaphragm, and performs many vital functions in the human body. Its secretory and excretory functions are most related to the process of digestion, particularly with respect to the syn- thesis and secretion of bile. Once bile is synthesized in the liver, it is then carried to the gallbladder

Biliary system

Right hepatic duct Left hepatic duct

Pancreas Liver

Stomach

Gallbladder

Cystic duct Common hepatic duct

Common bile duct Pancreatic duct

Duodenum

FIGURE 1.9 Accessories of the digestive tract, including the pancreas, liver, and gallbladder, assist in the process of digestion. (From http://www.biologycorner.com/anatomy/digestive/notes_digestive.html) Major Components of the Gastrointestinal System and Their Role in Digestion 7 where it is stored. The gallbladder is a pear-shaped sac, located under the liver, which receives bile from the liver and concentrates and stores it until being released into the small intestine via the com- mon bile duct. Bile is important in digestion because it emulsi˜es fats, making them susceptible to enzymatic breakdown.

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36. Whorwell, P. J. et al. 2006. Ef�cacy of an encapsulated probiotic Bi�dobacterium infantis 35624 in women with irritable bowel syndrome. Am J Gastroenterol 101 (7): 1581–90.

37. Gawronska, A. et al. 2007. A randomized double-blind placebo-controlled trial of Lactobacillus GG for abdominal pain disorders in children. Aliment Pharmacol Ther 25 (2): 177–84.

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47. McFarland, L. V. 2006. Meta-analysis of probiotics for the prevention of antibiotic associated diarrhea and the treatment of Clostridium dif�cile disease. Am J Gastroenterol 101 (4): 812–22.

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5. Messing, B., P. Crenn, P. Beau et al. 1999. Long-term survival and parenteral nutrition dependence in adult patients with the short bowel syndrome. Gastroenterology 117 (5): 1043–50.

6. Wilmore, D. W. 2003. Indications for speci�c therapy in the rehabilitation of patients with the shortbowel syndrome. Best Practice & Research in Clinical Gastroenterology 17 (6): 895–906.

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19. Buchman, A. L., J. Scolapio, and J. Fryer. 2003. AGA technical review on short bowel syndrome and intestinal transplantation. Gastroenterology 124:1111–34

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32. Nightingale, J. M., J. E. Lennard-Jones, D. J. Gertner et al. 1992. Colonic preservation reduces need for parenteral therapy, increases incidence of renal stones, but does not change high prevalence of gall stones in patients with a short bowel. Gut 33 (11): 1493–97.

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52. Remington, M., J. R. Malagelada, A. Zinsmeister, and C. R. Fleming. 1983. Abnormalities in gastrointestinal motor activity in patients with short bowels: Effect of a synthetic opiate. Gastroenterology 85 (3): 629–36.

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58. Sagor, G. R., M. A. Ghatei, D. J. O’Shaughnessy et al. 1985. In�uence of somatostatin and bombesin on plasma enteroglucagon and cell proliferation after intestinal resection in the rat. Gut 26 (1): 89–94.

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67. Wilmore, D. W., J. M. Lacey, R. P. Soultananis et al. 1997. Factors predicting a successful outcome after pharmacologic bowel compensation. Annals of Surgery 226:288–92.

68. Ellegarrd, L., I. Bosaeus, S. Nordgren, and B. A. Bengtsson. 1997. Lowdose recombinant human growth hormone increase body weight and lean body mass in patients with short bowel syndrome. Annals of Surgery 225:88–96.

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70. Scolapio, J. S. 1999. Effect of growth hormone, glutamine, and diet on body composition in short bowel syndrome: A randomized, controlled study. Journal of Parenteral and Enteral Nutrition 23:309–12.

71. Szkudlarek, J., P. B. Jeppesen, and P. B. Mortensen. 2000. Effect of high dose growth hormone with glutamine and no change in diet on intestinal absorption in short bowel patients: A randomised, double blind, crossover, placebo-controlled study. Gut 47:199–205.

72. Byrne, T. A., S. Cox, M. Karimbakas et al. 2002. Bowel rehabilitation: An alternative to long-term parenteral nutrition and intestinal transplantation for some patients with short bowel syndrome. Transplant Proceedings 34:887–90.

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74. Seguy, D., V. Kouroche, K. Nathalie et al. 2003. Low-dose growth hormone in adult home parenteral nutrition dependent short bowel syndrome patients: A positive study. Gastroenterology 124 (2): 293–302.

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79. Guan, X., B. Stoll, X. Lu et al. 2003. GLP-2-mediated up-regulation of intestinal blood �ow and glucose uptake is nitric oxide-dependent in TPN-fed piglets 1. Gastroenterology 125:136–47.

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88. Bianchi, A. 1984. Intestinal lengthening: An experimental and clinical review. Journal of the Royal Society of Medicine 77 (3): 35–41.

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90. Kim, H. B., D. Fauza, J. Garza et al. 2003. Serial transverse enteroplasty (STEP): A novel bowel lengthening procedure. Journal of Pediatric Surgery 38 (3): 425–29.

91. Abu-Elmagd, K. M., G. Costa, G. J. Bond et al. 2009. Five hundred intestinal and multivisceral transplantations at a single center: Major advances with new challenges. Annals of Surgery 250 (4): 567–81. 5 Chapter 5: Celiac Disease

Abdo, A., J. Meddings, and M. Swain. 2004. Liver abnormalities in celiac disease. Clin Gastroenterol Hepatol 2:107–12.

Askling, J., M. Linet, G. Gridley et al. 2002. Cancer incidence in a population-based cohort of individuals hospitalized with celiac disease or dermatitis herpetiformis. Gastroenterology 123:1428–35.

Barton, S. H., D. G. Kelly, and J. A. Murray. 2007. Nutritional de�ciencies in celiac disease. Gastroenterol Clin N Am 36 (1): 93–108.

Bingley, P. J., A. J. Williams, A. J. Norcross et al. 2004. Undiagnosed coeliac disease at age seven: Population based prospective birth cohort study. BMJ 328:322–23.

Bonamico, M., P. Mariani, E. Thanasi et al. 2004. Patchy villous atrophy of the duodenum in childhood celiac disease. J Pediatr Gastroenterol Nutr 38:204–7.

Catassi, C., I. M. Rätsch, L. Gandol� et al. 1999. Why is coeliac disease endemic in the people of the Sahara? Lancet 354:647–48.

Chin, R. L., H. W. Sander, T. H. Brannagan et al. 2003. Celiac neuropathy. Neurol 60:1581–85.

Ciacci, C., M. Cirillo, G. Auriemma et al. 1996. Celiac disease and pregnancy outcome. Am J Gastroenterol 91:718–22.

Collin, P., K. Kaukinen, M. Valimaki, and J. Salmi. 2002. Endocrinological disorders and celiac disease. Endocr Rev 23:464–83.

Culliford, A., J. Daly, B. Diamond et al. 2005. The value of wireless capsule endoscopy in patients with complicated celiac disease. Gastrointest Endosc 62:55–61. insufficiency disease Irritable bowel syndrome N Lactose intolerance Eosinophilic gastroenteritis Autoimmune enteropathy Microscopic colitis No response Bacterial overgrowth Intestinal lymphoma Tropical sprue Small bowel stricture True refractory sprue

FIGURE 5.7 Nonresponders to gluten-free diet. J Gastroenterol Dieterich, W., T. Ehnis, M. Bauer et al. 1997. Identi�cation of tissue transglutaminase as the autoantigen of celiac disease. Nat Med 3:797–801.

Farrell, R. J., and C. P. Kelly. 2002. Celiac sprue. N Engl J Med 346:180–88.

Fasano, A., and C. Catassi. 2001. Current approaches to diagnosis and treatment of celiac disease: An evolving spectrum. Gastroenterology 120:636–51.

Fasano, A., I. Berti, T. Gerarduzzi et al. 2003. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: A large multicenter study. Arch Intern Med 163:286–92.

Fine, K. D. 1996. The prevalence of occult gastrointestinal bleeding in celiac sprue. N Eng J Med 334:1163–67.

Gasbarrini, A., E. Sanz Torre et al. 2000. Recurrent spontaneous abortion and intrauterine fetal growth retardation as symptoms of celiac disease. Lancet 256:399–400.

Gomez, J. C., G. S. Selvaggio, M. Viola et al. 2001. Prevalence of celiac disease in Argentina: Screening of an adult population in the La Plata area. Am J Gastroenterol 96:2700–4.

Greco, L., R. Romino, I. Coto et al. 2002. The �rst large population-based twin study of celiac disease. Gut 50:624–28.

Green, P. H., E. Shane, H. Rotterdam et al. 2000. Signi�cance of unsuspected celiac disease detected at endoscopy. Gastroint Endosc 51:60–65.

Green, P. H., S. N. Stavropoulos, S. G. Panagi et al. 2001. Characteristics of adult celiac disease in the USA: Results of a national survey. Am J Gastroenterol 96:126–31.

Green, P. H., and B. Jabri. 2003. Celiac disease. Lancet 362:383–91.

Green, P. H., and B. Jabri. 2006. Celiac disease. Annu Rev Med 57:207–21.

Green, P. H., and C. Cellier. 2007. Celiac disease. N Engl J Med 357:1731–43. Hadjivassiliou, M., A. Gibson, G. A. Davies-Jones et al. 1996. Does cryptic gluten sensitivity play a part in neurological illness? Lancet 347:369–71.

Haines, M. L., R. P. Anderson, and P. R. Gibson. 2008. Systematic review: The evidence base for long-term management of celiac disease. Aliment Pharmacol Ther 28 (9): 1042–66.

Hovell, C. J., J. A. Collett, G. Vautier et al. 2001. High prevalence of celiac disease in a population-based study from Western Australia: A case for screening? Med J Aust 175:247–50.

Howdle, P. D., P. K. Jalal, G. K. Holmes, and R. S. Houlston. 2003. Primary small-bowel malignancy in the UK and its association with coeliac disease. QJM 96:345–53.

Karpati, S. 2004. Dermatitis herpetiformis: Close to unraveling a disease. J Dermatol Sci 34:83–90.

Kaukinen, K., L. Halme, P. Collin et al. 2002. Celiac disease in patients with severe liver disease: gluten-free diet may reverse hepatic failure. Gastroenterology 122:881–88.

Lee, S. K., W. Lo, L. Memeo et al. 2003. Duodenal histology in patients with celiac disease after treatment with a gluten-free diet. Gastrointest Endosc 57:187–91.

Lee, S. K., and P. H. Green. 2005. Endoscopy in celiac disease. Curr Opin Gastroenterol 21:589–94.

Logan, R. F. 1996. Screening for celiac disease: Has the time come for mass screening? Acta Paediatrica Suppl 412:15–19.

Mäki, M., K. Mustalahti, J. Kokkonen et al. 2003. Prevalence of celiac disease among children in Finland. N Engl J Med 348:2517–24.

Meyer, D., S. Stavropoulos, B. Diamond et al. 2001. Osteoporosis in a North American adult population with celiac disease. Am J Gastroenterol 96:112–19.

Moreno, M. L., H. Vazquez, R. Mazure et al. 2004. Strati�cation of bone fracture risk in patients with celiac disease. Clin Gastroenterol Hepatol 2:127–34.

Norris, J. M., K. Barriga, E. J. Hoffenberg et al. 2005. Risk of celiac disease autoimmunity and timing of gluten introduction in the diet of infants at increased risk of disease. JAMA 293:2343–51.

Oxentenko, A. S., S. W. Grisolano, J. A. Murray et al. 2002. The insensitivity of endoscopic markers in celiac disease. Am J Gastroenterol 97:933–38.

Peräaho, M., K. Kaukinen, K. Mustalahti et al. 2004. Effect of an oats-containing gluten-free diet on symptoms and quality of life in coeliac disease: A randomized study. Scand J Gastroenterol 39:27–31.

Persson, L. A., A. Ivarsson, and O. Hernell. 2002. Breastfeeding protects against celiac disease in childhood: Epidemiological evidence. Adv Exp Med Biol 503:115–23.

Rampertab, S. D., K. A. Forde, and P. H. Green. 2003. Small bowel neoplasia in coeliac disease. Gut 52:1211–14.

Rampertab, S. D., N. Pooran, P. Brar et al. 2006. Trends in the presentation of celiac disease. Am J Med 119 (4): e9–e14.

Rampertab, S. D. and P. H. Green. 2011. Celiac disease. In Integrative Gastroenterology, ed. G. Mullin, Ch. 40. New York, NY: Oxford University Press.

Rea, F., C. Polito, A. Marotta et al. 1996. Restoration of body composition in celiac children after one year of gluten-free diet. J Pediatr Gastroenterol Nutr 23 (4): 408–12.

Reinken, L., and H. Zieglauer. 1978. Vitamin B6 absorption in children with acute celiac disease and in control subjects. J Nutr 108 (10): 1562–65.

Reunala, T. L. 2001. Dermatitis herpetiformis. Clin Dermatol 19:728–36.

Rostom, A., C. Dubé, A. Cranney et al. 2005. The diagnostic accuracy of serologic tests for celiac disease: A systematic review. Gastroenterology 128 (suppl 1): S38–S46.

Sedlack, R. E., T. C. Smyrk, A. J. Czaja et al. 2002. Celiac disease-associated autoimmune cholangitis. Am J Gastroenterol 97:3196–98.

Scott, E. M., I. Gaywood, and B. B. Scott. 2000. Guidelines for osteoporosis in celiac disease and in�ammatory bowel disease. British Society of Gastroenterology. Gut 46 (suppl 1): i1–8.

Shah, V. H., H. Rotterdam, D. P. Kotler et al. 2000. All that scallops is not celiac disease. Gastrointest Endosc 51 (6): 717–20.

Shahbazkhani, B., R. Malekzadeh, M. Sotoudeh et al. 2003. High prevalence of celiac disease in apparently healthy Iranian blood donors. Eur J Gastroenterol Hepatol 15:475–78.

Smedby, K. E., M. Akerman, H. Hildebrand et al. 2005. Malignant lymphomas in coeliac disease: Evidence of increased risks for lymphoma types other than enteropathy-type T cell lymphoma. Gut 54:54–59.

Sood, A., V. Midha, N. Sood, and V. Malhotra. 2003. Adult celiac disease in northern India. Indian J Gastroenterol 22:124–26.

Tata, L. J., T. R. Card, R. F. Logan et al. 2005. Fertility and pregnancy-related events in women with celiac disease: A population based cohort study. Gastroenterology 128:849–55.

Tatar, G., R. Elsurer, H. Simsek et al. 2004. Screening of tissue transglutaminase antibody in healthy blood donors for celiac disease screening in the Turkish population. Dig Dis Sci 49:1479–84.

Thompson, T. 2003. Oats and the gluten-free diet. J Am Diet Assoc 103:376–79.

Tommasini, A., T. Not, V. Kiren et al. 2004. Mass screening for coeliac disease using antihuman transglutaminase antibody assay. Arch Dis Child 89:512–15.

Valdimarsson, T., O. Lofman, G. Toss et al. 1996. Reversal of osteopenia with diet in adult celiac disease. Gut 38:322–27.

Volta, U, L. Rodrigo, A. Granite et al. 2002. Celiac disease in autoimmune cholestatic liver disorders. Am J Gastroenterol 97:2609–13.

West, J., R. F. Logan, P. G. Hill et al. 2003. Seroprevalence, correlates, and characteristics of undetected coeliac disease in England. Gut 52:960–65. 6 Chapter 6: Food Allergy and Food Intolerance

1. Bischoff, S., and S. E. Crowe. 2005. Gastrointestinal food allergy: New insights into pathophysiology and clinical perspectives. Gastroenterol 128 (4): 1089–113.

2. Chafen, J. J. S., S. J. Newberry, M. A. Riedl et al. 2010. Diagnosing and managing common food allergies: A systematic review. JAMA 303 (18): 1848–56.

3. Sampson, H. A. 2004. Update on food allergy. J Allergy Clin Immunol 113 (5): 805–19; quiz 820.

4. Sicherer, S. H., A. Muñoz-Furlong, and H. A. Sampson. 2003. Prevalence of peanut and tree nut allergy in the United States determined by means of a random digit dial telephone survey: A 5-year follow-up study. J Allergy Clin Immunol 112 (6): 1203–7.

5. Jansen, J. J., A. F. Kardinaal, G. Huijbers et al. 1994. Prevalence of food allergy and intolerance in the adult Dutch population. J Allergy Clin Immunol 93 (2): 446–56.

6. Bock, S. A., and F. M. Atkins. 1990. Patterns of food hypersensitivity during sixteen years of doubleblind, placebo-controlled food challenges. J Pediatr 117 (4): 561–67.

7. Bock, S. A. 1987. Prospective appraisal of complaints of adverse reactions to foods in children during the �rst 3 years of life. Pediatrics 79 (5): 683–88.

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Eastell, R., E. R. Dickson, S. F. Hodgson et al. Aug 1991. Rates of vertebral bone loss before and after liver transplantation in women with primary biliary cirrhosis. Hepatology 14 (2): 296–300.

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Harrison, J., J. McKiernan, and J. M. Neuberger. 1997. A prospective study on the effect of recipient nutritional status on outcome in liver transplantation. Transpl Int 10 (5): 369–74.

Hasse, J. 1996. Liver Transplantation: The bene�ts of nutrition therapy in the liver transplant patient. In Recent developments in transplantation medicine: Volume III. Liver transplantation, ed. G. Klintmalm, 81–100. Glenview, IL: Physicians and Scientists Publishing Co.

Hasse, J. M., L. S. Blue, and G. U. Liepa. Nov–Dec 1995. Early enteral nutrition support in patients undergoing liver transplantation. JPEN J Parenter Enteral Nutr 19 (6): 437–43.

Hasse, J., S. Strong, M. A. Gorman, and G. Liepa. Jul–Aug 1993. Subjective global assessment: Alternative nutrition-assessment technique for liver-transplant candidates. Nutrition 9 (4): 339–43.

Hanouneh, I. A., A. E. Feldstein, A. J. McCullough et al. Sep 2008. The signi�cance of metabolic syndrome in the setting of recurrent hepatitis C after liver transplantation. Liver Transpl 14 (9): 1287–93.

Jiménez, F. J., J. C. Montejo González, and R. Nuñez Ruiz. Jun 2005. Arti�cial nutrition in liver failure. Nutr Hosp 20 (Suppl 2): 22–24 (Spanish).

Murray, K. F., and R. L. Carithers, Jr. 2005 AASLD practice guidelines: Evaluation of the patient for liver transplantation. Hepatology 41 (6): 1407–32.

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Stegall, M. D., G. Everson, G. Schroter et al. Nov 1995. Metabolic complications after liver transplantation. Diabetes, hypercholesterolemia, hypertension, and obesity. Transplantation 60 (9): 1057–60.

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Wallia, A., N. D. Parikh, M. E. Molitch et al. Jan 2010. Post-transplant hyperglycemia is associated with increased risk of liver allograft rejection. Transplantation 89 (2): 222–26.

Wicks, C., S. Somasundaram, and I. Bjarnason. Sep 1994. Comparison of enteral feeding and total parenteral nutrition after liver transplantation. Lancet 344 (8926): 837–40.

Zamboni, F., A. Franchello, E. David et al. Feb 2001. Effect of macrovesicular steatosis and other donor and recipient characteristics on the outcome of liver transplantation. Clin Transplant 15 (1): 53–57. 12 Chapter 12: Nutritional Considerations in Acute and Chronic Pancreatitis

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Ammori, B. J. 2002. Gut barrier dysfunction in patients with acute pancreatitis. J Hepatobiliary Pancreat Surg 9:411–12.

Andriulli, A., E. Botteri, P. L. Almasio, I. Vantini, G. Uomo, and P. Maisonneuve. 2010. Smoking as a cofactor for causation of chronic pancreatitis: A meta-analysis. Pancreas 39 (8): 1205–10.

Aoun, E., A. Slivka, D. J. Papachristou, F. C. Gleeson, D. C. Whitcomb, and G. I. Papachristou. 2007. Rapid evolution from the �rst episode of acute pancreatitis to chronic pancreatitis in human subjects. JOP 8 (5): 573–78.

Atkinson, S., E. Sieffert, and D. Bihari. 1998. A prospective, randomized, double-blind, controlled clinical trial of enteral immunonutrition in the critically ill. Crit Care Med 26:1164–72.

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Bollen, T. L., H. C. van Santvoort, M. G. Besselink, M. S. van Leeuwen, K. D. Horvath, P. C. Freeny, and H. G. Gooszen. 2008. The Atlanta Classi�cation of acute pancreatitis revisited. Br J Surg 95:6–21.

Bradley 3rd, E. L. 1993. A clinically based classi�cation system for acute pancreatitis. Summary of the International Symposium on Acute Pancreatitis, Atlanta, Ga, September 11 through 13, 1992. Arch Surg 128:586–90.

Brown, A., J. D. Baillargeon, M. D. Hughes, and P. A. Banks. 2002. Can �uid resuscitation prevent pancreatic necrosis in severe acute pancreatitis? Pancreatol 2 (2): 104–7.

Bruno, M. J. 2001. Current insights into the pathogenesis of acute and chronic pancreatitis. Scand J Gastroenterol Suppl 234:103–108.

DiMagno, M. J., E. J. Wamsterker, and A. T. DeBenedet. 2009. Advances in managing acute pancreatitis. F1000 Med Rep 1:59.

Eatock, F. C., P. Chong, N. Menezes, L. Murray, C. J. McKay, C. R. Carter, and C. W. Imrie. 2005. A randomized study of early nasogastric versus nasojejunal feeding in severe acute pancreatitis. Am J Gastroenterol 100 (2): 432–39.

Eckerwall, G., H. Olin, B. Andersson, and R. Andersson. 2006. Fluid resuscitation and nutritional support during severe acute pancreatitis in the past: What have we learned and how can we do better? Clin Nutr 25 (3): 497–504.

Ellis, M. P., J. J. French, and R. M. Charnley. 2009. Acute pancreatitis and the in�uence of socioeconomic deprivation. Br J Surg 96 (1): 74–80.

Fuentes-Orozco, C., G. Cervantes-Guevara, I. Muciño-Hernández, A. López-Ortega, G. Ambriz-González, J. L. Gutiérrez-de-la-Rosa, E. Gómez-Herrera, J. M. Hermosillo-Sandoval, and A. González-Ojeda. 2008. L-alanyl-L-glutamine-supplemented parenteral nutrition decreases infectious morbidity rate in patients with severe acute pancreatitis. JPEN J Parenter Enteral Nutr 32 (4): 403–11.

Gardner, T. B., S. S. Vege, R. K. Pearson, and S. T. Chari. 2008. Fluid resuscitation in acute pancreatitis. Clin Gastroenterol Hepatol 6:1070–76.

Gianotti, L., R. Meier, D. N. Lobo, C. Bassi, C. H. Dejong, J. Ockenga, O. Irtun, J. MacFie; ESPEN. 2009. ESPEN Guidelines on Parenteral Nutrition: Pancreas. Clin Nutr 28 (4): 428–35.

Girish, B. N., G. Rajesh, K. Vaidyanathan, and V. Balakrishnan. 2009. Zinc status in chronic pancreatitis and its relationship with exocrine and endocrine insuf�ciency. JOP 10:651–56.

Havala, T., E. Shronts, and F. Cerra. 1989. Nutritional support in acute pancreatitis. Gastroenterol Clin North Am 18 (3): 525–42.

Hebuterne, X., P. Hastier, J. L. Peroux, N. Zeboudj, J. P. Delmont, and P. Rampal. Resting energy expenditure in patients with alcoholic chronic pancreatitis. Dig Dis Sci 41:533–39.

Jabbar, A., W. K. Chang, G. W. Dryden, and S. A. McClave. 2003. Gut immunology and the differential response to feeding and starvation. Nutr Clin Pract 18:461–82.

Karakan, T., M. Ergun, I. Dogan, M. Cindoruk, and S. Unal. 2007. Comparison of early enteral nutrition in severe acute pancreatitiswith prebiotic �ber supplementation versus standard enteral solution: A prospective randomized double blind-study. World J Gastroenterol 13:2733–37.

Karsenti, D., P. Bourlier, E. Dorval, B. Scotto, B. Giraudeau, R. Lanotte, L. de Calan, J. Mesnyr, F. Lagarrigue, and E. Metman. 2002. Morbidity and mortality of acute pancreatitis. Prospective study in a French university hospital. Press Med 31:727–34.

Lati�, R., J. K. McIntosh, and S. J. Dudrick. 1991. Nutritional Management of acute and chronic pancreatitis. Surg Clin North Am 71:579–95.

Lévy, P., P. Mathurin, A. Roqueplo, B. Rueff, and P. Bernades. 1995. A multidimensional case-control study of dietary, alcohol, and tobacco habits in alcoholic men with chronic pancreatitis. Pancreas 103:231–38.

Lewis, S. J., H. K. Andersen, and S. Thomas. 2009. Early enteral nutrition within 24h of intestinal surgery versus later commencement of feeding: A systematic review and meta-analysis. J Gastrointest Surg 13:569–75.

Lewis, S. J., M. Egger, P. A. Sylvester, and S. Thomas. 2001. Early enteral feeding versus ‘nil by mouth’ after gastrointestinal surgery: Systematic review and meta-analysis of controlled trials. BMJ 323:773–76.

Makola, D., J. Krenitsky, and C. R. Parrish. 2007. Enteral feeding in acute and chronic pancreatitis. Gastrointest Endosc Clin N Am 17 (4): 747–64.

Marik, P. E., and G. P. Zaloga. 2001. Early enteral nutrition in acutely ill patients: A systematic review. Crit Care Med 29: 2264–70.

Marik, P. E., and G. P. Zaloga. 2004. Meta-analysis of parenteral nutrition versus enteral nutrition in patients with acute pancreatitis. BMJ 328:1407–13.

McClave, S. A., W. K. Chang, R. Dhaliwal, and D. K. Heyland. 2006. Nutrition support in acute pancreatitis: A systematic review of the literature. JPEN J Parenter Enteral Nutr 30:143–56.

McClave, S. A., H. Snider, N. Owens, and L. K. Sexton. 1997. Clinical nutrition in pancreatitis. Dig Dis Sci 42:2035–44.

Meier, R. F., and C. Beglinger. 2006. Nutrition in pancreatic disease. Best Pract Res Clin Gastroenterol 20:507–29.

Meier, R. F., and L. Sobotka. 2010. Basics in clinical nutrition: Support in acute and chronic pancreatitis. J Clin Nutr Metabol 5:58–62.

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Norman, J. G. 1999. New approaches to acute pancreatitis: Role of in�ammatory mediators. Dig 60 (1): 57–60.

O’Keefe, S. J., W. Foody, and S. Gill. 2003. Transnasal endoscopic placement of feeding tubes in the intensive care unit. JPEN J Parenter Enteral Nutr 27:349–54.

Olah, A., T. Belagyi, A. Issekutx, and G. Olgyai. 2005. Combination of early nasojejunal feeding with modern symbiotic therapy in treatment of severe acute pancreatitis (prospective, randomizsed, double blind study). Magy Seb 58:173–78.

Olah, A., and L. Romics. 2008. Early enteral nutrition in acute pancreatitis—bene�ts and limitations. Arch Surg 393:261–69.

Pearce, C. B., S. A. Sadek, A. M. Walters, P. M. Goggin, S. S. Somers, S. K. Toh, T. Johns, and H. D. Duncan. 2006. A double-blind, randomized, controlled trial to study the effects of an enteral feed supplemented with glutamine, arginine, and omega-3 fatty acid in predicted acute severe pancreatitis. JOP 7:361–71.

Petrov, M. S., V. A. Atduev, and V. E. Zagainov. 2008. Advanced enteral therapy in acute pancreatitis: Is there a room for immunonutrition? A meta-analysis. Int J Surg 6 (2): 119–24.

Petrov, M. S., M. I. Correia, and J. A. Windsor. 2008. Nasogastric tube feeding in predicted severe acute pancreatitis. A systematic review of the literature to determine safety and tolerance. JOP 9 (4): 440–48.

Petrov, M. S., B. P. Loveday, R. D. Pylypchuk, K. McIlroy, A. R. Phillips, and J. A. Windsor. 2009. Systematic review and meta-analysis of enteral nutrition formulations in acute pancreatitis. Br J Surg 96 (11): 1243–52.

Petrov, M. S., R. D. Pylypchuk, and A. F. Uchugina. 2009. A systematic review on the timing of arti�cial nutrition in acute pancreatitis. Br J of Nutr 101:787–93.

Petrov, M. S., and V. E. Zagainov. 2007. In�uence of enteral versus parenteral nutrition on blood glucose control in acute pancreatitis: A systematic review. Clin Nutr 26:514–23.

Powell, J. J., J. T. Murchison, K. C. H. Fearon, J. A. Ross, and A. K. Sieiwarden. 2000. Randomized controlled trial of the effect of early enteral nutrition on markers of the in�ammatory response in predicted severe acute pancreatitis. Br J Surgery 87:1375–81.

Ranson, J. H. C. 1982. Etiological and prognostic factors in human acute pancreatitis: A review. AM J Gastroenterol 77:633–38.

Schneider, A., and D. C. Whitcomb. 2002. Hereditary pancreatitis: A model for in�ammatory diseases of the pancreas. Best Pract Res Clin Gastroenterol 16:347–63.

Singh, S., S. Midha, N. Singh, Y. K. Joshi, and P. K. Garg. 2008. Dietary counseling versus dietary supplements for malnutrition in chronic pancreatitis: A randomized controlled trial. Clin Gastroenterol Hepatol 63:353–59.

Sitzmann, J. V., P. A. Steinborn, M. J. Zinner, and J. L. Cameron. 1989. Total parenteral nutrition and alternate energy substrates in treatment of severe acute pancreatitis. Surg Gynecol Obstet 168 (4): 311–17.

Sobotka, L. 1996. Acurte pancreatitis–pancreatic perfusion and �uid resuscitation in ICU. Nutr 12:844.

Thomson, A. 2008. The enteral vs parenteral nutrition debate revisited. J Parenter Enteral Nutr 32 (4): 474–81. Toyama, M. T., M. P. Lewis, A. M. Kusske, P. U. Reber, S. W. Ashley, and H. A. Reber. 1996. Ischaemiareperfusion mechanisms in acute pancreatitis. Scand J Gastroenterol Suppl 219:20–23.

Waljee, A. K., M. J. Dimagno, B. U. Wu, P. S. Schoenfeld, and D. L. Conwell. 2009. Systematic review: Pancreatic enzyme treatment of malabsorption associated with chronic pancreatitis. Aliment Pharmacol Ther 29:235–46.

Whitcomb, D. C. 2004. Mechanisms of disease: Advances in understanding the mechanisms leading to chronic pancreatitis. Nat Clin Pract Gastroenterol Hepatol 1:46–52.

Whitlock, T. L., K. Repas, A. Tignor, D. Conwell, V. Singh, P. A. Banks, and B. U. Wu. 2010. Early readmission in acute pancreatitis: Incidence and risk factors. Am J Gastroenterol 105:2492–7.

Whitlock, T.L., A. Tignor, E.M. Webster, K. Repas, D. Conwell, P.A. Banks, and B.U. Wu. 2011. A scoring system to predict readmission of patients with acute pancreatitis to the hospital within thirty days of discharge. Clin Gastroenterol Hepatol 9 (2): 175–80

Windsor, J. A., and H. Hammodat. 2000. Metabolic management of severe acute pancreatitis. World J Surg 24:664–72.

Winsler, M. C., C. Hall, N. J. M. London, and J. P. Neoptolemus. 1992. Relationship of diagnostic serum amylase to aetiology and prognosis in acute pancreatitis. Gut 33:982–86.

Wu, B.U., J. Hwang, T.Gardner, K. Repas, R. DeLee, S. Yu, P. Banks, and D. Conwell. 2010. Early resuscitation with lactated ringer’s reduces systemic in�ammation in acute pancreatitis: A multi-center randomizedcontrolled trial. Am J Gastroenterol 105 (S1): S70.

Yadav D., R.H. Hawes, R.E. Brand, M.A. Anderson, M.E. Money. P.A. Banks et al. 2009. Alcohol consumption, cigarette smoking, and the risk of recurrent acute and chronic pancreatitis. Arch Intern Med 169 (11): 1035–45. 13 Chapter 13: Nutrition in Irritable Bowel Syndrome

1. Whitehead, W. E., and D. A. Drossman. 2010. Validation of symptom-based diagnostic criteria for irritable bowel syndrome: A critical review. Am J Gastroenterol 105 (4): 814–20; quiz 813, 821.

2. Klooker, T. K. et al. 2010. The mast cell stabiliser ketotifen decreases visceral hypersensitivity and improves intestinal symptoms in patients with irritable bowel syndrome. Gut 59 (9): 1213–21.

3. Petitpierre, M., P. Gumowski, and J. P. Girard. 1985. Irritable bowel syndrome and hypersensitivity to food. Ann Allergy 54 (6): 538–40.

4. Shaw, A. D. et al. 1998. Dietary triggers in irritable bowel syndrome. Nutr Res Rev 11 (2): 279–309.

5. Jones, V. A. et al. 1982. Food intolerance: A major factor in the pathogenesis of irritable bowel syndrome. Lancet 2 (8308): 1115–17.

6. Shepherd, S. J. et al. 2008. Dietary triggers of abdominal symptoms in patients with irritable bowel syndrome: Randomized placebo-controlled evidence. Clin Gastroenterol Hepatol 6 (7): 765–71.

7. Simonato, B. et al. 2001. IgE binding to soluble and insoluble wheat �our proteins in atopic and nonatopic patients suffering from gastrointestinal symptoms after wheat ingestion. Clin Exp Allergy 31 (11): 1771–78.

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APPENDIX A

Common Predictive Energy Equations Harris-Benedict Equation (best for BMI between 18.5 and 24.9)

Males: 13.397 × weight (lbs.) + 4.799 × height (cm) − 5.677 × age (years) + 88.362

Females: 9.247 × weight (lbs.) + 3.098 × height (cm) − 4.33 × AGE + 477.593 Mifflin Equation (best for BMI between 25 and 40)

Males and Females: 9.99 × weight () + 6.25 × height (cm) − 4.92 × AGE + 166 × SEX − 161

Source: From Weiss, P. J., Am J Clin Nutr 88 (4): 959, 2008.

A

P P

E N

D

I X

B B o d y M a s s I n d e x T a b l e N o r m a l O v e r w e i g h t O b e s e E x t r e m e O b e s i t y B M I 1 9 2 0 2 1 2 2 2 3 2 4 2 5 2 6 2 7 2 8 2 9 3 0 3 1 3 2 3 3 3 4 3 5 3 6 3 7 3 8 3 9 4 0 4 1 4 2 4 3 4 4 4 5 4 6 4 7 4 8 4 9 5 0 5 1 5 2 5 3 H e i g h t ( i n c h e s ) B o d y W e i g h t ( p o u n d s ) 5 8 9 1 9 6 1 0 0 1 0 5 1 1 0 1 1 5 1 1 9 1 2 4 1 2 9 1 3 4 1 3 8 1 4 3 1 4 8 1 5 3 1 5 8 1 6 2 1 6 7 1 7 2 1 7 7 1 8 1 1 8 6 1 9 1 1 9 6 2 0 1 2 0 5 2 1 0 2 1 5 2 2 0 2 2 4 2 2 9 2 3 4 2 3 9 2 4 4 2 4 8 2 5 3 5 9 9 4 9 9 1 0 4 1 0 9 1 1 4 1 1 9 1 2 4 1 2 8 1 3 3 1 3 8 1 4 3 1 4 8 1 5 3 1 5 8 1 6 3 1 6 8 1 7 3 1 7 8 1 8 3 1 8 8 1 9 3 1 9 8 2 0 3 2 0 8 2 1 2 2 1 7 2 2 2 2 2 7 2 3 2 2 3 7 2 4 2 2 4 7 2 5 2 2 5 7 2 6 2 6 0 9 7 1 0 2 1 0 7 1 1 2 1 1 8 1 2 3 1 2 8 1 3 3 1 3 8 1 4 3 1 4 8 1 5 3 1 5 8 1 6 3 1 6 8 1 7 4 1 7 9 1 8 4 1 8 9 1 9 4 1 9 9 2 0 4 2 0 9 2 1 5 2 2 0 2 2 5 2 3 0 2 3 5 2 4 0 2 4 5 2 5 0 2 5 5 2 6 1 2 6 6 2 7 1 6 1 1 0 0 1 0 6 1 1 1 1 1 6 1 2 2 1 2 7 1 3 2 1 3 7 1 4 3 1 4 8 1 5 3 1 5 8 1 6 4 1 6 9 1 7 4 1 8 0 1 8 5 1 9 0 1 9 5 2 0 1 2 0 6 2 1 1 2 1 7 2 2 2 2 2 7 2 3 2 2 3 8 2 4 3 2 4 8 2 5 4 2 5 9 2 6 4 2 6 9 2 7 5 2 8 0 6 2 1 0 4 1 0 9 1 1 5 1 2 0 1 2 6 1 3 1 1 3 6 1 4 2 1 4 7 1 5 3 1 5 8 1 6 4 1 6 9 1 7 5 1 8 0 1 8 6 1 9 1 1 9 6 2 0 2 2 0 7 2 1 3 2 1 8 2 2 4 2 2 9 2 3 5 2 4 0 2 4 6 2 5 1 2 5 6 2 6 2 2 6 7 2 7 3 2 7 8 2 8 4 2 8 9 6 3 1 0 7 1 1 3 1 1 8 1 2 4 1 3 0 1 3 5 1 4 1 1 4 6 1 5 2 1 5 8 1 6 3 1 6 9 1 7 5 1 8 0 1 8 6 1 9 1 1 9 7 2 0 3 2 0 8 2 1 4 2 2 0 2 2 5 2 3 1 2 3 7 2 4 2 2 4 8 2 5 4 2 5 9 2 6 5 2 7 0 2 7 8 2 8 2 2 8 7 2 9 3 2 9 9 6 4 1 1 0 1 1 6 1 2 2 1 2 8 1 3 4 1 4 0 1 4 5 1 5 1 1 5 7 1 6 3 1 6 9 1 7 4 1 8 0 1 8 6 1 9 2 1 9 7 2 0 4 2 0 9 2 1 5 2 2 1 2 2 7 2 3 2 2 3 8 2 4 4 2 5 0 2 5 6 2 6 2 2 6 7 2 7 3 2 7 9 2 8 5 2 9 1 2 9 6 3 0 2 3 0 8 6 5 1 1 4 1 2 0 1 2 6 1 3 2 1 3 8 1 4 4 1 5 0 1 5 6 1 6 2 1 6 8 1 7 4 1 8 0 1 8 6 1 9 2 1 9 8 2 0 4 2 1 0 2 1 6 2 2 2 2 2 8 2 3 4 2 4 0 2 4 6 2 5 2 2 5 8 2 6 4 2 7 0 2 7 6 2 8 2 2 8 8 2 9 4 3 0 0 3 0 6 3 1 2 3 1 8 6 6 1 1 8 1 2 4 1 3 0 1 3 6 1 4 2 1 4 8 1 5 5 1 6 1 1 6 7 1 7 3 1 7 9 1 8 6 1 9 2 1 9 8 2 0 4 2 1 0 2 1 6 2 2 3 2 2 9 2 3 5 2 4 1 2 4 7 2 5 3 2 6 0 2 6 6 2 7 2 2 7 8 2 8 4 2 9 1 2 9 7 3 0 3 3 0 9 3 1 5 3 2 2 3 2 8 6 7 1 2 1 1 2 7 1 3 4 1 4 0 1 4 6 1 5 3 1 5 9 1 6 6 1 7 2 1 7 8 1 8 5 1 9 1 1 9 8 2 0 4 2 1 1 2 1 7 2 2 3 2 3 0 2 3 6 2 4 2 2 4 9 2 5 5 2 6 1 2 6 8 2 7 4 2 8 0 2 8 7 2 9 3 2 9 9 3 0 6 3 1 2 3 1 9 3 2 5 3 3 1 3 3 8 3 4 4 6 8 1 2 5 1 3 1 1 3 8 1 4 4 1 5 1 1 5 8 1 6 4 1 7 1 1 7 7 1 8 4 1 9 0 1 9 7 2 0 3 2 1 0 2 1 6 2 2 3 2 3 0 2 3 6 2 4 3 2 4 9 2 5 6 2 6 2 2 6 9 2 7 6 2 8 2 2 8 9 2 9 5 3 0 2 3 0 8 3 1 5 3 2 2 3 2 8 3 3 5 3 4 1 3 4 8 3 5 4 6 9 1 2 8 1 3 5 1 4 2 1 4 9 1 5 5 1 6 2 1 6 9 1 7 6 1 8 2 1 8 9 1 9 6 2 0 3 2 0 9 2 1 6 2 2 3 2 3 0 2 3 6 2 4 3 2 5 0 2 5 7 2 6 3 2 7 0 2 7 7 2 8 4 2 9 1 2 9 7 3 0 4 3 1 1 3 1 8 3 2 4 3 3 1 3 3 8 3 4 5 3 5 1 3 5 8 3 6 5 7 0 1 3 2 1 3 9 1 4 6 1 5 3 1 6 0 1 6 7 1 7 4 1 8 1 1 8 8 1 9 5 2 0 2 2 0 9 2 1 6 2 2 2 2 2 9 2 3 6 2 4 3 2 5 0 2 5 7 2 6 4 2 7 1 2 7 8 2 8 5 2 9 2 2 9 9 3 0 6 3 1 3 3 2 0 3 2 7 3 3 4 3 4 1 3 4 8 3 5 5 3 6 2 3 6 9 3 7 6 7 1 1 3 6 1 4 3 1 5 0 1 5 7 1 6 5 1 7 2 1 7 9 1 8 6 1 9 3 2 0 0 2 0 8 2 1 5 2 2 2 2 2 9 2 3 6 2 4 3 2 5 0 2 5 7 2 6 5 2 7 2 2 7 9 2 8 6 2 9 3 3 0 1 3 0 8 3 1 5 3 2 2 3 2 9 3 3 8 3 4 3 3 5 1 3 5 8 3 6 5 3 7 2 3 7 9 3 8 6 7 2 1 4 0 1 4 7 1 5 4 1 6 2 1 6 9 1 7 7 1 8 4 1 9 1 1 9 9 2 0 6 2 1 3 2 2 1 2 2 8 2 3 5 2 4 2 2 5 0 2 5 8 2 6 5 2 7 2 2 7 9 2 8 7 2 9 4 3 0 2 3 0 9 3 1 6 3 2 4 3 3 1 3 3 8 3 4 6 3 5 3 3 6 1 3 6 8 3 7 5 3 8 3 3 9 0 3 9 7 7 3 1 4 4 1 5 1 1 5 9 1 6 6 1 7 4 1 8 2 1 8 9 1 9 7 2 0 4 2 1 2 2 1 9 2 2 7 2 3 5 2 4 2 2 5 0 2 5 7 2 6 5 2 7 2 2 8 0 2 8 8 2 9 5 3 0 2 3 1 0 3 1 8 3 2 5 3 3 3 3 4 0 3 4 8 3 5 5 3 6 3 3 7 1 3 7 8 3 8 6 3 9 3 4 0 1 4 0 8 7 4 1 4 8 1 5 5 1 6 3 1 7 1 1 7 9 1 8 6 1 9 4 2 0 2 2 1 0 2 1 8 2 2 5 2 3 3 2 4 1 2 4 9 2 5 6 2 6 4 2 7 2 2 8 0 2 8 7 2 9 5 3 0 3 3 1 1 3 1 9 3 2 6 3 3 4 3 4 2 3 5 0 3 5 8 3 6 5 3 7 3 3 8 1 3 8 9 3 9 6 4 0 4 4 1 2 4 2 0 7 5 1 5 2 1 6 0 1 6 8 1 7 6 1 8 4 1 9 2 2 0 0 2 0 8 2 1 6 2 2 4 2 3 2 2 4 0 2 4 8 2 5 6 2 6 4 2 7 2 2 7 9 2 8 7 2 9 5 3 0 3 3 1 1 3 1 9 3 2 7 3 3 5 3 4 3 3 5 1 3 5 9 3 6 7 3 7 5 3 8 3 3 9 1 3 9 9 4 0 7 4 1 5 4 2 3 4 3 1 7 6 1 5 6 1 6 4 1 7 2 1 8 0 1 8 9 1 9 7 2 0 5 2 1 3 2 2 1 2 3 0 2 3 8 2 4 6 2 5 4 2 6 3 2 7 1 2 7 9 2 8 7 2 9 5 3 0 4 3 1 2 3 2 0 3 2 8 3 3 6 3 4 4 3 5 3 3 6 1 3 6 9 3 7 7 3 8 5 3 9 4 4 0 2 4 1 0 4 1 8 4 2 6 4 3 5 4 4 3 S o u r c e : A d a p t e d f r o m C l i n i c a l G u i d e l i n e s o n t h e I d e n t i � c a t i o n , E v a l u a t i o n , a n d T r e a t m e n t o f O v e r w e i g h t a n d O b e s i t y i n A d u l t s : T h e E v i d e n c e R e p o r t . 19 Chapter 19: Micronutrients

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2. Lefton, J., D. Halasa Esper, and M. Kochevar. 2007. Enteral formulations. In The ASPEN nutrition support core curriculum: A case based approach—the adult patient, ed. M. Gottschlich, 488–504. United States of America: American Society of Parenteral and Enteral Nutrition.

3. Marian, M., and S. Carlson. 2005. Enteral formulations. In ASPEN nutrition support manue, 2nd ed., ed. R. Merritt, 63–75. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition.

4. Chen, Y., and S. Peterson. 2009. Enteral nutrition formulas: Which formula is right for your adult patient? Nutr Clin Prac 24:344–555.

5. Barrett, J. S., S. J. Shepard, and P. R. Gibson. 2009. Strategies to manage gastrointestinal symptoms complicating enteral feeding. JPEN 33:21–26.

7. Wiesen, P., A. Gossum, and J. Preiser. 2006. Diarrhea in the critially ill. Curr Opin Crit Care 12:149–54.

8. Zimmaro, D. M., R. H. Rolandelli, M. J. Koruda et al. 1989. Isotonic tube feeding formula induces liquid stool in normal subjects: Reversal by pectin. JPEN 13:117–23.

9. Bliss, D. Z., S. Johnson, K. Savik et al. 1998. Acquistion of clostridium dif�cile and clostridium dif�cileassociated diarrhea in hospitalized patients receiving tube feeding. Annals of Inter Med 129:1012–19.

10. Barrett, J., S. Shepherd, and P. Gibson. 2009. Strategies to manage gastrointestinal symptoms complicating enteral feeding. JPEN 33:21–26.

11. Klessen, B., L. Hartmann, and M. Blaut. 2003. Fructans in the diet cause alterations of intestinal mucosal architecture, released mucin and mucosa-associated bi�dobacteria in gnotobiotic rats. Brit J Nutr 89:597–606.

12. Sobotka, L., M. Bratowa, and M. Slemrova. 1997. Inulin as the soluble �ber in liquid enteral nutrition. Nutr 13:21–25.

13. Rushdi, T. A., C. Pichard, and Y. H. Khater. 2004. Control of diarrhea by �ber-enriched diet in ICU patients on enteral nutrition: A prospective randomized controlled trial. J Clin Nutr 23:1344–52.

14. Spapen, H., M. Diltoer, C. Van Malderen et al. 2001. Soluble �ber reduces the incidence of diarrhea in septic patients receiving total enteral nutrition: A prospective, double-blind, randomized, and controlled trial. J Clin Nutr 20:301–5.

15. Guenter, T. A., R. G. Settle, S. Perlmutter et al. 1991. Tube feeding related diarrhea in acutely ill patients. JPEN 15:277–80.

16. Yang, G., X.-T. Wu, and Y. Zhou et al. 2005. Application of dietary �ber in clinical enteral nutrition: A meta-analysis of randomized controlled trials. World J Gastroenterol 11:3935–38.

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20. Elia, M., A. Ceriello, H. Laube et al. 2005. Enteral nutritional support and use of diabetes-speci�c formulas for patients with diabetes. Diabetes Care 28:2267–79.

21. Pohl, M., P. Mayr, M. Mertl-Roetzer et al. 2009. Glycemic control in patients with type II diabetes mellitus with a disease-speci�c enteral formula: Stage II of a randomized, controlled multicenter trial. JPEN 33:37–49.

22. León-Sanz, M., P. P. García-Luna, A. Sanz-París et al. 2005. Glycemic and lipid control in hospitalized type 2 diabetic patients: Evaluation of 2 enteral nutrition formulas (low carbohydrate-high monounsaturated fat vs high carbohydrate). JPEN 29:21–29.

23. Mesejo, A., J. A. Acosta, C. Ortega et al. 2003. Comparison of a high-protein disease-speci�c enteral formula with a high-protein enteral formula in hyperglycemic critically ill patients. Clin Nutr 22:295–305.

24. Krenitsky, J. 2004. Nutrition in renal failure: Myths and management. Practical Gastroenterol 20:40–59.

25. Rodriguez, D., and W. Sandoval. 1997. Nutrition support in acute renal failure patients: current prospectives. Support Line 14:3–10.

26. Wooley, J., I. Btaiche, and K. Good. 2005. Metabolic and nutritional aspects of acute renal failure in critically ill patients requiring continuous renal replacement therapy. NCP 20:176–91.

27. Aparicio, M., P. Chauveciu, and C. Combe. 2001. Low protein diets and outcome of renal patients. J Nephrol 14:433–39.

28. Patton, K., and J. Aranda-Michel. 2002. Nutritional aspects in liver disease and liver transplantation. Nutr Clin Prac 17:332–40.

29. Ariyan, W. 2004. Nutrition management in liver disease. Support Line 26:3–8.

30. Krenitsky, J. 2003. Nutrition for patients with hepatic failure. Practical Gastroenterol 6:23–42.

31. Davis, G. 2006. Thoughts on nutrition and liver disease. Nutr Clin Pract 21:243–44.

32. Srivastava, N., N. Singh, and Y. K. Joshi. 2003. Nutrition in the management of hepatic encephalopathy. Trop Gastroenterol 24:59–62.

33. Teran, C. 1999. Nutrition and liver diseases. Curr Gastroenterol Rep 19:335–40.

34. Btaiche, I. 2003. Branched chain amino acids in patients with hepatic encephalopathy. Nutr Clin Prac 18:97–100.

36. Schwartz, D., and R. DiMaria. 2007. Pulmonary and cardiac failure. In The ASPEN nutrition support core curriculum: A case based approach—the adult patient, ed. M. Gottschlich, 488–504. United States of America: American Society of Parenteral and Enteral Nutrition.

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41. Lee, S., K. Gura, S. Kim et al. 2006. Current clinical applications of ω-6 and ω-3 fatty acids. Nutr Clin Pract 21:323–41.

42. Grimble, R. 2007. Immunomodulatory impact of dietary lipids. Clin Nutr Highlights 3:2–8.

43. Alexander, J. 1998. Immunonutrition: The role of ω-3 fatty acids. Nutr 14:627–33.

44. Gadek, J., S. DeMichele, M. Karlstad et al. 1999. Effect of enteral feeding with eicosapentaenoic acid, γ-linolenic acid, and antioxidants in patients with acute respiratory distress syndrome. Crit Care Med 27:1409–20.

45. Pacht, E., S. DeMichele, J. Nelson et al. 2003. Enteral nutrition with eicosapentaenoic acid, γ-linolenic acid, and antioxidants reduces alveolar in�ammatory mediators and protein in�ux in patients with acute respiratory distress syndrome. Crit Care Med 31:491–500.

46. Pontes-Arruda, A., A. Aragao, and J. Albuquerque. 2006. Effects of enteral feeding with eicosapentaenoic acid, γ-linolenic acid, and antioxidants in mechanically ventilated patients with severe sepsis and septic shock. Crit Care Med 34:2325–33.

47. McClave, S., R. Martindale, V. Vanek et al. 2009. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of critical care medicine and American society for parenteral and enteral nutrition. JPEN 33:277–316.

48. Strickland, A., A. Brogan, J. Krauss et al. 2005. Is the use of specialized nutritional formulations a cost effective strategy? A national database evaluation. JPEN 29:S81–91.

49. Schloerb, P. 2001. Immune-enhancing diets: Products, components, and their rationales. JPEN 25:S3–7.

50. Todd, S., R. Kozar, and F. Moore. 2006. Nutrition support in adult trauma patients. Nutr Clin Prac 21:421–29.

51. Weitzel, L., W. Mayles, P. Sandoval et al. 2009. Effects of pharmaconutrients on cellular dysfunction and the microcirculation in critical illness. Curr Opin Anaesthesiol 22:177–83.

52. Heyland, D. K., F. Novak, J. W. Drover et al. 2001. Should immunonutrition become routine in critically ill patients? A systematic review of the literature. JAMA 286:944–53.

53. Bruzzone, R., and D. Radrizzani. 2003. Early enteral immunonutrition in patients with severe sepsis: Results of an interim analysis of a randomized multicenter clinical trial. Intensive Care Med 29:834–40.

54. Yan, H., X. Peng, Y. Huang et al. 2007. Effects of early enteral arginine supplementation on resuscitation of severe burn patients. Burns 33:179–84.

55. Farber, M., J. Moses, and M. Korn. 2005. Reducing costs and patient morbidity in the enterally fed intensive care unit patient. JPEN 29:S62–69.

56. Wischmeyer, P. 2003. Clinical applications of L-Glutamine: Past, present, and future. Nutr Clin Prac 18:377–85.

57. Novak, F., D. Heyland, A. Avenell et al. 2002. Glutamine supplementation in serious illness: A systematic review of the evidence. Crit Care Med 30:2022–29.

58. Garrell, D., J. Patenaude, B. Nedelec et al. 2003. Decreased mortality and infectious morbidity in adult burn patients given enteral glutamine supplements: A prospective, controlled, randomized clinical trial. Crit Care Med 31:2444–49.

59. Jurkovich, G. 2001. Outcome studies using immune-enhancing diets: Blunt and penetrating torso trauma patients. JPEN 25:S14–18.

60. Sax, H. 2001. Effect of immune enhancing formulas (IEF) in general surgery patients. JPEN 25:S19–23.

61. Cresci, G. 2001. Targeting the use of specialized nutritional formulas in surgery and critical care. JPEN 25:S92–95. outcome and cost-comparison analysis in surgical patients. Crit Care Med 25:1489–96.

64. Silk, D. B., P. D. Fairclough, M. L. Clark et al. 1980. Use of a peptide rather than free amino acid nitrogen source in chemically de�ned “elemental” diets. JPEN 4:548–53.

65. Silk, D. M., G. K. Grimble, and R. G. Rees. 1985. Protein digestion and amino acid and peptide absorption. Proc Nutr Soc 44:63–72.

66. Friedrich, M. 1982. The intestinal phase of peptide absorbtion. Nahrung 26:887–901.

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68. Heyland, D., R. Dhaliwal, J. Drover et al. 2003. Canadian clinical practice guidelines for nutrition support in mechanically ventilated, critically ill adult patients. JPEN 27:355–73.

69. Krenitsky, J., D. Makola, and C. R. Parrish. 2007. Parenteral nutrition in pancreatitis is passé: But are we ready for gastric feeding? A practical guide to jejunal feeding: Revenge of the cyst—part II. Practical Gastroenterology 55:54–72.

70. Duerksen, D., S. Bector, and D. Parry. 2001. A comparison of the effect of elemental and immune enhancing polymeric jejunal feeding on exocrine pancreatic function. JPEN 26:205–8.

71. Duszak, R., and M. A. Mabry. 2003. National trends in gastrointestinal access procedures: An analysis of Medicare services provided by radilologists and other specialists. J Vasc Interv Radiol 14:1031–36. 72. Burtch, C. D., and C. H. Shatney. 1987. Feeding jejunostomy (versus gastrostomy) passes the test of time. Am Surg 53:54–57.

73. Baskin, A. I. N., and J. F. Johansen. 1995. An improved approach to the delivery of enteral nutrition in the intensive care unit. Gastrointest Endosc 42:161–65.

74. Neumann, D. A., and M. H. DeLegge. 2002. Gastric versus small-bowel tube feeding in the intensive care unit. Crit Care Med 7:1436–39.

75. McClave, S. A., M. T. DeMeo, M. H. DeLegge et al. 2002. North American summit on aspiration in the critically ill patient: Consensus statement. JPEN 26:S80–85.

76. Caul�eld, K. A., C. P. Page, and C. Pestana. 1991. Technique for intraduodenal placement of transnasal enteral feeding catheters. NCP 6:23–26.

77. Roubenoff, R., and W. J. Ravich. 1989. The technique of avoiding feeding tube misplacement. J Crit Illness 4:75–79.

78. Cataldi-Belcher, E. L., M. H. Selzer, B. A. Slocumb et al. 1983. Complications during enteral nutrition therapy: A prospective study. JPEN 7:546–52.

79. Thurlow, P. M. 1986. Bedside enteral feeding tube placement into duodenum and jejunum. JPEN 10:104–5.

80. Zaloga, G. P. 1991. Bedside method for placing small bowel feeding tubes in critically ill patients. Chest 100:1643–46.

81. Ugo, P. J., P. A. Mohler, and G. L. Wilson. 1992. Bedside postpyloric placement of weighted feeding tubes. NCP 7:284–87.

82. Lord, L. M., A. Weiser-Mamone, M. Pulhamus et al. 1993. Comparison of weighted vs unweighted enteral feeding tubes for ef�cacy or transpyloric passage. JPEN 17:271–73.

83. Kittinger, J. M., R. S. Sandler, and W. D. Heizer. 1987. Ef�cacy of metoclopramide as an adjunct to duodenal placement of small bore feeding tubes: A randomized, placebo controlled, double blind study. JPEN 11:33–37.

84. Selfert, C. S., P. G. Cuddy, B. Pemberton et al. 1987. A randomized trial of metoclopramide’s effects on the transpyloric intubation of weighted feeding tubes. Nutr Supp Serv 11:11–13.

85. Whatley, K., W. W. Turner Jr., M. Dey et al. 1984. When does metoclopramide facilitate transpyloric intubation? JPEN 8:679–81.

86. Kalafarentzos, F., V. Alivizatos, K. Panagopoulos et al. 1987. Nasoduodenal intubation with the use of metoclopramide. Nutr Supp Sev 7:33–34.

87. Silva, C. C., H. Saconato, and A. N. Attalah. 2004. Metocloramide for migration of naso-enteral tube (Cochrane Review). In The cochrane library, Issue 1, 1–15. Chester, UK: John Wiley & Sons, Ltd.

88. Grif�th, D. P., A. T. McNally, C. H. Battey et al. 2003. Intravenous erythromycin facilitates bedside placement of postpyloric feeding tubes in critically ill adults: A double-blind, placebo-controlled study. Crit Care Med 31:39–44.

89. Berger, M. M., M. D. Bollmann, J. P. Revelly et al. 2002. Progression rates of self-propelled feeding tubes. Int Care Med 28:1768–74.

91. Phang, J., W. Marsh, and R. Prager. 2006. Feeding tube placement with the use of a new electromagnetic transmitter. JPEN J Parent Enteral Nutr 30:S082.

92. Gatt, M., and J. MacFie. 2009. Bedside postpyloric feeding tube placement: a pilot series to validate this novel technique. Crit Care Med 37:523–27.

93. Baskin, W. N., and J. F. Johansen. 1995. An improved approach to the delivery of enteral nutrition in the intensive care unit. Gastrointest Endosc 42:161–65.

94. Lovell, M. A., M. Y. Mudaliar, and P. L. Klineberg. 2001. Intrahospital transport of critically ill patients: Complications and dif�culties. Anaesth Inten Care 29:400–5.

95. Patrick, P. G., S. Marulenmdra, D. F. Kirby, and M. H. Delegge. 1997. Endoscopic naso-gastric jejunal feeding tube placement in critically ill patients. Gastrointest Endosc 45:72–76.

96. Fang, J.C., K. Hilden, R. Holubkov et al. 2005. Transnasal endoscopy vs �uoroscopy for the placment of nasoenteric feeding tubes in critically ill patients. Gastrointest Endosc 62:661–66.

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99. Park H. R. H., M. C. Allison, J. Long et al. 1992. Randomized comparison of percutaneous endoscopic gastrostomy vs nasogastric feedings in patients with persistent neurological dyspbagia. Br Med J 304:1406–9.

100. Gauderer, M. W. L., J. Ponsky Jr., R. J. Izant. 1980. Gastrostomy without laparotomy: A percutaneous endoscopic approach. J Pediatr Surg 15:872–75.

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108. Dennis, M. S., S. C. Lewis, and C. Warlow. 2005. FOOD trial collaboration. Effect of timing and method of enteral tube feeding for dysphagic stroke patients (FOOD): A muulitcentre randomised controlled trial. Lancet 365:764–72.

109. Gillick, M. R. 2000. Rethinking the role of tube feeding in patients with advanced dementia. New Engl J Med 342:206–10.

110. Sanders, D. S., M. J. Carter, J. D’Silva et al. 2000. Survival analysis in percutaneous endoscopic gastrostomy feeding: A worse outcome in patients with dementia. Am J Gastroenterol 95:1472–75.

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115. Marcuard, S. P., J. L. Finley, and K. G. MacDonald. 1993. Large-bore feeding tube occlusion by yeast colonies. JPEN 17:187–90.

116. Marcuard, S. P., and K. S. Stegall. 1990. Unclogging feeding tubes with pancreatic enzymes. JPEN 14:198–200.

117. Safadi, B. Y., J. M. Marks, and J. L. Ponsky. 1998. Percutaneous endoscopic gastrostomy. Gastrointest Endosc Clin Am 8:551–68.

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28. Eatock, F. C., P. Chong, M. Menezes et al. 2005. A randomized study of early nasogastric versus nasojejunal feeding in severe acute pancreatitis. Am J Gastroenterol 100:432–39.

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Newton, A. H., and M. DeLegge. 2007. Home initiation of parenteral nutrition. Nutrition in Clinical Practice 22 (1): 57–64.

Opilla, M. T., D. F. Kirby, and M. B. Edmond. 2007. Use of ethanol lock therapy to reduce the incidence of catheter-related bloodstream infections in home parenteral nutrition patients. Journal of Parenteral and Enteral Nutrition 31:302–7.

Siepler, J. 2007. Principles and strategies for monitoring home parenteral nutrition. Nutrition in Clinical Practice 22 (3): 340–50.

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