Pediatric Lactose Intolerance Clinical Presentation

  • Author: Stefano Guandalini, MD; Chief Editor: Carmen Cuffari, MD   more...
 
Updated: May 11, 2012
 

History

Symptoms of lactose intolerance include the following:

  • GI symptoms
    • Bloating, abdominal discomfort, meteorism, and flatulence that occur from 1 hour to a few hours after ingestion of milk or dairy products may signify lactose intolerance; however, other disorders such as milk-protein sensitivity, allergic-type reactions to other substances in the meal, or other saccharide intolerance may cause similar symptoms.
    • Many individuals with lactose intolerance are concerned about the presence of lactose in many orally administered drugs; however, one investigation concluded that no side effects are experienced by adults with hypolactasia upon ingestion of lactose-containing drugs.[4]
    • Adults and adolescents who have been diagnosed with lactose malabsorption appear able to tolerate as much as 12 g of lactose in a single dose (equivalent to the lactose content found in 1 cup of milk). Even larger amounts can be tolerated if they are ingested with meals and distributed throughout the day. However, 50 g of lactose (the lactose content found in 1 quart of milk) usually causes symptoms in adults with lactose malabsorption when administered as a single dose outside of meals.[2]
    • Although lactose intolerance is often suspected in children with functional recurrent abdominal pain, strong evidence suggests that lactose intolerance plays no role in such condition.
  • Associated food
    • The rate of gastric emptying is important in the development of symptoms, which may develop if lactose moves quickly to an intestine that is low in lactase. Fats decrease the rate of gastric emptying, whereas carbohydrates increase the rate of gastric emptying. Thus, if dairy products that contain lactose are ingested with carbohydrates, especially simple carbohydrates, symptoms are more likely.
    • Allergies to food proteins, particularly milk and grain proteins, can mimic lactose intolerance in part.
    • Inflammation of the intestinal mucosa due to infection or protein-sensitive enteritis causes secondary lactose intolerance.
  • Stool characteristics: Loose, watery, acidic stool often with excessive flatus and associated with urgency that occurs a few hours after the ingestion of lactose-containing substances is typical.
  • Gastroenteritis: Infectious diarrhea, particularly viral gastroenteritis in younger children, may damage the intestinal mucosa enough to reduce the quantity of the lactase enzyme. This does not result in any significant problem and does not require any changes in formula. However, intolerance is rarely more evident, especially in malnourished infants, and requires a few days of lactose-free feedings. Abundant literature conclusively shows that breastfeeding can and should always be continued throughout an episode of gastroenteritis, despite the high content of lactose in breast milk.
  • Food avoidance: Many people with lactose intolerance instinctively avoid products that contain lactose.
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Physical

  • Abdominal pain: Nonspecific, nonfocal abdominal pain and cramping are common and are sometimes associated with bloating and flatus. This pain may mildly increase with palpation. Focal abdominal pain significantly worsened by palpation, the presence of rebound tenderness, or guarding should alert the clinician to a more serious and possibly surgical GI diagnosis.
  • Borborygmi: A significant increase in peristaltic activity in the small bowel can cause an audible or palpable increase in bowel activity.
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Causes

  • Lactose intolerance: This is caused by a low or absent activity of the enzyme lactase.
  • Adult-onset lactose intolerance
    • This deficiency results from an unusual mechanism that involves a developmentally regulated change of the lactase gene product, resulting in a reduced synthesis of the precursor protein.
    • Differences in the rate of gene transcription account for much of the differences in lactose intolerance observed among racial groups.
  • Low lactase activity in the small intestine: This allows undigested lactose to pass into the colon. In the colon, bacteria ferment the sugar to hydrogen gas and organic acids. The gas produces distention of the bowel, creating the sensation of bloating, cramping, and abdominal pain. Organic acids can be absorbed, but the quantity produced is rarely large enough to cause systemic symptoms or metabolic acidosis.
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Contributor Information and Disclosures
Author

Stefano Guandalini, MD  Director, Celiac Disease Center, Chief, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, University of Chicago Medical Center; Professor, Department of Pediatrics, Section of Gastroenterology, Hepatology and Nutrition, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

Stefano Guandalini, MD is a member of the following medical societies: American Gastroenterological Association, European Society for Paediatric Gastroenterology, Hepatology & Nutrition, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Coauthor(s)

Richard E Frye, MD, PhD  Assistant Professor, Departments of Pediatrics and Neurology, University of Texas Medical School at Houston

Richard E Frye, MD, PhD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, Child Neurology Society, and International Neuropsychological Society

Disclosure: Nothing to disclose.

Delia M Rivera, MD  Assistant Professor, Department of Pediatrics, Division of Infectious Disease and Immunology, University of Miami Leonard M Miller School of Medicine

Delia M Rivera, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Stephen Borowitz, MD  Professor of Pediatrics and Public Health Sciences, Department of Pediatrics, Division of Gastroenterology and Nutrition, University of Virginia School of Medicine

Stephen Borowitz, MD is a member of the following medical societies: American Academy of Pediatrics, American Gastroenterological Association, American Pediatric Society, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Specialty Editor Board

Alan D Schmetzer, MD  Professor and Vice-Chair for Education, Director of Residency Training, Department of Psychiatry, Indiana University School of Medicine

Alan D Schmetzer, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Society of Transplant Surgeons, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

B UK Li, MD  Professor of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, Director, Pediatric Fellowships and Gastroenterology Fellowship, Medical Director, Functional Gastrointestinal Disorders and Cyclic Vomiting Program, Medical College of Wisconsin; Attending Gastroenterologist, Children's Hospital of Wisconsin

B UK Li, MD is a member of the following medical societies: Alpha Omega Alpha, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Steven M Schwarz, MD, FAAP, FACN, AGAF  Professor of Pediatrics, Children's Hospital at Downstate, State University of New York Downstate Medical Center

Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research

Disclosure: Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor; Johnson & Johnson, Inc. Grant/research funds Independent contractor

Chief Editor

Carmen Cuffari, MD  Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

References
  1. Campbell AK, Waud JP, Matthews SB. The molecular basis of lactose intolerance. Sci Prog. 2009;92:241-87. [Medline].

  2. [Best Evidence] [Guideline] Brannon PM, Carpenter TO, Fernandez JR, et al. NIH Consensus Development Conference Statement: Lactose Intolerance and Health. NIH Consens State Sci Statements. Feb 24 2010;27(2):[Medline].

  3. Seppo L, Tuure T, Korpela R, et al. Can primary hypolactasia manifest itself after the age of 20 years? A two-decade follow-up study. Scand J Gastro. 2008;43:1082-1087. [Medline].

  4. Montalto M, Gallo A, Santoro L, et al. Low-dose lactose in drugs neither increases breath hydrogen excretion nor causes gastrointestinal symptoms. Aliment Pharmacol Ther. Oct 15 2008;28(8):1003-12. [Medline].

  5. Krawczyk M, Wolska M, Schwartz S, et al. Concordance of genetic and breath tests for lactose intolerance in a tertiary referral centre. J Gastrointestin Liver Dis. Jun 2008;17(2):135-9. [Medline].

  6. Hovde O, Farup PG. A comparison of diagnostic tests for lactose malabsorption--which one is the best?. BMC Gastroenterol. Oct 31 2009;9:82. [Medline].

  7. Griffin MP, Hansen JW. Can the elimination of lactose from formula improve feeding tolerance in premature infants?. J Pediatr. Nov 1999;135(5):587-92. [Medline].

  8. Lactose intolerance and African Americans: implications for the consumption of appropriate intake levels of key nutrients. J Natl Med Assoc. Oct 2009;101(10 Suppl):5S-23S. [Medline].

  9. Bacsi K, Kosa JP, Lazary A, et al. LCT 13910 C/T polymorphism, serum calcium, and bone mineral density in postmenopausal women. Osteoporos Int. Aug 13 2008;[Medline].

  10. Bodlaj G, Stocher M, Hufnagl P, et al. Genotyping of the lactase-phlorizin hydrolase -13910 polymorphism by LightCycler PCR and implications for the diagnosis of lactose intolerance. Clin Chem. 2006;52:148-151. [Medline].

  11. Guandalini S. Treatment of acute diarrhea in the new millennium. J Pediatr Gastroenterol Nutr. 2000;30:486-9. [Medline].

  12. He T, Venema K, Priebe MG, Welling GW, Brummer RJ, Vonk RJ. The role of colonic metabolism in lactose intolerance. Eur J Clin Invest. Aug 2008;38(8):541-7. [Medline].

  13. Kuokkanen M, Kokkonen J, Enattah NS. Mutations in the Translated Region of the Lactase Gene (LCT) Underlie Congenital Lactase Deficiency. Am J Hum Genet. 2006;78:339-44. [Medline].

  14. Montalto M, Curigliano V, Santoro L. Management and treatment of lactose malabsorption. World J Gastroenterol. 2006;14:187-91. [Medline].

  15. Savaiano DA, Boushey CJ, McCabe GP. Lactose intolerance symptoms assessed by meta-analysis: a grain of truth that leads to exaggeration. J Nutr. 2006;136:1107-13. [Medline].

  16. Shulman RJ,, Wong WW, Smith EO. Influence of changes in lactase activity and small-intestinal mucosal growth on lactose digestion and absorption in preterm infants. Am J Clin Nutr. 2005;81:472-9. [Medline].

  17. Srinivasan R, Minocha A. When to suspect lactose intolerance. Symptomatic, ethnic, and laboratory clues. Postgrad Med. Sep 1998;104(3):109-11, 115-6, 122-3. [Medline].

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The small intestine is a major site of absorption.
 
 
 
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