Malabsorption
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Malabsorption is a clinical term that refers to the impaired absorption of nutrients. It encompasses defects that occur during the digestion and absorption of food nutrients by, and infections of, the gastrointestinal tract. The digestion or absorption of a single nutrient component may be impaired (eg, lactose intolerance due to lactase deficiency). When a diffuse disorder, such as celiac disease or Crohn disease, affects the intestine, the absorption of almost all nutrients is impaired.
Although presenting symptoms, such as diarrhea and weight loss, may be common, the specific causes of malabsorption are usually established based on physiologic evaluations. The treatment often depends on the establishment of a definitive etiology for malabsorption.
For patient education resources, see the Digestive Disorders Center as well as Celiac Sprue and Crohn Disease.
To understand the mechanisms of malabsorption, knowledge of the normal physiologic process of digestion and absorption by the intestinal tract is necessary.
In general, the digestion and absorption of food materials can be divided into three major phases: luminal, mucosal, and postabsorptive. [1] The luminal phase is the stage in which dietary fats, proteins, and carbohydrates are hydrolyzed and solubilized by secreted digestive enzymes and bile. The mucosal phase relies on the integrity of the brush-border membrane of intestinal epithelial cells to transport digested products from the lumen into the cells. In the postabsorptive phase, reassembled lipids and other key nutrients are transported via the lymphatics and portal circulation from epithelial cells to other parts of the body.
When disease processes perturb any of these phases, malabsorption frequently results.
The best way to classify the numerous causes of malabsorption is to consider the three phases of digestion and absorption.
Impaired nutrient hydrolysis
The most common cause for impaired nutrient hydrolysis is pancreatic insufficiency due to chronic pancreatitis, pancreatic resection, pancreatic cancer, or cystic fibrosis. The resultant deficiencies in lipase and proteases lead to lipid and protein malabsorption, respectively.
Inactivation of pancreatic enzymes by gastric hypersecretion, as seen in Zollinger-Ellison syndrome, is another cause.
Inadequate mixing of nutrients, bile, and pancreatic enzymes, as seen in rapid intestinal transit, gastrojejunostomy, total and partial gastrectomy, or intestinal resection after mesenteric emboli or thrombosis, also causes impaired hydrolysis.
Rarely, a failure to convert a proenzyme to its active form, such as enterokinase and trypsinogen deficiencies, also can cause protein maldigestion and malabsorption.
Impaired micelle formation
Impaired micelle formation causes a problem in fat solubilization and subsequent fat malabsorption. The origin of this impairment varies, including the following
Stasis of intestinal content caused by a motor abnormality (eg, scleroderma, diabetic neuropathy, intestinal obstruction), an anatomic abnormality (eg, small bowel diverticula, stricture, ischemia, blind loops), or small bowel contamination from enterocolonic fistulas can cause bacterial overgrowth.
Luminal availability and processing
Luminal bacterial overgrowth can cause a decrease in the availability of substrates, including carbohydrates, proteins, and vitamins (eg, vitamin B-12, folate).
Vitamin B12 (cobalamin) deficiency due to pernicious anemia is caused by a lack of intrinsic factor and by pancreatic enzyme deficiency.
Impaired brush-border hydrolase activity
Disaccharidase deficiency can lead to disaccharide malabsorption.
Lactase deficiency, either primary or secondary, is the most common form of disaccharidase deficiency. Genetic factors determine the primary form; C/T-13910 AND G/A-22018 mutations have been implicated. [2, 3] Secondary lactase deficiency can be result from acute gastroenteritis (rotavirus and giardia infection), chronic alcoholism, celiac sprue, radiation enteritis, regional enteritis, or acquired immunodeficiency syndrome (AIDS) enteropathy.
Immunoglobulin A (IgA) deficiency (the most common immunodeficiency) is due to decreased or absent serum and intestinal IgA, which clinically appears similar to celiac disease and is unresponsive to a gluten-free diet.
Acrodermatitis enteropathica is an autosomal recessive disease with selective inability to absorb zinc, leading to villous atrophy and acral dermatitis.
Autoimmune enteropathy is primarily diagnosed in children presenting with intractable secretory diarrhea and villous atrophy. Autoimmune enteropathy is occurs as a result of antibodies directed against intestinal epithelial and goblet cells. Additional cell types affected by autoantibodies include islet and parietal cells.
Other carbohydrase deficiencies, such as sucrase-isomaltase deficiency, may be the cause.
Impaired nutrient absorption
Nutrient malabsorption is due to inherited or acquired defects. Inherited defects include glucose-galactose malabsorption, abetalipoproteinemia, cystinuria, and Hartnup disease.
Acquired disorders are far more common and are caused by the following:
Obstruction of the lymphatic system, both congenital (eg, intestinal lymphangiectasia, Milroy disease) and acquired (eg, Whipple disease, neoplasm [including lymphoma], tuberculosis), impairs the absorption of chylomicrons and lipoproteins and may cause fat malabsorption or a protein-losing enteropathy.
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Muhammad Bader Hammami, MD Fellow in Inflammatory Bowel Disease, St Louis University School of Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Douglas M Heuman, MD, FACP, FACG, AGAF Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, American Gastroenterological Association
Disclosure: Received grant/research funds from Novartis for other; Received grant/research funds from Bayer for other; Received grant/research funds from Otsuka for none; Received grant/research funds from Bristol Myers Squibb for other; Received none from Scynexis for none; Received grant/research funds from Salix for other; Received grant/research funds from MannKind for other.
Praveen K Roy, MD, AGAF Chief of Gastroenterology, Presbyterian Hospital; Medical Director of Endoscopy, Presbyterian Medical Group; Adjunct Associate Research Scientist, Lovelace Respiratory Research Institute; Clinical Assistant Professor of Medicine, University of New Mexico School of Medicine
Praveen K Roy, MD, AGAF is a member of the following medical societies: American Gastroenterological Association, American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Tushar Patel, MB, ChB Professor of Medicine, Ohio State University Medical Center
Tushar Patel, MB, ChB is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association
Disclosure: Nothing to disclose.
Stephan U Goebel, MD Assistant Professor of Gastroenterology and Hepatology, Department of Medicine, Emory University School of Medicine
Stephan U Goebel, MD is a member of the following medical societies: American Gastroenterological Association, American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Jan-Michael A Klapproth, MD Assistant Professor, Department of Medicine, Division of Digestive Diseases, Emory University School of Medicine
Jan-Michael A Klapproth, MD is a member of the following medical societies: American College of Gastroenterology, American Federation for Medical Research, American Gastroenterological Association, and Crohns and Colitis Foundation of America
Disclosure: Nothing to disclose.
Vincent W Yang, MD, PhD R Bruce Logue Professor, Director, Division of Digestive Diseases, Department of Medicine, Professor of Hematology and Oncology, Winship Cancer Institute, Emory University School of Medicine
Vincent W Yang, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Gastroenterological Association, American Society for Clinical Investigation, and Association of American Physicians
Disclosure: Nothing to disclose.
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