Malabsorption

Updated: Jan 24, 2019
  • Author: Muhammad Bader Hammami, MD; Chief Editor: Praveen K Roy, MD, AGAF  more...
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Overview

Background

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.

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Pathophysiology

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.

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Etiology

The best way to classify the numerous causes of malabsorption is to consider the three phases of digestion and absorption.

Luminal phase

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

  • Decreased bile salt synthesis from severe parenchymal liver disease (eg, cirrhosis)
  • Impaired bile secretion from biliary obstruction or cholestatic jaundice (eg, primary biliary cirrhosis, primary sclerosing cholangitis)
  • Impaired enterohepatic bile circulation, as seen in small bowel resection or regional enteritis
  • Bile salt deconjugation due to small bowel bacterial overgrowth

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.

Mucosal phase

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:

  • Decreased absorptive surface area, as seen in intestinal resection of intestinal bypass
  • Damaged absorbing surface, as seen in celiac sprue, tropical sprue, Crohn disease, AIDS enteropathy, chemotherapy, or radiation therapy
  • Infiltrating disease of the intestinal wall, such as lymphoma and amyloidosis
  • Infections, including bacterial overgrowth, giardiasis, Whipple disease, cryptosporidiosis, and microsporidiosis

Postabsorptive phase

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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