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.

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

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:

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.


Malabsorption can present in a variety of ways, depending on the cause, nature, and severity of the underlying disorder.

The osmotic load resulting from the inability of the intestine to absorb certain nutrient elements causes the presenting symptoms. On occasion, the products of digestion produced by bacterial flora also result in a secretory reaction by the intestine.


Diarrhea is the most common symptomatic complaint.[4, 5, 6, 7, 8]  It is frequently is watery, reflecting the osmotic load received by the intestine. Bacterial action producing hydroxy fatty acids from undigested fat also can increase the net fluid secretion from the intestine, further worsening the diarrhea.


Steatorrhea is the result of fat malabsorption. The hallmark of steatorrhea is the passage of pale, bulky, and malodorous stools. Such stools often float on top of the toilet water and are difficult to flush. Also, patients often find floating oil droplets in the toilet following defecation.

Weight loss and fatigue

Weight loss is common and may be pronounced; however, patients may compensate by increasing their caloric consumption, masking weight loss from malabsorption. The chance of weight loss increases in diffuse diseases involving the intestine, such as celiac disease and Whipple disease.

Flatulence and abdominal distention

Bacterial fermentation of unabsorbed food substances releases gaseous products, such as hydrogen and methane, causing flatulence. Flatulence often results in uncomfortable abdominal distention and cramps.


Hypoalbuminemia from chronic protein malabsorption or from protein loss into the intestinal lumen causes peripheral edema. Extensive obstruction of the lymphatic system, as seen in intestinal lymphangiectasia, can result in protein loss.

With severe protein depletion, ascites may develop.


Depending on the cause, anemia resulting from malabsorption can be either microcytic (iron deficiency) or macrocytic (vitamin B12/cobalamin deficiency).[9]  

Iron deficiency anemia often is a manifestation of celiac disease.[10]  Ileal involvement in Crohn disease or ileal resection can cause megaloblastic anemia due to vitamin B12 deficiency.

Bleeding disorders

Bleeding usually is a consequence of vitamin K malabsorption and subsequent hypoprothrombinemia. Ecchymosis usually is the manifesting feature, although occasionally, melena and hematuria occur.

Metabolic defects of bones

Vitamin D deficiency can cause bone disorders, such as osteopenia or osteomalacia. Bone pain and pathologic fractures may be observed.

Malabsorption of calcium can lead to secondary hyperparathyroidism.

Neurologic manifestations

Electrolyte disturbances, such as hypocalcemia and hypomagnesemia, can lead to tetany, manifesting as the Trousseau sign and/or the Chvostek sign.

Vitamin malabsorption can cause generalized motor weakness (vitamin B5/pantothenic acid, vitamin D) or peripheral neuropathy (vitamin B1/thiamine), a sense of loss for vibration and position (vitamin B12/cobalamin), night blindness (vitamin A), and seizures (vitamin B7/biotin).

Physical Examination

General physical examination

Patients may have orthostatic hypotension, complain of fatigue, and/or have signs of loss of subcutaneous fat.

Signs of weight loss, muscle wasting, or both may be present.

Abdominal examination

The abdomen may be distended, and bowel sounds may be hyperactive.

Ascites may be present in severe hypoproteinemia.

Dermatologic manifestations

Pale skin may reveal anemia. The following may also be present:

Neurologic examination

Motor weakness, peripheral neuropathy, or ataxia may be present.

The Chvostek sign or the Trousseau sign may be evident due to hypocalcemia or hypomagnesemia.

Other findings

Cheilosis, glossitis, or aphthous ulcers of the mouth

Peripheral edema

Laboratory Studies

The choice and order of diagnostic testing should be individualized and guided by the patient’s history and physical examination.

Hematologic tests indicated in the workup of malabsorption include the following:

Levels of electrolytes and studies of serum chemistries may be indicated in the workup of malabsorption. Note the following:

No serologic tests are specific for malabsorption. Note the following:

Imaging Studies

Small bowel barium studies may reveal the following findings:

A computed tomography (CT) scan of the abdomen may help detect evidence of chronic pancreatitis, such as pancreatic calcification or atrophy. Enlarged lymph nodes are seen in Whipple disease and lymphoma.

CT enterography and magnetic resonance (MR) enterography are used to detect small bowel mucosal disease and neoplasms.

A plain abdominal radiograph may reveal pancreatic calcifications indicative of chronic pancreatitis.

Magnetic resonance cholangiopancreatography (MRCP) or endoscopic ultrasound (EUS) can help detect the cause of malabsorption due to pancreatic disease such as chronic pancreatitis or pancreatic malignancy.

Wireless capsule endoscopy allows for visualization of the entire small bowel and evaluation of small bowel mucosal disease.

Other Tests

Fat malabsorption studies

Fat malabsorption is usually the first test obtained because many disease processes result in fat malabsorption. Instruct patients to consume a normal amount (80-100 g/d) of fat before and during the collection. Based on this intake, fecal fat excretion in healthy individuals should be less than 7 g/d.

For a quantitative measurement of fat absorption, a 72-hour fecal fat collection is often performed and is considered the criterion standard. Raman et al have suggested that a novel clinical test that uses levels of serum retinyl palmitate to identify severe cases of fat malabsorption may be useful relative to the 72-hour fecal fat test.[11]

Qualitative tests include the acid steatocrit test and Sudan III staining of stool, but these tests are less reliable.

D-xylose test

If the 72-hour fecal fat collection results demonstrate fat malabsorption, the D-xylose test is used to document the integrity of the intestinal mucosa.

Facilitated diffusion in the proximal intestine primarily absorbs D-xylose. Approximately half of the absorbed D-xylose is excreted in urine, unmetabolized. If the absorption of D-xylose is impaired due to either a luminal factor (eg, bacterial overgrowth) or a reduced or damaged mucosal surface area (eg, surgical resection, celiac disease), urinary excretion is lower than normal.

Cases of pancreatic insufficiency usually result in normal urinary excretion because the absorption of D-xylose remains intact.

Carbohydrate absorption studies

A simple sensitive test for carbohydrate malabsorption is the hydrogen breath test, in which patients are given an oral solution of lactose.[12, 13]  In cases of lactase deficiency, colonic flora digest the unabsorbed lactose, resulting in an elevated hydrogen content in the expired air. Bacterial overgrowth or rapid transit also can cause an early rise in breath hydrogen, necessitating the use of glucose instead of lactose to make a diagnosis. However, 18% of patients are hydrogen nonexcretors, causing a false-negative test result.

Bile salt absorption studies

The bile salt breath test can determine the integrity of bile salt metabolism. The patient is given oral conjugated bile salt, such as glycine cholic acid with the glycine radiolabeled in the carbon position. The bile salt is deconjugated and subsequently metabolized by bacteria, leading to a radioactively labeled elevated breath carbon dioxide level in the presence of interrupted enterohepatic circulation, such as bacterial overgrowth, ileal resection, or disease.

Schilling test

Malabsorption of vitamin B12 (cobalamin) may occur as a consequence of a deficiency of intrinsic factor (eg, pernicious anemia, gastric resection), pancreatic insufficiency, bacterial overgrowth, ileal resection, or disease. The three-stage Schilling test results often can help differentiate these conditions.

13C-D-xylose breath test

Hope et al suggested that small intestinal malabsorption in chronic alcoholism may be determined by a 13C-D-xylose breath test.[14] The investigators evaluated the 13C-D-xylose breath test in 14 alcoholics, compared the breath test results with those of untreated celiac patients and healthy controls, and correlated the breath test findings to morphologic findings of the duodenal mucosa.[14] Their findings showed significantly reduced absorption of 13C-D-xylose in the alcoholic individuals relative to the healthy controls, whereas the time curve of 13C-D-xylose absorption in the alcoholics was similar in appearance to that of the untreated celiac patients. In addition, despite few light microscopic changes in the alcoholic individuals, morphologic pathology, primarily a reduced surface area of microvilli, was observed under electron microscopy in the majority of the patients.[14]


Upper endoscopy with small bowel mucosal biopsy

Establishing a definitive diagnosis of malabsorption of the mucosal phase often can be achieved by histologic examination of biopsied mucosal specimens obtained during routine upper endoscopy.

Examples of conditions that can be diagnosed this way include celiac sprue, giardiasis, Crohn disease, Whipple disease, amyloidosis, abetalipoproteinemia, and lymphoma.

Magnification narrow band imaging with upper endoscopy for the evaluation of duodenal villi may be predictive for the presence of villous atrophy or normal villi, which could be helpful for targeted biopsies.[15] In a prospective study, 16 of 100 patients who underwent upper endoscopy with magnification narrow band imaging for suspected malabsorption had histologically confirmed villous atrophy. Two endoscopists independently demonstrated this technique had a greater than 80% sensitivity (87.5% vs 81.3%) and a more than 92% specificity (95.2% vs 92.9%) for detecting villous atrophy; the interobserver agreement was very good (kappa = 0.87).[15]


Colonoscopy with intubation of the terminal ileum may be useful in the evaluation of ileal Crohn disease.

Histologic Findings

Depending on the cause, the histologic features of malabsorption vary. A frequently encountered histologic finding is villous atrophy, which is seen in celiac disease, tropical sprue, viral gastroenteritis, bacterial overgrowth, inflammatory bowel disease, immunodeficiency syndromes, lymphoma, and radiation enteritis.

Medical Care

Two basic principles underlie the management of patients with malabsorption, (1) the correction of nutritional deficiencies, and (2) when possible, the treatment of causative diseases.

Nutritional support

Caloric and protein replacement is essential. It is crucial to supplement the patient with various minerals, such as calcium, magnesium, iron, and vitamins, which may be deficient in malabsorption. 

Medium-chain triglycerides can be used as fat substitutes, because they do not require micelle formation for absorption and their route of transport is portal rather than lymphatic.

In severe intestinal disease, such as extensive regional enteritis and following a massive resection, parenteral nutrition may become necessary.

Treatment of causative diseases

A gluten-free diet helps treat celiac disease. Similarly, a lactose-free diet helps correct lactose intolerance; supplementing the first bite of milk-containing food products with a product such as Lactaid also helps.

The use of protease and lipase supplements are the therapy for pancreatic insufficiency. Antibiotics are used to treat small intestinal bacterial overgrowth. Corticosteroids, anti-inflammatory agents, such as mesalamine, and other therapies are used to treat regional enteritis. Pancreatic enzymes supplementation is the treatment for pancreatic insufficiency.


Muhammad Bader Hammami, MD, Fellow in Inflammatory Bowel Disease, St Louis University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editors

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

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.

Chief Editor

Praveen K Roy, MD, AGAF, Clinical Assistant Professor of Medicine, University of New Mexico School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Stephan U Goebel, MD, Assistant Professor of Gastroenterology and Hepatology, Department of Medicine, Emory University School of Medicine

Disclosure: Nothing to disclose.

Tushar Patel, MB, ChB, Professor of Medicine, Ohio State University Medical Center

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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