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Malabsorption can affect macronutrients (eg, proteins, carbohydrates, fats), micronutrients (eg, vitamins, minerals), or both, causing excessive fecal excretion, nutritional deficiencies, and gastrointestinal (GI) symptoms. Malabsorption may be global, with impaired absorption of almost all nutrients, or partial (isolated), with malabsorption of only specific nutrients.

Pathophysiology of Malabsorption

Digestion and absorption occur in three phases:

Intraluminal hydrolysis of fats, proteins, and carbohydrates by enzymes—bile salts enhance the solubilization of fat in this phase

Digestion by brush border enzymes and uptake of end-products

Lymphatic transport of nutrients

The term malabsorption is commonly used when any of these phases is impaired, but, strictly speaking, impairment of phase 1 is maldigestion rather than malabsorption.

Digestion of fats

Pancreatic enzymes (lipase and colipase) split long-chain triglycerides into fatty acids and monoglycerides, which combine with bile acids and phospholipids to form micelles that pass through jejunal enterocytes. Absorbed fatty acids are resynthesized and combined with protein, cholesterol, and phospholipid to form chylomicrons, which are transported by the lymphatic system. Medium-chain triglycerides are absorbed directly.

Unabsorbed fats trap fat-soluble vitamins (A, D, E, K) and possibly some minerals, causing deficiency. Bacterial overgrowth results in deconjugation and dehydroxylation of bile salts, limiting the absorption of fats. Unabsorbed bile salts stimulate water secretion in the colon, causing diarrhea.

Digestion of carbohydrates

The pancreatic enzyme amylase and brush border enzymes on microvilli lyse carbohydrates and disaccharides into constituent monosaccharides. Colonic bacteria ferment unabsorbed carbohydrates into carbon dioxide, methane, hydrogen, and short-chain fatty acids (butyrate, propionate, acetate, and lactate). These fatty acids cause diarrhea. The gases cause abdominal distention and bloating.

Digestion of proteins

Gastric pepsin initiates digestion of proteins in the stomach (and also stimulates release of cholecystokinin that is critical to the secretion of pancreatic enzymes). Enterokinase, a brush border enzyme, activates trypsinogen into trypsin, which converts many pancreatic proteases into their active forms. Active pancreatic enzymes hydrolyze proteins into oligopeptides, which are absorbed directly or hydrolyzed into amino acids.


Abdominal pain.

Abdominal distension.



Nausea and vomiting.


Steatorrhea (fatty stools).


Cystic fibrosis (the number one cause in the United States)

Chronic pancreatitis.

Lactose intolerance.

Celiac disease.

Whipple disease.

Shwachman-Diamond syndrome (a genetic disease affecting the pancreas and bone marrow)

Cow's milk protein intolerance.

Risk factors

a family history of cystic fibrosis or malabsorption.

drinking large amounts of alcohol.

intestinal surgery.

use of certain medications, including laxatives or mineral oil.

travel to the Caribbean, India, and parts of Southeast Asia.

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 The complications associated with malabsorption depend upon the severity of the underlying condition. Malabsorption can lead to weight loss, malnutrition, and even failure to thrive in many people. A person can also experience impaired wound healing, a deficient immune system, and low energy levels.


ingesting proper amounts of fluids.

taking antimalarial medication for 12 to 18 months.

using iron supplements to assist with anemia.

taking vitamin D, vitamin K, calcium, and magnesium supplements.

maintaining a high-calorie diet to help with nutrient absorption.