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Malabsorption


Anatomic Classification of Malabsorption

Carbohydrate digestion requires a functioning pancreas and small bowel brush border enzymes. Normal protein digestion requires adequate gastric and pancreatic function and small bowel brush border enzymes. Fat digestion requires normal hepatic, biliary, exocrine, pancreatic, and small bowel function. An anatomic classification of malabsorption based on abnormalities of the liver, biliary tree, pancreas, stomach, and small intestine aids the radiologist in understanding malabsorption ( Table 29.1 ).

TABLE29.1
Anatomically Oriented Classification of Malabsorption
Organ Disease or Condition Pathophysiology
Stomach Zollinger-Ellison syndrome Pancreatic enzyme inactivation by acid
Postgastrectomy Rapid transit of nutrients, dilution of pancreatic enzymes
Pernicious anemia Intrinsic factor deficiency (vitamin B 12 malabsorption)
Pancreas Chronic pancreatitis, cystic fibrosis, pancreatic cancer Decreased pancreatic enzyme and bicarbonate secretion
Liver, biliary tree Severe parenchymal liver disease Decreased bile salt formation
Cholestatic liver disease (primary biliary cirrhosis, drug-induced cholestasis), bile duct obstruction (bile duct carcinoma, pancreatic cancer, gallstones, sclerosing cholangitis) Decreased bile salt delivery to duodenum
Small intestine Jejunal diverticulosis, scleroderma, small intestinal fistulas, stricture in Crohn’s disease, diabetes, pseudo-obstruction Stasis with bacterial overgrowth, bile salt deconjugation
Crohn’s disease, small intestinal resection, cholecystocolonic fistula Increased bile salt loss
Lactase deficiency, Crohn’s disease Disaccharidase deficiency
Celiac disease, tropical sprue, Whipple’s disease, eosinophilic gastroenteritis, radiation enteropathy, Crohn’s disease, intestinal ischemia, ileal resection Loss of normal epithelial cells
Abetalipoproteinemia Lack of formation of chylomicrons
Lymphangiectasia, lymphoma, tuberculosis, carcinoid Lymphatic obstruction
Diabetes mellitus, giardiasis, adrenal insufficiency, hyperthyroidism, hypogammaglobulinemia, amyloidosis, AIDS Multiple causes
From Rubesin SE, Rubin RA, Herlinger H. Small bowel malabsorption: Clinical and radiological perspectives. Radiology. 1992;184:297–305.

HEPATOBILIARY AND PANCREATIC DISORDERS

Bile salt insufficiency caused by biliary obstruction or decreased hepatic synthesis can lead to malabsorption. Any disease resulting in loss of pancreatic exocrine tissue decreases bicarbonate and pancreatic enzyme secretion, but maldigestion does not occur until 90% of pancreatic exocrine tissue has been lost. The most common pancreatic cause of maldigestion is alcohol-related pancreatitis. Patients with cystic fibrosis have malabsorption, but this disease is much less common.

GASTRIC DISORDERS

Diseases of the stomach may cause mild malabsorptive states. Patients with pernicious anemia have decreased production of intrinsic factor, leading to vitamin B 12 deficiency. Patients with Zollinger-Ellison syndrome have inflammation and ulceration of the duodenum and proximal jejunum, causing diarrhea without malabsorption. About one-third of patients with Zollinger-Ellison syndrome also have diarrhea because of gastric hypersecretion and intestinal mucosal damage. Mild malabsorption results from inactivation of pancreatic enzymes by excess acid entering the duodenum.

SMALL BOWEL DISORDERS

Small bowel disorders cause malabsorption through a wide variety of mechanisms involving the small bowel lumen or wall or even the small bowel mesentery (see Table 29.1 ).

Intraluminal Stasis with Bacterial Overgrowth

Any disease that causes small bowel stasis can lead to bacterial overgrowth and subsequent malabsorption ( Box 29.1 ). Stasis may be caused by chronic small bowel obstruction (SBO) from conditions such as Crohn’s disease and adhesions or by small bowel hypomotility from conditions such as diabetes, scleroderma, and jejunal diverticulosis. Stasis and bacterial overgrowth may also occur in surgically created blind small bowel loops or in the afferent loop of a gastrojejunostomy.

BOX 29.1
DISEASES CAUSING SMALL BOWEL HYPOMOTILITY AND MALABSORPTION a

GENETIC DISORDERS

  • Familial visceral neuropathies

  • Familial visceral myopathies

  • Muscular dystrophy

COLLAGEN-VASCULAR DISORDERS

  • Progressive systemic sclerosis

  • Dermatomyositis, polymyositis

  • Periarteritis nodosa

  • Systemic lupus erythematosus

ENDOCRINE DISORDERS

  • Diabetes mellitus

  • Hypothyroidism

  • Hypoparathyroidism

NEUROLOGIC DISEASES

  • Spinal cord injury

  • Parkinson’s disease

  • Multiple sclerosis

  • Chagas’ disease

DRUGS

  • Narcotics

  • Phenothiazines

  • Antiparkinson medications

  • Ganglionic blockers

  • Tricyclic antidepressants

OTHER

  • Celiac disease

  • Radiation enteritis

  • Jejunal diverticulosis

  • Amyloidosis

  • Lead poisoning

a Disorders typically causing a malabsorptive state are highlighted in bold. Data from Rubesin SE. Diseases of the small bowel causing malabsorption. In: Taveras JM, Ferrucci JT, eds. Radiology: Diagnosis, Imaging, Intervention . Philadelphia: JB Lippincott; 1993:1–17.

Bacterial overgrowth causes malabsorption by several mechanisms, including intraluminal bacterial deconjugation of bile salts and fermentation of carbohydrates. Concomitant epithelial cell dysfunction may be present. Bacterial digestion of malabsorbed fat forms compounds that can stimulate small bowel or colonic secretion. Solutes of malabsorbed carbohydrates and deconjugated bile salts are also osmotically active, resulting in water and electrolyte loss.

Brush Border Disease

Brush border enzyme deficiencies or transport mechanism deficiencies may cause osmotic diarrhea, malabsorption, or both. The most common example of osmotic diarrhea caused by brush border disaccharidase deficiency is so-called lactase deficiency (lactose-phlorizin hydrolase deficiency) with lactose intolerance. Brush border lactose-phlorizin hydrolase levels normally decline in older children and adolescents to 5% to 10% of early childhood levels, resulting in a high frequency of lactase-phlorizin hydrolase deficiency by adulthood. Ingestion of dairy products therefore causes diarrhea, flatulence, and crampy abdominal discomfort in most adults.

Mucosal Damage

Inflammation or necrosis of crypt cells and immature villous cells causes secretory diarrhea, whereas blood, pus, or mucus in the intestinal lumen leads to osmotic diarrhea. Widespread epithelial damage is therefore characterized by a combination of secretory and osmotic diarrhea and nutrient malabsorption. Diseases that destroy proximal small bowel epithelium cause generalized malabsorption of fats, proteins, carbohydrates, iron, and folate, whereas diseases that damage distal ileal mucosa primarily cause malabsorption of fat because of bile salt loss and vitamin B 12 deficiency. Mucosal diseases causing malabsorption typically involve long segments of small bowel. These conditions, which are relatively uncommon, include celiac disease, tropical sprue, Whipple’s disease, and eosinophilic enteritis.

Postmucosal Disease

Any disorder that obstructs lacteals in small bowel villi or lymphatics in the small bowel mesentery may cause fat malabsorption. In primary lymphangiectasia, for example, abnormal formation of lymphatics results in impaired absorption of chylomicrons and fat-soluble vitamins and loss of lymph into the intestinal lumen from lymphoenteric fistulas.

Diseases with Multifactorial Causes

Malabsorption is often multifactorial. In amyloidosis, for example, malabsorption is attributed to stasis with bacterial overgrowth, mucosal ischemia, and disruption of nutrient absorption by amyloid deposition in the lamina propria. In contrast, malabsorption in hyperthyroidism is attributed to rapid small bowel transit.

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