Malabsorption refers to a state arising from abnormality in absorption of food nutrients across the gastrointestinal tract.
Malabsorption constitutes the interference of the normal physiological sequence of digestion, absorption, and transport of nutrients.
Intestinal malabsorption can be due to Congenital or acquired reduction in absorptive surfaces, defects of ion transport,
defects of specific hydrolysis, Impaired enterohepatic circulation,
mucosal damage, and pancreatic insufficiency.
Absorption impairment can be of single or multiple nutrients depending on the abnormality.
Malabsorption may lead to malnutrition and a variety of anemias.
Causes of malabsorption:
Coeliac disease; short bowel syndrome; lactase deficiency; exocrine pancreatic insufficiency; small intestinal bacterial overgrowth; Whipple’s disease; genetic diseases; certain medications
Treatment depends on the cause of the malabsorption.
Normally the human gastrointestinal tract digests and absorbs dietary nutrients with remarkable efficiency.
A typical Western diet ingested by an adult in one day includes approximately 100 g of fat, 400 g of carbohydrate, 100 g of protein, 2 L of fluid, and the required sodium, potassium, chloride, calcium, vitamins, and other elements.
Salivary, gastric, intestinal, hepatic, and pancreatic secretions add an additional 7–8 L of protein-, lipid-, and electrolyte-containing fluid to intestinal contents.
Gastrointestinal tract secretions:
Saliva 500-1500 cc/d
Stomach 1500-2500 cc/d
Bile 500-1000 cc/d
Pancreas 600-1500cc/d
Intestine 1000-1800cc/d
The above is reduced by the small and large intestines to less than 200 g of stool that contains less than 8 g of fat, 1–2 g of nitrogen, and less than 20 mmol each of Na+, K+, Cl–, HCO3–, Ca2+, or Mg2+.
If impairment in any of the many steps involved in nutrient digestion and absorption, intestinal malabsorption may ensue.
If the abnormality involves a single step in the absorptive process, as in primary lactase deficiency, or if the disease process is limited to the very proximal small intestine, then selective malabsorption of only a single nutrients may occur.
With generalized malabsorption, deficiencies in multiple dietary nutrients develop when the disease process is extensive, thus disturbing several digestive and absorptive processes.
Gastrointestinal manifestations depend
on the nature of the underlying disease process causing malabsorption, and its extent.
Gastrointestinal symptoms with malabsorption may range from severe to subtle or may even be totally absent.
Diarrhea, weight loss, flatulence, abdominal bloating, abdominal cramps, and pain may be present.
Although diarrhea is a common complaint.
With malabsorption the character and frequency of stools may vary considerably ranging from over 10 watery stools per day to less than one voluminous putty-like stool.
Stool mass is invariably increased in patients with steatorrhea
and generalized malabsorption: above the normal with 150–200 g/day.
Unabsorbed nutrients contribute to stool mass.
Mucosal fluid and electrolyte secretion is also increased in diseases associated with mucosal inflammation such as coeliac disease.
Unabsorbed fatty acids, converted to hydroxy-fatty acids by colonic flora, as well as unabsorbed bile acids both impair absorption and induce secretion of water and electrolytes by the colon adding to stool mass.
Weight loss is common among patients with significant intestinal malabsorption.
Some patients unabsorbed nutrients by significantly increasing their oral intake.
Excessive flatus and abdominal bloating may be a result of excessive gas production due to fermentation of unabsorbed carbohydrate, especially with a primary or secondary disaccharidase deficiency, such as lactose intolerance or sucrose intolerance.
Malabsorption of dietary nutrients and excessive fluid secretion in an inflamed small intestine also contribute to abdominal distention and bloating.
The prevalence, severity, and character of
abdominal pain varies considerably among the various disease processes: pain is common in patients with chronic pancreatitis or pancreatic cancer and Crohn’s disease, but it is absent in many patients with coeliac disease or postgastrectomy malabsorption.
Extraintestinal manifestations in patients with intestinal malabsorption, frequently present with symptoms or laboratory abnormalities that point to other organ systems in the absence of or overshadowing symptoms referable to the gastrointestinal tract:
coeliac disease present with anemia and osteopenia in the absence of significant classic gastrointestinal symptoms,
anemia may reflect impaired iron, folate, or vitamin B12 absorption, purpura, subconjunctival hemorrhage, or even frank bleeding may reflect hypoprothrombinemia secondary to vitamin K malabsorption.
Osteopenia is common, especially in the presence of steatorrhea.
With malabsorption there is Impaired calcium and vitamin D absorption and chelation of calcium by unabsorbed fatty acids resulting in fecal loss of calcium.
Prolonged malnutrition may induce amenorrhea, infertility, impotence, and edema.
Ascites may reflect hypoproteinemia associated with protein losing enteropathy caused by lymphatic obstruction or extensive mucosal inflammation.
Dermatitis may be caused by malabsorption of specific vitamins or micronutrients and essential fatty acids.
Symptoms predominates in severe malabsorption.
Diarrhea, often steatorrhea, are the most common features of malabsorption.
The clinical hallmark of overt malabsorption: Watery, diurnal and nocturnal, bulky, frequent stools, caused
by impaired water, carbohydrate and electrolyte absorption or irritation from unabsorbed fatty acid.
Malabsorption results in bloating, flatulence and abdominal discomfort.
Cramping pain usually suggests obstructive intestinal segment.
Cramping abdominal pain is seen with Crohn’s disease, especially if it persists after defecation.
Weight loss with malabsorption can be significant despite increased oral intake of nutrients.
Growth retardation, failure to thrive, and delayed puberty in children may be seen.
Edema from loss of protein can occur.
Anemia from vitamin B12, folic acid and iron deficiency presenting as fatigue and weakness can be present.
Muscle cramps from decreased vitamin D, calcium absorption are seen, leading to osteomalacia and osteoporosis.
Bleeding tendencies from vitamin K and other coagulation factor deficiencies are seen in malabsorption.
Causes of malabsorption:
Due to infection
HIV related malabsorption
Intestinal tuberculosis
Parasites: diphyllobothrium (fish tape worm) leading to B12 malabsorption), giardiasis (Giardia lamblia), hookworm (Ancylostoma duodenale roundworm, and Necator americanus.
Traveler’s diarrhea
Tropical sprue
Whipple’s disease
Due to structural defects
Blind loops
Fistulae, diverticula and strictures
Infiltrative conditions such as amyloidosis, lymphoma, eosinophilic gastroenteritis
Inflammatory bowel diseases, as in Crohn’s disease
Radiation enteritis
Short bowel syndrome
Systemic sclerosis and collagen vascular diseases
Due to surgical structural changes
Bariatric surgery
Gastrectomy; Vagotomy
Due to mucosal abnormalities
Coeliac disease
Cows’ milk intolerance
Fructose malabsorption
Soya milk intolerance
Due to enzyme deficiencies
Lactase deficiency inducing lactose intolerance
Intestinal disaccharidase deficiency
Intestinal enteropeptidase deficiency
Sucrose intolerance
Due to digestive failure
Bile acid/Bile salt malabsorption
Bacterial overgrowth
Obstructive jaundice
Primary bile acid diarrhea
Terminal ileal disease such as Crohn’s disease
Pancreatic insufficiencies:
Carcinoma of pancreas
Chronic pancreatitis
Cystic fibrosis
Zollinger-Ellison syndrome
Other systemic diseases affecting GI tract
Abetalipoproteinaemia
Addison’s disease
Carcinoid syndrome
Coeliac disease
Common variable immunodeficiency (CVID)
Fiber Deficiency
Hypothyroidism and hyperthyroidism
Diabetes mellitus
Hyperparathyroidism and Hypoparathyroidism
Malnutrition
Chronic Proton Pump Inhibitor Use
The main purpose of the gastrointestinal tract is to digest and absorb nutrients including fat, carbohydrate, protein, micronutrients (vitamins and trace minerals), water, and electrolytes.
Digestion involves both mechanical and enzymatic breakdown of food.
Chewing, gastric churning, and the to-and-fro mixing in the small intestine are the mechanical processes of the GI tract.
Enzymatic hydrolysis is initiated by intraluminal processes requiring gastric, pancreatic, and biliary secretions, with the final products of digestion are absorbed through the intestinal epithelial cells.
DIAGNOSIS:
Evaluation is guided by symptoms and signs.
Because a number of different conditions can produce malabsorption and it is necessary to evaluate each of these specifically.
Many tests have been advocated, and some, such as tests for pancreatic function are complex, vary between centers and have not been widely adopted. However, better tests have become available with greater ease of use, better sensitivity and specificity for the causative conditions.
Tests are also needed to detect the systemic effects of deficiency of the malabsorbed nutrients vitamin B12 malabsorption.
Malabsorption may be selective, as seen in lactose malabsorption.
partial, as observed in abetalipoproteinaemia.
total, as in celiac disease.
Laboratory tests:
CBC may reveal anemia, high CRP or low albumin; which shows a high correlation for the presence of an organic disease.
Microcytic anaemia usually implies iron deficiency and macrocytosis can be caused by impaired folic acid or B12 absorption or both.
Low cholesterol or triglyceride may suggest fat malabsorption.
Low calcium and phosphate may cause osteomalacia from low vitamin D absorption.
Fat soluble vitamins (A, D, E and K) are affected in fat malabsorption.
Prolonged prothrombin time can be caused by vitamin K deficiency.
IgA Anti-transglutaminase antibodies or IgA Anti-endomysial antibodies for celiac disease
Stool studies:
Microscopy is particularly useful in diarrhea, may show protozoa like Giardia, ova, cyst and other infective agents.
Fecal fat study to diagnose steatorrhoea
Low fecal pancreatic elastase is indicative of pancreatic insufficiency.
Chymotrypsin and pancreolauryl can be assessed
Barium follow through is useful in delineating small intestinal anatomy.
Barium enema may be undertaken to see colonic or ileal lesions.
CT abdomen is useful in ruling out structural abnormality, and visualising pancreas.
Magnetic resonance cholangiopancreatography (MRCP) to complement or as an alternative to ERCP.
Biopsy of small bowel showing coeliac disease manifested by blunting of villi, crypt hyperplasia, and lymphocyte infiltration of crypts.
Esophago-gastro-duodenoscopy to detect duodenal pathology and obtain biopsy for coeliac disease, tropical sprue, Whipple’s disease, abetalipoproteinaemia.
Enteroscopy for enteropathy and jejunal aspirate and culture for bacterial overgrowth
Capsule endoscopy is able to visualize the whole small intestine and is occasionally useful.
Colonoscopy is necessary in colonic and ileal disease.
ERCP will show pancreatic and biliary structural abnormalities.
75SeHCAT test to diagnose bile acid malabsorption in ileal disease or primary bile acid diarrhea.
Glucose hydrogen breath test for bacterial overgrowth
Lactose hydrogen breath test for lactose intolerance
Sugar probes or 51Cr-EDTA to determine intestinal permeability.
Treatment is directed largely towards management of underlying cause:
Replacement of nutrients, electrolytes and fluid may be necessary.
In severe deficiency, nutritional support is required.
Use of enteral nutrition by naso-gastric or other feeding tubes may be sufficient nutritional supplementation.
If intestinal absorptive surfaces are severely limited from disease or surgery, long term total parenteral nutrition may be needed.
Pancreatic enzymes are supplemented orally in pancreatic insufficiency.
Dietary modifications:
Gluten-free diet in celiac disease.
Lactose avoidance in lactose intolerance.
Antibiotic therapy to treat Small Bowel Bacterial overgrowth.
Cholestyramine or other bile acid sequestrants will help reducing diarrhoea in bile acid malabsorption.