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Malabsorption From Wikipedia, the free encyclopedia Jump to: navigation, search Malabsorption Classification and external resources Whipple's disease: Alcian blue with apparently eosin counterstain enlarged villus with many macrophages  ICD-10 (K90) ICD-9 579 DiseasesDB 7698 MedlinePlus 000299 eMedicine med/1384MeSH D008286 Malabsorption is a state arising from abnormality in  absorption  of  food nutrients  across the gastrointestinal (GI) tract . Impairment can be of single or multiple nutrients depending on the abnormality. This may lead to malnutrition  and a variety of  anaemias . [1]  

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Malabsorption

From Wikipedia, the free encyclopedia

Jump to: navigation, search 

Malabsorption

Classification and external resources 

Whipple's disease: Alcian blue with apparently eosin 

counterstain enlarged villus with many macrophages 

ICD-10  (K90) 

ICD-9  579

DiseasesDB 7698

MedlinePlus 000299

eMedicine med/1384 

MeSH D008286

Malabsorption is a state arising from abnormality in absorption of  food nutrients across the

gastrointestinal (GI) tract. 

Impairment can be of single or multiple nutrients depending on the abnormality. This may lead

to malnutrition and a variety of  anaemias.[1] 

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Contents

[hide] 

  1 Classification 

  2 Pathophysiology 

  3 Causes 

  4 Clinical features 

  5 Diagnosis 

o  5.1 Blood tests 

o  5.2 Stool studies o  5.3 Radiological studies 

o  5.4 Interventional studies 

o  5.5 Other investigations 

o  5.6 Obsolete tests no longer used clinically 

  6 Management 

  7 See also   8 References 

  9 External links 

[edit] Classification

Some prefer to classify malabsorption clinically into three basic categories:[2]

 

(1) selective, as seen in lactose malabsorption;

(2) partial, as observed in a-Beta-lipoproteinaemia, and(3) total as in coeliac disease. 

[edit] Pathophysiology

The main purpose of the gastrointestinal tract is to digest and absorb nutrients (fat, carbohydrate, 

protein, and fiber), micronutrients (vitamins and trace minerals), water, and electrolytes. Digestion involves both mechanical and enzymatic breakdown of food. Mechanical processes 

include chewing, gastric churning, and the to-and-fro mixing in the small intestine. Enzymatic

hydrolysis is initiated by intraluminal processes requiring gastric, pancreatic, and biliary

secretions. The final products of digestion are absorbed through the intestinal epithelial cells.

Malabsorption constitutes the pathological interference with the normal physiological sequence

of  digestion (intraluminal process), absorption (mucosal process) and transport (postmucosalevents) of nutrients.[3] 

Intestinal malabsorption can be due to:[4]

 

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  Mucosal damage (enteropathy) 

  Congenital or acquired reduction in absorptive surface

  Defects of specific hydrolysis 

  Defects of  ion transport

  Pancreatic insufficiency

 Impaired enterohepatic circulation 

[edit] Causes

Due to infective agents 

  Whipple's disease 

  Intestinal tuberculosis 

  HIV related malabsorption

  Tropical sprue 

  traveller's diarrhoea 

  Parasites e.g. Giardia lamblia, fish tape worm (B12 malabsorption); roundworm ,hookworm ( Ancylostoma duodenale and Necator americanus)

Due to structural defects[5]

 

  Blind loops 

  Inflammatory bowel diseases commonly in Crohn's Disease 

  Intestinal hurry from Post-gastrectomy; post-vagotomy, gastro-jejunostomy 

  Fistulae, diverticulae and strictures, 

  Infiltrative conditions such as amyloidosis, lymphoma, Eosinophilic gastroenteropathy 

  Radiation enteritis 

  Systemic sclerosis and collagen vascular diseases

  Short bowel syndrome 

Due to mucosal abnormality 

  Coeliac disease 

  Cows' milk intolerance

  Soya milk intolerance

  Fructose malabsorption 

Due to enzyme deficiencies 

  Lactase deficiency inducing lactose intolerance (constitutional, secondary or rarely

congenital)

  Sucrose intolerance 

  Intestinal disaccharidase deficiency

  Intestinal enteropeptidase deficiency

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Due to digestive failure 

  Pancreatic insufficiencies:

o  cystic fibrosis 

o  chronic pancreatitis 

o  carcinoma of pancreas o  Zollinger-Ellison syndrome 

  Bile salt malabsorption 

o  terminal ileal disease

o  obstructive jaundice 

o  bacterial overgrowth 

o  primary bile acid diarrhea 

Due to other systemic diseases affecting GI tract 

  Coeliac disease 

  Hypothyroidism and hyperthyroidism   Addison's disease 

  Diabetes mellitus 

  Hyperparathyroidism and Hypoparathyroidism 

  Carcinoid syndrome 

  Malnutrition

  Fiber Deficiency

  Abeta-lipoproteinaemia 

[edit] Clinical features

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 Small intestine : major site of absorption

They can occur in a variety of ways and features might give a clue to the underlying condition.

Symptoms can be intestinal or extra-intestinal - the former predominates in severe

malabsorption.

  Diarrhoea, often steatorrhoea is the most common feature. Watery, diurnal and nocturnal,

bulky, frequent stools are the clinical hallmark of overt malabsorption. It is due to

impaired water, carbohydrate and electrolyte absorption or irritation from unabsorbed

fatty acid. Latter also results in bloating, flatulence and abdominal discomfort. Crampingpain usually suggests obstructive intestinal segment e.g. in Crohn's disease, especially if 

it persists after defecation.[3]

 

  Weight loss can be significant despite increased oral intake of nutrients.[6]

 

  Growth retardation, failure to thrive, delayed puberty in children

  Swelling or oedema from loss of  protein 

 Anaemias, commonly from vitamin B12, folic acid and iron deficiency presenting asfatigue and weakness.

  Muscle cramp from decreased vitamin D, calcium absorption. Also lead to osteomalacia 

and osteoporosis 

  Bleeding tendencies from vitamin K and other coagulation factor deficiencies.

[edit] Diagnosis

There is no specific test for malabsorption. As for most medical conditions, investigation isguided by symptoms and signs. A range of different conditions can produce malabsorption and it

is necessary to look for each of these specifically. Many tests have been advocated, and some,

such as tests for pancreatic function are complex, vary between centres and have not been widelyadopted. However, better tests have become available with greater ease of use, better sensitivity

and specificity for the causative conditions. Test are also needed to detect the systemic effects of 

deficiency of the malabsorbed nutrients (such as anaemia with vitamin B12 malabsorption).

[edit] Blood tests

  Routine blood tests may reveal anaemia, high CRP or low albumin; which shows a highcorrelation for the presence of an organic disease.[7][8] In this setting, 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 give a clue toward fat

malabsorption as low calcium and phosphate toward osteomalacia from low vitamin D.  Specific vitamins like vitamin D or micro nutrient like zinc levels can be checked. Fat

soluble vitamins (A, D, E & K) are affected in fat malabsorption. Prolonged prothrombin

time can be caused by vitamin K deficiency.

  Serological studies

Specific tests are carried out to determine the underlying cause.

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IgA Anti-transglutaminase antibodies or IgA Anti-endomysial antibodies for Coeliac

disease(gluten sensitive enteropathy).

[edit] Stool studies

  Microscopy is particularly useful in diarrhoea, may show protozoa like Giardia, ova, cystand other infective agents.

  Fecal fat study to diagnose steatorrhoea is rarely performed nowadays.

  Low fecal pancreatic elastase is indicative of pancreatic insufficiency. Chymotrypsin and

pancreolauryl can be assessed as well[9] 

[edit] Radiological studies

  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, done in pancreatic protocol

when visualising pancreas.   Magnetic resonance cholangiopancreatography (MRCP) to complement or as an

alternative to ERCP 

[edit] Interventional studies

Biopsy of  small bowel showing coeliac disease manifested by blunting of  villi, crypt hyperplasia, 

and lymphocyte infiltration of crypts.

  OGD to detect duodenal pathology and obtain D2 biopsy (for coeliac disease, tropical

sprue, Whipple's disease, abetalipoproteinaemia etc.)  Enteroscopy for enteropathy and  jejunal aspirate and culture for bacterial overgrowth

  Capsule Endoscopy is able to visualise the whole small intestine and is occasionally

useful.

  Colonoscopy is necessary in colonic and ileal disease.

  ERCP will show pancreatic and biliary structural abnormalities.

[edit] Other investigations

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  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 or51

Cr-EDTA to determine intestinal permeability.[3]

 

[edit] Obsolete tests no longer used clinically

  D-xylose absorption test for mucosal disease or bacterial overgrowth. Normal in

pancreatic insufficiency.

  Bile salt breath test (14

C-glycocholate) to determine bile salt malabsorption.

  Schilling test to establish cause of B12 deficiency.

[edit] Management

Treatment is directed largely towards management of underlying cause:

  Replacement of nutrients, electrolytes and fluid may be necessary. In severe deficiency,hospital admission may be required for parenteral administration, often advice from

dietitian is sought. People whose absorptive surface are severely limited from disease or

surgery may need long term total parenteral nutrition. 

  Pancreatic enzymes are supplemented orally in insufficiencies.

  Dietary modification is important in some conditions:

o  Gluten-free diet in coeliac disease. 

o  Lactose avoidance in lactose intolerance. 

  Antibiotic therapy will treat Small Bowel Bacterial overgrowth. 

  Cholestyramine or other bile acid sequestrants will help reducing diarrhoea in bile acid

malabsorption. 

[edit] See also