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Fat Malabsorption Syndrome

Fat Malabsorption Syndrome

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A short writeup on fat malabsorption syndrome
A short writeup on fat malabsorption syndrome

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Published by: Vytheeshwaran Vedagiri on Jul 12, 2010
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02/21/2013

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Fat Malabsorption SyndromeFat malabsorption syndrome is caused by functional or organiccauses. Symptoms and signs include fatigue, weight changes, steatorrhea,abdominal distention, cramps, gas, explosive diarrhea with foul smellingstools, malnutrition and weight loss, and biochemical abnormalities. Under normal dietary conditions, less than 5% of the ingested fat is observed in thefeces. An increase in this value might indicate fat malabsorption. Thedigestive process of fat in the digestive system involves the pancreatic stage,the biliary stage and the cellular and delivery stage into the small intestines.A lingual lipase is responsible for the first partial hydrolysis of triglycerides; this enzyme becomes active in persons with low gastric pHlevels and is active even in premature infants. However, the largest part of triglyceride digestion is accomplished in the duodenojejunal lumen becauseof a complex of pancreatic enzymes, the most important of which is thelipase–colipase complex. Like amylase, these enzymes also develop slowly,and this accounts for the known low capacity of babies to absorb lipids,termed physiologic steatorrhea of the newborn. Additionally, adequateconcentrations of intraluminal conjugated bile salts are needed to formmicelles, and the secretion of bile acids may also be partially inadequate invery young patients.Disorders of these processes can be congenital (cystic fibrosis andShwachman–Diamond syndrome, which cause lipase and colipasedeficiency; the uncommon isolated deficiency of lipase and colipase; theextremely rare congenital primary bile acid malabsorption, which results inlow bile acids concentrations) or acquired (secondary mostly to disorders of the liver and the biliary tract or to chronic pancreatitis).Some of the conditions which are associated with the malabsorptionof lipids are tabulated as follows:
Stage Conditions
Pancreatic stage
Isolated pancreatic lipase or colipasedeficiency (inherited)
Pancreatic insufficiency
o
Cystic fibrosis
o
Chronic pancreatitis
 
o
Obstruction of pancreatic duct
o
Pancreatic cancer 
o
Pancreatic resection
o
Shwachman–Diamond syndrome
o
Johnson–Blizzard syndrome
o
Pearson syndromeBiliary stage
Decreased bile salt synthesis in severehepatic insufficiency
Decreased delivery of bile salts in biliarytract obstruction or cholestatic biliarydisease
Decreased concentration of conjugated bile salts due to increased acidity, drugsaffecting micelle formation
Increased intestinal loss of bile salts due tosurgery or diseased terminal ileumCellular and delivery stage
Rapid transit, dumping syndrome
Improper emulsification, following certaintypes of gastrectomy
Zollinger–Ellison syndrome (alteredduodenal pH)
Decrease in small intestine lymphaticsDefects in multiple stages of digestions and absorption
Decreased CCK release due to mucosaldestruction as in sprue or regional enteritis(Crohn’s disease)
Conditions associated with malabsorption of lipids (Modified from Tietz. Textbook of Clinical Chemistry)
Apart from the aforementioned conditions fat malabsorption couldalso be resultant of abetalipoproteinemia is a rare disorder with autosomalrecessive inheritance. Absence of the lipoproteins results in cytoplasmiclipid accumulation in the enterocyte. Lymphatic transport of long-chain fatsis impaired in patients with abetalipoproteinemia, lymphangiectasia, and protein-losing enteropathy, resulting in moderate fat malabsorption.Individuals with malabsorption syndrome must be monitored for dehydration (dry tongue, mouth, and skin, increased thirst, low, concentratedurine output, feeling weak and dizzy when standing). An individual should be evaluated for nutrient depletion and should be evaluated for signs
 
including nausea or vomiting, fissures at the corners of mouth, fatigue or weakness, and dry pluckable hair.Individuals who have inflammatory bowel disease have an increasedrisk of nephrolithiasis; enteric hyperoxaluria is the major risk factor with fatmalabsorptive states, and use of probiotics to decrease oxalate levels is beingstudied and considered.Long term nutritional monitoring is necessary after gastric bypasssurgery for morbid obesity which can lead to fat malabsorption and vitamindeficiencies for Vitamin A, D, E, and K. In addition, altered calciummetabolism can lead to decline in bone health. In addition, malabsorption of dietary and biliary phosphatidylcholine may result in choline deficiency.To avoid nutritional deterioration, early screening for fatmalabsorption should be recommended using the acid steatocrit, a reliableand inexpensive test. Intake of 40g of olestra can cause false positive resultson tests for steatorrhea and can lead to an erroneous diagnosis of malabsorption syndrome. Low total cholesterol (120mg/dL) or low serumcarotene levels may be typical of fat malabsorption but not necessarilydiagnostic. Altered stools characterize different types of malabsorption.Fecal fat study may be useful.The clinical analysis of fat malabsorption can be mapped as follows(From Modern Nutrition In Health & Disease- M. Shils, 10
th
ed (pg 1150):

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