Malabsorption of lipids

Several diseases, called malabsorption syndromes, result in the lack of absorption of a number of nutrients. Their consequent loss in the feces dearly is not desirable. Malabsorption of lipids, which occurs more frequently than malabsorption of any other class of nutrient, can result in diarrhea and steatorrhea. Steatorrhea, production of feces with a high fat content, derives its name from "stearic add," a fatt> acid, With severe steatorrhea, over 30 g fat may appear in the feces per day. The problem can be elicited by liver diseases that piev ent the pn>duction of bile salts and thus impair the absorption of fats. 

Deficiencies. The current model for the cause of vitamin E deficiencies points to malabsorption of lipids. Thus, there may be malabsorption of other lipid-soluble vitamins. Little is known regarding the pharmacokinetics of the tocopherols. Part of the reason for this may be attributed to lack of a specific storage organ for the vitamin. 

The consequences of such injury are, of course, not only malabsorption because of the reduction in the surface epithelium and in microvilli, but ineffective digestion because of reduction in enzyme secretion and breakdown of conjugated bile acids. The result is total malabsorption of lipid, protein, sugar, electrolytes, calcium, and both lipid-soluble and water-soluble vitamins. 

Steatorrhea, the clinical result of insufficient intraluminal lipid hydrolysis, is the most important digestive malfunction in pancreatic exocrine insufficiency. As a rule, concomitant malabsorption of the lipid-soluble vitamins A, D, E, and K must be suspected in these patients. Naturally, potential differential diagnoses have to be considered in patients who present with steatorrhea (Table 26-1). The pivotal role of fat malabsorption in chronic pancreatitis is due to several interacting mechanisms ... 

Endoscopic analysis and intestinal biopsies are useful to rule out other diseases of the intestine and to confirm ABL. In ABL, the intestinal lumen has a gelee blanche or white frothy appearance from massive accumulation of lipids within the mucosa, which persists even in the setting of a low-fat diet. On microscopic evaluation of a biopsy sample taken from this region, inflammation commonly observed in other malabsorption syndromes is usually ab-... 

Persons at risk for EFA deficiency tend to be the same as those at risk for vitamin E deficiency. Some signs are shared by both defidencies. Premature infants may be at risk for EFA deficiency because of their low stores of lipids and their rapid growth, especially when they are fed diets that do not contain EFAs. For example, fats have been omitted from diets used to feed preterm infants (to avoid a variety of complications). EFA deficiency may develop later in life with fat malabsorption syndromes, EFA deficiency has presented in adults fed by total parenteral nutrition for longer periods, where EFAs had not been included in the liquid diet. 

It has been recommended for many years that the use of liquid paraffin should be discontinued because of its propensity to cause malabsorption of fat-soluble vitamins, to leak and soil the perineal skin, and to cause lipid pneumonia if aspirated at the very least it should be avoided in young children (35). 

Blockage of the bile duct caused by problems such as cholesterol-containing gallstones or duodenal or pancreatic tumors can lead to an inadequate concentration of bile salts in the intestine. Digestion and absorption of dietary lipids is diminished. Certain diseases that affect the pancreas can lead to a decrease in bicarbonate and digestive enzymes in the intestinal lumen. (Bicarbonate is required to raise the intestinal pH so that bile salts and digestive enzymes can function.) If dietary fats are not adequately digested, steatorrhea may result. Malabsorption of fats can lead to caloric deficiencies and lack of fat-soluble vitamins and essential fatty acids. 

Normally more than 95% of ingested lipid is absorbed. When a large fraction is excreted in the feces, it is called steatorrhea. Measurement of fecal lipid with adequate lipid intake is a sensitive indicator of lipid malabsorption. Malabsorption can result from impairment in lipolysis (Table 12-6), micelle formation (Table 12-7), absorption, chylomicron formation, or transport of chylomicrons via the lymph to blood. 

Vitamin E is absorbed as free tocopherol, along with other fat-soluble vitamins and dietary lipids. Tocopheryl acetate, the form commonly used for dietary supplementation, is hydrolyzed before absorption. Uptake requires bile salts. A selective impairment of vitamin E absorption without malabsorption of other fat-soluble vitamins has been identified it was corrected after a large oral intake of the vitamin. Patients with chronic fat malabsorption and abetalipoproteinemia (Chapter 20) may develop vitamin E deficiency. 

Xenobiotic-induced pancreatitis may be accompanied by gross plasma lipid changes that may result from marked changes of carbohydrate metabolism (see Chapter 9). The observation of the presence of gross macroscopic fecal fat content (steatorrhea) can indicate effects on pancreatic function, biliary dysfunction, or intestinal malabsorption. In longer-term studies, malabsorption of fat-soluble vitamins may be reflected by the clinical condition of vitamin-deficient animals. 

The vitamin is absorbed through the intestine by a mechanism similar to that involved in the absorption of other liposoluble vitamins consequently, intestinal disorders leading to lipid malabsorption are associated with malabsorption of vitamin E. Humans with such malabsorption syndromes have reduced levels of vitamin E in their tissues. They do not show classical symptoms of muscular dystrophy, although a certain degree of muscular fatigue may be observed. 

Vitamin E deficiency is seen rarely in humans. However, there may be a risk of vitamin E deficiency in premature infants because the placenta does not transfer a-tocopherol to the fetus in adequate amounts. When it occurs in older children and adults, it is usually a result of lipoprotein deficiencies or a lipid malabsorption syndrome. These include patients with abetalipoproteinemia or homozygous hypobeta-lipoproteinemia, those with cholestatic disease, and patients receiving total parenteral nutrition. There is also an extremely rare disorder in which primary vitamin E deficiency occurs in the absence of lipid malabsorption. This disorder is a rare autosomal recessive neurodegenerative disease caused by mutations in the gene for a-TTP. This disorder is known as ataxia with vitamin E deficiency (AVED). Patients with AVED have extraordinary low plasma vitamin E concentrations (<5pgml ) and have an onset between 4 and 18 years, with progressive development of peripheral neuropathy,... 

Since B12 only occurs in meat, deficiendes are likely to result firom a strict vegetarian diet containing no animal produrts. Vitamin B12 defidency is also estimated to affect 10-15% of individuals over the age of 60. Vitamin B12 is absorbed firom the small intestine as a complex with a protein called intrinsic factor (IF). The most common cause of vitamin B12 defidency is pernicious anaemia which is an autoimmune disease where the cells of the stomach become inflamed and do not secrete the required amounts of add and enzymes to release vitamin B12 firom food. In addition, antibodies to IF further prevent B12 absorption. The condition is treated with high doses of vitamin B12 supplements or by intramuscular injection of vitamin B12. A similar condition occurs in the elderly where there is malabsorption of vitamin B12 horn food due to decreased secretion of stomach add. This condition is easier to treat with supplementation since IF levds are still normal. Symptoms indude megaloblastic anaemia, neuropathy, memory loss and abnormalities of lipid metabolism. 

Malabsorption of fat can also occur in a number of inherited disorders in which the biosynthesis of different apoproteins in the enterocytes is impaired. Without the apoproteins, the stabilization of the lipid droplets cannot occur and the fat cannot be transported out of the cell. Triacylglycerols then begin to accumulate in the enterocyte. 

Hypolipoproteinemias Abetaiipoproteinemia No chylomicrons, VLDL, or LDL are formed because of defect in the loading of apo B with lipid. Rare blood acylglycerols low intestine and liver accumulate acylglycerols. Intestinal malabsorption. Early death avoidable by administration of large doses of fat-soluble vitamins, particularly vitamin E. 

As patients lose exocrine function of the pancreas, they have decreased ability to absorb lipids and protein ingested with normal dietary intake. Weight loss from nutritional malabsorption is a common symptom of chronic pancreatitis not often seen in acute pancreatitis. Fatty- or protein-containing stools are also common carbohydrate absorption is usually unaffected. Even though patients with chronic pancreatitis have decreased ability to absorb lipid from the gastrointestinal tract, there does not appear to be an increased incidence of fat-soluble vitamin deficiency in these patients.34... 

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