Vitamin Steatorrhea

Weight loss, steatorrhea, and vitamin B12 and fat-soluble vitamin deficiencies... 

Abetalipoproteinemia or Bassen-Kornzweig syndrome, a potentially disabling, familial disease characterized by lack of plasma TGs, malabsorption of fat-soluble vitamins, liver steatosis, steatorrhea, and other symptoms, is linked to mutations in the MTP functional subunit [52,53],... 

B4. Barnes, B. C., Wollaeger, E. E., and Mason, H. L., The comparative absorption of vitamin A from a water-miscible and an oily preparation by normal human adults and patients with steatorrhea. J. Clin. Invest. 29, 982-987 (1950). 

G9. Grasbeck, R., Kantero, I., and Srurala, M., Influence of calcium ions on vitamin B12 absorption in steatorrhea and pernicious anaemia. Lancet i, 234 (1959). 

Bile. The liver forms a thin secretion (bile) that is stored in the gallbladder after water and salts have been extracted from it. From the gallbladder, it is released into the duodenum. The most important constituents of bile are water and inorganic salts, bile acids and bile salts (see p. 314), phospholipids, bile pigments, and cholesterol. Bile salts, together with phospholipids, emulsify insoluble food lipids and activate the lipases. Without bile, fats would be inadequately cleaved, if at all, resulting in fatty stool (steatorrhea). Resorption of fat-soluble vitamins would also be affected. 

Oral As a dietary supplement when calcium intake may be inadequate. Conditions that may be associated with calcium deficiency include the following Vitamin D deficiency, sprue, pregnancy and lactation, achlorhydria, chronic diarrhea, hypoparathyroidism, steatorrhea, menopause, renal failure, pancreatitis, hyperphosphatemia, and alkalosis. Some diuretics and anticonvulsants may precipitate hypocalcemia, which may validate calcium replacement therapy. Calcium salt therapy should not preclude the use of other corrective measures intended to treat the underlying cause of calcium depletion. 

Enhanced anticoagulant effects Endogenous factors that may be responsible for increased PT/INR response include the following Blood dyscrasias cancer collagen vascular disease CHF diarrhea elevated temperature hepatic disorders (eg, infectious hepatitis, jaundice) hyperthyroidism poor nutritional state steatorrhea vitamin K deficiency. 

Abuse/Dependency Chronic use of laxatives, particularly stimulants, may lead to laxative dependency, which in turn may result in fluid and electrolyte imbalances, steatorrhea, osteomalacia, vitamin and mineral deficiencies, and a poorly functioning colon. Also known as laxative abuse syndrome (LAS), it is difficult to diagnose. Cathartic colon Cathartic colon, a poorly functioning colon, results from the chronic abuse of stimulant cathartics. 

A major symptom of fat malabsorption is steatorrhea, production of bulky, foul-smelling feces that float due to high fat content, which may be accompanied by diarrhea and abdominal pain, and if sustained for a period of days or weeks, lead to deficiencies of the fat-soluble vitamins. 

The answer is B. This patient s greasy, foul-smelling stools indicate steatorrhea. Her vision problems may be a manifestation of vitamin A deficiency due to fat malabsorption. The most likely explanation is biliary insufficiency, ie, decreased bile salt production leading to poor emulsification of dietary fats. Active ileal disease is a possibility, but the WBC count would likely be elevated unless her condition was in remission. Infection with Giardia is less likely due to the absence of pathogenic organisms in her stool. Lactose intolerance can produce diarrhea but not steatorrhea. 

Deficiency of vitamin E is characterized by low serum tocopherol levels and a positive hydrogen peroxide hemolysis test. This deficiency is believed to occur in patients with biliary, pancreatic, or intestinal disease that is characterized by excessive steatorrhea. Premature infants with a high intake of fatty acids exhibit a deficiency syndrome characterized by edema, anemia, and low tocopherol levels. This condition is reversed by giving vitamin E. 

In patients who have preexisting bowel disease or cholestasis, steatorrhea may occur. Malabsorption of vitamin occurs rarely, leading to hypoprothrombinemia. Prothrombin time should be measured frequently in patients who are taking resins and anticoagulants. Malabsorption of folic acid has been reported rarely. Increased formation of gallstones, particularly in obese persons, was an anticipated adverse effect but has rarely occurred in practice. 

Adverse effects of octreotide therapy include nausea, vomiting, abdominal cramps, flatulence, and steatorrhea with bulky bowel movements. Biliary sludge and gallstones may occur after 6 months of use in 20-30% of patients. However, the yearly incidence of symptomatic gallstones is about 1%. Cardiac effects include sinus bradycardia (25%) and conduction disturbances (10%). Pain at the site of injection is common, especially with the long-acting octreotide suspension. Vitamin B12 deficiency may occur with long-term use of octreotide. 

Exocrine pancreatic insufficiency is most commonly caused by cystic fibrosis, chronic pancreatitis, or pancreatic resection. When secretion of pancreatic enzymes falls below 10% of normal, fat and protein digestion is impaired and can lead to steatorrhea, azotorrhea, vitamin malabsorption, and weight loss. Pancreatic enzyme supplements, which contain a mixture of amylase, lipase, and proteases, are the mainstay of treatment for pancreatic enzyme insufficiency. Two major types of preparations in use are pancreatin and pancrelipase. Pancreatin is an alcohol-derived extract of hog pancreas with relatively low concentrations of lipase and proteolytic enzymes, whereas pancrelipase is an enriched preparation. On a per-weight basis, pancrelipase has approximately 12 times the lipolytic activity and more than 4 times the proteolytic activity of pancreatin. Consequently, pancreatin is no longer in common clinical use. Only pancrelipase is discussed here. 

In chylomicron retention disease (Anderson s disease) the secretory defect is restricted to intestinal apoB-containing lipoproteins (i.e., chylomicrons). This very rare recessively inherited disorder results from defects in a GTPase, Sarlb, which plays a critical role in the intracellular assembly and trafficking of chylomicrons. The affected patients present with fat malabsorption resulting in steatorrhea and deficiency of fat-soluble vitamins [46, 52, 54]. 

It should be noted that deficiency states for some vitamins (e.g., pantothenic acid) are practically unknown in human beings. In such cases, deficiency states may be simulated by feeding the subject an appropriate vitamin antagonist. In another series of situations, vitamin deficiencies can be brought about by interfering with their absorption intentionally or may be the result of a disease process. Thus, fat-soluble vitamin deficiency may develop in cases of fat malabsorption syndromes (steatorrhea) sprue, pancreatic insufficiency, and bile duct obstruction. 

Normally there is very little fat in the feces. However, fat content in stools may increase because of various fat malabsorption syndromes. Such increased fat excretion is steatorrhea. Decreased fat absorption may be the result of failure to emulsify food contents because of a deficiency in bile salts, as in liver disease or bile duct obstruction (stone or tumor). Pancreatic insufficiency may result in an inadequate pancreatic lipase supply. Finally, absorption itself may be faulty because of damage to intestinal mucosal cells through allergy or infection. An example of allergy-based malabsorption is celiac disease, which is usually associated with gluten intolerance. Gluten is a wheat protein. An example of intestinal infection is tropical sprue, which is often curable with tetracycline. Various vitamin deficiencies may accompany fat malabsorption syndromes. 

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 ... 

Abetalipoproteinemia (ABL) is a rare, autosomal recessive disease first described by Bassen and Kornsweig in 1950. It is characterized by the absence of plasma apoB lipoproteins, fat-soluble vitamin deficiencies (A, E, and K), and the presence of acanthocytosis (Table 27-1). Other signs include fat malabsorption presenting as steatorrhea, flatus, abdominal discomfort, and progressive ataxic neuropathy. The key diagnostic feature is an extremely low plasma total cholesterol and absence of all apoB lipoproteins (chylomicrons, VLDL, and LDL). 

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. 

The bacteria colonizing the small bowel (such as Escherichia coli and Bacteroides species) deconjugate and dehydroxylate bde salts, leading to conjugated bde salt deficiency, which causes fat malabsorption. Bacterial metabolism of vitamin B12 may also occur, leading to vitamin B,2 deficiency. The clinical symptoms of bacterial overgrowth are abdominal pain, diarrhea, and steatorrhea. ... 

Ion exchange resins (colestipol,colestyramine), which complex with the brie salts and can interfere with the absorption of the oil-soluble vitamins Aluminum antacids can complex with some of the vitamins and, when used chronically, most definitely can cause hypophosphatemia Cystic fibrosis, which can cause fat malabsorption (steatorrhea) attributed to inadequate production of pancreatic lipases... 

In cholestasis, bile salts and bile pigments are retained and appear in the circulation, and steatorrhea and deficiencies of fat-soluble vitamins may occur. These deficiencies are often manifested as hypoprothrombinemia (from lack of vitamin K) and osteomalacia (from lack of vitamin D). The magnitude depends on the degree of obstruction. If blockage is complete, urinary urobilinogen will be absent and the stools will have a pale, clay-like color. 

In addition to nutritional inadequacy, vitamin deficiency may result from malabsorption, effects of pharmacological agents, and abnormalities of vitamin metabolism or utilization. Thus, in biliary obstruction or pancreatic disease, the fat-soluble vitamins are poorly absorbed despite adequate dietary intake because of steatorrhea. Absorption, transport, activation, and utilization of vitamins require the participation of enzymes or other proteins whose synthesis is under genetic control. Dysfunction or absence of one of these proteins can produce a disease that is clinically indistinguishable from one caused by dietary deficiency. In vitamin-dependent or vitamin-responsive... 

The fat-soluble vitamins share many properties despite their limited chemical similarity. They are absorbed into the intestinal lymphatics, along with other dietary lipids, after emulsification by bile salts. Lipid malabsorption accompanied by steatorrhea usually results in poor uptake of all the fat-soluble vitamins. Deficiency disease (except in the case of vitamin K) is difficult to produce in adults because large amounts of most fat-soluble vitamins are stored in the liver and in adipose tissue. The fat-soluble vitamins are assembled from isoprenoid units this fact is apparent from examination of the structures of vitamins A, E, and K cholesterol, the precursor of vitamin D, is derived from six isoprenoid units (Chapter 18). Specific biochemical functions for vitamins A, D, and K are known, but a role for vitamin E, other than as a relatively nonspecific antioxidant, remains elusive. 

Because of the lipase deficiency, fat-soluble vitamin (A, D, E, and K) deficiencies may occur. Whether lipase activity or bile acids (e.g., in micelle formation) are involved in fat-soluble vitamin absorption with steatorrhea is unclear. Vitamin and zinc deficiencies also may occur as aresult of pancreatic enzyme deficiency. Although pancreatic involvement is predominantly exocrine in nature, insulin deficiency with glucose intolerance also occurs in CF patients, especially as they advance in age. Carbohydrate intolerance is characterized by low insulin concentrations and enhanced peripheral sensitivity to insulin but not by the presence of islet cell or anti-insulin antibodies. Carbohydrate intolerance in CF is not usually associated with the ketosis as commonly occurs in type 1 diabetes. This complication involves an increase in the number of insulin receptors with decreased affinity for insulin. Despite a concomitant increase in tissue affinity for insulin, 8% of CF children over 12 years of age require insulin therapy. 

Lanthanum carbonate Decreased dietary phosphorus intake Glucocorticoids Vitamin D deficiency/resistance Hypoparathyroidism Chronic diarrhea Steatorrhea... 

Bile has long been attributed an important role in medicine [1]. The effect of an impaired bile flow to the intestine has been known to result in steatorrhea — fat malabsorption — and defective absorption of fat-soluble vitamins, notably vitamin K [2], Thus, it is obvious that bile is important for fat assimilation from the intestine. However, it is equally apparent that when fat absorption after bile obstruction or diversion could be studied by quantitative methods, the malabsorption was found to be only partial [3]. In fact, it has seemed surprising that some 60-70% of a normal fat load is absorbed in man and the experimental animal in the absence of bile in the intestine. The absorption of nonpolar lipids, however, is much less efficient, and cholesterol absorption has been reported to have an absolute requirement for the presence of bile salts [4]. Of the bile components important for fat absorption bile salts have been ascribed the main role although experimental results are accumulating regarding the role of bile phospholipids in the specific uptake of sterols by the intestine [5]. 

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