Under malabsorption refers to an inadequate assimilation of food components due to disturbances of digestion, absorption and transport.

The malabsorption can macronutrients (eg., Proteins, carbohydrates and fats), micronutrients (eg. As vitamins, minerals) or both concern and leads to the excretion of large amounts of stool and deficiencies and gastrointestinal symptoms. Malabsorption may be global, with reduced intake of almost all nutrients, or partially (isolated), with malabsorption only certain nutrients.

Under malabsorption refers to an inadequate assimilation of food components due to disturbances of digestion, absorption and transport. The malabsorption can macronutrients (eg., Proteins, carbohydrates and fats), micronutrients (eg. As vitamins, minerals) or both concern and leads to the excretion of large amounts of stool and deficiencies and gastrointestinal symptoms. Malabsorption may be global, with reduced intake of almost all nutrients, or partially (isolated), with malabsorption only certain nutrients. Pathophysiology digestion and absorption occur in three phases: intraluminal hydrolysis of fat, proteins and carbohydrates by enzymes – Increase bile salts the emulsification of fat in this phase digestion by brush border and recording of final lymphatic transport of nutrients. The term malabsorption is often used when one of these phases is impaired, but strictly speaking is meant by an impairment of the Phase 1 rather maldigestion instead malabsorption. The digestion of fats, the pancreatic enzymes lipase and colipase cleave the long-chain triglycerides into fatty acids and monoglycerides, which combine with bile acids and phospholipids form micelles and be absorbed by the jejunal enterocytes. Absorbed fatty acids are resynthesized and forming after connection with protein, cholesterol and phospholipids chylomicrons which are transported through the lymphatic system. Medium chain triglycerides can be absorbed directly. Unabsorbed fat retains fat-soluble vitamins (A, D, E, K) and possibly some minerals, causing deficiencies. A bacterial overgrowth leads to deconjugation and dehydroxylation of bile salts and limits the fat absorption. Unabsorbed bile salts stimulate water secretion in the colon and cause Diarrhö.Verdauung of carbohydrates The amylase enzyme pancreatic and brush border of microvilli lyse carbohydrates and disaccharides to monosaccharides. Colonic bacteria to ferment carbohydrates to unabsorbed Carbondioxid, methane, hydrogen and short-chain fatty acids (butyrate, propionate, acetate and lactate). These fatty acids cause diarrhea. The intestinal gases cause a bloated abdomen and Blähungen.Verdauung of proteins initiates the pepsin digestion of proteins in the stomach (and also stimulates the release of cholecystokinin, which is critical for the secretion of pancreatic enzymes). Enterokinase, a Bürstensaumenzym activates trypsinogen to trypsin, which converts a number of pancreatic proteases in their active form. Active pancreatic enzymes hydrolyze proteins to oligopeptides that are directly absorbed or hydrolyzed to amino acids. Etiology Malabsorption has many causes (see Table: Causes of malabsorption). Some malabsorptive diseases (eg. As the celiac disease) impair the absorption of most nutrients, vitamins and trace elements (global malabsorption), others (eg. As pernicious anemia) are more selective. Pancreatic insufficiency causes malabsorption, if> 90% of the function are lost. An increased luminal acidic environment (eg. As Zollinger-Ellison syndrome) inhibits lipase and fat digestion. Cirrhosis and cholestasis reduce the hepatic bile acid synthesis or the release of bile salts into the duodenum and cause malabsorption. Other causes are addressed elsewhere in this chapter. Acute bacterial, viral and parasitic infections (see p. A. Overview of the gastroenteritis) can cause a temporary malabsorption, probably as a result of a temporary superficial damage to the villi and microvilli. Chronic bacterial infection of the small intestine are rare, apart from blind loops, scleroderma, and diverticula. Intestinal bacteria consume vitamin B12 and other nutrients and interfere possibly with enzyme systems and cause mucosal damage. Causes of malabsorption mechanism cause insufficient mixing in the stomach and / or rapid emptying Billroth II gastrectomy Gastrokolische fistulas gastroenterostomy Insufficient digestive enzymes biliary obstruction and cholestasis cirrhosis Chronic pancreatitis Cholestyramininduzierter bile acid loss cystic fibrosis lactase deficiency pancreatic pancreatectomy sucrose isomaltase deficiency variation of the environment Abn orme motility in diabetes, scleroderma, hypothyroidism or hyperthyroidism Bacterial overgrowth by blind intestinal loops (deconjugation of bile acids), diverticula in the small intestine Zollinger-Ellison syndrome (low duodenal pH) Acute epithelial Acute enteric infections alcohol neomycin Chronic epithelial amyloidosis celiac disease Crohn’s disease ischemia radiation enteritis Tropical sprue Whipple’s short bowel bowel resection (eg. As in Crohn’s disease, volvulus, intussusception, or infarction) Jejunoileal bypass in obesity Impaired transport Abetalipoproteinemia Addison Clogged lymph due to lymphoma or TB intrinsic factor deficiency (as in pernicious anemia) Lymphangiectasia symptoms and complaints The consequences nichtresorbierter substances insbesonder at the global malabsorption are diarrhea, steatorrhea, Darmblähungen and increased air. Other symptoms are due to the lack of nutrients. Patients often lose weight, even though their food intake is adequate. Chronic diarrhea is the most common symptom and the one that is usually a clarification of patients occasion. Steatorrhea – fatty stools, an essential feature of malabsorption – occur when> 7 g fat excreted per day. The steatorrhea caused foul-smelling, pale, bulky and greasy stools. The symptoms depend on the particular nutrient deficiency (see Table: Symptoms of malabsorption). Severe vitamin and mineral deficiencies occur in advanced malabsorption. Vitamin B12 deficiency occurs when so-called blind loop syndrome or after extensive resection of the distal ileum or Magens.p.p1 {margin: 0.0px 0.0px 0.0px 0.0px;. font: 16.0px Helvetica; -webkit-text-stroke: # 000000} span.s1 {font-kerning: none} iron deficiency may be the only symptom in a patient with mild malabsorption. Symptoms of malabsorption symptoms Malabsorbierter nutritional anemia (hypochromic, microcytic) iron anemia (macrocytic) Vitamin B12, folic acid bleeding, bruising, petechiae vitamins K and C Karpopedalspasmen Ca, Mg edema Protein glossitis vitamins B2 and B12, folic acid, niacin, iron night blindness Vitamin A pain in limbs, bone, pathological fractures K, Mg, Ca, vitamin D Peripheral neuropathy vitamins B1, B6, B12 amenorrhea may arise as a result of malnutrition and an important manifestation of celiac disease in young women. Diagnosis Diagnosis usually clinically obvious from a detailed history of blood tests to check the consequences of malabsorption stool tests to confirm the malabsorption (when unclear) establishing the cause is made by endoscopy, X-ray contrast images or other tests based on the findings Suspected malabsorption is often the patient chronic diarrhea, weight loss and anemia. The etiology is sometimes obvious. For example, patients with malabsorption due to chronic pancreatitis usually mode already earlier episodes of acute pancreatitis. In patients with celiac disease is dermatitis herpetiformis can live long exhibit diarrhea, which is reinforced by gluten products, as well as occasionally. In patients with cirrhosis and a pancreatic jaundice may be present. A strained abdomen, excessive bloating and watery diarrhea that occurs 30-90 min after carbohydrate digestion is suggestive of a lack of Disaccharidaseenzymen, usually lactase. Earlier extensive abdominal operations can think of a short bowel syndrome. When the history leads to a specific cause, should in this respect be diagnosed (Recommended clarification malabsorption.). If a cause is not clear, blood tests can be used as screening tools (eg. As total blood count, erythrocyte indices, ferritin, vitamin B12, folic acid, calcium, albumin, cholesterol, PT). The test results may suggest a diagnosis and guide further investigation. Recommended clarification malabsorption. The existence of a macrocytic anemia induced the determination of folic acid and vitamin B12 in serum. A folic acid deficiency (celiac disease, tropical sprue, Whipple’s disease z. B.) in diseases of the mucosa, relating to the proximal small intestine, often. Low vitamin B12 levels occur in pernicious anemia in chronic pancreatitis, with bacterial overgrowth and disease in the terminal ileum. A combination of low vitamin B12 and folate levels high is suggestive of bacterial overgrowth because intestinal bacteria use vitamin B12 and folic acid synthesis. A microcytic anemia directs the suspicion of an iron deficiency, which can occur in a celiac disease. Albumin is a general indicator of the nutritional status. A low serum albumin may be the result of too low intake, decreased synthesis in cirrhosis or protein deficiency. A low serum carotene (a precursor of vitamin A) directs the Malabsorption when recording is adequate with the food. The diagnosis malabsorption Diagnostic tests to ensure the malabsorption are appropriate when the symptoms vague and the etiology is not obvious. Most tests for malabsorption capture the fat malabsorption because it is relatively easy to determine. Securing a Carbohydrate is not helpful if the Steatorrhea is already documented. There are few testing procedures for Proteinmalabsorption because nitrogen in the stool is difficult to measure. A direct measurement of the Stuhlfettsim 72-h chair is the gold standard for the diagnosis of steatorrhea, but it is not necessary if a massive steatorrhea already represents the apparent cause. However, this test is routinely available only in a few centers. The chair is collected over 3 days, during which the patient takes ? 100 g fat / day to himself. In the chair, the total fat is measured. A fecal fat content of> 7 g / day is pathological. Although the severe fat malabsorption suggests a pancreatic insufficiency or a disease of the small intestine (fecal fat ? 40 g / day), this test can not yet reveal the specific cause of malabsorption. Because the test is dirty, uncomfortable and time-consuming, it is not acceptable and therefore difficult to perform for most patients. A Sudan III staining of Stuhlausstrichs is a simple and direct, but no quantitative screening test for fecal fat. The Säuresteatokrit is a gravimetric test on a single fecal sample; its sensitivity and specificity (72-h chair as standard) are used as highly valued. The infrared reflectance analysis (Near-infrared reflectance analysis, NIRA) simultaneously investigated chair fat, nitrogen and carbohydrates and may be the preferred test zurkünftig. Currently, this test is only available in selected centers. A measurement of elastase and chymotrypsin in the stool can also help to distinguish the pancreatic and intestinal causes of malabsorption; both values ??are reduced in pancreatic insufficiency, whereas they are normal in intestinal cause. The d-xylose absorption test can be performed when the etiology should not be obvious. However, this test is used because of the advent of modern endoscopic and imaging techniques currently rare. Though he may allow a non-invasive assessment of the integrity of the intestinal mucosa and help distinguish diseases of the mucosa of pancreatic diseases, a striking result in the d-xylose test requires an endoscopic examination with biopsies of the small intestine mucosa. To determine a disease of the intestinal mucosa, small intestinal biopsy has therefore replaced this test. D-xylose is taken up by passive diffusion and does not require pancreatic enzymes for their digestion. A normal d-xylose test at the same time existing moderate to severe steatorrhea has more indicative of exocrine pancreatic insufficiency as a Mukosaerkrankung the small intestine. The syndrome of bacterial overgrowth can result in pathological results, because the intestinal bacteria metabolize pentose and reduce in this way be absorbed d-xylose. After fasting the patient is 25 g D-xylose in 200-300 ml water p.o. given. Urine is collected over a period of 5 h and extracted a venous blood sample after 1 h. Serum-d-xylose <20 mg / dl or <4 g in the urine sample is a sign of abnormal absorption. Falsely low levels may auftreten.Diagnostik the causes of malabsorption more specific diagnostic tests (eg. As upper endoscopy, colonoscopy, barium swallow) even with kidney disease, in portal hypertension, ascites or delayed gastric emptying are indexed to diagnose veschiedene causes of malabsorption , An upper endoscopy with small bowel biopsy is performed when a Mukosaerkrankung of the small intestine is suspected or when the d-xylose-test result is abnormal in a patient with massive fatty stools. Endoscopy allows visual assessment of the intestinal mucosa and enables direct biopsies of the affected areas. Aspirate from the small intestine can be sent for bacterial culture and colony count to document bacterial overgrowth when a clinical suspicion. A video capsule endoscopy can be used to study areas of the distal small intestine now that are beyond the reach of a regular endoscope. Use the histological findings of small bowel biopsy (see Table: Histology of the small intestinal mucosa in certain Malabsorptionskrankheiten) can diagnose the specific mucosal disease. Histology of the intestinal mucosa for certain disease Malabsorptionskrankheiten Histological peculiarities normal finger-shaped villi with a villous crypts ratio of about 4: 1; Epithelial numerous regular microvilli (brush); small round cells infiltration in the lamina propria celiac disease (untreated) Practically missing villi and crypts extended; increased intraepithelial lymphocytes and round cells (v a plasma cells..) in the lamina propria; cuboidal epithelial cells with poor, irregular microvilli Intestinal lymphangiectasia dilation and ectasia of the lymphatic vessels in the mucosa Tropical sprue areas of minimal changes in the villous height and moderate epithelial cell damage up to virtually lack of villi and elongated crypts with lymphocyte infiltration into the lamina propria Morbus Whipple lamina propria with dense infiltration of PAS-positive macrophages; Villous in severe cases, missing the help of X-ray examinations of the small intestine (eg. As small bowel barium enema, enteroclysis, CT Enterographie) can be the anatomical conditions that predispose to bacterial overgrowth elicit. These are: jejunal diverticula, fistulas, surgically created blind loops and anastomoses, ulceration and stricture. A radiograph of the abdomen may show calcifications in the pancreatic area, and indicates that a chronic pancreatitis. Bariumkontrasteinläufe in the small intestine are neither sensitive nor specific, but may yield results that are at least on a Mukosaerkrankung suspicious (z. B. expanded bowel loops, too thin or thickened mucosal folds, coarse speckled Bariumsäule). CT, magnetic resonance cholangiopancreatography (MRCP) and ERCP can confirm the diagnosis of chronic pancreatitis. Testing for pancreatic insufficiency (Pankreozymin secretin test, Bentiromidtest, pancreolauryl, Serumtrypsinogen, Stuhlelastase, Stuhlchymotrypsin) are indicated when the history leaves this suspect but are not sensitive at only slightly more pronounced disease of the pancreas. The 14C-xylose breath test is useful in the diagnosis of bacterial overgrowth. 14C-xylose administered orally and determines the secreted 14CO2 concentration. The degradation of recorded xylose by a bacterial overgrowth leads to the enrichment of 14CO2 in the exhaled air. The hydrogen (H2) 2atemtest measures exhaled hydrogen, which is produced by bacterial degradation of carbohydrates. In patients with a Disaccharidasemangel intestinal bacteria build nichtresorbierte carbohydrates in the colon, and thus increase the concentration of exhaled hydrogen. The lactose hydrogen breath test is only useful to confirm a lactase deficiency, and is not used for initial diagnosis of the Malabsorptionsabklärung. The 14C-xylose and the hydrogen breath test were replaced by bacterial cultures from aspirates, obtained during endoscopy for the diagnosis of bacterial overgrowth. The Schilling test detects a malabsorption of vitamin B12. Its four stages differentiate whether the defect is caused by a pernicious anemia, exocrine pancreatic insufficiency, bacterial overgrowth or intestinal diseases. Stage 1: The patient is 1 ug radioactive cyanocobalamin p.o. zusammnen 1000 ug "nonlabeled" cobalamin i.m. administered to saturation of hepatic binding sites. 24-h urine is examined for radioactivity; a urinary excretion of <8% of the oral dose suggests a malabsorption of cobalamin. Stage 2: If Stage 1 is abnormal, the test is repeated with the addition of intrinsic factor. Pernicious anemia is when the intrinsic factor normalized absorption. Stage 3: This stage 3 is carried out after the addition of pancreatic enzymes; normalization at this stage shows a cobalamin malabsorption as a result of pancreatic insufficiency. Stage 4: This stage 4 is performed by treatment with an antimicrobial cover the anaerobes; a normalization after treatment with antibiotics is suggestive of bacterial overgrowth. Cobalamin deficiency as a result of the small intestine disease or ileal resection leads to noticeable results at all stages. Examinations for less common causes of malabsorption, the serum gastrin (Zollinger-Ellison syndrome), intrinsic factor and parietal cell antibodies include (pernicious anemia), chloride in sweat (cystic fibrosis), lipoprotein (Abetalipoproteinemia) and Serum cortisol (Addison's disease). In order to diagnose a bile acid malabsorption, which in diseases of the terminal ileum (z. B. Crohn's disease, extensive resection of terminal ileum) may occur in the patient a therapeutic experiment can with a bile acid-binding resin (eg., Cholestyramine) be taken. Alternatively, a selenium homocholic acid taurine (SeHCAT) test can be performed. In this test, 75 Se-labeled synthetic bile acid is administered orally and measured after 7 days the stored bile acid with a whole body scan or a gamma camera. When the bile acid is disturbed, the retention is less than 5%.

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