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Malabsorption

From Wikipedia, the free encyclopedia
Abnormality in absorption of food nutrients across the gastrointestinal tract

Medical condition
Malabsorption
Whipple's disease: Alcian blue with apparentlyeosin counterstain enlargedvillus with manymacrophages
SpecialtyGastroenterology
ComplicationsMalnutrition;anaemia;steatorrhoea;diarrhoea
CausesCoeliac disease;short bowel syndrome;lactase deficiency;exocrine pancreatic insufficiency;small intestinal bacterial overgrowth;Whipple's disease; genetic diseases; certain medications[1]
TreatmentDepends on cause

Malabsorption is a state arising from abnormality inabsorption offood nutrients across thegastrointestinal (GI) tract. Impairment can be of single or multiple nutrients depending on the abnormality. This may lead tomalnutrition and a variety ofanaemias.[1]

Normally the human gastrointestinal tract digests and absorbs dietary nutrients with remarkable efficiency. A typical Western diet ingested by an adult in one day includes approximately 100 g of fat, 400 g of carbohydrate, 100 g of protein, 2 L of fluid, and the requiredsodium,potassium,chloride,calcium,vitamins, and other elements.[citation needed]Salivary,gastric,intestinal,hepatic, andpancreatic secretions add an additional 7–8 L of protein-, lipid-, and electrolyte-containing fluid to intestinal contents. This massive load is reduced by the small and large intestines to less than 200 g of stool that contains less than 8 g of fat, 1–2 g of nitrogen, and less than 20 mmol each ofNa+,K+,Cl,HCO3,Ca2+, orMg2+.

If there is impairment of any of the many steps involved in the complex process of nutrient digestion and absorption, intestinalmalabsorption may ensue. If the abnormality involves a single step in the absorptive process, as in primarylactase deficiency, or if the disease process is limited to the very proximal small intestine, then selective malabsorption of only a single nutrient may occur. However, generalizedmalabsorption of multiple dietary nutrients develops when the disease process is extensive, thus disturbing several digestive and absorptive processes, as occurs incoeliac disease with extensive involvement of thesmall intestine.[1]

Signs and symptoms

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Gastrointestinal manifestations

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Depending on the nature of the disease process causing malabsorption and its extent, gastrointestinal symptoms may range from severe to subtle or may even be totally absent.Diarrhea,weight loss,flatulence, abdominalbloating, abdominalcramps, and pain may be present. Although diarrhea is a common complaint, the character and frequency of stools may vary considerably ranging from over 10 watery stools per day to less than one voluminous putty-like stool, the latter causing some patients to complain of constipation. On the other hand, stool mass is invariably increased in patients withsteatorrhea and generalized malabsorption above the normal with 150–200 g/day. Not only do unabsorbed nutrients contribute to stool mass but mucosal fluid and electrolyte secretion is also increased in diseases associated with mucosal inflammation such ascoeliac disease. In addition, unabsorbed fatty acids, converted to hydroxy-fatty acids by colonic flora, as well as unabsorbedbile acids both impair absorption and induce secretion of water and electrolytes by the colon adding to stool mass. Weight loss is common among patients with significant intestinal malabsorption but must be evaluated in the context of caloric intake. Some patients compensate for fecal wastage of unabsorbed nutrients by significantly increasing their oral intake. Eliciting a careful dietary history from patients with suspected malabsorption is therefore crucial. Excessive flatus and abdominal bloating may reflect excessive gas production due to fermentation of unabsorbed carbohydrate, especially among patients with a primary or secondarydisaccharidase deficiency, such aslactose intolerance orsucrose intolerance. Malabsorption of dietary nutrients and excessive fluid secretion by inflamed small intestine also contribute to abdominal distention and bloating. Prevalence, severity, and character of abdominal pain vary considerably among the various disease processes associated with intestinal malabsorption. For example, pain is common in patients with chronic pancreatitis or pancreatic cancer andCrohn's disease, but it is absent in many patients with coeliac disease or postgastrectomy malabsorption.[1]

Extraintestinal manifestations

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Substantial numbers of patients with intestinal malabsorption present initially with symptoms or laboratory abnormalities that point to other organ systems in the absence of or overshadowing symptoms referable to the gastrointestinal tract. For example, there is increasing epidemiologic evidence that more patients with coeliac disease present withanemia andosteopenia in the absence of significant classic gastrointestinal symptoms. Microcytic,macrocytic, or dimorphic anemia may reflect impairediron, folate, orvitamin B12 absorption.Purpura,subconjunctival hemorrhage, or even frank bleeding may reflect hypoprothrombinemia secondary to vitamin K malabsorption. Osteopenia is common, especially in the presence ofsteatorrhea. Impaired calcium and vitamin D absorption and chelation of calcium by unabsorbed fatty acids resulting in fecal loss of calcium may all contribute. If calcium deficiency is prolonged, secondary hyperparathyroidism may develop. Prolonged malnutrition may induce amenorrhea, infertility, and impotence. Edema and even ascites may reflect hypoproteinemia associated with protein losing enteropathy caused bylymphatic obstruction or extensive mucosal inflammation. Dermatitis and peripheral neuropathy may be caused by malabsorption of specific vitamins or micronutrients and essential fatty acids.[2]

Presentation

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Small intestine : major site of absorption

Symptoms can manifest in a variety of ways and features might give a clue to the underlying condition. Symptoms can beintestinal or extra-intestinal - the former predominates in severe malabsorption.[citation needed]

Causes

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Due to infective agents[citation needed]
Due to structural defects[5]
Due to surgical structural changes
Due to mucosal abnormality
Due to enzyme deficiencies
Due to digestive failure
Due to othersystemic diseases affecting GI tract
Other Possible Causes
  • Chronic Proton Pump Inhibitor Use[7]

Pathophysiology

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The main purpose of thegastrointestinal tract is todigest andabsorb nutrients (fat,carbohydrate,protein, micronutrients (vitamins andtrace minerals), water, andelectrolytes.Digestion involves both mechanical andenzymatic breakdown of food.Mechanical processes include chewing, gastric churning, and the to-and-fro mixing in thesmall intestine.Enzymatic hydrolysis is initiated by intraluminal processes requiring gastric, pancreatic, and biliary secretions. The final products of digestion are absorbed through theintestinal epithelial cells.[citation needed]

Malabsorption constitutes the pathological interference with the normal physiological sequence ofdigestion (intraluminal process), absorption (mucosal process) and transport (postmucosal events) of nutrients.[3]

Intestinal malabsorption can be due to:[8]

Diagnosis

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There is no single, specific test for malabsorption. As for most medical conditions, investigation is guided bysymptoms 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 centers and have not been widely adopted. However, better tests have become available with greater ease of use, better sensitivity and specificity for the causative conditions. Tests are also needed to detect the systemic effects of deficiency of the malabsorbed nutrients (such as anaemia with vitamin B12 malabsorption).[citation needed]

Classification

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Some[who?] prefer to classify malabsorption clinically into three basic categories:[9]

  1. selective, as seen inlactose malabsorption.
  2. partial, as observed inabetalipoproteinaemia.
  3. total, as in exceptional cases ofcoeliac disease.[10]

Blood tests

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Stool studies

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  • Microscopy is particularly useful in diarrhoea, may show protozoa likeGiardia, ova, cyst and other infective agents.
  • Fecal fat study to diagnosesteatorrhoea is rarely performed nowadays.
  • Low fecal pancreaticelastase is indicative of pancreatic insufficiency.Chymotrypsin and pancreolauryl can be assessed as well[13]

Radiological studies

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Interventional studies

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Biopsy ofsmall bowel showingcoeliac disease manifested by blunting ofvilli, crypthyperplasia, andlymphocyte infiltration of crypts.

Other investigations

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Obsolete tests no longer used clinically

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  • D-xylose absorption test for mucosal disease or bacterial overgrowth. Normal in pancreatic insufficiency.
  • Bile salt breath test (14C-glycocholate) to determinebile salt malabsorption.
  • Schilling test to establish cause of B12 deficiency.

Management

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Treatment is directed largely towards management of underlying cause:[1]

See also

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References

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  1. ^abcde"Malabsorption Syndrome". MedlinePlus. Retrieved29 April 2018.
  2. ^Fine KD, Schiller LR (1999). "technical review on the evaluation and management of chronic diarrhea".Gastroenterology.116 (6):1464–1486.doi:10.1016/s0016-5085(99)70513-5.PMID 10348832.S2CID 12239612.
  3. ^abcBai J (1998). "Malabsorption syndromes".Digestion.59 (5):530–46.doi:10.1159/000007529.PMID 9705537.S2CID 46786949.
  4. ^health a to z"Malabsorption syndrome". Archived fromthe original on 2007-05-22. Retrieved2007-05-10.
  5. ^Losowsky, M.S. (1974).Malabsorption in clinical practice. Edinburgh: Churchill Livingstone.ISBN 0-443-01007-2.
  6. ^Afrin LB, Butterfield JH, Raithel M, Molderings GJ (2016)."Often seen, rarely recognized: mast cell activation disease--a guide to diagnosis and therapeutic options".The American Journal of the Medical Science.48 (3):190–201.doi:10.3109/07853890.2016.1161231.PMID 27012973.
  7. ^Heidelbaugh JJ (June 2013)."Proton pump inhibitors and risk of vitamin and mineral deficiency: evidence and clinical implications".Therapeutic Advances in Drug Safety.4 (3):125–133.doi:10.1177/2042098613482484.ISSN 2042-0986.PMC 4110863.PMID 25083257.
  8. ^Walker-Smith J, Barnard J, Bhutta Z, Heubi J, Reeves Z, Schmitz J (2002)."Chronic diarrhea and malabsorption (including short gut syndrome): Working Group Report of the First World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition".J. Pediatr. Gastroenterol. Nutr.35 (Suppl 2): S98–105.doi:10.1097/00005176-200208002-00006.PMID 12192177.S2CID 10373517.
  9. ^Gasbarrini G, Frisono M: Critical evaluation of malabsorption tests; inDobrilla G, Bertaccini G (1986). Langman G (ed.).Problems and Controversies in Gastroenterology. New York: Raven Pr. pp. 123–130.ISBN 88-85037-75-5.
  10. ^Newnham ED (2017)."Coeliac disease in the 21st century: paradigm shifts in the modern age".J Gastroenterol Hepatol (Review).32 (Suppl 1):82–85.doi:10.1111/jgh.13704.PMID 28244672.
  11. ^Bertomeu A, Ros E, Barragán V, Sachje L, Navarro S (1991). "Chronic diarrhea with normal stool and colonic examinations: organic or functional?".J. Clin. Gastroenterol.13 (5):531–6.doi:10.1097/00004836-199110000-00011.PMID 1744388.
  12. ^Read N, Krejs G, Read M, Santa Ana C, Morawski S, Fordtran J (1980)."Chronic diarrhea of unknown origin".Gastroenterology.78 (2):264–71.doi:10.1016/0016-5085(80)90575-2.PMID 7350049.
  13. ^abcThomas P, Forbes A, Green J, Howdle P, Long R, Playford R, Sheridan M, Stevens R, Valori R, Walters J, Addison G, Hill P, Brydon G (2003)."Guidelines for the investigation of chronic diarrhoea, 2nd edition".Gut. 52 Suppl 5 (90005): v1–15.doi:10.1136/gut.52.suppl_5.v1.PMC 1867765.PMID 12801941.
  14. ^Sankararaman S, Hendrix SJ, Schindler T (October 2022)."Update on the management of vitamins and minerals in cystic fibrosis".Nutrition in Clinical Practice.37 (5):1074–1087.doi:10.1002/ncp.10899.ISSN 0884-5336.PMC 9544449.PMID 35997322.
  15. ^Silvester JA, Kurada S, Szwajcer A, Kelly CP, Leffler DA, Duerksen DR (2017-09-01)."Tests for Serum Transglutaminase and Endomysial Antibodies Do Not Detect Most Patients With Celiac Disease and Persistent Villous Atrophy on Gluten-free Diets: a Meta-analysis".Gastroenterology.153 (3): 689–701.e1.doi:10.1053/j.gastro.2017.05.015.PMC 5738024.PMID 28545781.

External links

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Classification
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