Lactose intolerance classification: Difference between revisions
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==Overview== | ==Overview== | ||
There is no established system for the classification of lactose intolerance. Lactose intolerance may be classified according to its causes into 2 groups: primary lactose malabsorption and secondary lactose malabsorption. Primary lactose malabsorption may be classified into 3 subtypes: acquired primary lactase deficiency, congenital lactase deficiency and developmental lactase deficiency. Secondary lactose malabsorption occurs as a result of the underlying intestinal diseases such as [[small intestinal bacterial overgrowth]], small intestinal infection such as | There is no established system for the classification of lactose intolerance. Lactose intolerance may be classified according to its causes into 2 groups: primary lactose malabsorption and secondary lactose malabsorption. Primary lactose malabsorption may be classified into 3 subtypes: acquired primary lactase deficiency, congenital lactase deficiency and developmental lactase deficiency. Secondary lactose malabsorption occurs as a result of the underlying [[Intestine|intestinal]] diseases such as [[small intestinal bacterial overgrowth]], [[Small intestine|small intestinal]] [[infection]] such as [[giardiasis]] and [[Small intestine|small intestinal]] [[inflammation]]. | ||
==Classification== | ==Classification== | ||
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** Fermentation of [[lactose]] in the small bowel may be increased and leads to symptoms of lactose intolerance | ** Fermentation of [[lactose]] in the small bowel may be increased and leads to symptoms of lactose intolerance | ||
** Breath hydrogen levels peaks very early in lactose challenge test | ** Breath hydrogen levels peaks very early in lactose challenge test | ||
* Small intestinal infection such as giardiasis | * [[Small intestine|Small intestinal]] [[infection]] such as giardiasis | ||
* Small intestinal inflammation:<ref name="pmid24917953">{{cite journal |vauthors=Misselwitz B, Pohl D, Frühauf H, Fried M, Vavricka SR, Fox M |title=Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment |journal=United European Gastroenterol J |volume=1 |issue=3 |pages=151–9 |year=2013 |pmid=24917953 |pmc=4040760 |doi=10.1177/2050640613484463 |url=}}</ref><ref name="pmid120188073">{{cite journal |vauthors=Swagerty DL, Walling AD, Klein RM |title=Lactose intolerance |journal=Am Fam Physician |volume=65 |issue=9 |pages=1845–50 |year=2002 |pmid=12018807 |doi= |url=}}</ref><ref name="pmid9219788">{{cite journal |vauthors=Mishkin B, Yalovsky M, Mishkin S |title=Increased prevalence of lactose malabsorption in Crohn's disease patients at low risk for lactose malabsorption based on ethnic origin |journal=Am. J. Gastroenterol. |volume=92 |issue=7 |pages=1148–53 |year=1997 |pmid=9219788 |doi= |url=}}</ref><ref name="pmid6895202">{{cite journal |vauthors=Kirschner BS, DeFavaro MV, Jensen W |title=Lactose malabsorption in children and adolescents with inflammatory bowel disease |journal=Gastroenterology |volume=81 |issue=5 |pages=829–32 |year=1981 |pmid=6895202 |doi= |url=}}</ref> | * [[Small intestine|Small intestinal]] [[inflammation]]:<ref name="pmid24917953">{{cite journal |vauthors=Misselwitz B, Pohl D, Frühauf H, Fried M, Vavricka SR, Fox M |title=Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment |journal=United European Gastroenterol J |volume=1 |issue=3 |pages=151–9 |year=2013 |pmid=24917953 |pmc=4040760 |doi=10.1177/2050640613484463 |url=}}</ref><ref name="pmid120188073">{{cite journal |vauthors=Swagerty DL, Walling AD, Klein RM |title=Lactose intolerance |journal=Am Fam Physician |volume=65 |issue=9 |pages=1845–50 |year=2002 |pmid=12018807 |doi= |url=}}</ref><ref name="pmid9219788">{{cite journal |vauthors=Mishkin B, Yalovsky M, Mishkin S |title=Increased prevalence of lactose malabsorption in Crohn's disease patients at low risk for lactose malabsorption based on ethnic origin |journal=Am. J. Gastroenterol. |volume=92 |issue=7 |pages=1148–53 |year=1997 |pmid=9219788 |doi= |url=}}</ref><ref name="pmid6895202">{{cite journal |vauthors=Kirschner BS, DeFavaro MV, Jensen W |title=Lactose malabsorption in children and adolescents with inflammatory bowel disease |journal=Gastroenterology |volume=81 |issue=5 |pages=829–32 |year=1981 |pmid=6895202 |doi= |url=}}</ref> | ||
** It causes malabsorption through flattening of the [[Villus|villi]] of the intestinal epithelium. | ** It causes malabsorption through flattening of the [[Villus|villi]] of the intestinal epithelium. | ||
** [[Lactase]] enzyme is affected first because it is located at the distal part of the villi. | ** [[Lactase]] enzyme is affected first because it is located at the distal part of the villi. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]
Overview
There is no established system for the classification of lactose intolerance. Lactose intolerance may be classified according to its causes into 2 groups: primary lactose malabsorption and secondary lactose malabsorption. Primary lactose malabsorption may be classified into 3 subtypes: acquired primary lactase deficiency, congenital lactase deficiency and developmental lactase deficiency. Secondary lactose malabsorption occurs as a result of the underlying intestinal diseases such as small intestinal bacterial overgrowth, small intestinal infection such as giardiasis and small intestinal inflammation.
Classification
- There is no established system for the classification of lactose intolerance.
- Lactose intolerance may be classified according to its causes into 2 groups:
- Primary lactose malabsorption
- Secondary lactose malabsorption
- Primary lactose malabsorption may be classified into 3 subtypes include:
- Acquired primary lactase deficiency
- Congenital lactase deficiency
- Developmental lactase deficiency
Acquired primary lactase deficiency ( lactase nonpersistence, adult-type hypolactasia)
- The most common cause of primary lactase malabsorbtion
- Autosomal recessive trait[1]
- Intestinal lactase levels is deceresed at preschool age in many populations especially in Asia and Africa.
- Elevated lactase activity is maintained in Caucasians such as northern European.
- Convergent evolution of lactase persistence is seen in some populations in Africa that domesticate cows and consume milks product into adulthood [2]
- Persistence of intestinal lactase until adulthood is inherited as autosomal dominant characteristic[3]
Congenital lactase deficiency
- Rare autosomal recessive[4]
- Absence of lactase activity
- Characteristic findings:[5]
- Watery diarrhea
- Medullary nephrocalcinosis
- Hypercalcemia that will be ceased after one week lactose free diet.
- More in Finnish population
Developmental lactase deficiency
- Low lactase levels in premature infants that born at 28 to 32 weeks of gestation[6]
- Clinical lactose intolerance is uncommon because colonic flora ferment lactose to hydrogen gas and short chain fatty acids and then fatty acids are absorbed by the colon.
Secondary lactose malabsorption
Secondary lactose malabsorption occurs as a result of the underlying intestinal diseases such as:[7]
- Small intestinal bacterial overgrowth:
- Fermentation of lactose in the small bowel may be increased and leads to symptoms of lactose intolerance
- Breath hydrogen levels peaks very early in lactose challenge test
- Small intestinal infection such as giardiasis
- Small intestinal inflammation:[8][9][10][11]
- It causes malabsorption through flattening of the villi of the intestinal epithelium.
- Lactase enzyme is affected first because it is located at the distal part of the villi.
- Following are a few disease that are related to small intestinal inflammation:
- Whipple's disease (intestinal lipodystrophy)
- Celiac sprue
- Tropical sprue
- Inflammatory bowel disease more in pateints with crohn disease
- Drug induced enteritis
- Radiation induced enteritis
- Severe gastroenteritis
References
- ↑ Enattah NS, Sahi T, Savilahti E, Terwilliger JD, Peltonen L, Järvelä I (2002). "Identification of a variant associated with adult-type hypolactasia". Nat. Genet. 30 (2): 233–7. doi:10.1038/ng826. PMID 11788828.
- ↑ Tishkoff SA, Reed FA, Ranciaro A, Voight BF, Babbitt CC, Silverman JS, Powell K, Mortensen HM, Hirbo JB, Osman M, Ibrahim M, Omar SA, Lema G, Nyambo TB, Ghori J, Bumpstead S, Pritchard JK, Wray GA, Deloukas P (2007). "Convergent adaptation of human lactase persistence in Africa and Europe". Nat. Genet. 39 (1): 31–40. doi:10.1038/ng1946. PMC 2672153. PMID 17159977.
- ↑ Scrimshaw NS, Murray EB (1988). "The acceptability of milk and milk products in populations with a high prevalence of lactose intolerance". Am. J. Clin. Nutr. 48 (4 Suppl): 1079–159. PMID 3140651.
- ↑ Saarela T, Similä S, Koivisto M (1995). "Hypercalcemia and nephrocalcinosis in patients with congenital lactase deficiency". J. Pediatr. 127 (6): 920–3. PMID 8523189.
- ↑ Kuokkanen M, Kokkonen J, Enattah NS, Ylisaukko-Oja T, Komu H, Varilo T, Peltonen L, Savilahti E, Jarvela I (2006). "Mutations in the translated region of the lactase gene (LCT) underlie congenital lactase deficiency". Am. J. Hum. Genet. 78 (2): 339–44. doi:10.1086/500053. PMC 1380240. PMID 16400612.
- ↑ Mobassaleh M, Montgomery RK, Biller JA, Grand RJ (1985). "Development of carbohydrate absorption in the fetus and neonate". Pediatrics. 75 (1 Pt 2): 160–6. PMID 2578223.
- ↑ Srinivasan R, Minocha A (1998). "When to suspect lactose intolerance. Symptomatic, ethnic, and laboratory clues". Postgrad Med. 104 (3): 109–11, 115–6, 122–3. doi:10.3810/pgm.1998.09.577. PMID 9742907.
- ↑ Misselwitz B, Pohl D, Frühauf H, Fried M, Vavricka SR, Fox M (2013). "Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment". United European Gastroenterol J. 1 (3): 151–9. doi:10.1177/2050640613484463. PMC 4040760. PMID 24917953.
- ↑ Swagerty DL, Walling AD, Klein RM (2002). "Lactose intolerance". Am Fam Physician. 65 (9): 1845–50. PMID 12018807.
- ↑ Mishkin B, Yalovsky M, Mishkin S (1997). "Increased prevalence of lactose malabsorption in Crohn's disease patients at low risk for lactose malabsorption based on ethnic origin". Am. J. Gastroenterol. 92 (7): 1148–53. PMID 9219788.
- ↑ Kirschner BS, DeFavaro MV, Jensen W (1981). "Lactose malabsorption in children and adolescents with inflammatory bowel disease". Gastroenterology. 81 (5): 829–32. PMID 6895202.