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__NOTOC__
__NOTOC__
{{Esophageal stricture}}
{{Lactose intolerance}}


{{CMG}}; {{AE}} {{MA}}
{{CMG}}; {{AE}} {{MA}}
==Overview==
==Overview==
There is no established system for the classification of [disease name].
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]].


OR
==Classification==
 
{{familytree/start }}
[Disease name] may be classified according to [classification method] into [number] subtypes/groups: [group1], [group2], [group3], and [group4].
{{familytree | | | | | | | | | | | | | | | | A01 |A01=''lactose intolerance''}}
 
{{familytree | | | | | |,|-|-|-|-|-|-|-|-|-|-|^|-|-|-|-|-|-|-|-|-|.| | | }}
OR
{{familytree | | | | | B01 | | | | | | | | | | | | | | | | | | | B02 | | |B01=Primary lactose malabsorption |B02=Secondary lactose malabsorption}}
{{familytree | |,|-|-|-|+|-|-|-|.| | | | | | | | | | | | |,|-|-|-|+|-|-|-|.|}}
{{familytree | D01 | | D02 | | D03 | | | | | | | | | | | D04 | | D05 | | |D06|D01=Acquired primary lactase deficiency |D02=Congenital lactase deficiency|D03=Developmental lactase deficiency|D04=[[Small intestinal bacterial overgrowth]]|D05=[[Small intestinal]] [[infection]]|D06=[[Small intestinal]] [[inflammation]]}}


[Disease name] may be classified into [large number > 6] subtypes based on [classification method 1], [classification method 2], and [classification method 3].
[Disease name] may be classified into several subtypes based on [classification method 1], [classification method 2], and [classification method 3].


OR
{{familytree/end}}


Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.


OR


If the staging system involves specific and characteristic findings and features:
*There is no established system for the classification of lactose intolerance.  
According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].


OR
*Lactose intolerance can be classified according to its causes into 2 groups:  
 
The staging of [malignancy name] is based on the [staging system].
 
OR
 
There is no established system for the staging of [malignancy name].
 
==Classification==
 
*There is no established system for the classification of [disease name].
OR
*Lactose intolerance may be classified according to its causes into 2 groups:  
**Primary lactose malabsorption 
**Primary lactose malabsorption 
**Secondary lactose malabsorption
**Secondary lactose malabsorption


* Primary lactose malabsorption may be classified into 3 subtypes include:
* Primary lactose malabsorption can be classified into 3 subtypes:
** Acquired primary lactase deficiency 
** Acquired primary lactase deficiency 
** Congenital lactase deficiency
** Congenital lactase deficiency
** Developmental lactase deficiency
** Developmental lactase deficiency
'''Acquired primary lactase deficiency (adult-type hypolactasia, lactase nonpersistence)'''
* The most common cause of primary lactase malabsorbtion


* Intestinal lactase levels is deceresed at preschool age in many populations especially in Asia and Africa
=== Primary lactose intolerance ===
* 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 <ref name="pmid17159977">{{cite journal |vauthors=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 |title=Convergent adaptation of human lactase persistence in Africa and Europe |journal=Nat. Genet. |volume=39 |issue=1 |pages=31–40 |year=2007 |pmid=17159977 |pmc=2672153 |doi=10.1038/ng1946 |url=}}</ref> 
* Persistence of intestinal lactase is inherited as autosomal-dominant characteristic<ref name="pmid3140651">{{cite journal |vauthors=Scrimshaw NS, Murray EB |title=The acceptability of milk and milk products in populations with a high prevalence of lactose intolerance |journal=Am. J. Clin. Nutr. |volume=48 |issue=4 Suppl |pages=1079–159 |year=1988 |pmid=3140651 |doi= |url=}}</ref> 
OR
*[Disease name] may be classified into [large number > 6] subtypes based on:
**[Classification method 1]
**[Classification method 2]
**[Classification method 3]
*[Disease name] may be classified into several subtypes based on:
**[Classification method 1]
**[Classification method 2]
**[Classification method 3]
OR
*Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.
OR
*If the staging system involves specific and characteristic findings and features:
*According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].
OR
*The staging of [malignancy name] is based on the [staging system].
OR
*There is no established system for the staging of [malignancy name].


==References==
==== '''Acquired primary lactase deficiency ( lactase nonpersistence, adult-type hypolactasia)''' ====
{{Reflist|2}}
* The most common cause of primary lactase malabsorbtion.
{{WH}}
* In this type of disease, environmental and genetic factors collaborate with each other to develop lactose intolerance. 
{{WS}}
* [[Autosomal recessive]] trait.<ref name="pmid11788828">{{cite journal |vauthors=Enattah NS, Sahi T, Savilahti E, Terwilliger JD, Peltonen L, Järvelä I |title=Identification of a variant associated with adult-type hypolactasia |journal=Nat. Genet. |volume=30 |issue=2 |pages=233–7 |year=2002 |pmid=11788828 |doi=10.1038/ng826 |url=}}</ref>
[[Category: (name of the system)]]
 
__NOTOC__
* [[Intestine|Intestinal]] [[lactase]] levels are decreased at preschool age in many populations especially in Asia and Africa.
{{Lactose intolerance}}
* Elevated [[lactase]] activity is maintained in Caucasians such as Northern European.
{{CMG}}
* Convergent evolution of lactase persistence is seen in some populations in Africa that domesticate cows and consume milk product into adulthood. <ref name="pmid17159977">{{cite journal |vauthors=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 |title=Convergent adaptation of human lactase persistence in Africa and Europe |journal=Nat. Genet. |volume=39 |issue=1 |pages=31–40 |year=2007 |pmid=17159977 |pmc=2672153 |doi=10.1038/ng1946 |url=}}</ref> 
* Persistence of intestinal [[lactase]] until adulthood is inherited in an [[autosomal dominant]] manner.<ref name="pmid3140651">{{cite journal |vauthors=Scrimshaw NS, Murray EB |title=The acceptability of milk and milk products in populations with a high prevalence of lactose intolerance |journal=Am. J. Clin. Nutr. |volume=48 |issue=4 Suppl |pages=1079–159 |year=1988 |pmid=3140651 |doi= |url=}}</ref> 
 
'''Congenital lactase deficiency'''
* Rare [[autosomal recessive]] disorder.<ref name="pmid8523189">{{cite journal |vauthors=Saarela T, Similä S, Koivisto M |title=Hypercalcemia and nephrocalcinosis in patients with congenital lactase deficiency |journal=J. Pediatr. |volume=127 |issue=6 |pages=920–3 |year=1995 |pmid=8523189 |doi= |url=}}</ref>
* Absence of [[lactase]] activity since birth 
* Characteristic findings:<ref name="pmid16400612">{{cite journal |vauthors=Kuokkanen M, Kokkonen J, Enattah NS, Ylisaukko-Oja T, Komu H, Varilo T, Peltonen L, Savilahti E, Jarvela I |title=Mutations in the translated region of the lactase gene (LCT) underlie congenital lactase deficiency |journal=Am. J. Hum. Genet. |volume=78 |issue=2 |pages=339–44 |year=2006 |pmid=16400612 |pmc=1380240 |doi=10.1086/500053 |url=}}</ref>
** Watery [[diarrhea]] 
** Medullary [[nephrocalcinosis]]
** [[Hypercalcemia]] that will be ceased after one week lactose free diet.
* More in Finnish population


==Overview==
==== '''Developmental lactase deficiency''' ====
There are three major types of lactose intolerance.<ref name="Melvin">[http://aappolicy.aappublications.org/cgi/content/full/pediatrics;118/3/1279|Melvin B. Heyman. ''Lactose Intolerance in Infants, Children, and Adolescents''. PEDIATRICS Vol. 118 No. 3 September 2006, pp. 1279-1286 (doi:10.1542/peds.2006-1721)]</ref> They are primary lactose intolerance, secondary lactose intolerance and congenital lactase deficiency.
* Low [[lactase]] levels in [[premature]] infants that were born at 28 to 32 weeks of [[gestation]]<ref name="pmid2578223">{{cite journal |vauthors=Mobassaleh M, Montgomery RK, Biller JA, Grand RJ |title=Development of carbohydrate absorption in the fetus and neonate |journal=Pediatrics |volume=75 |issue=1 Pt 2 |pages=160–6 |year=1985 |pmid=2578223 |doi= |url=}}</ref> 
* Clinical lactose intolerance is uncommon because colonic flora ferment lactose to hydrogen and short chain fatty acids and then fatty acids are absorbed by the colon.


==Classification==
=== '''Secondary lactose malabsorption''' ===
There are three major types of lactose intolerance:<ref name="Melvin">[http://aappolicy.aappublications.org/cgi/content/full/pediatrics;118/3/1279|Melvin B. Heyman. ''Lactose Intolerance in Infants, Children, and Adolescents''. PEDIATRICS Vol. 118 No. 3 September 2006, pp. 1279-1286 (doi:10.1542/peds.2006-1721)]</ref>
Secondary lactose malabsorption occurs as a result of the underlying intestinal diseases such as:<ref name="pmid9742907">{{cite journal |vauthors=Srinivasan R, Minocha A |title=When to suspect lactose intolerance. Symptomatic, ethnic, and laboratory clues |journal=Postgrad Med |volume=104 |issue=3 |pages=109–11, 115–6, 122–3 |year=1998 |pmid=9742907 |doi=10.3810/pgm.1998.09.577 |url=}}</ref>
#Primary lactose intolerance: Environmentally induced by weaning in non dairy consuming societies. In most Asian and African cultures, mother's milk is the only commonly available milk and so milk consumption beyond infancy is not commonplace, therefore children become weaned, which is the same weaning process for all mammals (domesticated and wild).  However societies such as the japanese where milk consumption has been on the increase, demonstrate that notwithstanding the genetic predisposition to lactose intolerance, they now present lower prevalence of lactose intolerance.<ref name="Yoshida">[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1234085&dopt=Abstract ''Studies on the etiology of milk intolerance in Japanese adults'', Yoshida Y, Sasaki G, Goto S, Yanagiya S, Takashina K, Gastroenterol Jpn.;10(1):29–34, 1975]</ref> For any given individual the degree of weaning is probably genetically influenced.
* [[Small intestinal bacterial overgrowth]]: 
#Secondary lactose intolerance: Environmentally induced, resulting from certain [[gastrointestinal diseases]], including exposure to [[intestinal parasites]] such as [[giardia]].<ref>[http://www.tulane.edu/~wiser/protozoology/notes/intes.html "Intestinal Protozoa" Mark Wiser 2000] </ref><ref>[http://www.emedicine.com/emerg/topic215.htm "Giardiasis" Andre Pennardt February 22, 2006] </ref> In such cases the production of lactase may be permanently disrupted.<ref name="urlLactose Intolerance - May 1, 2002 - American Family Physician">{{cite web |url=http://www.aafp.org/afp/20020501/1845.html |title=Lactose Intolerance - May 1, 2002 - American Family Physician |format= |work= |accessdate=2013-04-01}}</ref>
** Fermentation of [[lactose]] in the small bowel may be increased and this leads to symptoms of lactose intolerance
#Congenital lactase deficiency present at birth and diagnosed in early infancy.
** Breath hydrogen levels peak very early in lactose challenge test
* [[Small intestine|Small intestinal]] [[infection]] such as giardiasis 
* [[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.
** [[Lactase]] enzyme is affected first because it is located at the distal part of the villi.
** Following are some disease that cause small intestinal inflammation:
*** [[Whipple's disease]] ([[intestinal lipodystrophy]])
*** [[Celiac disease|Celiac sprue]]
*** [[Tropical sprue]]
*** [[Inflammatory bowel disease]] (more in pateints with [[Crohn's disease|crohn's disease]])
*** [[Drug]] induced enteritis
*** [[Radiation]] induced enteritis
*** Severe [[gastroenteritis]]


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
{{WH}}
{{WS}}
{{WS}}
{{WH}}


[[Category:Gastroenterology]]
[[Category:Gastroenterology]]
[[Category:Endocrinology]]
[[Category:Medicine]]
[[Category:Up-To-Date]]

Latest revision as of 22:28, 29 July 2020

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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


 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
lactose intolerance
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Primary lactose malabsorption
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Secondary lactose malabsorption
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Acquired primary lactase deficiency
 
Congenital lactase deficiency
 
Developmental lactase deficiency
 
 
 
 
 
 
 
 
 
 
Small intestinal bacterial overgrowth
 
Small intestinal infection
 
 
Small intestinal inflammation


  • There is no established system for the classification of lactose intolerance.
  • Lactose intolerance can be classified according to its causes into 2 groups:
    • Primary lactose malabsorption 
    • Secondary lactose malabsorption
  • Primary lactose malabsorption can be classified into 3 subtypes:
    • Acquired primary lactase deficiency 
    • Congenital lactase deficiency
    • Developmental lactase deficiency

Primary lactose intolerance

Acquired primary lactase deficiency ( lactase nonpersistence, adult-type hypolactasia)

  • The most common cause of primary lactase malabsorbtion.
  • In this type of disease, environmental and genetic factors collaborate with each other to develop lactose intolerance.
  • Autosomal recessive trait.[1]
  • Intestinal lactase levels are decreased 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 milk product into adulthood. [2]
  • Persistence of intestinal lactase until adulthood is inherited in an autosomal dominant manner.[3]

Congenital lactase deficiency

Developmental lactase deficiency

  • Low lactase levels in premature infants that were born at 28 to 32 weeks of gestation[6] 
  • Clinical lactose intolerance is uncommon because colonic flora ferment lactose to hydrogen 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]

References

  1. ↑ 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.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ Saarela T, Similä S, Koivisto M (1995). "Hypercalcemia and nephrocalcinosis in patients with congenital lactase deficiency". J. Pediatr. 127 (6): 920–3. PMID 8523189.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ 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.
  8. ↑ 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.
  9. ↑ Swagerty DL, Walling AD, Klein RM (2002). "Lactose intolerance". Am Fam Physician. 65 (9): 1845–50. PMID 12018807.
  10. ↑ 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.
  11. ↑ Kirschner BS, DeFavaro MV, Jensen W (1981). "Lactose malabsorption in children and adolescents with inflammatory bowel disease". Gastroenterology. 81 (5): 829–32. PMID 6895202.

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