LACTOSE INTOLERANCE

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LACTOSE INTOLERANCE

• Tova Rainis
• Gastroenterolgy unit
• Bnai-Zion

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• Common problem
• Europe and U.S.A 7-20 - Caucasians (lowest in
  north Europe) , 80-95 Native American, 65-75
  Africans and African Americans, 50 Hispanics
• Eastern Asia, Jewish descent gt 90

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Lactose intake

• Varies with age
• Infants 35-55 of daily calories ingested
• Lactose intake falls as weaning foods are
  introduced
• Average adult ingests 300 gram of carbohydrates
  per day (52 starch, 37 sucrose, 5 lactose
  (mainly in milk), 3 fructose)

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Lactose digestion and colonic salvage of
nonabsorbed lactose
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Etiology of lactose malabsorption

• Primary lactose malabsorption
• Racial or ethnic lactose malabsorption
• Developmental lactase deficiency
• Congenital lactase deficiency

• Secondary lactose malabsorption
• Bacterial overgrowth/stasis
• Mucosal injury of GIT that causes villus
  flattening

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Racial or ethnic lactose malabsorption

• Genetically determined reduction of lactase
  activity
• Most common form of lactose malabsorption
• The great majority of the worlds population
  develop low intestinal lactase during
  mid-childhood (approximately at age 5 yrs)
• This finding is most prominent in Asian and
  African populations rare in Caucasians of
  Scandinavian background
• Molecular basis remains unknown

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Developmental lactase deficiency

• Low lactase levels as a consequence of
  prematurity
• Lactase activity in the fetus increases late in
  gestation
• Premature infants born at 28-32 weeks of
  gestation have a reduced lactase activity

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Congenital lactase deficiency

• Rare autosomal recessive disorder (Finnish
  population)
• Characterized by the absence of lactase activity
  in the small intestine, with normal histologic
  findings
• A gene located on the same chromosome of the
  lactase gene, is responsible for CLD
• Affected infants have diarrhea from birth,
  hypercalcemia and nephrocalcinosis

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Secondary lactose malabsorption

• Bacterial overgrowth or stasis syndromes
• Increased fermentation of dietary lactose in the
  small bowel, leading to symptoms of lactose
  intolerance
• Suspected from clinical history and from a very
  early peak of breath hydrogen during lactose
  challenge

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Secondary lactose malabsorption - 2

• Mucosal injury
• Villus flattening or damage to the intestinal
  epithelium
• Celiac disease
• Crohns disease
• Radiation enteritis, chemotherapy
• HIV enteropathy
• Whipples disease

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Secondary lactose malabsorption -3

• Lactase usually first affected disaccharidase in
  these disorders, because of its distal location
  on the villus
• Treatment of the primary disorder can lead to
  restoration of lactase activity
• Restoration of lactase activity lags behind the
  return of normal intestinal morphology

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Clinical manifestations

• Abdominal pain crampy, localized to
  periumbilical area, or lower quadrant
• Bloating
• Flatulence
• Diarrhea
• Vomiting
• Stools are usually bulky, frothy and watery

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Clinical manifestations - 2

• Meals with higher osmolality and fat content slow
  gastric emptying and reduce the severity of
  symptoms
• Rapid intestinal motility ? rapid movement of
  sugar are more symptomatic
• Individuals have variable sensitivity to the
  abdominal distention produced when undigested
  lactose stimulates an influx of water into the
  lumen or to gas production

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Differential diagnosis

• Irritable bowel disease
• Inflammatory bowel disease
• Cystic fibrosis
• Diverticulitis
• Celiac sprue
• Acute gastroenteritis
• Giardiasis

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Diagnosis

• Test absorption (lactose absorption test) or
  malabsorption (lactose breath hydrogen test)
• Lactose tolerance test
• Oral administration of 50 gram lactose
• Blood glucose levels 0, 60 and 120 min
• Increase of blood glucose by less than 20mg/dl
  symptoms diagnostic
• False negative diabetes, bacterial overgrowth,
  delayed gastric emptying
• Sensitivity of 75, specificity of 96

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Diagnosis - 2

• Lactose breath hydrogen test
• Oral lactose (2g/kg)
• Breath hydrogen sampled at baseline and at 30 min
  intervals for three hours
• Breath hydrogen value of 10ppm normal, 10-20ppm
  indeterminate unless symptomatic, gt20ppm
  diagnostic
• False positive recent smoking, false negative
  recent use of antibiotics, lung disorders, 1
  non-hydrogen producers

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Diagnosis -3

• Under the age of 5 years abnormal test reflects
  an abnormal intestinal mucosa or bacterial
  overgrowth, both of which require further
  evaluation by appropriate diagnostic tests
• Normal breath hydrogen test psychologic
  factors, intolerance to other factors in milk

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Treatment

• In the absence of a correctable underlying
  disease, the treatment includes four general
  principles
• Reduced dietary lactose intake
• Substitution of alternative nutrient sources to
  maintain energy and protein intake
• Administration of a commercially available enzyme
  substitute
• Maintenance of calcium intake

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Dietary lactose restriction

• Highest concentration in milk and ice-cream, much
  lower quantities in cheese
• Complete restriction of lactose-containing foods
  should be necessary for a limited period to
  ascertain the specificity of the diagnosis
• Since patients can tolerate graded increases in
  lactose intake, small quantities of lactose may
  subsequently be reintroduced into the diet, with
  careful attention to development of symptoms

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Enzyme replacement

• Commercially available lactase preparations
  (bacterial or yeast beta galactosidases)
• Lactaid, Lactrase, LactAce, DairyEase and Lactrol
• Start with two Lactaid tablets with lactose
  ingestion, and adjust both the Lactaid dose and
  the lactose load to tolerance

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Calcium intake

• Avoidance of milk and other dairy products can
  lead to reduced calcium intake, and increase in
  risk of osteoporosis and fracture
• Calcium carbonate
• Tums popular and effective
• Infants and young children liquid calcium
  gluconate
• Yogurt containing lactose is well tolerated by
  the patients. The yogurt contains live cultures
  of bacteria that produce lactase

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