Upload
khaleda-fatmawati
View
228
Download
5
Embed Size (px)
Citation preview
LACTOSE INTOLERANCE
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 > 90%
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)
Lactose digestion and colonic salvage of nonabsorbed lactose
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
Racial or ethnic lactose malabsorption
Genetically determined reduction of lactase activity
Most common form of lactose malabsorption The great majority of the world’s 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
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
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
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
Secondary lactose malabsorption - 2
Mucosal injuryVillus flattening or damage to the intestinal
epithelium
Celiac disease Crohn’s disease Radiation enteritis, chemotherapy HIV enteropathy Whipple’s disease
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
Clinical manifestations Abdominal pain – crampy, localized to periumbilical area, or
lower quadrant
Bloating
Flatulence
Diarrhea
Vomiting
Stools are usually bulky, frothy and watery
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
Differential diagnosis
Irritable bowel disease Inflammatory bowel disease Cystic fibrosis Diverticulitis Celiac sprue Acute gastroenteritis Giardiasis
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%
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, >20ppm – diagnostic
False positive – recent smoking, false negative – recent use of antibiotics, lung disorders, 1% non-hydrogen producers
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
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
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
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
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