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