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Lactose intolerance in infants

VOL: 102, ISSUE: 17, PAGE NO: 43

Cathy Taylor, BSc, CHS(HV), MSc, RGN, DipN, is tutor - health visiting, University of Wales, Swansea

Diarrhoeal disease in infants is extremely common in the United Kingdom and is one of the most important causes of ...

Diarrhoeal disease in infants is extremely common in the United Kingdom and is one of the most important causes of global infant mortality and morbidity, according to the World Health Organization's World Health Report in 1998 (www.who.int).

In developed countries, infant deaths associated with diarrhoea are rare, but chronic diarrhoea remains a major cause of illness in infants.

The investigation into the causes of persistent or chronic diarrhoea in infants is complex, but in the past 50 years lactose intolerance has been recognised and diagnosed as a true medical phenomenon (Matthews et al, 2005). However, its true incidence remains uncertain, as the term is often used synonymously with other conditions, such as lactose maldigestion, cow's milk protein intolerance and cow's milk allergy (Curran, 2005, Wilson 2005). These conditions are not the same (McBean and Miller, 1998).

Prevalence

The prevalence of lactose intolerance in the UK remains relatively low - affecting an estimated 2% of the population (Buttriss, 2001). Interestingly, the decline of the enzyme lactase in the human body is a normal physiological process that occurs following weaning, however the rate that this happens varies widely and often depends on cultural and ethnic backgrounds.

McBean and Miller (1998) report that approximately 75% of the world population are 'lactase non-persistent' and therefore find it difficult to digest lactose. However, this is particularly significant in Asian and African populations, where lactase deficiency can be as high as 100%. In contrast, people in northern Europe (including the UK), usually retain their ability to produce lactase throughout their life, possibly because of a continued use of dairy products after weaning or as a direct result of genetic inheritance (Swagerty et al, 2002).

Pathophysiology

Lactose is the unique sugar found in both breast and formula milk and is a major source of carbohydrate for infants (Rosado, 1997). It cannot be absorbed directly by the body but must be hydrolysed into its monosaccharide components of glucose and galactose.

This process is assisted in the body by the enzyme lactase (Beta-galactosidase) which is situated in the brush border cells in the microvilli in the small intestine. Once absorbed, these simple sugars enter the bloodstream and act as nutrients.

Lactose intolerance occurs when the lactase enzyme is absent (alactasia) or deficient (hypolactasia), leading to reduced activity in the normal functioning of the small intestine. The undigested sugars are unable to participate in the normal absorption process and remain in the intestinal lumens and draw fluid into the intestine by a process of osmosis. In addition, the bacteria in the colon act on the undigested sugars, causing hydrogen gas and lactic acid to be produced. The outcome of this fermentation process initiates the main signs and symptoms associated with lactose intolerance. These include the following:

- Diarrhoeal stools - frequent, explosive, acidic and watery (may be green or yellow in colour depending on severity);

- A persistently unsettled, crying infant;

- Pain and distension of the abdomen;

- Excess gas/flatus - 'a windy baby' with loud bowel sounds;

- Vomiting;

- Possible dehydration and weight loss;

- Acidic breath.

Aetiology

Lactose intolerance may be present in healthy people or it may be associated with a diseased state (Shukla, 1997). Regardless of its effect, it is usually identified and categorised in three discrete ways:

- Congenital lactose intolerance - This is rare, but some infants may be born with a genetic defect where there is absence of the lactase enzyme (alactasia). The infant presents with severe feeding problems, along with diarrhoea, vomiting and poor weight gain;

- Primary lactose intolerance - A genetically inherited condition associated with the developmental decline of the lactase enzyme. For this reason, primary lactose intolerance normally becomes apparent at a later age as an infant matures (normally between five and 20 years of age);

- Secondary lactose lntolerance - This temporary but common condition can occur in infants due to a transient state of lactase deficiency following damage to the lining of the intestine, normally as a result of infection. Fortunately, this type of intolerance is usually temporary and symptoms will normally subside when the lining of the intestine returns to normal, which is usually within two to four weeks.

Diagnosis

The effects of the disease in a young infant can cause a great deal of anxiety and stress for parents. Early diagnosis can help to minimise this and can normally be achieved through a full medical history and physical examination.

Premature infants may be more prone to the disease, with infants born at 34 weeks' gestation having only 30% lactase activity compared to that of a full-term baby (Griffin and Hansen, 1999).

An accurate history of the infant and family is essential, together with a detailed picture of feeding patterns and bowel habits. A thorough physical examination is required to determine the infant's overall condition, and should include hydration and nutrition status. Baseline observations of temperature, pulse, respirations and blood pressure are required, together with growth and development measurements in relation to weight, height and head circumference.

If the infant is acutely unwell, an acid stool test may be a preferred choice of investigation for paediatricians to assist with diagnosis. This test measures the amount of acid in the infant's stools. If lactose is undigested in the bowel, the fermentation process creates lactic acid, which can then be measured.

A stool pH of (lt) 5.5 can be an indication of lactose intolerance and can be a useful aid to diagnosis, especially in infants and young children.

Management

If the infant is acutely unwell and is admitted to hospital, initial treatment will focus on rehydration and control of electrolyte imbalance. This will depend on the degree of intolerance and the severity and duration of the symptoms.

In the case of secondary lactose intolerance, when these acute symptoms have been alleviated management should continue in a supportive way. Milk, whether breast or formula, should be reintroduced to the infant, but the response of the child should be observed and the feeding regime manipulated in a controlled way.

WHO (1997) infers that lactose intolerance is rare when breast milk is the only source of lactose entering the infant's body. This is interesting, as breast milk contains a higher proportion of lactose than some formula milks (approximately 7g per 100ml), but it tends to be well tolerated - possibly because the amount of lactose reaching the intestine at any one time is low.

This is not to say that breastfed infants never become lactose intolerant; Woolridge and Fisher (1988) suggest that lactose intolerance can occur in breastfed infants when lactose overload occurs due to low-fat feeds. This may arise if infants have insufficient feeds, are unable to milk the breast well and therefore fail to extract the fattier hind milk from the breast. The resulting feed is often low in fat, causing fast gastric clearance, which overloads the small intestine with lactose.

If this is the case, it is essential that assessment of a breast feed is performed, noting in particular the positioning and attachment of the infant. Exclusive breastfeeding in the first year of life should be supported, and parents need reassurance from health visitors and other members of the primary health care team to continue with breastfeeding.

By suggesting simple changes in breastfeeding patterns the effects of lactose intolerance can be eliminated. Infants should be encouraged to nurse fully on one breast before being offered the second.

An individual assessment of the mother's diet (in consultation with the dietitian) may prove useful, and modifications, such as a lactose-free diet for the mother with the addition of calcium supplements, may be suggested.

Low lactose or lactose-free formula milks may be recommended for those infants who are predominantly formula fed. Numerous commercial formulas can be obtained over the counter, but it is important that parents are advised by the health professional about the correct nutritional milk substitutes for their infant. Infants who are intolerant can be prescribed formula milk.

Conclusion

Congenital lactase deficiency is rare. Typically, lactose intolerance in developed countries is more likely to exist following infections (such as gastroenteritis) that affect the normal functioning of the intestinal tract.

Symptoms of chronic, persistent diarrhoea and dehydration may lead to a period of hospitalisation for an infant, which can be distressing for parents. However, for infants managed at home, nurses, health visitors and other members of the primary health care team are pivotal in providing ongoing advice, support and education.

Reassurance should be given that symptoms can often be minimised through nutritional support, with dietary control preventing further complications for the infant.

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