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Lactose Intolerance & Milk Allergy
 

Lactose intolerance is one example of food intolerance. The term "food intolerance" denotes a non-immunologic adverse reaction to a food.

In the case of lactose intolerance it is due to an inability to digest significant amounts of lactose, the predominant sugar of milk. This inability results from a shortage of the enzyme lactase, which is normally produced by the cells that line the small intestines. Lactase breaks down milk sugar into simpler forms that can be absorbed into the blood stream.

Congenital Lactase Deficiency

This is a rare condition (less than 50 cases are known) in which the individual cannot produce lactase. Watery diarrhoea occurs after breast-feeding or milk ingestion.

Primary (Late-onset) Lactase Deficiency

Lactase levels are high in all mammals following birth. In most mammals, however, lactase levels decline after the infant is weaned. Man is the only mammal that may retain lactase activity into adulthood. The gradual lactase disappearance usually does not begin until the child reaches pre-school age (2-6 years), although it can also begin at virtually any time later in life. The timing and rate of decline is genetically determined.

The ability of adults to drink milk is known as lactase persistence. Lactase persistence is mainly confined to northwest Europeans and certain African subpopulations. This was a survival trait from times of meat famine, when milk was required as a rich source of protein and the gene for lactase persistence was passed along. These groups include the Germans and British, who engaged in cattle farming and dairying by the late first millennium AD.

Primary lactase deficiency is mostly seen in those racial/geographic groups whose ancestors did not drink milk as a nutrient. Groups that cannot usually digest milk include people from:

Africa
East & South Asia
Pacific & Mediterranean Countries
Native Americans
Jews & Eskimos

Secondary Lactase Deficiency

This type of lactase deficiency is secondary to a medical problem or use of certain therapies. For instance, an episode of acute infectious diarrhoea (gastroenteritis) can leave the patient lactase deficient through damage and temporary loss of the relatively shallow intestinal villous section of the intestine. While other enzymes (eg, sucrase and maltase) may be affected, lactase is the earliest to be lost and the slowest to regenerate. Average recovery time is 4 weeks.

HIV infection can cause lactase deficiency, as do rotavirus and giardiasis.

Drugs, like Neomycin, Kanamycin, tetracycline and Methotrexate can cause villous atrophy, leading to secondary lactase deficiency.

Alcohol can also inhibit disaccharidases (lactase & others enzymes) and cause or worsen a lactase deficiency.

Prevalence

It is estimated that 25% of Americans and 75% of adults worldwide have lactose intolerance.

81% of black adults and 100% of Asian adult have this problem.

Age

Age is predictive of LA. At least 46% of those over 50 have the problem, in contrast to only 25% of those under the age of 50.

Sex

Both affected equally.

Inheritance

Autosomal recessive single gene inheritance. Therefore, having 2 parents with lactose intolerance virtually guarantees that the children will develop the disorder.

Symptoms

Two main reasons for symptoms.

  1. Undigested lactose acts as an osmotic laxative. This leads to diarrhoea and abdominal pain.
  2. Intestinal bacteria are able to use lactose as a growth substrate. The rapid growth of intestinal bacteria leads to the production of large volumes of gas. The gas is responsible for the flatulence, dyspepsia, abdominal distension and stomach rumbling.

Vomiting, which is a common feature of milk allergy, is rare in lactose intolerance.

Diagnosis

The age of presentation is usually after two, in contrast with cow’s milk allergy that usually manifests during breast-feeding or shortly after weaning.

Often in LA the patient can tolerate small amounts of some dairy products whereas in milk allergy even traces of any will cause symptoms.

Lactose elimination & lactase supplementation (in the form of tablets or liquid) will usually differentiate this problem from milk allergy.

Fermentation of lactose produces hydrogen as a by-product. Breath hydrogen excretion can be measured after a lactose challenge, and compared with baseline.

Treatment of Lactose Intolerance

Dietary Modification

Since milk allergy can be life-threatening even in trace amount, it is important to differentiate lactose intolerance (which is not life-threatening) from milk allergy.

Very few people are so lactase deficient that the remedy is total restriction of dietary lactose. The disorder is often dose-dependent. Many adults with primary lactose deficiency can drink 100ml — 200ml of milk (5g —10g of lactose) without having symptoms. However, a little too much causes mild symptoms and a great deal of excess lactose cause severe symptoms.

The severity of symptoms is product-dependent for many patients as well. Skim milk causes more severe symptoms than whole milk. Chocolate milk may help the condition. These differences are attributed to the fat content, osmolality and the delayed gastric emptying augmented by additional ingredients in the different products. In one study milk with breakfast cereals prevented symptoms completely.

Lactase supplementation

There are several ways of giving lactase.

Yoghurt has lactase activity. Lactase enzymes are available without a prescription. One form is a liquid to add to milk. A few drops are added to milk, and then after 24 hours in the refrigerator, the lactose is reduced by 70%.

There are also chewable lactase tablets that help people digest solid foods that have lactose.

Infants and young children can have dairy based lactose-free formulas or non-dairy formulas like soy.

Cow’s Milk Allergy (CMA)

Cow’s milk allergy is one of the commonest food allergies in children, perhaps because it is usually the first highly allergenic foreign protein encountered by infants. CMA is a "true allergy" since it is an immunologically-mediated reaction

Prevalence

Between 2% and 7.5% of infants and young children suffer CMA.

Natural History & Prognosis of CMA

Most children will outgrow their milk allergy by age 3 years: 50% by 1 year of age, 70% by 2 years of age, and 85% by 3 years of age.

Unfortunately, in CMA patients, 50% will develop an allergy to other food proteins (e.g., egg, soy, peanut) and 50-80% will develop an allergy against one or more inhalant allergens (pollens, house dust mites, cat) before puberty. Milk allergy is therefore a high risk factor for predicting infants who will develop asthma and eczema.

Milk Allergens

The two main protein fractions of milk are whey (20%) and casein (80%), and an individual can be allergic to one or both. The casein is the curd that forms when milk goes sour, and the whey is the watery fraction, which is left after the curd is removed.

The whey fraction contains mainly alpha-lactalbumin and beta-lactoglobulin and is the most allergenic fraction and therefore causes the most clinical problem. The whey fraction is altered by heat, and so the whey sensitive person may be able to tolerate evaporated, boiled or sterilised (Long Life) milk & milk powder.

Casein is heat stable and is the most important allergen in cheese. The harder the cheese, the more casein is formed. Extensive heating will reduce only, but not eliminate the allergenicity of casein.

Exposure & Sensitisation to CM

Exposure to CM proteins may occur prenatally, as indicated by the demonstration of milk-specific IgE antibodies in cord blood.

Recently, specific IgE against individual cow’s milk protein was demonstrated in 76% of selected infants in whom CMA later developed. This data indicate that prenatal sensitisation occurs and may play a role in the pathogenesis of food allergy.

Postnatally, breast fed infants are exposed to CM and other food proteins ingested by the mother and excreted by the mammary gland. Bovine beta-lactoglobulin can be detected in the breast milk in 95% of lactating women. Exclusively breast fed infants in whom CMA develops may react to minute amounts of CM protein in human milk. Also, sensitisation to foods during exclusive breast-feeding is likely to result from ingestion of hidden CM protein and possibly from inhalant and skin contact.

The very small amount of cow’s milk protein in breast milk may induce tolerance rather than allergic sensitisation and development of allergic disease. On the other hand, a significant relationship exists between early neonatal exposure to CM formula feeding and subsequent development of CMA.

With the introduction of CM-based formula into the infant’s diet, the antigenic load of CM proteins becomes enormous. Macromolecular absorption is increased in preterm infants and in newborns and has also been demonstrated in infants with CMA. Whether increased macromolecular absorption is part of an allergic constitution or is due to temporal mucosal damage is not clear

Development of Clinical Disease

There is increasing evidence that intrauterine sensitisation to foods as well as to inhalants may occur. However, such weak intrauterine sensitisation may be a normal phenomenon as is the well-known weak postnatal IgE response in infants without allergic disease. Neonatal exposure to "high dose" of foreign protein may be necessary for the development of allergic disease. Clinical symptoms of CMA may appear during breast-feeding, but most infants have symptoms shortly after introduction of CMA formula. Many studies have shown that CMA develops mostly during early infancy and rarely afterwards.

Clinical Types of Milk Allergic Reactions

Reactions vary from mild hives to life-threatening anaphylaxis.

Reactions can be immediate, following very small quantities of milk or start several hours or even days after the intake of moderate to large amounts of CM.

Type 1 (Immediate)

Symptoms start within minutes of intake of small volumes of CM. Mainly cause skin symptoms – eczema or urticaria (hives).

Respiratory – runny nose, cough or wheezing

Gastrointestinal – vomiting and diarrhoea

This is the most serious type as anaphylaxis and death is possible.

Type 2 (Intermediate)

Symptoms start several hours after intake of modest volumes of CM.

Main symptoms are vomiting and Diarrhoea

Type 3 (Delayed)

Symptoms develop after more than 20 hours, or even days after intake of large volumes of CM.

Symptoms include, diarrhoea with or without eczema and asthma

Cross-reactivity

There is cross-reactivity among milk from cows, goats and sheep. Only the whey fraction in goat’s milk differs from that in cow’s milk. Goat’s milk is tolerated by only 40% of CMA children.

Diagnosis of Milk Allergy

Only the immediate (Type 1) milk reactions that develop after a few minutes are most likely to give a positive skin prick test or RAST (blood test) to milk.

Skin Prick Tests (SPT)

SPT is especially accurate in the young child with immediate (type 1) reaction. The skin is pricked through a small drop of milk placed on the forearm. A wheal and flare reaction after 15 minutes will indicate that the patient is allergic to milk.

The positive predictive accuracies of SPTs are less than 50% compared with DBPCFCs, whereas negative SPT responses virtually exclude IgE-mediated reactions (negative predictive accuracy is greater than 95%)

Nearly 60% of milk reactions in the young child are the delayed type (intolerant, non-immunologic) and therefore unlikely to give positive results.

The diagnosis is then made by the Elimination-Challenge Test. This should show the relief of symptoms on the removal of milk and the recurrence of symptoms when re-introduced. This test should never be done at home. It should be done under the supervision of the doctor and the dietitian.

An open challenge and careful follow-up may be adequate for practical clinical purpose to diagnose the Type 1 (Immediate) Milk Reactions.

Double-blind Placebo-controlled Food Challenge (DBPCFC) remains the gold standard for diagnosing milk allergy/intolerance, especially in the Intermediate & delayed groups.

Patch Tests

Milk is applied to the back in a special Finn chamber for 48 hours. A positive response suggests a delayed hypersensitivity & is useful in intermediate & delayed milk reactions.

In one study of patients with atopic dermatitis, it was demonstrated that Patch Testing could identify many patients with negative skin prick test and delayed clinical reactions. Parallel skin testing with combined prick and patch tests can significantly enhance the accuracy of specific food allergies in patients with atopic dermatitis.

Blood Tests (RAST & CAP RAST)

The CAP RAST is newer & more accurate than the RAST. It tests for milk proteins as whole, or individual fractions of milk (casein, whey, beta-lactoglobulin).

A recent study with CAP RAST in children with atopic dermatitis showed that the positive predictive value for milk, if the level is above 32 kuA/l is 95%. Therefore for results above 32kUA/l a DBPCFC is not warranted.

 

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