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Contents A. Case study B. More information C. Editors' comments D. References E. CEU questions

Index

A. Case study
A mother brought her 7-and-a-half-month-old baby girl to her doctor. The baby had suffered from loose, watery stools for 5 days, and the mother was concerned, as the baby clinic had confirmed weight loss. The doctor took a stool sample to assess for pathogens but felt the problem could a viral infection; he had seen a number of cases of viral gastroenteritis that week. The mother was advised to continue oral rehydration therapy and to monitor the stool frequency and consistency.

The diarrhea seemed to improve for approximately 3 days, but then reappeared and was accompanied by abdominal pain and bloating. Stools were large and watery and occasionally had a frothy appearance.

WHAT SHOULD BE CONSIDERED AT THIS STAGE?
a. Viral or bacterial infection
b. Urinary tract infection, causing secondary symptoms in the digestive tract
c. Intolerance to food secondary to diarrhea
d. Onset of food allergy

a. Tests were negative for microorganisms, and a viral infection seemed unlikely.
b. A urinary tract infection was ruled out.
c. The mother said she had given her daughter very little food over the period of the first diarrhea. Once it had started improving, she gave her yoghurt and her cow’s milk-based infant formula. The doctor attributed the diarrhea to a secondary lactose intolerance and advised avoidance of dairy products in favour of a soya formula for 2 weeks to allow for gastrointestinal repair.
d. The baby had received breastmilk and then a cow’s milk-based formula since birth without any noticeable allergic reactions. Complementary foods had been introduced between 5 and 6 months. The mother had given her maize cereal mixed with her infant formula, yoghurt, pears, and recently orange vegetables such as squash, pumpkin, carrot and butternut. The foods seemed to be relatively non-allergenic, apart from the yoghurt; but since the child had had no reaction to cow’s milk-based infant formula, there was no reason to avoid it. She had shown no change in condition after eating yoghurt, so an allergy seemed unlikely.

With the soya formula and without dairy products, the diarrhea did not improve, and the little girl continued to demonstrate weight loss and was at risk of failure to thrive.

QUESTIONS AT THIS STAGE
a. Was she demonstrating a food allergy or food allergy enteropathy?
b. Had she consumed anything else that could have precipitated the diarrhea?
c. Was she consuming something currently that could be aggravating the diarrhea?

a. Food allergy enteropathy to cow’s milk or soya seemed unlikely, as she had been on a cow’s milk-based infant formula from the age of 2 months and had been eating a maize- and soy-based infant cereal from the age of 5 months with no reactions. In order to rule out a sudden onset of soy or cow’s milk allergy, skin prick tests and food-specific IgE tests were done. Both were negative for reactions to cow’s milk and soya proteins; however, an open food challenge was also conducted to confirm the absence of a clinical reaction or a non-IgE mediated allergy.
b. On questioning, the mother revealed that at approximately 7 months she had also started giving her daughter infant fruit juice and introduced apples and apricots into her diet. As previously mentioned, she had also been consuming infant maize cereal with her cow’s milk-based infant formula, yoghurt, water, pears and orange vegetables. An analysis of the child’s diet therefore showed lactose-containing foods and recently introduced foods which happened to be higher in sucrose and fructose – the apples, apricots, fruit juice and carrots.
c. Analysis of the soya formula revealed that although it was lactose-free, it contained large quantities of sucrose.

THOUGHT PROCESS
A secondary lactose intolerance had been ruled out. Could the child be demonstrating a primary carbohydrate intolerance to lactose, fructose or sucrose? Could she have a secondary fructose or sucrose intolerance due to severe diarrhea?

DISCUSSION
It is often difficult to distinguish carbohydrate intolerances from each other. Dietary restriction is the best diagnostic tool in identifying the culprit disaccharide as well as in determining whether the condition is secondary and thus temporary.

Complete removal of fructose- and sucrose-containing foods did result in improvement of the diarrhoea, which resumed after reintroduction of these sugars. The reducing substances test came back positive, which meant that lactose and sucrose (disaccharides) could be present in the stools. The doctor felt that a primary carbohydrate intolerance should be investigated.

Diagnosis of lactase deficiency is made on the basis of a history of gastrointestinal symptoms, occurring after or aggravated by milk ingestion; response to an empirical trial of dietary lactose reduction or avoidance; a breath test demonstrating abnormal hydrogen levels; an abnormal lactose tolerance test; a stool sample showing reducing substances or acidic pH; and/or a small intestinal biopsy to assess direct lactase enzyme activity. Symptoms are alleviated by complete elimination or reduced consumption of lactose-containing foods. Fructose and sucrose malabsorption can also be confirmed by testing the breath hydrogen response to a challenge with fructose, or by checking for reducing substances in the stools.

A primary enzyme deficiency can be demonstrated directly only by intestinal mucosal biopsy assays - findings in a biopsy tend to be representative of the whole small gut in patients with genetically determined enzyme deficiencies.

A biopsy revealed that the child’s small intestinal mucosa had normal levels of lactase enzyme as well as of fructose. The biopsy showed an absence of sucrase enzyme and extremely depleted levels of isomaltase. This corresponded with her clinical presentation and diet history. It appeared that, from about 7 months, with the treatment of the suspected secondary lactose intolerance, she had ingested more sucrose than usual – apple, apricot and carrots are high in sucrose, fruit juice contains sucrose, and the soya formula contained large amounts of sucrose. She was diagnosed with a congenital sucrase-isomaltase deficiency, and sucrose, glucose polymer and starch were initially restricted in her diet.

TIP for Allergy Advisor users: The Management section of Allergy Advisor contains a diet sheet for the management of fructose intolerance. The diet sheet includes foods that are allowed and foods restricted, as well as a patient information sheet on the topic that can be printed for the patient to take home.

B. More information:
Disaccharides include the following sugars: sucrose, lactose, maltose, maltotriose, isomaltose, some starch molecules, and trehalose.

Disaccharide intolerance may be primary or secondary.
Primary intolerance may occur as a result of the following:
• immaturity of the digestive tract;
• congenital deficiencies in digestive enzymes; and
• congenital absence of components of the transport systems needed to digest sugars.

Secondary disaccharide intolerance may occur in the course of a variety of conditions that damage the tissues lining the intestinal tract. These conditions include:
• deficiencies in digestive enzymes;
• cow’s milk and soy protein allergy or enteropathy;
• gluten-sensitive enteropathy;
• infections of the digestive tract caused by parasites,or other organisms;
• (immaturity of the digestive tract)
In all cases, symptoms are confined to the gastrointestinal tract.^1,2,3

The best-known and commonest disaccharide intolerance is lactose intolerance (concerning which see http://www.allergyadvisor.com/educational/June05.htm). This review will also discuss intolerance of other disaccharides, such as sucrose (table sugar, syrup and fruit sugar), isomaltose, trehalose (found in mushrooms) and maltose (sugar derived from grains, a less common trigger) will be discussed. Due to similar clinical presentation, fructose intolerance (although a monosaccharide) should not be overlooked in practice. (Please refer to http://www.allergyadvisor.com/educational/sept2002.htm for an overview on fructose intolerance.)

1. What is disaccharide intolerance?
In the brush border of the small intestine, there are four disaccharidase enzymes: sucrase-isomaltase, maltase-glucoamylase, lactase and trehelase, with the highest level of activity occurring in the jejunum and the second-highest in the ileum.² Maltase, sucrase and isomaltase activity in the fetus reach the lower range of normal adult levels by 28-32 weeks of gestation. In both healthy premature and full-term infants, sucrose, maltose and isomaltose digestion should therefore be adequate.³ Deficiencies of these enzymes can be primary in nature, due to a congenital enzyme defect; or can be secondary to some other gastrointestinal insult.^2,3

Enzymes in the small intestines and their respective disaccharide sugar substrates ²:
Enzyme: Sucrase-isomaltase (accounts for 80% of maltase activity)
Substrate – disaccharide: Sucrose, alpha 1-6 glucoside bonds in starch molecules, Isomaltose, Maltose, Maltotriose

Enzyme: Maltase-glucoamylase (accounts for 20% of maltase activity)
Substrate – disaccharide: Maltose, Maltotriose, Starch

Enzyme: Lactase
Substrate – disaccharide: Lactose

Enzyme: Trehelase
Substrate – disaccharide: Trehalose

Disaccharides, sugars made up of two sugar molecules, comprise 50% of the usual dietary carbohydrate intake in humans and in addition are the by-products of amylase digestion of polysaccharides such as starch.³

There are various types of disaccharides, which include:
• Lactose – the sugar in breast milk and cow’s milk, which occurs mainly in the whey (liquid) fraction of milk, although some casein-dominant foods (such as some cheeses) may still contain a small amount of lactose. Lactase is the enzyme which breaks this sugar down into the monosaccharides glucose and galactose.¹
• Sucrose – found in table sugar and syrups. Table sugar usually comes from sugar beets or sugar cane but can also be found in fruits, grains and vegetables. Syrups can be made from various plants and grains. The enzyme responsible for the breakdown of sucrose into glucose and fructose is sucrase.¹
• Maltose and starches – mainly found in grains and starchy vegetables. Maltase and isomaltase are needed to split maltose and starches into molecules of glucose.¹
• Trehalose – found mainly in mushrooms, insect hemolymph and algae. Intestinal trehelase is the brush border enzyme that hydrolyses trehalose into two glucose molecules.⁴
• Oligosaccharides – products of luminal starch digestion, hydrolysed to glucose monomers by the following membrane-bound brush border digestive enzymes: maltase-glucoamylase, sucrase and isomaltase. Maltase-glucoamylase removes single glucose residues from the a (1-4) chains of oligosaccharides and from maltotriose and maltose.⁴

2. Causes of disaccharide intolerance
Disaccharide intolerance occurs due to an inability to digest disaccharide sugars, which require degradation by disaccharidase enzymes, usually produced in the microvilli of the small intestinal mucosa. Damage to the microvilli leads to inadequate production of the enzymes, and the disaccharide sugars remain intact and undigested, passing into the large bowel where bacteria cause fermentation to occur. Products of the microbial fermentation result in the clinical symptoms.^1,3

Most children with disaccharidase deficiency may be placed in one of two groups. In the first, the enzyme deficit is genetically determined, and in the second it is due to some other cause, most commonly disease of the small intestine. The terms ‘primary’ and ‘secondary’ are applied to describe these two groups respectively.⁵

Reasons why the cells lining the small intestine stop producing disaccharidases include ^1,2:
Primary:
• Inherited tendency. This is most commonly seen in lactose intolerance. The ability to produce the lactase enzyme usually diminishes after the age of five years in most of the world’s population.
• Congenital disaccharidase deficiency. An individual can either be deficient in one specific disaccharidase or in two, resulting in intolerance of one or both disaccharides. An example is congenital sucrase-isomaltase deficiency.

Secondary:
• Inflammation resulting from an intestinal infection (enteritis), due to a virus (a rotavirus), a bacterium (Giardia lamblia) or an intestinal parasite (amoebae, helminthes, nematode worms).
• A food allergy
• Gluten enteropathy
• Chrohn’s disease
• Use of strong oral drugs and medications (antibiotics), which may cause damage to the fragile cells.
• Chronic diarrhea
• Pathology of the gastrointestinal tract, e.g., short bowl syndrome

3. Types of disaccharidase deficiencies
a. Congenital sucrase-isomaltase deficiency (CSID)
Congenital sucrase-isomaltase deficiency (CSID) is an autosomal recessively inherited disease, which is a rare but frequently misdiagnosed cause of chronic diarrhea in infants and children. It is characterised by a complete lack of sucrase activity and a marked reduction (occasionally an absence) of isomaltase activity, resulting in differing degrees of dietary intolerance.²

While being breast-fed or given a normal infant formula, the infant tends to remain asymptomatic and thrives. The introduction of starch or sucrose into the diet – often the change in formula to one containing glucose polymer or sucrose – initiates symptoms.²

b. Glucoamylase deficiency
A disorder of absorption of short polymers of glucose and starch resulting from primary glucoamylase deficiency has been described. It was detected in 1.8% of children with chronic diarrhea.^4,6 Also, a recent report of a patient with congenital maltase-glucoamylase deficiency with associated lactase and sucrase deficiencies raises the possibility of a rare global carbohydrate digestive disorder caused by a shared regulator.^4,7

c. Trehalase deficiency
Trehalase deficiency, as a distinct and isolated condition, is almost unknown outside of Greenland, where at least 8% of the population have been reported to have it.^4,8 An extremely low prevalence of trehalose intolerance has been confirmed in the UK.⁹ Intestinal examination for trehalose in cases of unexplained diarrhea is therefore not routinely recommended.⁴

4. Aetiology, symptoms and duration of the condition
Fluid is drawn into the colon to normalize the increased osmotic pressure caused by excess undigested sugars. Gases are produced due to increased microbial growth and fermentation in the bowel, leading to abdominal pain, bloating and flatulence. Microbial fermentation in the bowel also produces organic acids (lactic acid and short-chain fatty acids), making the stools acidic and contributing to a further increase in osmotic pressure and more water retention in the bowel. The increased fluid in the large bowel causes watery diarrhea or loose stools which may actually be fatal in infants with a congenital deficiency.^1,2,3

A lifelong disaccharide intolerance or primary deficiency results from an inherited disaccharidase deficiency. Foods responsible for symptoms require permanent avoidance unless the deficient enzyme can be artificially provided from medication, which would allow ingestion of a certain amount of the culprit food.^1,5

A secondary deficiency, as a result of damage to the intestinal cells from infection, food allergy or strong drugs, is usually temporary. Removal of the primary cause will enable the cells to heal and resume production of disaccharide enzymes, and tolerance to previously problematic foods will develop over time.^1,5 Clinical manifestations will depend on the underlying disease.^2,5

Intolerance of disaccharides almost always leads to digestive-tract symptoms. Abdominal bloating, pressure and pain are often accompanied by diarrhea (frequently frothy), which sometimes alternates with constipation. There is occasionally nausea and vomiting.^1,3 Symptoms may be dose-dependent, appearing inconsistently and making diagnosis difficult.

The clinical presentation of CSID is variable. Chronic diarrhea and failure to thrive are common in infants and toddlers, and symptoms often become manifest once sucrose in fruits and juice is introduced.² The inability to digest sugars may also result in increased gas production and abdominal distention.⁴

As previously mentioned, disaccharide intolerance should not be mistaken for fructose intolerance, which may present in a similar manner. Fructose is a monosaccharide, abundant in fruits, honey and some root vegetables. It is also formed from the digestion of sucrose to fructose and glucose. It is not as well digested and absorbed as glucose; consequently, ingestion of high levels of fructose can lead to carbohydrate intolerance. In children, drinking excessive amounts of juice high in fructose may result in diarrhea, excessive intestinal gas and recurrent abdominal pain. Carbohydrate malabsorption appears to be most frequently provoked by fruit juices containing sorbitol and a high fructose-to-glucose ratio (e.g., by apple juice more than by grape juice). In children and adults, fructose malabsorption has been associated with previously unexplained gastrointestinal symptoms. In a recent report, the prevalence of fructose malabsorption detected by hydrogen breath test ranged from 38 to 80%, depending on the fructose dose, in adult patients presenting with unexplained gastrointestinal symptoms. The possibility of fructose intolerance should therefore be considered in adults and children with persistent unexplained gastrointestinal symptoms.⁴

5. Diagnosis
A disaccharidase deficiency can be demonstrated directly only by intestinal mucosal biopsy assays. There are problems, however, with accuracy, as only a minute sample of tissue is usually available, and enzyme levels in the sample may not reflect the disaccharidase activity of the whole small bowel in vivo. This is particularly problematic when pathological changes are unevenly distributed along the small bowel, e.g., in celiac disease or regional enteritis. But findings in a biopsy are probably representative of the whole small gut in patients with genetically determined enzyme deficiencies.⁵

It is often difficult to distinguish different disaccharide intolerances, other than lactose intolerance, from each other. Dietary restriction is the best diagnostic tool in determining the culprit disaccharide as well as whether the condition is primary, or secondary and thus temporary.¹ In most cases, a disaccharide intolerance is dose-related. Usually the cells produce a limited amount of the disaccharidase enzyme, and small quantities of the relevant disaccharide in the food can be digested. Problems will occur when the threshold is exceeded. Patients’ individual disaccharide tolerance capacity should be determined to ensure they remain symptom-free.¹

CSID diagnosis usually occurs later in infancy or even in childhood, once sucrose-containing foods are introduced. A delay in the diagnosis of CSID tends to be related to the introduction of a low-sucrose diet by parents, which controls symptoms. Some children attain relatively normal growth before diagnosis, despite chronic symptoms of intermittent diarrhea, bloating and abdominal cramps. In older children, symptoms may be misdiagnosed as irritable bowel syndrome. CSID has been diagnosed as late as in adulthood.²

6. Treatment and supplementation
Restriction of all disaccharides is initially required. The disaccharide-free diet can be divided into two phases. The first phase, in which all probable culprit foods are withheld, should be followed for at least 4 weeks. This will help distinguish whether the deficiency is primary, or secondary due to diarrhea. When the diarrhea improves, an individual’s tolerance for each disaccharide is tested in the second phase: every other day, one food is introduced from the ‘restricted’ list until diarrhea recurs. Maltose tolerance is tested by introducing grains, especially ‘white’ grains and flours. Sucrose tolerance is tested by introducing vegetables and fruits high in sucrose, nuts and seeds, and finally sugars. (Fruits contain sucrose as well as fructose. Once they are digested, the predominant sugars remaining are fructose and glucose).¹

In a secondary disaccharide deficiency, it is usually necessary to eliminate the offending carbohydrates and treat the primary disorder causing the mucosal damage.²

In a disaccharide-intolerant baby, infant formulas free of lactose and sucrose can be given. Cow’s milk-based formulas free from lactose and sucrose are suitable for babies who are not allergic to cow’s milk proteins. Sucrose-free soya-based formulas are also suitable for infants, as long as they do not have a combined cow’s milk and soya allergy (commonly seen in infants with non-IgE-mediated cow’s milk hypersensitivity). Infants allergic to both cow’s milk and soya proteins should tolerate a casein hydrolysate, formula which is free from lactose and sucrose.¹

Treatment of CSID consists primarily of avoidance of sucrose in the diet. In the first year of life, treatment generally requires the elimination of sucrose, glucose polymers and starch from the diet. The lactose in normal infant formula and breast milk (and after a year, cow’s milk) will be well tolerated.^2,4

With age, the tolerance of starch and of foods containing lower amounts of sucrose should improve; by the age of 2-3 years, the restriction of starch should no longer be needed. Tolerance can be titrated against dietary intake – if the capacity to absorb carbohydrate is exceeded, this will cause osmotic diarrhea. Fruits with higher amounts of sucrose can be included in the diet according to tolerance. Reducing the starch to the previously tolerated level should result in normal stools. Soy flour (15g starch per 100g) can be used in recipes to replace wheat flour (75g starch per 100g) for children with low starch tolerance. Parents need reassurance that occasional dietary indiscretions will not cause long-term problems.²

Older children diagnosed with CSID should initially be advised to avoid dietary sources of sucrose only. If this does not lead to prompt improvement in symptoms, then the starch content of the diet can be reduced, particularly in the case of foods with a high amylopectin content, such as wheat and potatoes. Advice needs to be given to increase the energy from protein and fat to replace the loss in energy from carbohydrate. Glucose tablets and Lucozade can be included in the diet.²

Enzyme substitution therapy has recently been applied to patients with CSID. Baker’s yeast has been shown to improve sucrose tolerance, although it is unpalatable and poorly accepted. A tasteless liquid preparation, Sacrosidase (a fructofuranoside fructohydrolase), containing high concentrations of yeast-derived invertase (sucrase), has recently been used in treatment, as it hydrolyses sucrose and has been found to be safe and effective in preventing symptoms of intolerance in patients with sucrase-isomaltase deficiency. Sacrosidase may allow the consumption of a more normal diet by children with CSID and decrease the high incidence of chronic gastrointestinal complaints.^2,4,10

Micronutrient supplementation is not indicated in individuals with secondary (temporary) deficiencies who are eating a relatively wide range of allowed foods. The need for supplementation will ultimately depend on individual tolerance to disaccharide-containing foods. For those with primary (permanent) deficiencies or needing to adhere to a restrictive diet for a prolonged period, supplements may be necessary. Additional vitamin C and vitamin B complex should be given in cases of restriction of sucrose and maltose respectively.¹ It may be that adequate vitamin intake in infants and young children with CSID can be achieved only be achieved by continuing an infant formulas after 1 year of age, as all medications should be sucrose free.²

Below is an example of low sucrose, low starch foods which can be included in the elimination diet used for treating CSID during the first year of life²:

Low sucrose, low starch solids (<1 g per 100g):
Protein: Meat, poultry, egg*, fish
Fats: Margarine, butter, lard, vegetable oils
Vegetables: Most vegetables except potato (unless stored for a week or two – lowers amounts of sucrose), sweet potato, parsnip, peas, carrots, onion, sweetcorn and beetroot, mixed vegetables, tomato paste (generally 1-2 teaspoons can be used in cooking)
Fruits: Initially use fruits with less than 1 g sucrose per 100 g fruit (see table below), fruit juices and drinks. Most fruits contain negligible amounts of starch.
Milk: Breast milk, infant formula (free of glucose polymer and sucrose), cow’s milk, unsweetened natural yoghurt, cream
Others: Marmite, Oxo, Bovril, vinegar, salt, pepper, herbs, spices, 1-2 teaspoons tomato puree, gelatine, essences and food colourings, sugar-free jelly, sugar-free drinks, fructose, glucose
* Soft eggs should not be given to babies under 1 year of age

Sucrose content of some common fruits (per 100 g edible portions) ²:
Less than 1 g sucrose:
Blackcurrants, cherries, bilberries, damsons, gooseberries, grapes, lemons, loganberries, lychees, melon (except Gallia), pears, raisins, raspberries, redcurrants, rhubarb, strawberries, sultanas
Less than 3 g sucrose:
Gallia melon, grapefruit, kiwi fruit, passion fruit, plums
Less than 5 g sucrose:
Apples, apricots, oranges, clementines, satsumas

C. Comments by our editors

Dr. Harris Steinman M.B.Ch.B. The disaccharide intolerances may appear at first glance to be complex and difficult to diagnose. In essence, the purpose of this review is to heighten your index of suspicion in considering these conditions in patients where symptoms are clearly not that of allergy, or where management has not resulted in resolution of the complaints. I am acutely aware that as health professionals dealing with patients who have seen multiple other health professionals for ongoing symptoms, that we may lose sight of these other "hidden" causes. In some instances, they may even be iatrogenic, i.e., in children who are allergic and that are prescribed an additive and preservative free diet, the replacement food or drink may the cause of symptoms. For example, children who replace preservative- and color-containing softdrinks may replace these with pure fruit juice which may result in diarrhea. This review therefore will heighten your index of suspicion for these conditions and give you a clear structure of how to approach the assessment and management of these patients. Our other editor, Janice Joneja has discussed this topic in her book "Digestion, Diet and Disease", published by Rutgers University Press in 2004 in the chapter "Abnormalities of the Large Intestine: Maldigestion of Carbohydrates" (Chapter 8). Appendix A of the same book discussed "Dietary Management of Disaccharidase Deficiency".

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D. References
1. Joneja JV. Dealing with food allergies. A practical guide to detecting culprit foods and eating a healthy enjoyable diet. Chapter 18 - Disaccharide intolerance. Bull Publishing, Colorado. 2003: 223-232
2. Shaw V, Lawson M. Clinical Paediatric Dietetics. Second edition. Chapter 6 - The Gastrointestinal Tract. Blackwell publishing, Oxford. 2001: 79-81
3. Bayless TM, Christopher NL. Disaccharidase deficiency. Am J Clin Nutr 1969; 22(2): 181-190
4. Sibley E. Carbohydrate Intolerance. Curr Opin Gastroenterol 2004; 20: 162-167
5. Townley RRW. Disaccharidase deficiency in infancy and childhood. Pediatrics 1966; 38(1): 127-141
6. Lebanthal E, Khin Maung U, Zheng BY et al. Small intestinal glucoamylase deficiency and starch malabsorption: a newly recognized alpha-glucosidase deficiency in children. J Pediatr 1994; 124:541–546.
7. Nichols BL, Avery SE, Karnsakul W et al. Congenital maltase-glucoamylase deficiency associated with lactase and sucrase deficiencies. J Pediatr Gastroenterol Nutr 2002; 35:573–579.
8. Gudmand-Hoyer E. The clinical significance of disaccharide maldigestion. Am J Clin Nutr 1994; 59(Suppl): 735S-741S
9. Murray IA, Coupland K, Smith JA et al. Intestinal trehalase activity in a UK population: establishing a normal range and the effect of disease. Br J Nutr 2000; 83:241–245.
10. Treem WR, McAdams L, Stanford L et al. Sacrosidase therapy for congenital sucrase-isomaltase deficiency. J Pediatr Gastroenterol Nutr 1999, 28:137–142.

E. CPD Questions (For South African dietitians only. Australian dietitians: where you have relevant learning goals, CEU hours related to this resource can be included in your APD log.)

PLEASE ANSWER ALL THE QUESTIONS
(There is only one correct answer per question.)

1. Disaccharides include the following:
a. Lactose, sucrose, fructose, glucose and galactose
b. Lactose, sucrose, maltose, isomaltose and trehalose
c. Lactose, sucrose, glucose, maltose and starch
d. None of the above

2. True or false: The jejunum and ileum contain the highest levels of enzymes in the small intestine.
a. True
b. False

3. Lactose occurs mainly in which fraction of milk?
a. Both casein and whey
b. Casein
c. Whey
d. Curd

4. Intestinal trehelase hydrolyses trehalose into the following molecules:
a. Fructose and glucose
b. Glucose and galactose
c. Two glucose molecules
d. Two galactose molecules

5. True or false: A food allergy can result in primary disaccharide intolerance.
a. True
b. False

6. True or false: Congenital sucrase-isomaltase deficiency (CSID) is usually diagnosed immediately at birth.
a. True
b. False

7. True or false: Dietary restriction of starch is not a lifelong requirement in the treatment of CSID.
a. True
b. False

8. What is the starch content of soya flour and wheat flour respectively?
a. 10g starch per 100g and 75g starch per 100g
b. 15g starch per 100g and 55g starch per 100g
c. 25g starch per 100g and 75g starch per 100g
d. 15g starch per 100g and 75g starch per 100g

9. Initial dietary restriction in older children diagnosed with CSID includes avoidance of the following:
a. Starch only
b. Starch and sucrose
c. Sucrose only
d. Starch, sucrose and glucose
e. None of the above

10. True or false: Sacrosidase hydrolyses sucrose, as it contains high concentrations of yeast-derived invertase (sucrase)
a. True
b. False

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Disaccharide Intolerance
CEU Reference number: DT/A01/2007/00066

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This issue was sponsored by Abbott Laboratories S.A (PTY) LTD All Abbott products are lactose and gluten free Tel: 011-8582054