Caballero B. (ed.) Encyclopaedia of Food Science, Food Technology and Nutrition. Ten-Volume Set

Подождите немного. Документ загружается.

Nutritional Impact of Regeneration and

Warm-Holding of Foods

0047 Traditionally catering systems either operated on a

basis of ‘making-to-order,’ where there is no delay

between cooking and service of food, such as in

quality restaurant operations, or bulk production,

when food may be held warm for considerable

periods prior to service, as in hospital and canteen

feeding operations. In relatively recent times inter-

rupted catering systems, such as cook-chill and

cook-freeze operations, have been introduced (See

Catering: Catering Systems) where foods are cooked,

then rapidly chilled or frozen, to be reheated later just

prior to use. These different methods have implica-

tions for retention of nutritional value of foods that

must be considered by caterers.

Traditional Catering Methods and Warm-Holding

Foods

0048 Where food is made-to-order and served, and pre-

suming quality stock has been purchased originally

and stored, prepared, and cooked efficiently, then it is

likely that consumers will receive food with optimal

palatable, digestible, and nutritional characteristics.

However, for those large-scale operations where it is

necessary to hold food warm for any length of time,

the outcome can be significantly different.

0049 Whilst some unstable nutrients are irredeemably

destroyed during the cooking process, as discussed,

due to the action of heat and oxidation, this may be

seen as a necessary trade-off to achieve improved

digestibility and hence give access to the vast majority

of nutrients remaining in the food, and liquors pro-

duced during cooking. Should food have to be held

warm for any period after cooking and before con-

sumption, the only nutritional effect is adverse.

0050 Maintaining foods at safe temperatures (above



C, and usually much higher) and further exposure

to atmospheric oxygen results in rapid and unrecover-

able depletion of unstable nutrients. Warm-holding of

cooked vegetables, for instance, which are the key

dietary sources of vulnerable nutrients such as vita-

min C, can result in typical permanent losses of up to

20% h

1

and 10–15% h

1

for folic acid. Prolonged

warm-holding also results in deteriorating organolep-

tic (flavor, texture, aroma) and visual properties. This

reduction in the palatability of foods may lead to less

food being consumed, hence further reducing utiliza-

tion of remaining nutritional potential.

Cold-Holding and Regeneration of Foods

0051 In interrupted catering systems, food is chilled rapidly

immediately upon completion of cooking. The

process of chilling itself has no adverse impact on

nutritional value of food. However, if foods are only

chilled and not frozen, a significant reduction of un-

stable nutrients continues to occur during chilled

storage. Vitamin C levels have been shown to fall by

around 10% per day during such holding, although

this varies depending on the particular food. If foods

are frozen then further vitamin losses are virtually

halted, although losses may occur during the thawing

process, if foods are not regenerated from frozen,

when liquid containing vitamins may run off.

0052Frozen or chilled foods will need to be regenerated

prior to service and brought to a safe temperature in

excess of 63



C. During this second heating, further

permanent vitamin losses will occur, as in primary

cooking, due to the effects of heat and oxidation.

Foods that have been regenerated must then be served

and consumed as swiftly as possible, to reduce to

a minimum the warm-holding effects previously

discussed.

The Importance of Catering in Relation to

Nutritional Intakes

0053Whilst there are many influences that can affect the

final nutritional value of a meal or food item before it

reaches the consumer, it should be noted that the

contribution that catering makes to the overall nutri-

tion of individuals varies greatly.

0054Catering systems operate either as welfare-related

concerns within the cost sector, or as commercial

operations within the profit sector (See Catering:

Catering Systems). Where customers are captive,

such as in hospitals, schools, or prisons, then the

catering provision may be an important contributor

to daily nutritional intakes. Just how important this

becomes to individuals will depend on the length of

time for which they are reliant on catering provisions

for all or a major part of their daily diet. Long-stay

hospital patients, boarders at schools, and those

retained at Her Majesty’s Pleasure for prolonged

periods will need to acquire satisfactory nutritional

benefit from the food provided by the caterers in their

respective environments.

0055In the UK the National Food Survey, conducted

by the Ministry of Agriculture, Fisheries and Food

(MAFF), indicated that households were spending

almost £24 per person per week on average on food

and drink in 1999. Of this sum, just over £7 per

person per week was spent on meals and beverages

eaten out – around 30% of total expenditure. Be-

tween 1998 and 1999 expenditure on eating out

rose by just over 5%, whereas the total spent on

food and drink at home remained almost static.

Whilst the economic climate is generally positive it

is likely that such a tend will continue, as consumers

986 CATERING/Nutritional Implications

may not feel the need to ‘tighten their belts.’ In terms

of nutrition, the implication must be that, as the

proportion of expenditure on food and drink eaten

outside the home increases, so the relative importance

of catering and food service operations to the national

diet increases.

0056 The National Food Survey indicated that the pat-

tern of consumption of food away from the home

varies considerably between socioeconomic groups

in respect of total amount spent and nature of foods

consumed. Gender and age differences also influence

individuals, food consumption patterns. This means

that it is difficult to make any generalizations

about the impact of commercial catering on the nu-

trition of the community at large. However, some

observations relating to the nutritional value of food

and drink consumed include the fact that fats and

alcohol provide a considerably higher proportion of

the total energy (caloric value) of food eaten out.

Overall, food eaten away from the home accounted

for just over 12% of total energy intake for the

average person in the UK in 1999.

0057 There are increasing concerns about the increasing

prevalence of obesity in developed countries such as

the UK. Medical practitioners and nutritionists regu-

larly confirm this growing problem, exemplified by

the fact that nearly one in five adults in the UK are

classified as clinically obese. Because obesity is recog-

nized as contributing to a range of health problems

such as cardiovascular disease, it is suggested that

caterers should make any efforts that they can to

contribute to the general dietary goals of reducing

fats, sugar, and salt by examining and modifying

recipes whenever they can.

See also: Catering: Catering Systems; Chill Foods: Effect

of Modified-atmosphere Packaging on Food Quality

Further Reading

Department of Health (1995) Nutrition Guidelines for

Hospital Catering – Prepared by Nutrition Task Force

of Health of the Nation. London: HMSO.

Hunt C (1984) Nutrient losses in cook-freeze and cook-chill

catering. Human Nutrition Applied Nutrition 38A:

50–59.

Hunt C (1990) Vitamins in institutional feeding. Journal of

Micronutrient Analysis 7: 193–206.

MAFF (2000) National Food Survey 1999 – Annual Report

on Food Expenditure, Consumption and Nutrient

Intakes. London: Stationery Office.

West A, Walker A and Lawson JM (1998) The effects of

food processing in hospital catering systems. In:

Edwards JSA (ed.) Culinary Arts and Sciences 2. Global

and National Perspectives, pp. 283–289. London: Com-

putational Mechanics Publications.

Williams PG, Ross H and Brand Miller JC (1995) Ascorbic

acid and 5-methyltetrahydrofolate losses in vegetables

with cook-chill or cook/hot-hold foodservice systems.

Journal of Food Science 60(3): 541–546.

CELIAC (COELIAC) DISEASE

P D Howdle, St. James’s University Hospital, Leeds,

Introduction

0001 Celiac disease, or gluten-sensitive enteropathy, is a

common condition in which the principal abnormal-

ity is in the small intestine. This abnormality is related

to the ingestion of a cereal protein, gluten, and leads

to a variety of clinical problems. The pathogenesis of

the abnormality is thought to be an immune reaction

to gluten in a genetically predisposed individual.

0002 The clinical presentation varies from a normal state

to a severely malnourished state, and there are a

number of associated diseases.

0003 Treatment is with a gluten-free diet and, in the

majority of patients, is very effective.

Epidemiology

0004The most comprehensive data on the prevalence of

celiac disease are from Western Europe. The preva-

lence of clinically apparent disease ranges from one in

300 to one in 1000. The disease has thus been de-

scribed principally in Caucasian peoples, although

cases have been diagnosed in all other ethnic groups.

Any variation between ethnic groups may be due to a

genetic variation between different populations, the

availability of diagnostic facilities, and the consump-

tion of the relevant cereals, since the disease can only

present in wheat-eating populations.

0005In recent years, serological antibody tests have been

used to screen for the disease in the general popula-

tion of several European countries. Such studies sug-

gest that the true prevalence may be as high as one in

140, although the majority of the subjects have no

apparent symptoms of the disease.

CELIAC (COELIAC) DISEASE 987

0006 Such screening studies have led to the concept of

the celiac iceberg (see Figure 1). This suggests that a

minority of patients have clinical evidence of the

disease, others have the small intestinal abnormality

but are asymptomatic (silent disease), and others have

the genetic predisposition but have not yet developed

the pathological changes that could lead to symptoms

(potential disease). There are normal individuals

who have the genetic predisposition as described at

present, but who never develop the disease. There is

presumably an as-yet unidentified factor that distin-

guishes these normal individuals from the potential

celiac patient.

Pathogenesis

Genetics

0007 Celiac disease has been recognized as being a familial

condition for many years. Approximately 10% of

first degree relatives have the condition. The mode

of inheritance is not understood.

0008 It is also known that a particular haplotype in the

MHC region of chromosome 6 is necessary in

order to develop the disease. The extended haplotype

concerned is B8, DR3, DQ2 but it is the DQ2 haplo-

type that is specifically associated with the disease,

being present in 95% of patients. The 5% of patients

who are DQ2-negative are DQ8-positive. It should

be noted that other genes must be involved, since

approximately 30% of the general population

carry these genes, and the majority of these do

not develop the disease. Hence, DQ2 or DQ8 is ne-

cessary, but not sufficient in terms of the genetic

constitution of an individual in order to develop the

disease. For this reason, other genes are being sought

elsewhere in the genome that might predispose to the

disease, but to date, no consistent results have been

produced.

Gluten

0009The term ‘gluten’ is the generic name applied to the

storage proteins found in wheat, rye, and barley.

Gluten is responsible for the visco-elastic properties

of these cereals, which make them good for baking. It

is the insoluble material (a complex mixture of pro-

teins, with small amounts of lipids, sugars, and min-

erals) obtained when flour is washed in tap-water to

remove the soluble substances (albumins, globulins,

and starch). Gluten is thus an ill-defined mixture that

varies between different flours and is even dependent

upon the solubilizing properties of the tap-water

used. Gliadin is the ethanol-soluble component of

wheat flour, usually solubilized in 70% ethanol; the

same component can be extracted from wheat gluten.

Gliadin, although a complex mixture of proteins, is

thus more homogenous than gluten. The comparable

ethanol-soluble components from rye and barley are

termed secalin and hordein, respectively. Collectively,

these proteins are prolamins. All these prolamins are

related phylogenetically and are rich in the amino

acids proline and glutamine. All are capable of pro-

voking the pathological changes in the small intestine

characteristic of celiac disease.

0010Most is known about wheat gluten or gliadin, and

the terms are often used interchangeably when refer-

ring to their involvement in celiac disease. Gliadin

comprises approximately 50% of wheat proteins,

and a single variety of wheat may have 45 different

gliadins. Their complexity has made them difficult to

Clinical

celiac disease

Silent

celiac

disease

Mucosal

abnormality

of celiac

disease

Normal

small

intestinal

mucosa

Genetic

predisposition

Potential

celiac

disease

Healthy individuals

fig0001 Figure 1 ‘Celiac iceberg’ showing the spectrum of disease and small intestinal abnormality.

988 CELIAC (COELIAC) DISEASE

investigate, but some gliadins have been sequenced,

and synthetic or chemically derived peptides from

gliadin have been tested in in-vitro or in-vivo experi-

ments in celiac disease. It appears that short peptides,

approximately 10–20 amino acids in length, which

are particularly rich in glutamine, are capable of

producing small-intestinal damage. It is believed,

therefore, that ultimately, several peptides from the

prolamins of wheat, rye, and barley, with similar

amino acid sequences, will be found to be responsible

for initiating the disease process in predisposed

individuals.

0011 Oats are a major related cereal, but the prolamin in

oats (avenin) only accounts for 5–15% of the oats’

protein. It is thought that because of this low prola-

min content and possible dissimilarities between the

amino acid structures of avenins and the other prola-

mins, oats are nontoxic to the vast majority of celiac

patients.

Immunology

0012 There is much evidence of enhanced immunological

activity in celiac disease. In the small-intestinal

mucosa where the characteristic pathology develops,

there is an increase in T-lymphocytes, principally of

the helper (CD4) type in the lamina propria, resulting

in the production of pro-inflammatory cytokines, and

of the cytotoxic-suppressor (CD8) type in the epithe-

lium, the so-called intra-epithelial lymphocytes. Con-

comitantly, the plasma cell numbers increase, leading

to the production of immunoglobulins, particularly

antibodies to gliadin and tissue auto-antigens. Re-

cently, tissue transglutaminase (tTG), a ubiquitous

enzyme present particularly in the lamina propria,

which catalyzes the cross-linking of proteins, has

been reported to be an auto-antigen in celiac disease.

The antibody against this antigen is termed the ‘anti-

endomysial antibody’ and is very specific for the

disease when measured in the serum of untreated

patients. Interestingly, gliadin is an excellent substrate

for tTG because of its high glutamine content. It is

currently hypothesized that in celiac patients, tTG

reacts with gliadin, thus forming a deaminated

gliadin and a gliadin–tTG complex. This neo-antigen

could then be involved in the initiation of an immune

reaction in a predisposed individual.

Pathophysiological pathway

0013A possible pathway leading to the small intestinal

mucosal damage in celiac disease is shown in Figure 2.

This scheme takes into account the pathogenetic

factors discussed above. The products of the

enterocyte

gliadin

gliadin peptides

activation

intraepithelial

lymphocyte

tTG

Antigen presenting cell

Processed and deaminated gliadin

presented to T cell receptor on T helper cell

T helper

cell

Immunoglobulins (antigliadin antibodies)

Plasma

cell

mucosal

damage

pro-inflammatory

cytokines

stimulation

Epithelium

Lamina

propria

fig0002 Figure 2 Schematic representation of the immune mechanisms leading to the mucosal abnormalities in celiac disease.

CELIAC (COELIAC) DISEASE 989

HLA-DQ2 genes are proteins located on the mem-

brane of antigen-presenting cells (e.g., macrophages

in the lamina propria). These HLA molecules form a

groove in which short peptides (i.e., digested gliadins)

can be specifically bound. Deamination by tTG may

unmask neo-antigens, which bind more effectively

to the HLA-DQ2 molecules. The bound peptides are

presented to the T-cell receptor on the CD4 lympho-

cytes, and the lymphocytes are activated to proliferate

and to produce pro-inflammatory cytokines. This pro-

motes the inflammatory cascade and leads to an

immune reaction, with resulting tissue damage.

Mucosal pathology

0014 The normal appearance of the small intestinal

mucosa has finger-like villi (see Figure 3a), which,

on microscopic sections, appear as tall villi covered

with a layer of regular epithelial cells supported by

a lamina propria (Figure 3b). In untreated celiac

disease, the villi are lost, and the surface looks ‘flat’

(Figure 4a). Microscopically, there are no villi, the

crypts between the villi are deeper, and the lamina

propria has a vastly increased number of inflamma-

tory cells (Figure 4b). Careful studies of serial biopsies

have shown that these changes develop in a sequential

fashion related to the amount of gluten in the diet.

Hence, in celiac patients, one can see a range of

abnormalities from the severe, as can be seen in

Figure 4, to the normal, as can be seen in Figure 3

when the patient is well treated, or in potential

patients before the mucosal abnormalities develop.

Clinical Features

0015Celiac disease can present at any age, in both adults

and children. The clinical features are protean (see

Table 1), although since it is a disease affecting the

small intestine, symptoms of gastrointestinal disease

predominate in classical descriptions of the disease.

Patients may have diarrhoea, anorexia, nausea,

fig0004Figure 4 (see color plate 23) (a) Dissecting-microscopic

appearance of biopsy from untreated celiac patient with total

absence of villi and a ‘flat’-looking mucosal surface; (b) light-

microscopic appearance of untreated celiac mucosa with ab-

sence of villi, deep crypts, and an increase in inflammatory cells.

fig0003 Figure 3 (see color plate 22) (a) Dissecting-microscopic ap-

pearance of normal mucosal biopsy showing finger-like villi;

(b) light-microscopic appearance of normal mucosal biopsy.

990 CELIAC (COELIAC) DISEASE

vomiting, abdominal distention and pain, flatulence,

a sore tongue, or mouth ulcers. As well as these

gastrointestinal symptoms, patients commonly have

constitutional symptoms of lassitude and malaise,

weakness, and weight loss. Children may fail to thrive

as infants and be underdeveloped, not reaching their

expected height. Apart from these general symptoms,

there are symptoms that arise as a result of poor

absorption of various vitamins and minerals due

to the small intestinal mucosal abnormality, which

causes ‘malabsorption’. Such symptoms include

features of anemia (malabsorption of iron and/or

folic acid), a bleeding tendency (vitamin K) cramps,

paraesthesiae, rickets, and proximal muscle weakness

(vitamin D). Finally, there are rare symptoms that

may result from the chronicity of the disease or mal-

absorption of undiscovered factors; these include dis-

orders of the nervous system, reproductive system,

and skin.

0016 It is important to stress that many of these symp-

toms are described in untreated patients with celiac

disease, and almost all are reversible with treatment.

It is also of note that as physicians have become more

aware of the disease, the diagnosis is being made

more quickly, and patients nowadays do not present

with such gross features. In fact, the majority of

patients are diagnosed with mild symptoms and

minor biochemical or hematological abnormalities.

Recently, it has become apparent that previously

unrecognized osteopenia and osteoporosis are present

in a significant minority of celiac patients.

0017When untreated patients are examined, the find-

ings on physical examination reflect the symptoms

referred to above. For example, a patient with

major symptoms may be thin and wasted, with

muscle weakness, bruising of the skin, a sore tongue,

and a distended abdomen. Patients diagnosed at an

early stage may be apparently normal on physical

examination.

Associated Disorders

0018Many disorders have been described to occur in asso-

ciation with celiac disease. The explanation may be

that the underlying predisposition to celiac disease

enhances the possibility of other disorders occurring,

particularly those that have an immunological eti-

ology. The most common of the associated disorders

are shown in Table 2.

Diagnostic Tests

Hematological investigations

0019The majority of untreated patients are anemic.

Anemia is caused by iron or folic acid deficiency, or

both, and is a result of the malabsorption of these

factors. Vitamin B

may be low but rarely causes the

features of B

deficiency. Unexplained anemia may

therefore alert the physician to the possibility of celiac

disease.

Biochemical investigations

0020Similarly, other nutritional factors are often low in

the serum of untreated celiac patients, e.g., the fat-

soluble vitamins A, E, D, and K, deficiency of the

latter two being responsible for the features of osteo-

malacia and a bleeding tendency referred to above.

Calcium and magnesium, as well as water-soluble

vitamins such as Vitamin C, may be low, although

scurvy is rare in celiac disease. Albumin is often low,

owing to loss into the gastrointestinal tract from the

tbl0001 Table 1 The presenting symptoms encountered in patients

with celiac disease

General Lassitude, malaise, weakness, weight loss

Gastrointestinal Diarrhea (+ features of steatorrhea)

Anorexia

Nausea and vomiting

Flatulence and abdominal distention

Abdominal pain

Constipation

Glossitis/aphthous ulcers

Metabolic Features of anemia

Bleeding tendency

Edema

Cramps/tetany

Paresthesiae

Nocturnal diuresis

Musculoskeletal Increased risk of fracture

Bone pain

Rickets

Proximal myopathy

Neuropsychiatric Peripheral neuropathy

Cerebrospinal degenerations

Anxiety/depression

Reproductive Menstrual irregularities

Reduced fertility (male and female)

Relapse associated with pregnancy

Skin Variety of rashes

Dermatitis herpetiformis

tbl0002Table 2 Disorders known to be associated with celiac disease

Insulin-dependent diabetes mellitus

Autoimmune liver disease

Thyroid disorders

Pulmonary alveolitis

Inflammatory bowel disease

Connective-tissue disorders

Immunoglobulin A (IgA) deficiency

Down’s syndrome

Osteoporosis

Epilepsy

CELIAC (COELIAC) DISEASE 991

blood, rather than malabsorption. This can lead to

peripheral edema in the patient. Immunoglobulin A

(IgA) deficiency may be found since this is 10 times

more common in celiac disease than in the general

population. None of these measurements is specific

for celiac disease, and therefore, they are not used in

diagnosis.

Tests of malabsorption

0021 Apart from finding low levels of various nutrients in

the serum, as outlined above, absorption can be

assessed more formally. For example, the absorption

of fat can be assessed by measuring the dietary intake

and fecal output over a period of days. A more indir-

ect method measures the serum levels and urinary

excretion of d-xylose, a carbohydrate not normally

found in the diet. Such tests can indicate malabsorp-

tion but are not specific for celiac disease and are

rarely used routinely.

Serological screening tests

0022 IgA and immunoglobulin G (IgG)-class antigliadin

antibodies are present in the serum of many patients

with celiac disease. Their measurement has been used

particularly as a screening test. The sensitivity and

specificity of these tests approach 90%. False positive

results limit their use as a definitive diagnostic test.

0023 IgA-class anti-endomysial antibodies are also

found. As outlined above, tTg is the auto-antigen

responsible for anti-endomysial antibody positivity.

This antibody test has more than 95% sensitivity

and specificity in celiac disease and thus is an ideal

screening test. It cannot, however, be regarded as

definitely diagnostic.

0024 tTg itself has been used as the substrate in an

enzyme-linked immunosorbent assay (ELISA) test,

and tTg antibodies are now coming into use as an-

other serological screening test for celiac disease, with

a similar accuracy to anti-endomysial antibodies.

0025 These serological tests are useful as screening tests

in case-finding studies, particularly in at-risk groups

such as patients with disorders associated with celiac

disease, or first-degree relatives. They are also useful

for follow-up of patients to monitor treatment and to

indicate the timing of follow-up intestinal biopsies,

since the tests usually become negative when treat-

ment is being effective (see below).

Small-intestinal mucosal biopsies

0026 Celiac disease is defined as that disease in which there is

an abnormality of the small intestinal mucosa, made

manifest by contact with the gluten fraction of wheat

and related cereals. The cornerstone of diagnosis must

therefore be the examination of a biopsy of this

mucosa. Such a biopsy can be obtained using a biopsy

tube or fiber-optic endoscope, which the patient

swallows, usually under sedation. Careful examination

of the biopsy will reveal the typical pathological fea-

tures, although these can vary in severity. Since there

are other, rarer causes of the same abnormality, the

diagnosis is only definite when a second biopsy is

obtained after a period (usually 6–12 months) on a

gluten-free diet, and the abnormality has been shown

to improve and return towards normal (Figures 3

and 4). If such an improvement in the pathological

features is seen, the diagnosis of celiac disease can be

firmly made. Such a scheme for diagnosis is suggested

in the definition of the disease, since this indicates

that the mucosal abnormality must be related to the

presence of gluten in the diet.

Management

Treatment: a gluten-free diet

0027The cornerstone of treatment is a gluten-free diet,

which should be taken for life. Patients should omit

foods containing wheat, rye, and barley from their

diet. In severely symptomatic untreated patients, ini-

tial treatment may also include replacement of nutri-

tional deficiencies such as iron, folate, calcium, and

Vitamins D and K. Rarely, severely ill patients may

require parenteral nutrition.

0028Once treatment with a gluten-free diet is estab-

lished, patients begin to respond quickly and usually

note a remarkable improvement within weeks. Pa-

tients vary in their sensitivity to gluten in the diet.

Some can eventually consume some gluten and appear

to remain clinically well; others have to adhere

strictly to their diet, even to the extent of avoiding

Communion wafers. They may need to omit oats

from their diet. If patients do consume gluten, they

can produce some damage to the small intestinal

mucosa, which may take months or years to produce

clinical symptoms. There is evidence that the malig-

nancy that can occur in celiac disease can be reduced

by strict adherence to a gluten-free diet.

0029Osteopenia will improve with a gluten-free diet,

but patients should have an adequate calcium intake

and take regular exercise.

0030If patients are to adhere to a gluten-free diet,

they need help from an experienced dietitian. Some

patients have problems once dietary treatment has

started. Initially, some put on weight, presumably as

a result of improved absorption. These patients need

advice about weight reduction. In this situation,

diabetes may be unmasked.

0031Constipation sometimes becomes a problem, re-

flecting the fact that bran from most cereals is omitted

from the diet. Defatted rice bran or soya bran has

992 CELIAC (COELIAC) DISEASE

been shown to help, and bulking agents such as

ispaghula husk or methyl cellulose may also help.

The dietitian can help with all these problems and

advise about a diet based around fresh meat, vege-

tables, fish, and fruit, with the gradual introduction

of other safe foods as the patient becomes more con-

fident about the gluten-free diet.

Prognosis

0032 The prognosis is good for celiac patients. Nearly all

respond clinically and pathologically to treatment

with a gluten-free diet, there being an improvement

in symptoms and in the small intestinal mucosa. Life-

long treatment with the diet is recommended, as is

follow-up in an out-patient clinic with the help of a

dietitian. Younger patients, particularly teenagers,

need sympathetic follow-up since they often find the

restrictions of the diet quite onerous.

0033 Some physicians recommend further intestinal bi-

opsies (after the first two that are necessary for diag-

nosis) every few years. This provides an objective

assessment of the patient’s condition and helps to

motivate patients to maintain a strict diet.

0034 Occasionally, the mucosa does not respond to a

gluten-free diet, and the physician must consider the

other, much rarer, causes of an abnormal small intes-

tinal mucosa (see Table 3). However, by far the most

common cause of failure to respond to the gluten-free

diet is inadequate dietary gluten exclusion. This may

be conscious or inadvertent. Dietary compliance

needs to be assessed by a well-informed dietitian.

Rarely, other foods (e.g., milk, eggs and soya) need

to be excluded as well as gluten, either temporarily or

permanently. Other causes preventing a mucosal re-

sponse to gluten exclusion may be pancreatic insuffi-

ciency, or contamination of the small intestine by

bacterial overgrowth. Such causes should be sought

and treated in this situation. Finally, nonresponse

may be associated with serious complications of the

disease, which, fortunately, occur only rarely. These

are the development of ulcers and strictures in

the small intestine and also malignancy, particularly

small intestinal lymphoma. Such complications may

be a cause not only of nonresponse but also of deteri-

oration in a previously well patient who has been

adequately treated for some time with a gluten-free

diet. As already suggested, there is good evidence

that the incidence of malignancy in celiac disease

may be reduced in patients who maintain a strict

gluten-free diet.

0035If no underlying cause is found for nonresponse to

a gluten-free diet, and the diagnosis has been carefully

considered, patients may be treated with oral steroids

in order to induce a remission. This should only be

done under careful supervision, and there are no long-

term studies, but the side-effects of steroid therapy

suggest that such a course of treatment has a limited

role in celiac disease.

See also: Anemia (Anaemia): Iron-deficiency Anemia;

Calcium: Properties and Determination; Cereals:

Contribution to the Diet; Folic Acid: Properties and

Determination; Immunology of Food; Iron: Properties

and Determination; Physiology; Magnesium; Vitamin K:

Properties and Determination; Vitamins: Overview;

Wheat: The Crop

Further Reading

Dieterich W, Ehnis T, Bauer M et al. (1997) Identification of

tissue transglutaminase as the autoantigen of coeliac

disease. Nature Medicine 3: 797–801.

Feighery C (1999) Coeliac disease. British Medical Journal

319: 236–239.

Hin H, Bird G, Fisher P et al. (1999) Coeliac disease in

primary care: case finding study. British Medical Journal

318: 164–167.

Holmes GKT and Catassi C (2000) Coeliac disease. Health

Press, Oxford.

Holmes GKT, Prior P, Lane MR et al. (1989) Malignancy in

coeliac disease – effect of a gluten-free diet. Gut 30:

333–338.

Howdle PD (1995) Coeliac Disease. Baillie

re’s Clinical

Gastroenterology, vol. 9. London: Baillie

re Tindall.

Janatuinen E, Pikkarainen PH, Kemppainen TA et al.

(1995) A comparison of diets with and without oats in

adult coeliac disease. New England Journal of Medicine

333: 1033–1037.

Maki M and Collin P (1997) Coeliac disease. Lancet 349:

1755–1759.

tbl0003 Table 3 Causes of an abnormal small-intestinal mucosa

Celiac disease (CD), including:

Non-responsive CD

Complications of CD (ulceration, malignancy)

Cow’s milk protein intolerance

Soya protein intolerance

Immunodeficiency syndromes

Eosinophilic gastroenteropathy

Immunoproliferative small-intestinal disease (IPSID)

Protein-energy malnutrition

Intractable diarrhea of infancy

Gastroenteritis in children

Infections:

Parasites, e.g., giardiasis

Tuberculosis

Human immunodeficiency virus

Contaminated bowel syndrome

Whipple’s disease

Tropical sprue

Arterial disease of small intestine

Drug and radiation damage

CELIAC (COELIAC) DISEASE 993

Marsh MN (1992a) Coeliac Disease. Oxford: Blackwell

Scientific.

Marsh MN (1992b) Gluten, major histocompatibility

complex, and the small intestine. A molecular and

immunobiologic approach to the spectrum of gluten

sensitivity (‘celiac sprue’). Gastroenterology 102:

330–354.

Trier JS (1998) Diagnosis of celiac sprue. Gastroenterology

115: 211–216.

CELLS

P McGrath, University of Newcastle, Callaghan,

Australia

Structure and Function of Human and

Animal Cells

0001 The cell is the fundamental functional unit of all

living organisms. Cells perform all of the body’s vital

physiological functions. Cells are ultimately respon-

sible for activities such as breathing, moving, combat-

ing infection, digesting food, thinking – in fact, all

bodily functions. These activities require energy. It

is inside cells that fuels are used to produce the energy

needed to drive these activities. This article examines

the structure inside the cell and the combined

activities of cells that make all of this possible.

Structure and Organization of Human

Animal Cells

Structure

0002 Common to nearly all cells are three compartments,

namely the cell membrane (also called the plasma

membrane), the cytoplasm, and the nucleus (mature,

human red blood cells have no nucleus). This basic

structure is evident in a wide variety of cells even

though they may differ dramatically in size and

shape (Figure 1). The plasma membrane not only

encloses the contents of the cell but performs many

vital functions. The cytoplasm is that compartment

between the nucleus and the cell membrane. It is

composed of a soluble component (the cytosol) in

which are immersed various microscopic components

called organelles. Among the many important bio-

chemical reactions that take place in the cytosol is

glycolysis, an energy-releasing process involving the

breakdown of glucose to pyruvic acid. (See Glucose:

Function and Metabolism.)

0003 The cellular organelles are a diverse group of struc-

tures that perform many different functions within the

cell. The nucleus of the cell is a membrane-bound

structure that contains within it the genetic material

of the cell. It is here that the genes reside in the form of

DNA (deoxyribonucleic acid) molecules grouped into

structures called chromosomes.

(d)

(a)

(b)

(c)

fig0001Figure 1 Different shapes of cells. The nucleus is darkly

shaded; the plasma membrane is represented by the outline of

the cell; the cytoplasm is represented by the clear space between

the plasma membrane and the nucleus. (a) Epithelial cell; (b)

smooth muscle cell; (c) neuron; (d) lymphocyte. Reproduced

from Cells, Encyclopaedia of Food Science, Food Technology and

Nutrition, Macrae R, Robinson RK and Sadler MJ (eds), 1993,

Academic Press.

994 CELLS

Organization

0004 In the body, cells often function in combination with

other cells of the same type and are held together with

varying degrees of tenacity and with varying amounts

of extracellular material between them. Clusters of

cells of the same type are called tissues. Four different

types of tissues are recognized:

0005 Epithelial tissue, in which the cells are held very

tightly together, and there is very little extracellu-

lar material between them. This tissue forms

glands and the linings of the body cavities and

surfaces.

0006 Connective tissue, in which the cells are not bound

closely to one another. There is much extracellular

material in such tissue, and the cells may be held

rigidly in place by this material, as in the case of

bone, or they may be freely moving, as in blood.

0007 Muscle tissue, in which the cells may be bound

to each other, as in cardiac muscle and smooth

muscle, or separate from each other but gathered

into bundles by connective tissue, as in skeletal

muscle. (See Exercise: Muscle.)

0008 Nervous tissue, which is composed of neurons

(nerve cells) that conduct electrical impulses from

one neuron to another. These cells are not physic-

ally coupled but are held in place by specialized

connective tissue cells.

The organs of the body are in turn composed of

different types of tissues. For example, the heart is

composed mainly of muscle tissue but also includes

connective tissue, epithelial tissue, and some nervous

tissue.

Cellular Components

0009 There are numerous chemical activities occurring

simultaneously inside the cell. Eukaryotic cells (cells

that have membrane-bound compartments) are able

to minimize interference of one chemical reaction

with another by confining certain chemical activities

to specific membrane-bound components of the cell.

This design also facilitates cellular specialization.

Prokaryotic cells (cells that lack membrane-bound

compartments) such as bacteria are disadvantaged

in this regard. These membrane-bound components

and other specific structures inside the cell are called

organelles. Although some of these (e.g., the nucleus)

can be seen under the light microscope, it has been

necessary to employ electron microscopy to clearly

visualize most of them. Not all of the organelles are

found in every cell, and the relative abundance of a

particular type of organelle varies from cell to cell,

depending on the activity of the cell. Figure 2 is a

drawing of a generalized cell with various organelles

represented.

Nuclear Components

0010The nucleus contains the chromosomes. In humans,

there are 46 chromosomes (23 pairs). The number in

other animals varies from species to species. The

chromosomes are very long, thin strands of DNA.

They also contain proteins called histones. They are

not easily seen under the light microscope until just

prior to cell division, when they shorten and coil up,

making them visible following appropriate staining.

The nucleus also contains other structures called nucle-

oli. These are roughly spherical structures containing

strands of RNA (ribonucleic acid) molecules, DNA,

and proteins. The nucleoli are responsible for manufac-

turing rRNA (ribosomal RNA) of the ribosome. The

nucleus is enclosed by a membrane that is perforated

by holes (nuclear pores) that are large enough to allow

large molecules, such as RNA, to pass through. There

are several different types of RNA, and each type has a

distinct role in the manufacture of proteins (protein

synthesis). Protein synthesis takes place in the cyto-

plasm. (See Nucleic Acids: Physiology.)

Cytoplasmic Components

0011There are many organelles or structures within the

cytoplasm that are involved with specific cell func-

tions. These are listed below with a brief description

of the structure and function of each.

0012Ribosomes Ribosomes are tiny granules (about

25 nm in diameter) composed of rRNA and protein.

A ribosome consists of two subunits, one about twice

the size of the other. Ribosomes play an integral role

in protein synthesis.

Microvilli

Microfilaments

Ribosomes

Microtubules

Nuclear

membrane

Nuclear pores

Nucleolus

Golgi complex

Plasma

membrane

Mitochondrion

Endoplasmic

reticulum

(smooth)

Endoplasmic

reticulum

(rough)

Lysosome

fig0002Figure 2 Drawing of a ‘generalized’ cell showing many of the

organelles found in human and animal cells. Reproduced from

Cells, Encyclopaedia of Food Science, Food Technology and Nutri-

tion, Macrae R, Robinson RK and Sadler MJ (eds), 1993, Aca-

demic Press.

CELLS 995