COELIAC DISEASE


CONTENTS

PAGE 1 COELIAC DISEASE: The Silent Destroyer
(A technical article written for use by the medical profession and allied health professional people)

PAGE 6 WHAT IS COELIAC DISEASE?
(Corrected version of a factual essay written for the Council of Adult Education course “Essay Writing”: submitted July 2005.)

PAGE 7 UNDERSTANDING COELIAC DISEASE
This paper is based on the article “Coeliac Disease; The hidden disease of adults” by the same author which was published in PROBUS NEWS Spring 2003
********************

**PAGE 1**

COELIAC DISEASE: The Silent Destroyer

By Phillipa Andrew
Former Senior Lecturer in Applied Biology: Royal Melbourne Institute of Technology

Coeliac disease [CD] is an autoimmune, progressive, potentially debilitating medical condition. It is also known popularly as non-tropical sprue or as coeliac sprue (Merck 2000). Medically, coeliac disease is termed “gluten enteropathy” or “gluten-sensitive enteropathy” [GSE]. CD was once considered to be mainly a disease of children who failed to thrive, showed poor weight gain, or even weight loss, and experienced gastroenteritis. Many died (Willett 2002).
It is now known that the condition is far more widespread than this, especially among the adult population (Hin et al 1999). Their symptoms may be totally different from those listed above and may be almost non-existent in the sub-clinical latent and silent stages (Cook 2002). Rarely are the very extreme cases met in children nowadays. Their condition is being recognised and treated at a much earlier stage as well (Bingley, et al 2004). Coeliac disease is uncommon during adolescence (Selby 2001), even in people who have coeliac disease in both childhood and adulthood.

People with CD react adversely to the alcohol-soluble fraction, gliadin, of the storage protein, gluten, in wheat, kamut (a large Egyptian wheat) and German spelt (Anderson 2002). Similar prolamines producing a similar toxicity are found in rye (secalin), triticale (an hybrid of wheat and rye) barley (hordein), and, to a lesser extent, oats (avenin) (Fraser and Ciclitira 2001). This toxicity includes an adverse reaction to the many by-products of these cereals.
The condition is found predominantly amongst Caucasians. It is found to a lesser degree amongst Arabs, Indians and Africans along the Mediterranean rim (Vale 2001, Willett 2002). It is absent from people native to Africa south of the Sahara, from Asians along the Pacific rim and from the native inhabitants of the American continents. However, people of Chinese and Japanese descent long resident in “European” cultures such as the USA and Australia eventually become prone to the condition (Shepherd 2000).
Coeliac disease is relatively common. Estimates of its frequency in various populations range from 1:100 to 1:500 (Shepherd 2000). However many fewer people than this have been diagnosed. In Australia almost 200,000 people have the condition. Over 170,000 people remain undiagnosed. Most of these people are older Australians. Many of them are experiencing chronic secondary symptoms which are not recognised as being linked to CD. This means that the primary cause of their condition remains undiagnosed.

**PAGE 2**

Wide variations in the number of symptoms and in their severity make diagnosis of coeliac disease difficult (Duggan 2004, Pruessner 1998). Reasons for these variations are still unknown. It is known, however, that the condition may remain in one phase for many years before it is suddenly triggered to progress from the almost silent stage to the more severe stages. These triggers include viral illness, physical trauma, including surgery, emotional stress and pregnancy.
The small intestine, about 3.5cm [1.5in] in diameter, is very folded internally to give it a velvet-like appearance. These fine, finger-like folds, called villi, are responsible for the absorption of digested food. Between them, like the sweat glands in the skin, are downward folds called crypts where the digestive enzymes are produced. In coeliac disease these villi are slowly destroyed. This destruction starts at the proximal end of the duodenum and gradually progresses down the duodenum over time. Four stages of the condition are recognised (Willett 2002).
In the latent or infiltration stage of coeliac disease antibodies [anti-gliadial, anti-endomysial and anti-tissue transglutaminase] are found in the blood. The duodenum is normal except for a small increase in the antibody- producing immune cells, the lymphocytes.
This stage can progress to the silent or inflammation stage in which more immune cells are present. Also the length and number of crypts increase. Symptoms, if present, are very mild; perhaps no more than loss of energy and increased tiredness.
The trigger factor can eventually turn on the third [deformed- hypoplastic] and fourth [destructive] stages in which the intestine is damaged. For this reason coeliac disease is classed as an autoimmune disease. With the third and fourth stages outward signs of illness become increasingly apparent. The villi become shorter, flatter, wider in stage three and are totally absent in stage four. Crypts, in contrast, are numerous and deeper than normal. In many people with CD there is a mosaic of two or more stages present simultaneously. Some doctors recognise a fifth, refractory, stage of the condition in which the patient no longer responds to the gluten-free diet.
In the undamaged intestine the ratio of villi to crypts is four to one. Even after a considerable period on a gluten-free diet this ratio is not fully restored but remains at a ratio of two villi to one crypt (Jewell 1996).

CD may suddenly manifest itself at any age although much less so in adolescence. However, late menarche in adolescent girls and short stature in both boys and girls may indicate the presence of coeliac disease. Initial diagnosis of coeliac disease is sometimes made in people in their 80’s and 90’s who suddenly exhibit symptoms such as excessive, rapid weight loss or, occasionally, weight gain amongst many other symptoms. After their diagnosis people frequently realise in retrospect that they have had mild symptoms of CD for many years prior to diagnosis: they have just accepted their feeling of unwellness as normal for them. Prior to diagnosis with coeliac disease patients may be underweight, of average weight or overweight (Catassi 1994, Dickey and Bodkin 1998).
CD should be suspected in people of short stature: in women under 162cm [5ft4in] and in men under 168cm [5ft6in], especially if they were low weight babies or exhibited slow growth as children; and in women who gave birth to low weight babies. Infertility in both sexes, miscarriages, difficulty with breast-feeding, delayed puberty and premature menopause can be among other reproductive expressions of undiagnosed CD.

**PAGE 3**

Frequently, excessive fatigue, tiredness or sleepiness may be the only or main symptom. Often such people are not tested for coeliac disease as a possible cause.
Likewise this lack of testing applies to emotional symptoms such as depression or lethargy, mood swings, irritability and crankiness (Bird 2004, Shepherd 2000). People of all ages with coeliac disease may be easily annoyed and upset.
Undiagnosed CD can also lead to sometimes subtle nerve/muscle problems such as peripheral neuropathy, muscle weakness, epileptic fits (especially those commencing in adulthood), other neurological problems and, eventually, dementia (Bird 2004, Skeen 2002, Tietge et al 1997,Volta, et al 2002; Wills and Unsworth 2002).
Some people experience mouth ulcers [red ring with pale top], a cracked corner of the lips, cold sores, hair loss to varying degrees, low thyroid function, and excessive bruising. These are due in part to the inadequate absorption of vitamins and minerals as a result of the CD. Other symptoms of vitamin and mineral deficiencies may also occur. Liver function tests reveal problems, especially elevated alkaline phosphatase Pruessner 1998).
Secondary lactose intolerance may occur in some people (Murray 1996). Usually these people can tolerate milk in theitr diet after some months, or longer, on a gluten-free diet. It is now recommended that all people diagnosed with osteoporosis and anaemia [due to lack of iron, vitamin B12 or folate] be tested for CD (Selby 2001). This also applies to people with Type 1 diabetes and other auto-immune diseases such as rheumatoid arthritis, thyroiditis, lupus, “dry eye/dry mouth” condition-Sjogren’s syndrome, scleroderma and vitiligo.
In Australia free bone-density tests are given regularly to people diagnosed with CD for the rest of their lives, whether or not they already have osteoporosis.

Chronic nausea, vomiting, reflux, abdominal cramps and bloating, diarrhoea and excessive flatulence may all suggest the need for testing for CD to eliminate it from other possible causes. Flatulence may be particularly smelly and offensive in some people. Unfortunately, testing for coeliac disease is often overlooked.
Screening is initially by blood tests for the antibodies followed by endoscopic examination. During this period a diet heavy in gluten must be maintained in spite of the illness it causes. False positives and false negatives mean that the blood tests alone are inadequate to diagnose coeliac disease.
Approximately 10% of close relatives of people with coeliac disease also have the condition. When a person is diagnosed with coeliac disease it is recommended that all close relatives should be screened for the condition as well.

Associated with coeliac disease in some patients, [1:10], is “coeliac disease of the skin”, Dermatitis Herpetiformis [DH]. DH may also occur without CD in up to 5% of patients. These people exhibit some damage to the intestines without symptoms of CD. DH is an intensely itchy rash consisting of little red lumps with or without blisters on top or just as clusters of blisters or large lumps [urticaria]. They are found mainly on the back of the arms, especially near the elbows and on the front of the legs, particularly near the knees, and also on the buttocks, shoulders and scalp. Extra dark or pale areas may mottle the skin on the arms and other parts of the body in many patients (Fry 2002, Wong 2004).

**PAGE 4**

Some doctors may be unfamiliar with CD and DH [and the information given above about them] and so may take some persuasion to test for CD and DH (Woods 2002). This is a not uncommon experience for those later diagnosed with coeliac disease.
People with CD and DH are more prone to certain cancers than the general population, particularly lymphoma. This increased incidence of cancer reduces gradually over time on the very strict gluten- free diet. After about five years the frequency of cancer in people with CD returns to normal. (Digestive Health Foundation 2001).
There are good internet sites on both conditions, including that of the Australian Coeliac Society, but note the American spelling “Celiac” used on many sites.

The only treatment for CD and DH is a lifelong gluten-free diet with strict attempts to avoid contamination. Surprisingly-many foodstuffs contain gluten in unexpected ways as by-products of the processing of the forbidden grains. There are, however, many alternative foods and plenty of variety available.

Emergency situations, such as evacuation during bushfire, are particularly serious for the person with CD and DH as that person cannot eat the mass- produced simple food such as sausages on bread. To do so could precipitate serious illness quite quickly and inconveniently not only personally but to others present as well, to the level of creating a personal emergency.
The impact on the infirm elderly is great, for carers, meals-on-wheels suppliers, hospitals and nursing homes often find it difficult to manage this strict diet and to avoid accidental contamination.

REFERENCES

Anderson, R. P. 2002.Coeliac disease: the past and the future. The Australian Coeliac December, 14(2): 11-13.
Bingley, P.J., Williams, A.J.K., Norcross, A.J., Unsworth, J., Lock, R.J., Ness A.R. and Jones, R.W. 2004. Undiagnosed coeliac disease at age seven: population base prospective birth cohort study. British Medical Journal 328 (7435): 322-323.
Bird, K. 2004. Neurological psychiatric complications of coeliac disease. The Australian Coeliac March, 15(3): 9-10.
Bramell,J Living with coeliac disease. www.studentbmj.com/backissues /1100/ reviews/ 433a.html.
Catassi, C., Ratsch, I.M., Fabiani, E., Rossini, M., Bordicchia, F., Candela, F., Coppa, G.V. and Giorgi, P.L. 1994. Coeliac disease in the year 2000: exploring the iceberg. The Lancet 343 (8891):200-203.
Cook, B. 2002. A Disease with many faces. The Australian Coeliac, September, 15(1): 10-13.
Cook, B., Oxner, R., Chapman, B., Whitehead, M. and Burt, M. 2004. A thirty-year (1970-1999) study of coeliac disease in the Canterbury region of New Zealand. www.nzma.org.nz/journal/abstract.php?id=772.
Dickey, W. and Bodkin, S. 1998. Prospective study of body mass index in patients with coeliac disease .British Medical Journal 317:1290-1290.
Digestive Health Foundation, 2001. www.gesa.org.au
Duggan, J.M. 2004.Coeliac disease: the great imitator. www.mja.com.au/public/issues/18o-10-170504/dug10818-fm.
Faulkner-Hogg. K. 2003. “Sensitive” coeliac disease: does it exist? The Australian Coeliac March: 12-13.

**PAGE 5**

Fraser,J.S. and Ciclitira, P.J. 2001.Pathogenesis of coeliac disease: implications for treatment. World Journal of Gastroenterology October 7(5): 772-776.
Fry, L. 2002. The Dermatitis Herpetiformis Online Community.
Wysiwyg://47http://www.dhcondition.plus.com/whatisdh.html
Hin, H., Bird, G., Fisher, P., Mahy, N. and Jewell, D.1999. Coeliac disease in primary care: case finding study. British Medical Journal 318 (7177): 164-167.
Jewell, P.D. 1996. Coeliac Disease. The Oxford Textbook of Medicine 3rd edition. Oxford University Press.
Johnson, M. 1999. Gluten for punishment. www.dotpharmacy.com/upgluten.html.
www.naspgn.org/sub/celiac-disease.asp.
Merck Manual of Medical Information, The, 2000.
Murray, Joseph 1996. The widening spectrum of Celiac disease. http://members.ozmail.com.au/~coeliac/sptue.htm.
Pruessner, Harold T. 1998. Detecting celiac disease in your patients. www.aafp.org/afp/980301ap/pruessn.html
Selby,W. 2001.Gluten Enteropathy. www.australianprescriber.com/magazines/vol24no2/gluten.htm.
Shepherd, S. 2000. Report on the 9th International Symposium on coeliac disease. The Australian Coeliac, December 12(2): 10-13.
Skeen, Mark B.2002. The Neurological manifestations of gluten sensitivity. Neurological Clinics 20 (1)
http://brain.hastypastry.net/forums/archives/index.php/t-2127.html
Stewart, J.S. History of the coeliac condition. http://osiris.sunderland.ac.uk/~cs0rel/hist.htm.
Tietge, et al, 1997. Neurological Complications of Celiac Disease. American Journal of Gastroenterology 92: 40
Vale, A. D. 2001. Coeliac disease in children of the Sahara. The Australian Coeliac, September, 13(1): 31.
Volta, U., De Giorgio, R., Petrolini, N., Stangbellini, V., Barbara, G., Granito, A., De ponti, F., Corinaldesi, R. and Bianchi, F. B. 2002. Clinical findings and anti-neuronal antibodies in coeliac disease with neurological disorders. Scand J Gastroenterol. 37 (11): 1276-1281.
Willett, I. 2002. An update on coeliac disease. The Australian Coeliac,
March ,13(3): 14.
Wills,A.J. and Unsworth, D.J. 2002. The neurology of gluten sensitivity: separating the wheat from the chaff. Current Opinion in Neurology, 15(5): 519-523.
www.otago.ac.nz/hunannutrition/.
Woods, W. 2002. Letter to the Editor. .Australian Doctor April 19, p428.
Wong, L. 2004. All about dermatitis herpetiformis. The Australian Coeliac,
December, 16(2): 9.

© 2005
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**PAGE 6**

WHAT IS COELIAC DISEASE?
(Corrected version of a factual essay written for the Council of Adult Education course “Essay Writing”: submitted July 2005.)

Coeliac disease [CD], is a potentially debilitating medical condition. In popular parlance it is also called coeliac sprue or non-tropical sprue. Medically, it is termed “gluten enteropathy” or “gluten-sensitive enteropathy”.
The condition is found worldwide in Caucasian populations. People from the Mediterranean rim and from India can also have coeliac disease. Hence CD is relatively common in Australia. About one person in one hundred has this medical condition, but only about one-eighth of these people are diagnosed currently in Australia.
Coeliac disease is an allergic reaction to the alcohol-soluble protein fraction of wheat (including Egyptian kamut and German spelt, dinkel and einkorn), triticale rye, barley, and, to a lesser extent, oats. As a result of this allergy the finger-like processes of the intestine, called villi, are gradually destroyed. Other relevant changes in the structure of the intestine also occur. These villi are necessary to absorb the food we eat. As more villi are destroyed the amount of food absorbed into the body is decreased, more symptoms develop and the person’s state of malnutrition increases.
Thus, coeliac disease is an auto-immune, progressive condition. It ranges from latent with no symptoms, through mild (silent and deformation stages) to severe (the destructive phase). The number of symptoms can vary from few to many and may increase over time. Hence, people can remain in one phase for many years before a trigger factor precipitates them into the next phase of the condition. Some of these trigger factors are trauma and stress, such as surgery or viral illness and pregnancy.
Over forty different symptoms of coeliac disease are known. Some symptoms are more common than others. The symptoms of coeliac disease in children usually differ from those in adults. Digestive upsets and/or tiredness in various guises are amongst the most common symptoms. In addition, the presence of mouth ulcers, excessive bruising, anaemia, fractures from simple accidents and having osteoporosis or its precursor, osteopaenia, also suggest the need for testing for coeliac disease. Unfortunately, testing is delayed for many years in many people even when they exhibit these symptoms, especially if the symptoms are comparatively mild.
Testing for coeliac disease involves a blood test followed by an endoscopy incorporating a biopsy of the intestine to look for the destruction of the villi and other tissue changes.
The only treatment for coeliac disease is a diet completely free from the cereals which precipitate the condition. This also includes products such as food additives derived from the grains. Moreover, it is necessary for people with coeliac disease to read thoroughly the labels on processed foods. They must carry a booklet of foods and food additives that they can and cannot consume.
When a person is diagnosed with coeliac disease it is estimated that one in ten of their close relatives will also have the condition. Consequently, it is recommended that all relatives of a person diagnosed with coeliac disease also
should be tested for the condition. Unfortunately, to their own detriment, some relatives refuse to be tested.
Coeliac disease affects more than a person’s general health and wellness. Social life and the ability to work, to drive or to play sport may be compromised eventually. Severe coeliac disease can cause considerable disruption to a person’s life. In its severest form, coeliac disease can be fatal. The rate of fatality from coeliac disease may be enhanced by the development of various cancers, especially of the digestive tract.
The widespread prevalence of coeliac disease in our society is largely unrecognised. Nor are its symptoms and consequences well known by the general public. Unfortunately, this ignorance also applies to some of the medical profession. Older people eventually diagnosed with coeliac disease may have been reporting symptoms of the condition for many years prior to this. Moreover, they may even have been treated unsuccessfully over long periods for symptoms such as mouth ulcers using palliative medications.
Considerable publicity about the coeliac disease and its symptoms is required. This would ensure that the about 170,000 Australians with undiagnosed coeliac disease will receive appropriate medical assistance, In the meantime some of these people are already experiencing increasingly severe medical conditions and all have the potential to become debilitated by the effects of coeliac disease on their lives.
********************

**PAGE 7**

UNDERSTANDING COELIAC DISEASE
By Phillipa Andrew

This paper is based on the article “Coeliac Disease; The hidden disease of adults” by the same author which was published in PROBUS NEWS Spring 2003

Coeliac disease [CD] is an auto-immune, progressive, potentially debilitating medical condition. It is also known popularly as non-tropical sprue or as coeliac sprue. Medically, coeliac disease is termed “gluten enteropathy” or “gluten-sensitive enteropathy” [GSE]. CD was once considered to be mainly a disease of children who failed to thrive, showed poor weight gain, or even weight loss, and experienced gastroenteritis. Many died.
It is now known that the condition is far more widespread than this, especially among the adult population where the symptoms may be totally different from those found in children, or even almost non-existent in the latent and silent stages.
People with CD react adversely to the alcohol-soluble protein fractions, known as gluten, found in some cereals. These cereals are wheat, rye, triticale [an hybrid of wheat and rye], barley, kamut [a large Egyptian wheat], German spelt and, to a lesser extent, oats. This includes an adverse reaction to their many by-products. Over time the toxic gluten destroys increasingly more of the gut. This increased destruction means that the amount of food absorbed into the body is gradually decreased, more symptoms develop and the person’s state of malnutrition increases.
The condition is found predominantly amongst Caucasians [1:100 to 1:500 in different populations] and to a lesser degree amongst Arabs, Indians and Africans along the Mediterranean rim. It is absent from people native to Africa south of the Sahara, from Asians along the Pacific Rim and from the native inhabitants of the American continents. However, people of Chinese and Japanese descent long resident in “European” cultures such as the USA and Australia eventually become prone to the condition.
Currently about 30,000 Australians are diagnosed with CD but nearer to 1:100 people actually have the condition. This means around 170,000 cases of CD are still undiagnosed. Those people with undiagnosed CD may be experiencing symptoms which are not recognised as being linked to CD. Most of these cases are amongst older Australians.
Wide variations in the number of symptoms and in their severity make diagnosis difficult. Reasons for these variations are still unknown. It is known, however, that the condition may remain in one phase for many years before it is suddenly triggered to progress from the almost silent stage to the more severe stages. These triggers include viral illness, physical trauma – including surgery, emotional stress and pregnancy.
The small intestine, about 3.5cm [1.5in] in diameter, is very folded to give it a velvet-like appearance such that a 2.5cm [1in] strip fully flattened would be about 26m [80ft] long. These fine, finger-like folds, called villi, are responsible for the absorption of digested food. Between them, like the sweat glands in the skin, are downward folds called crypts where the digestive enzymes are produced. In coeliac disease these villi are slowly destroyed, starting at the stomach end of the small intestine. Four stages of the condition are recognised.
In the latent or infiltration stage of CD antibodies [anti-gliadial, anti-endomysial and anti-tissue transglutaminase] are found in the blood but the small intestine is normal except for a small increase in the antibody-producing immune cells called lymphocytes.
This latent stage can progress to the silent or inflammation stage in which more immune cells are present and the length and number of crypts increase. Symptoms, if present, are very mild, perhaps no more than loss of energy and increased tiredness.

**PAGE 8**

The trigger factor can eventually turn on the third [deformed- hypoplastic] and fourth [destructive] stages in which the intestine is damaged. Outward signs of illness become increasingly apparent. The villi become shorter, flatter, wider in stage three and are totally absent in stage four. Crypts, in contrast, are numerous and deeper than normal. In many people with CD there is a mosaic of two or more stages present simultaneously.
In the undamaged intestine the ratio of villi to crypts is four to one. Even after a considerable period on a gluten-free diet this ratio is not fully restored but remains at a ratio of two villi to one crypt.

CD may suddenly manifest itself at any age although much less so in adolescence. Initial diagnosis is sometimes made in people in their 80’s and 90’s who suddenly exhibit symptoms such as excessive, rapid weight loss or, occasionally, weight gain amongst many other symptoms.
CD should be suspected in people of short stature (in women under 162cm [5ft4in] and in men under 168cm [5ft6in]), especially if they were low weight babies or exhibited slow growth as children; and in women who gave birth to low weight babies. Infertility in both sexes, miscarriages, difficulty with breast- feeding, delayed puberty and premature menopause can be among other reproductive expressions of undiagnosed CD.
Some people experience mouth ulcers [red ring with pale top], a cracked corner of the lips, cold sores, hair loss to varying degrees, low thyroid function, and excessive bruising, These problems are, in part, due to the inadequate absorption of vitamins and minerals as a result of the CD. Other symptoms of vitamin and mineral deficiencies may also occur.
Frequently, excessive fatigue, tiredness or sleepiness may be the only or main symptom but such people are often not tested for CD as a possible cause.
Likewise this lack of testing applies to emotional symptoms such as depression or lethargy, mood swings, crankiness, irritability or being easily annoyed and similar reactions of unknown cause.
Undiagnosed CD can also lead to sometimes subtle nerve/muscle problems such as nerve damage in the arms and legs, epileptic fits [especially those commencing in adulthood] and, eventually, dementia.
Secondary lactose intolerance may occur in some people. Usually these people can again tolerate milk in their diet after some months or longer of gluten-free diet.
It is now recommended that all people diagnosed with osteoporosis and anaemia [due it lack of iron, vitamin B12 or folate] be tested for CD. This also applies to people with Type 1 diabetes and other auto-immune diseases such as rheumatoid arthritis, thyroiditis, lupus, sclerodorma and “dry mouth/dry eye” condition-Sjogren’s syndrome and vitiligo. Free bone-density tests are given regularly to people diagnosed with CD for the rest of their lives whether or not they already have osteoporosis.
Chronic nausea, vomiting, reflux, abdominal cramps and bloating, diarrhoea and excessive flatulence may all suggest the need for testing for CD to eliminate it from other possible causes. Flatulence may be particularly smelly and offensive in some people.
Screening is initially by blood tests for the antibodies followed by endoscopic examination. During this period a diet heavy in gluten must be maintained in spite of the illness it causes. False positives and false negatives mean that the blood tests alone are inadequate to diagnose coeliac disease.

**PAGE 9**

Associated with coeliac disease in some [1:10] is “coeliac disease of the skin”, Dermatitis Herpetiformis [DH], which may also occur without CD in up to 5% of patients. These people exhibit some damage to the intestines without symptoms of CD. DH is an intensely itchy rash consisting of little red lumps with or without blisters on top or just as clusters of blisters or large lumps [urticaria]. They are found mainly on the back of the arms, especially near the elbows and on the front of the legs, particularly near the knees, and also on the buttocks, shoulders and scalp. Extra dark or pale areas may mottle the skin on the arms and other parts of the body in many patients.
Some doctors may be unfamiliar with CD and DH [and the information given above about them] and so may take some persuasion to test for CD and DH, as I have experienced personally. There are good internet sites on both conditions, including that of the Australian Coeliac Society, but note the American spelling “Celiac” used on many sites.
The only treatment for CD and DH is a lifelong gluten-free diet with strict attempts to avoid contamination. Surprisingly-many foodstuffs contain gluten in unexpected ways as by-products of the processing of the forbidden grains. There are, however, many alternative foods available, including buckwheat, millet and amaranth. A large number of special gluten-free products are now manufactured. I find the diet very easy in reality.
People with CD and DH are more prone to certain cancers than the general population. This gradually reduces over time on the very strict gluten- free diet.
Emergency situations, such as evacuation during bushfire, are particularly serious for the person with CD and DH as that person cannot eat the mass- produced simple food such as sausages on bread. To do so could precipitate serious illness quite quickly and inconveniently not only personally but also to others present as well, to the level of creating a personal emergency.
The impact of CD on the infirm elderly is great, for carers, meals-on-wheels suppliers, hospitals and nursing homes often find it difficult to manage this strict diet and to avoid accidental contamination.


References

Duggan, J.M. 2004.Coeliac disease: the great imitator. www.mja.com.au/public/issues/18o-10-170504/dug10818-fm.
Murray, Joseph. The widening spectrum of Celiac disease. http://members.ozmail.com.au/~coeliac/sptue.htm.

Pruessner, Harold T. 1998. Detecting celiac disease in your patients. www.aafp.org/afp/980301ap/pruessn.html
Selby,W. 2001.Gluten Enteropathy. www.australianprescriber.com/magazines/vol24no2/gluten.htm.






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