Archive for the ‘Symptoms’ Category

 

Cleo Libonati, RN, BSN

Making the Connection – in Celiac Disease

May 19th, 2008 by Cleo Libonati, RN, BSN


Advance For Nurses Magazine
Vol. 9 •Issue 11 • Page 21

Making the Connection

Underdiagnosed in the U.S., celiac disease can be identified and treated if the condition is understood

By Cleo Libonati, RN, BSN

Celiac disease is a common food sensitivity that can be the underlying source of hundreds of health problems mistakenly attributed to other causes. This insidious disorder has the potential to disfigure, disable and destroy lives at any age. Yet, of the 3 million affected Americans, only 3 percent are diagnosed and treated.1 Prevalence rates are higher in certain populations, such as blood relatives of a person with celiac disease and those with autoimmune disorders.

Unfortunately, people in the U.S. with this condition actively seeking help for their symptoms can go a lifetime without diagnosis and proper treatment. Typically, worldwide diagnosis is faster.
Genetic Susceptibility & Gluten

Celiac disease is also called celiac sprue, nontropical sprue, gluten-sensitive enteropathy or simply celiac by the public.

This immune-mediated disorder stems from an inherited lifelong intolerance to the gluten protein found in wheat, barley, rye and oats. When ingested, gluten resists the breakdown action of normal digestive enzymes into harmless amino acids. Undigested peptides precipitate hyperpermeability of the small intestinal lining (so-called “leaky gut”) to breach the intestinal barrier defense system. In this way, gluten unnaturally gains entrance to the lamina propria.

Within the lamina propria, gluten peptides encounter the enzyme transglutaminase and the local immune system. Transglutaminase deamidates, or breaks off, the rich glutamine residues in gluten. This deamidation creates the toxic molecular compounds, or epitopes, the immune system identifies as foreign.

These epitopes trigger autoimmune antibodies in genetically susceptible individuals. Ensuing inflammation swells affected portions of the small intestinal lining and damages its delicate structures, interfering with its function to finish digestion and absorb nutrients.

While gluten itself is the environmental cause for antibody development, some stressors that can trigger active disease include gluten overload, pregnancy, viral gastrointestinal infection, surgery and severe stress.
Recognizing Celiac Disease

Despite dramatic advancements in knowledge and testing procedures, recognition of this multifaceted disorder is lacking.1Celiac disease often is undiagnosed due to ignorance of the following:

Pathophysiology — The traditional description of celiac disease as an intestinal disorder with malabsorption as the primary defect is a shadow of the real condition.

Prevalence — In contrast to the historic belief celiac disease affected just one in 5,000 individuals, antibody testing demonstrated prevalence of one in 100.

Diagnostic tests — Healthcare providers are unfamiliar with new and improved testing methods.

Manifestations — Many patients do not have diarrhea and wasting symptoms of classic celiac disease. Extraintestinal symptoms predominate in people with atypical symptoms.
How It’s Diagnosed

Diagnosis of celiac disease is made by a positive serologic antibody study and confirmed by histological findings of small-bowel biopsy specimens obtained by endoscopy and improved clinical response following a gluten-free diet.

The single most important step in diagnosing celiac disease is to recognize its myriad clinical features. No single test can definitively diagnose or exclude celiac disease in every individual; there also is a continuum of laboratory and histopathologic results.1

Positive anti-endomysium antibodies and positive anti-tissue transglutaminase antibodies show celiac disease. Positive antigliadin antibodies demonstrate sensitivity to gliadin itself, the gluten in wheat.

Not all patients have positive antibodies at presentation. When symptoms are present but test results are negative, further testing is warranted, including selective immunoglobin A deficiency. In the event the patient started a gluten-free diet prior to testing, suggest a gluten challenge of 3 months or longer in the expectation of antibody development.

Positive small intestinal biopsy shows the degree of villous atrophy, yet this is not foolproof either. The gastroenterologist must be skilled in taking accurate specimens from multiple sites, and the pathologist must be skilled in examining them properly. In addition, damage may be submicroscopic, returning a level not yet detectable by histological examination.

Additional studies include sonogram and genetic testing. Sonogram shows edema and abnormal appearance of the bowel wall. This is especially helpful for children or those who cannot undergo an endoscopy.

More than 97 percent of people with celiac disease share the same genetic human leukocyte antigen (HLA) haplotype markers, HLA-DQ2 and HLA-DQ8. While HLA genotyping is not specific for celiac disease, it has a very high negative predictive value. If the markers are not present, genetic testing essentially rules out the disease.

Annual follow-up testing is warranted for patients with negative test results who continue to show symptoms.
Recognizing Symptoms

There are no typical symptoms of celiac disease, although the most common clinical presentation is unexplained iron-deficiency anemia with or without gastrointestinal symptoms.

Celiac disease, by way of malnutrition, immunity or the direct toxic effect of gluten on cellular structures, has the potential to produce a broad range of symptoms, associated disorders and complications that may affect any organ or body system. Manifestations vary and may appear at any age.

Nutrient deficits are responsible for many seemingly unrelated conditions, such as depression, inability to concentrate, anxiety, insomnia, defective tooth enamel, coagulopathies, hypertension, obesity, anorexia and excessive thirst.

Associated autoimmune disorders may affect any body tissue, including type I diabetes mellitus, hypothyroidism and Grave’s disease, to name a few. Further, severe complications include various cancers such as B-cell non-Hodgkin lymphoma, cryptic intestinal T cell lymphoma and enteropathy-associated T cell lymphoma.

Chronic diarrhea in childhood should provoke screening. Pediatric presentation for celiac disease could involve hypotonia, failure to thrive, growth retardation, short stature, convulsions, poor bone and tooth development, thymic atrophy and delayed puberty.
Treatment

Treatment is a gluten-free diet. Excluding gluten usually results in rapid healing of the small intestinal mucosa, resolution or improvement of nutritional deficiencies, and disappearance of many manifestations of celiac disease.

The gluten-free diet is challenging due to the plethora of gluten-containing foods in the standard American diet. To succeed, patients need detailed diet instruction, including how to read food labels and identify hidden sources of gluten, such as in medications and supplements. Refer patients to a qualified dietitian if possible; otherwise, nurses can teach appropriate information.

Inform patients about community help such as celiac support groups, which offer practical advice on how to shop and cook, and where to dine. Many support groups hold their meetings at local hospitals.
Prognosis

Clinical outcome depends on duration of exposure to gluten. The longer gluten is consumed, the more the body is damaged, and the greater the likelihood of health disorders and complications developing.

Intestinal permeability improves within 2 months of starting a gluten-free diet. Despite a good clinical response, abnormal endoscopic and histologic appearances persist in the majority of patients.2Patients who receive adequate education about celiac disease and treatment with the gluten-free diet are better able to prevent intestinal damage and improve their health by dietary self-management. Clearly, nursing intervention that uncovers hidden celiac disease, provides nutritional education and promotes regular follow-up will considerably improve prognosis. n
References for this article can be accessed at www.advanceweb.com/nurses. Click on Education, then References.
Cleo Libonati is author of Recognizing Celiac Disease, and co-founder, president and CEO of Gluten Free Works Inc., Ambler, PA.
This article copyrighted to Advance For Nurses and can be accessed online at their website at http://nursing.advanceweb.com/Editorial/Search/AViewer.aspx?AN=NW_08may12_n4p21.html&AD=05-12-2008


We have some very important information to share with you today.

While we were at Columbia University’s Topics in Gastroenterology, Dr. Steven Lobritto talked about cirrhosis of the liver and how he has actually seen people who were on the liver transplant list heal enough to be taken off once they started a gluten-free diet.

According to our new book, “Recognizing Celiac Disease”, 3.4% of people with non-alcoholic fatty liver disease have SILENT Celiac Disease. Most patients DO NOT have gastrointestinal symptoms.

Non-alcoholic fatty liver is a non-inflammatory hepatic (liver) disorder characterized by degenerative changes in the liver secondary to excessive accumulation of lipid in hepatocytes.

The good news is that studies showed liver enzymes normalize after 6 months on a gluten-free diet.

If you have patients or family members with non-alcoholic fatty liver (cirrhosis), who are not diagnosed with celiac disease, give them this information so they can get tested.

Related medical studies are referenced in “Recognizing Celiac Disease.” www.recognizingceliacdisease.com.

Celiac disease is a multi-system, hereditary, chronic, auto-immune disease estimated to affect 1% of the human population (3 million in the US) that is caused by the ingestion of wheat, barley, rye and oats. It is treated by removing these items from the diet. Signs, symptoms, associated disorders and complications can affect any part of the body and removal of the offending foods can result in complete recovery.  

Hyperthyroidism, also called Grave’s Disease, is an immunologically mediated thyroid disease.  That basically means it is brought on by the action of specific abnormal autoantibodies, called thyroid receptor antibodies (TRAb), that stimulate excessive release of normal thyroid hormones into the blood.  Thyroid hormones control body metabolism.

Features of hyperthyroidism are diffuse non-tender goiter (enlarged thyroid gland), elevated blood levels of thyroxine hormone, suppressed blood levels of thyrotropin hormone (TSH), and the presence of thyroid receptor antibodies in the blood.

Symptoms include various degrees of bulging eyeballs, staring, firm areas of edema or swellings of the lower legs in most patients, rapid pulse, increased blood pressure, palpitations, nervousness, depression, anxiety, heat intolerance, weight loss, thigh and upper arm weakness, brisk tendon reflexes, cardiac abnormalities and oligomenorrhea in females – infrequent or scanty menstruation. 

According to a recent medical study of 111 people with hyperthyroidism, 4.5% had positive celiac disease antibodies, 14% had anti-gliadin antibodies and 3% had IgA deficiency. Anti-gliadin antibodies demonstrate a normal reaction to the abnormal presence of gluten in the blood. The high presence of anti-gliadin antibodies in thyroid disorders is likely related to gluten entering the bloodstream through the small intestine via “leaky gut.”  Leaky gut can result from poorly digested gluten with or without celiac disease. 

An immune-linked reason for the co-existence of hyperthyroidism and celiac disease revolves around the fact that both disorders (and several other diseases) share the immune system genetic markers HLA B-8 and HLA DR3. Individuals having these genetic markers can develop one or more of a certain cluster of diseases associated with these genes.1

The good news is that a strict gluten free diet can successfully treat hyperthyroidism in celiac disease.

Thyroid function should be assessed in all celiac disease patients at diagnosis and follow-up if clinically indicated. Screening of high-risk groups such as those with autoimmune thyroid disease is a reasonable strategy.2

If you have hyperthyroidism, be sure your doctor tests you for celiac disease and gluten sensitivity. Anti-gliadin antibody (AGA-IgA and AGA-IgG) tests for gluten sensitivity while EMA-IgA and EMA-IgG or tTG-IgA and tTG-IgG  are specific tests for celiac disease.  Testing that is based on IgA only would give a false negative result for individuals who are unable to produce IgA antibodies, that is, in IgA deficiency.

If your physician refuses or dismisses the idea of testing for celiac disease, please get a second opinion from a medical provider who is knowledgeable about celiac disease.  The longer gluten is consumed, the greater will be its damaging effects on your body.

(This Health Alert was taken from information found in Issue #11 – “Gluten and the Thyroid” of the Gluten Free Gazette.)

Celiac disease is a hereditary, auto-immune disorder estimated to affect 1% of the human population (3 million in the US). Less than 3 % are estimated to be medically diagnosed, but numbers are expected to rapidly increase as diagnosis improves. Celiac disease is caused by the ingestion of wheat, barley, rye and oats and treated by removing these items from the diet. Signs, symptoms, associated disorders and complications can affect any part of the body and removal of the offending foods can result in complete recovery.  Visit Glutenfreeworks.com for more information.
Grave’s Disease and Gluten Sensitivity Enteropathy (GSE). Elaine Moore. http://www.suite101.com/article.cfm/graves_disease/54749
Ch’ng CL, Keston Jones M, Kingham JGC. Celiac disease and autoimmune thyroid disease. Clinical Medicine & Research. May 2007; 5(3)184-192.

John Libonati

Neurological Disorders, Gluten & Celiac Disease

March 13th, 2008 by John Libonati

The brain is a delicate organ, where billions of cells, electrical and chemical reactions have to interact correctly to function optimally.  When something unbalances brain chemistry, interrupts reactions or damages the cells, brain dysfunction results. Gluten does all these things – whether or not you have celiac disease.

Neurological disorders from gluten can arise in either, or both, of the following ways.  Gluten can penetrate the intestinal lining and enter the bloodstream, by its own mechanism, travel to the brain where it can damage or disrupt cells or cause inflammation.  This is the direct effect of gluten on the brain.  Gluten can also lead to malabsorption of nutrients in celiac disease.  In this case, the body does not absorb the nutrients it needs. Nutrients are chemicals. The brain, therefore, does not receive the chemicals it needs to function correctly and problems develop.

Nervous system disorders have been found in over 50% of newly diagnosed celiacs.  The list of nervous disorders is long: autism, gait ataxia, gluten ataxia, progressive myoclonic ataxia, chorea, tremors, brain atrophy, cerebral perfusion abnormalities, cortical calcifying angiomatosis (cerebral calcifications), dementia, headaches, epilepsy, chronic fatigue and chronic fatigue syndrome, migraines, multiple sclerosis, vasculitis of the central nervous system, chronic maladaptive anxiety, apathy, depression, inability to concentrate, insomnia, irritability, schizophrenia spectrum disorders, and peripheral neuropathy.  New disorders are being added as the link between

These nervous disorders can include either hard or soft disorders.

Examples of hard disorders would be epilepsy, ataxia (motor abnormalities), myoclonus, internuclear ophthalmoplegia, multifocal leukoencephlopathy, dementia and peripheral neuropathies.  Hard disorders, besides peripheral neuropathies, do not respond to gluten restriction – so identifying gluten sensitivity and/or celiac disease early is critical.

Soft disorders in celiac disease include a broad range of what are considered common neurological disorders.  Hypotonia (flaccid muscles in babies), developmental delay, learning disorders and ADHD, headaches and cerebellar ataxia are examples.  Importantly, there does not seem to be a difference in whether people with infantile-onset gastrointestinal symptoms, those with late onset symptoms or are asymptomatic (have no symptoms at all) develop soft disorders.

This means you may never experience a gastrointestinal symptom, yet still suffer from neurological disorder due to celiac disease.

Recovery from these neurological disorders usually depends on length of time gluten has been digested. The gluten-free diet can result in complete recovery, improvement or no recovery depending on the amount of damage incurred. This means the earlier gluten is removed from the diet, the greater the likelihood of successful recovery.

For these reasons, anyone with an unexplained neurological disorder that does or does not respond to traditional treatment should be screened for celiac disease and gluten sensitivity.

(This Health Alert was taken from information found in Issue #10 – “How Gluten Perturbs the Brain” of the Gluten Free Gazette.)

Celiac disease is a hereditary, auto-immune disorder estimated to affect 1% of the human population (3 million in the US). Less than 3 % are estimated to be medically diagnosed, but numbers are expected to rapidly increase as diagnosis improves. Celiac disease is caused by the ingestion of wheat, barley, rye and oats and treated by removing these items from the diet. Signs, symptoms, associated disorders and complications can affect any part of the body and removal of the offending foods can result in complete recovery.

Visit Glutenfreeworks.com for more information.

John Libonati

Celiac Disease, Diabetes Have Genetic Link

March 5th, 2008 by John Libonati

The article below discusses that similar genes are found in people with celiac disease and Type 1 Diabetes.  This supports the findings of a recent Danish study that showed 12.3% of children with Type 1 Diabetes tested positive for celiac disease. 

Published: March 4, 2008 at 5:48 PM

Print story Email to a friend Font size:LONDON, March 4 (UPI) — London researchers suggest celiac disease and diabetes may have common genetic origins.

David van Heel of Barts and The London School of Medicine and Dentistry demonstrated that of the nine celiac gene regions now known, four are also predisposing factors for type 1 diabetes.

The team of researchers, which also include Irish and Dutch scientists and the Wellcome Trust Sanger Institute, performed a genome-wide association study in celiac disease. Genetic markers across the genome were compared in celiac disease subjects versus healthy controls. The researchers identified seven new risk regions, six of which harbor important genes critical in the control of immune responses, highlighting their significance in the development of the disease.

Celiac disease, triggered by an intolerance to gluten — a protein found in wheat, barley and rye can lead to anemia, poor bone health, fatigue and weight loss.

The findings are published in the journal Nature Genetics.

© 2008 United Press International. All Rights Reserved.
This material may not be reproduced, redistributed, or manipulated in any form.

John Libonati

Bone Mineral Density and Celiac Disease in Women

January 4th, 2008 by John Libonati

The article below describes a study showing if a woman enters menopause with a low bone mineral density, the risk is 25% to develop fractures compared to 9% who had normal bone mineral density. This is a significant and important reason for women with celiac disease to: 

1) Keep a strict gluten-free diet to be able to absorb calcium, vitamin D and other nutrients vital to bone health,  

2) Influence disinterested relatives to get tested, and 

3) Get a baseline bone mineral density (BMD) test with follow-up for the appropriate supplementation.

Bone Density Tests Do Predict Women’s Fracture Risk
Largest, longest study ever supports screening and prevention of osteoporosis

By Amanda GardnerPosted 12/18/07

TUESDAY, Dec. 18 (HealthDay News) — One bone mineral density test can accurately predict a woman’s chance of spinal fractures 15 years down the line, new research shows.

And, according to the largest and longest prospective study of osteoporosis ever, women who had a spinal fracture at the beginning of the study had four times the risk of sustaining another fracture later on.

The bottom line: “Women need to talk to their doctors about the risk of osteoporosis,” according to Jane Cauley, lead author of the study and professor of epidemiology at the University of Pittsburgh Graduate School of Public Health.

Her team published the findings in the Dec. 19 issue of the Journal of the American Medical Association.

“I agree with the guidelines that all women after the age of 65 have bone density tests, and Medicare will pay for that,” Cauley said. “Women who are postmenopausal, 50 to 64 years of age, should consider having a bone density test if they have other risk factors for osteoporosis or if they want to know what their bone density is before they consider any other treatment.”

The findings don’t change current standard practice, experts said, and they don’t change the basic message to women: Don’t ignore bone health, especially in middle and old age.

“The only really major advance here is that it’s a longer term study. Mostly studies are five years typically. This one went out 15 years,” said Paul Brandt, associate professor of neuroscience and experimental therapeutics at Texas A&M Health Science Center College of Medicine in College Station. “Women need to get their bone mineral density tested after they start menopause and if they stay on hormone replacement therapy or an anti-osteoporotic treatment.” he said.

Postmenopausal women are particularly vulnerable to fractures resulting from osteoporosis, a degenerative weakening of the bones. Some 10 million Americans, including one in five American women over the age of 50, suffer from osteoporosis, which is the most common type of bone disease.

Spinal fractures are the most common type of fracture resulting from osteoporosis, affecting 35 percent to 50 percent of women over 50 (about 700,000 vertebral fractures annually in the

United States).
But many, if not most, of these fractures go undetected. “Osteoporosis is sometimes called the silent thief,” Cauley said. “It basically robs the skeleton of strength and resources, and women don’t really know about it. About 75 percent of all spine fractures actually occur silently.”

“Identifying risk factors for spine fractures is less well developed. You have to systematically look for them by repeated X-rays,” Cauley continued.

The findings from this study are based on bone mineral density data from 2,300 women over the age of 65 who enrolled in the Study of Osteoporotic Fractures (SOF), initiated in 1986.

After 15 years of follow-up, it was evident that 25 percent of women who had low BMD at the beginning of the study developed fractures of the spine, compared with only 9 percent of women with normal BMD.

“It was pretty much a strong gradient of risk,” Cauley explained. “If you had normal bone density when you entered and did not have an [existing] fracture, the risk of having a new spine fracture was about 9 percent, compared to a risk of 56 percent in women who had osteoporosis and who had an existing fracture. So, the range of risk varied dramatically depending on bone density and previous spine fractures.”

According to Brandt, one interesting finding from the study is that a previous vertebral fracture topped even bone mineral density as a predictor for future fracture.

This indicates that women with an existing vertebral fracture should be treated for osteoporosis regardless of their BMD, the authors reported.

“People think osteoporosis is an inevitable consequence of aging, but it is preventable and treatable,” she said.

More information There’s more on age-linked bone loss at the U.S. National Library of Medicine. Copyright © 2007 ScoutNews, LLC. All rights reserved.                  

John Libonati

Non-alcoholic fatty liver disease and gluten

November 16th, 2007 by John Libonati

non alcoholic cirrhosis fatty liver celiac disease gluten
This is super important for anyone with fatty liver disease!

While we were at Columbia University’s Topics in Gastroenterology, Dr. Steven Lobritto talked about cirrhosis of the liver and how he has actually seen people who were on the liver transplant list heal enough to be taken off once they started a gluten-free diet. That’s right.  People who needed liver transplants – their liver’s were basically done for – healed!

Non-alcoholic fatty liver is a non-inflammatory hepatic (liver) disorder characterized by degenerative changes in the liver secondary to excessive accumulation of lipid in hepatocytes.

According to research we found for our book, “Recognizing Celiac Disease” 3.4% of people with non-alcoholic fatty liver disease have SILENT Celiac Disease. That means they don’t have symptoms.  Most patients DO NOT have gastrointestinal symptoms.

The good news is that studies showed liver enzymes can normalize after 6 months on a gluten-free diet. If you or your family members have non-alcoholic fatty liver (cirrhosis), but have not been tested for celiac disease, get tested and give them this information so they can get tested.  And if they test negative, try the diet anyway because we’ve seen time and time again that the test are NOT 100% accurate.

Related medical studies are referenced in the celiac disease symptom guide “Recognizing Celiac Disease” .

——————–
Author Information: John Libonati, Philadelphia, PA
Publisher, Glutenfreeworks.com.
Editor & Publisher, Recognizing Celiac Disease.
John can be reached by e-mail here.