Gluten Sensitivity, Autoimmune and Neurological Disease

by Jeffrey Dach MD

This article is Part Three of a Series. For Other Parts, Click Here:
Part One , Part Two , Part Four

Two Very Mysterious and Complicated Cases caused by Gluten Sensitivity

What is wheat gluten?

Gluten is a protein in grains such as wheat, rye, barley, spelt, triticale, kamut,and possibly oats.  In susceptible individuals, about one per cent of the population, Wheat Gluten stimulates an immune response which may damage the inner lining of the gastrointestinal tract, or cross-react with other tissues in the body producing auto-immune, neurological and psychiatric illness.

Upper left image: A variety of foods made from wheat, all containing gluten. Courtesy of the USDA and Wikimedia Commons.

Celiac Disease or Gluten Sensitivity ?  Shag Carpet or Flat Carpet ?

The immune response to gluten may cause malabsorption, and damage to the mucosal lining of the GI tract which can be seen on endoscopic biopsy as villous atrophy (see left image).

Normally, the healthy small bowel looks like a  “shag carpet” under the microscope with a brush border.  However, with villous atrophy, the villi or fingers are lost or shortened, and the shag carpet turns into indoor-out door carpeting with a flat surface.

Left Image: Red Arrows point to Villous Atrophy.  Biopsy of small bowel showing Coeliac disease manifested by blunting of villi, crypt hyperplasia, and lymphocyte infiltration of crypts, consistent with Marsh classification III. Courtesy of wikimedia commons.

This advanced form is called Celiac Disease which may cause malabsorption of B12, Iron, and Calcium (leading to osteoporosis and stress fractures at a  young age) .  In addition, there may be malabsorption of fat with labs showing a low serum triglyceride level which may be “tip-off” for the diagnosis. (12-14)

However, in many people, there may be minimal or no gastrointestinal symptoms.  Rather the immune response may show up elsewhere in the body as an auto-immune disease, a neurological disease or a psychiatric manifestation.  This form of the disease is called Gluten Sensitivity, a diagnosis frequently missed or ignored by mainstream medicine.

Gluten Testing – Conventional Lab Panel

Since Gluten sensitivity leads to villous atrophy and malabsorption of vitamins, minerals and fats, various abnormalities may show up on the conventional lab panel: Low serum triglyceride level (below 75) is a marker for gluten sensitivity.(12-14)  Low Serum Iron, Ferritin and Vitamin B12 are frequently seen together as a “pattern”.  This pattern of malabsorption is strongly suggestive for gluten sensitivity.   A clinical history of stress fracture, and osteoporosis at a young age (from calcium malabsorption) is strongly suggestive for gluten sensitivity.

Enterolabs – Definitive Testing

After finding the conventional blood antibody testing to be useless, we have switched to stool antibody testing with a home test kit from Enterolabs.  This kit can be ordered by anyone, without a prescription, and the test performed at home.  The stool sample is sent into the lab for analysis which includes immunological response to gluten, anti-gliadin antibody and genetic testing for gluten sensitivity.  They offer additional panels which examine fat malabsorption (similar to the triglyreride test), and food sensitivity to dairy, egg, and soy.

Cyrex Labs- Dedicated to Gluten, Leaky Gut and Autoimmune Testing

Another excellent lab is Cyrex with a number of useful blood test arrays.
Array 2 – Intestinal Antigenic Permeability Screen
Array 3 – Wheat/Gluten Proteome Reactivity & Autoimmunity
Array 4 – Gluten-Associated Cross-Reactive Foods and Foods Sensitivity
Array 5 – Multiple Autoimmune Reactivity Screen
Array 6 – Diabetes Autoimmune Reactivity Screen
Array 7 – Neurological Autoimmune Reactivity Screen
Array 8 – Joint Autoimmune Reactivity Screen

Dietary Trial Off-Gluten

Another obvious test is a 6-week trial on a strict gluten-free diet, during which time symptoms are closely observed for improvement, indicating a gluten sensitivity.  These patient should remain on a strict gluten-free diet.

A 63 year old male with Recurring Cranial Nerve Palsies, Hypertransaminasemia, and Hashimotos Thyroiditis

A pleasant 63 year old gentleman came to the office for a “wellness physical and some vitamins”.  A few years past, he had Bell’s Palsy, a form of facial nerve paralysis, which had  resolved.  He also noticed intermittent loss of sensation involving the soles of his feet.

On physical exam, he had a mild residual facial paralysis (Bell’s Palsy), and a mild sensory polyneuropathy with loss of vibratory sense in the lower extremities. His lab studies showed mildly elevated liver enzymes which “had always been present over the years”,  and previous doctors have told him that it is “genetic”, and not to worry about it.

The patient also had elevated thyroid antibodies, with reduced thyroid function compatible with Hashimoto’s thyroiditis.  The patient was treated with thyroid hormone among other things, and did well over the next few years.

However a few years later, he reported eye problems.  He was unable to gaze laterally with his right eye. The opthalmologist made a diagnosis of Sixth Cranial Nerve palsy (abducens nerve to the lateral rectus eye muscle) with failure of lateral gaze.  Extensive neurological workup with MRI scans was unremarkable, and his neurologist suggested a test for Lyme’s Disease, which was done and found negative.

Gluten and Neurological Disease

The immunologic response to gluten may cross react with the nervous system, producing various neurological symptoms, such as cranial nerve palsy, and neuropathy.  These may be present in the absence of any gastrointestinal symptoms.  Neuropathies and psychiatric symptoms caused by consumption of wheat gluten have been reported in the medical literature.(5-7)  Recurrent cranial nerve palsy has also been reported caused by ingestion of gluten. (1)

Gluten Sensitivity Celiac Hashimoto’s Connection

Patients who have Hashimoto’s thyroiditis have about 15 times greater chance of also having gluten sensitivity.   One Dutch study published in 2007 showed 15% of Hashimoto’s patients tested positive for gluten sensitivity or celiac disease.(2).

Chronic Mild Elevation of Liver Enzymes

Chronic mild elevation of liver enzymes may be a tip off of underlying gluten sensitivity.(3-4)  These mild liver enzyme elevations will normalize 95% of the time by adhering to a strict gluten-free diet.(3)

Treatment- Gluten Free Diet

This patient ordered the Enterolabs test kit for gluten sensitivity which showed a markedly positive immunologic response to wheat gluten.  After adhering to a strict gluten-free diet, the patient’s symptoms of cranial nerve palsy and sensory neuropathy gradually resolved.  In addition, the liver enzyme elevations normalized.

A Young Patient with Systemic Lupus –  Gluten Connection

A 23 year old female college student with Lupus came to my office.   She had been previously  diagnosed with Systemic Lupus and started on Prednisone, a commonly used immune suppressive drug.  She was recently hospitalized and treated with IV antibiotics for pneumonia.

She was very ill, lost weight, and was amenorrheic, with menses stopping about 18 months ago.  Her symptoms included joint pains, and buccal ulcerations.  Physical examination showed a chronically ill, weak,  cachectic young woman, with typical increased pigmentation of the palms and Lupus Butterfly Rash of the face as shown above.

Above left image : Butterfly Facial Rash of Systemic Lupus Courtesy of Wikimedia Commons.  This is caused by low adrenal output which stimulates increased pituitary ACTH which has Melanocyte stimulating properties.  This patient needs adrenal hormones.

Acetyl Co-A Deficiency in Lupus

Lupus is an autoimmune disease, and blood testing shows circulating anti-nuclear antibodies as a main feature.

Acetyl Co-A Deficiency in Lupus

My previous article discussed the underlying defect in Lupus as an Acetyl Co-A Deficiency  and how this produces adrenal insufficiency, with reduced hormone production.

Adrenal insufficiency causes the pituitary to increase ACTH production which has melanocyte stimulating properties.  The melanin pigment accounts for the increased skin pigmentation and facial rash of lupus (see above image).  Vitamin B5, Pantothenic Acid is extremely beneficial for Lupus patients because B5 increases Acetyl-Co-A which helps the adrenals recover in their important job manufacturing adrenal hormones.

My Lupus treatment program includes high dose Pantothenic Acid (300 mg three times a day of Vitamin B5), as well as direct adrenal hormones replacement with cortisol or prednisone.  Over time, patients are slowly weaned off the prednisone and switched to low dose bioidentical hydro-cortisone (cortisol).

Since other hormones levels are typically low in Lupus patients, we will commonly give a bioidentical hormone topical cream containing DHEA, Estradiol, Estriol (Bi-Est), Testosterone and Progesterone.

Low vitamin D is frequently associated with autoimmune disease, correction is important. Her low Vitamin D levels were treated with Vitamin D3, 10,000 units per day.

LDN for Autoimmune Diseases including Systemic Lupus

Low Dose Naltrexone is an FDA approved drug which has been used off label in a variety of auto-immune diseases such as multiple sclerosis, crohn’s rheumatoid arthritis and systemic lupus, with considerable benefits for these patients.  See my previous articles on LDN: LDN Part One  and  LDN Part Two.

Lupus patients will frequently benefit from Low Dose Naltrexone Capsules 4.5 mg each evening before sleep.

Gluten Free Diet Benefits Systemic Lupus Patients

Medical science considers Lupus to be an incurable disease, and relies on prednisone, a powerful immune suppressing drug to control symptoms.  Prednisone is a synthetic form of hydro-cortisone, the main adrenal hormone.

Systemc Lupus Cured With a Gluten Free Diet

I was astounded to find a report by Jonathon Wright of 500 patients cured of Lupus with  a gluten free diet.

Jonathan Wright MD writes in a newsletter about how dietary exposure to wheat gluten may trigger autoimmune disease including systemic lupus. Here is an exerpt from  “A Simple Solution to an Incurable Disease”.  (15):

In 1989, my wife Holly and I visited the office of Dr. Christopher Reading in Dee Why, a suburb of Sydney, Australia. He showed us documentation of over 500 individuals who came to see him with a diagnosis of Systemic Lupus, a usually-thought-to-be incurable auto-immune disease.

With hard work on their own and with Dr. Reading’s treatment, these individuals eliminated all signs and symptoms of lupus as well as the patent and formerly patent medicines used to treat it.

How did over 500 individuals eliminate all signs and symptoms of lupus – and all patent medicines given for it, too – over 20 years ago? Dr. Reading had them totally eliminate all gluten, all milk and dairy products, and often other foods to which they were found to be allergic.(15)

Lupus is only one of a long list of auto-immune diseases triggered by Wheat Gluten Exposure.  (15)  Here is the complete list of auto-immune diseases triggered by gluten sensitivity:

Type One Diabetes
Hashimoto’s thyroiditis
Graves’s disease
Ulcerative Colitis
Systemic Lupus Erythematosis (lupus)
Vitiligo
Addison’s disease
Sjogren’s syndrome
Pernicious anemia
Scleroderma
Chronic auto-immune hepatitis
Dermatitis herpetiformis
Polymyalgia rheumatica
Celiac disease

The patient was advised to adhere to a strict gluten-free diet, and eliminate dairy products as well. (8-16)  She did well,  and eventually tapered off the prednisone without recurrence of joint pain, and resumption of normal menses.

How Many Cases of Gluten Sensitivity  Are Missed by the Mainstream Medical System ?   All of them.

Articles with Related Interest:

Wheat Gluten, Celiac Disease Part One

Gluten Sensitivity, Is Your Food Making You Sick? Part Two

Wheat Gluten Part Three, Autoimmune and Neurological Disease

Wheat Gluten Leaky Gut and Autoimmune Disease Part Four

Minefield at the Grocery Store

Fast Food in Hospitals, Selling Sickness in the Lobby

Jeffrey Dach MD
7450 Griffin Road, Suite 190
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Links and References

Gluten and nerve damage facial nerve ,  Bells palsy,  Abducens nerve.  6th cranial nerve

1) www.ncbi.nlm.nih.gov/pubmed/22383733
jnnp.bmj.com/content/early/2012/02/29/jnnp-2011-301921.short
J Neurol Neurosurg Psychiatry March 2012
Gluten-related recurrent peripheral facial palsy by Vincenzo Di Lazzaro, Istituto di Neurologia, Università Cattolica, L.go A. Gemelli 8, 00168 Rome, Italy;

Recurrent peripheral facial paralysis (PFP) is an uncommon disorder that often occurs in the setting of family history. In 2001, we observed a patient with recurrent PFP who manifested symptoms of coeliac disease (CD) several months later. Because of this observation and because neurological disorders may be the only manifestation of atypical forms of CD,1 we started to screen for gluten-related diseases all patients with at least two episodes of PFP who were referred to our department between 2001 and 2011. We performed initial screening serological tests (antigliadin, antitransglutaminase and antiendomysial antibodies), followed by a confirmatory small intestinal biopsy in positive cases. Testing for human leucocyte antigen (HLA) class 2 alleles was performed in patients with uncertain diagnosis2 in that positive HLA-DQ2 or HLA-DQ8 genotypes are useful to support the diagnosis of potential CD in patients with positive serology and mild or absent histological lesions.3 The frequency of CD in PFP population was compared by Fisher exact test with that observed in a control group of 100 consecutive patients admitted to out-patient clinic for several neurological disorder including multiple sclerosis, cranial neuropathies not involving facial nerve and neuromuscular disorders.

2) http://www.ncbi.nlm.nih.gov/pubmed/17461476
World J Gastroenterol. 2007 Mar 21;13(11):1715-22.
Coeliac disease in Dutch patients with Hashimoto’s thyroiditis and vice versa. Hadithi M, de Boer H, Meijer JW, Willekens F, Kerckhaert JA, Heijmans R, Peña AS, Stehouwer CD, Mulder CJ.
Department of Gastroenterology, Rijnstate Hospital, The Netherlands.

To define the association between Hashimoto’s thyroiditis and coeliac disease in Dutch patients. METHODS:A total of 104 consecutive patients with Hashimoto’s thyroiditis underwent coeliac serological tests (antigliadins, transglutaminase and endomysium antibodies) and HLA-DQ typing. Small intestinal biopsy was performed when any of coeliac serological tests was positive. On the other hand, 184 patients with coeliac disease were subjected to thyroid biochemical (thyroid stimulating hormone and free thyroxine) and thyroid serological tests (thyroglobulin and thyroid peroxidase antibodies).

RESULTS:Of 104 patients with Hashimoto’s thyroiditis, sixteen (15%) were positive for coeliac serology and five patients with documented villous atrophy were diagnosed with coeliac disease (4.8%; 95% CI 0.7-8.9). HLA-DQ2 (and/or -DQ8) was present in all the five and 53 patients with Hashimoto’s thyroiditis (50%; 95% CI 43-62). Of 184 patients with coeliac disease, 39 (21%) were positive for thyroid serology. Based on thyroid biochemistry, the 39 patients were subclassified into euthyroidism in ten (5%; 95% CI 2-9), subclinical hypothyroidism in seven (3.8%; 95% CI 1.8-7.6), and overt hypothyroidism (Hashimoto’s thyroiditis) in 22 (12%; 95% CI 8-16). Moreover, four patients with coeliac disease had Graves’ disease (2%; 95% CI 0.8-5) and one patient had post-partum thyroiditis.
CONCLUSION:The data from a Dutch population confirm the association between Hashimoto’s thyroiditis and coeliac disease. Screening patients with Hashimoto’s thyroiditis for coeliac disease and vice versa is recommended.

elevated liver enzymes – Sign of Gluten Sensitivity

3) www.ncbi.nlm.nih.gov/pubmed/7657290

Hepatology. 1995 Sep;22(3):833-6.
Prevalence of hypertransaminasemia in adult celiac patients and effect of gluten-free diet. Bardella MT, Fraquelli M, Quatrini M, Molteni N, Bianchi P, Conte D. Source Cattedra di Gastroenterologia, Università degli Studi di Milano, IRCCS Ospedale Maggiore, Italy.

Abstract The prevalence of hypertransaminasemia and the effect of gluten-free diet (GFD) were evaluated in 158 consecutive adult celiac patients, 127 women and 31 men, aged 18 to 68 years (mean, 32). At diagnosis, 67 patients (42%) had raised aspartate and/or alanine transaminase levels (AST and ALT; mean, 47 IU/L, range, 30 to 190; and 61 IU/L, range, 25 to 470, respectively), whereas 91 patients had normal liver function tests (LFT). Patients with and without hypertransaminasemia were comparable for epidemiological data, body mass index (18.5 vs. 19.6), and severity of intestinal histological involvement.

All patients were given a strict GFD and were followed for 1 to 10 years (median, 4). At 1 year, a highly significant improvement in intestinal histology was observed in both groups (P < .0001). In the 67 patients with raised transaminase levels body mass index (BMI) also increased significantly (from 18.5 to 21.0, P < .001), and transaminase levels normalized in 60 (95%). In the other seven cases liver biopsy showed fatty infiltration in two and chronic active hepatitis (CAH) in the other five, related to chronic infection with hepatitis B virus in three and hepatitis C virus in one, and to autoimmune type in the fifth.

We conclude that in adult celiac patients elevated serum transaminases are a frequent finding and normalize in most cases after GFD. When they persist, liver biopsy is mandatory to further investigate hepatic involvement, which is our series was mainly attributable to CAH.

Long Standing Elevated Liver Enzymes suggests gluten sensitivity

4) www.ncbi.nlm.nih.gov/pmc/articles/PMC3395124/
Gastroenterol Res Pract. 2012; 2012: 637187.
Atypical Celiac Disease: From Recognizing to Managing B. Admou, 1 , 2 ,* L. Essaadouni, 3 K. Krati, 4 K. Zaher, 2 M. Sbihi, 5 L. Chabaa, 6 B. Belaabidia, 7 and A. Alaoui-Yazidi 2 Moreover, a wider spectrum of neurologic syndromes may be the presenting extraintestinal manifestation of gluten sensitivity with or without intestinal pathology.

include headache, ataxia and psychiatric disorders [29], migraine, encephalopathy, chorea, brain stem dysfunction, myelopathy, mononeuritis multiplex, Guillain-Barré-like syndrome, and neuropathy with positive antiganglioside antibodies [37].

Additional studies showed high prevalence of gluten sensitivity in genetic neurodegenerative disorders such as hereditary spinocerebellar ataxia and Huntington’s disease [37].

As well, oral manifestations, mostly recurrent apthous ulcers or stomatitis and dental enamel hypoplasia or defects, are atypical signs of CD, and should be considered, even in the absence of any gastrointestinal symptom, at-risk subjects, and should therefore undergo diagnostic procedure for CD [28, 38]. Also, recurrent febrile infections associated to moderate neutropenia must be included in the diagnostic workup for atypical/silent CD in the general population [39]. Furthermore, many of biologic abnormalities either concur with CD or at times may reveal the disease such as anemia with iron, vitamin B12 and/or folate deficiencies, hypertransaminasemia (Table 1).

Neurological presentation of Gluten sensitivity

5) www.ncbi.nlm.nih.gov/pubmed/15825133
Gastroenterology. 2005 Apr;128(4 Suppl 1):S92-7.
Neurologic presentation of celiac disease.Bushara KO.
Neurology Department, Minneapolis VA Medical Center, University of Minnesota, Minneapolis, Minnesota, USA.

Neurological Disorders Associated with Gluten Sensitivity

6) www.ncbi.nlm.nih.gov/pubmed/21796607
Rev Neurol. 2011 Sep 1;53(5):287-300.

Neurological disorders associated with gluten sensitivity] Hernandez-Lahoz C, Mauri-Capdevila G, Vega-Villar J, Rodrigo L. Hospital Universitario Central de Asturias, 33006 Oviedo, Espana.

Gluten sensitivity is a systemic autoimmune disease that occurs in genetically susceptible individuals on ingesting gluten. It can appear at any age, then becoming a permanent condition. It is more frequent in women, as happens with other autoimmune diseases. Celiac disease is the intestinal form and the most important manifestation among a set of gluten-induced autoimmune pathologies that affect different systems.

Neurological manifestations of gluten sensitivity, with or without enteropathy, are also frequent, their pathogenesis including an immunological attack on the central and peripheral nervous tissue accompanied by neurodegenerative changes. The clinical manifestations are varied, but the most common syndromes are cerebellar ataxia and peripheral neuropathy. Finally, gluten sensitivity is associated to a varying degree, with other complex diseases and could influence their evolution. The early detection of cases of gluten sensitivity with neurological manifestations and subsequent treatment with the gluten-free diet could provide remarkable benefits to the patients.

www.ncbi.nlm.nih.gov/pubmed/21877216

7) Psychiatr Q. 2012 Mar;83(1):91-102.
Neurologic and psychiatric manifestations of celiac disease and gluten sensitivity. Jackson JR, Eaton WW, Cascella NG, Fasano A, Kelly DL. Maryland Psychiatric Research Center, University of Maryland School of Medicine, Box 21247, Baltimore, MD 21228, USA.

Celiac Disease (CD) is an immune-mediated disease dependent on gluten (a protein present in wheat, rye or barley) that occurs in about 1% of the population and is generally characterized by gastrointestinal complaints. More recently the understanding and knowledge of gluten sensitivity (GS), has emerged as an illness distinct from celiac disease with an estimated prevalence 6 times that of CD. Gluten sensitive people do not have villous atrophy or antibodies that are present in celiac disease, but rather they can test positive for antibodies to gliadin.

Both CD and GS may present with a variety of neurologic and psychiatric co-morbidities, however, extraintestinal symptoms may be the prime presentation in those with GS. However, gluten sensitivity remains undertreated and underrecognized as a contributing factor to psychiatric and neurologic manifestations. This review focuses on neurologic and psychiatric manifestations implicated with gluten sensitivity, reviews the emergence of gluten sensitivity distinct from celiac disease, and summarizes the potential mechanisms related to this immune reaction.

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Gluten Sensitivity Associated with Systemic Lupus
8) www.ncbi.nlm.nih.gov/pmc/articles/PMC1754806/pdf/v063p01501.pdf www.ncbi.nlm.nih.gov/pmc/articles/PMC1754806/

Ann Rheum Dis. 2004 November; 63(11): 1501–1503.

Gluten sensitivity masquerading as systemic lupus erythematosus
M Hadjivassiliou, D Sanders, R Grunewald, and M Akil

Conclusions: The immunological profile of IgA deficiency and/or raised double stranded DNA in the absence of antinuclear factor together with raised inflammatory markers and symptoms suggestive of an immune diathesis should alert the physician to the possibility of gluten sensitivity. The presence of an enteropathy is no longer a prerequisite for the diagnosis of gluten sensitivity, which can solely present with extraintestinal symptoms and signs. Knowledge of the diverse manifestations of gluten sensitivity is essential in avoiding such misdiagnosis.

False Positive Testing ?

9) www.ncbi.nlm.nih.gov/pubmed/11316156
Am J Gastroenterol. 2001 Apr;96(4):1113-5.
The prevalence of celiac disease autoantibodies in patients with systemic lupus erythematosus.

Rensch MJ, Szyjkowski R, Shaffer RT, Fink S, Kopecky C, Grissmer L, Enzenhauer R, Kadakia S. Department of Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas 78234-6200, USA.

AbstractOBJECTIVE: Systemic lupus erythematosus has been associated with false positive autoantibodies for primary biliary cirrhosis, chronic active hepatitis, Sjogren’s syndrome, rheumatoid arthritis, thyroid disorders, syphilis, and scleroderma. An increased prevalence of autoantibodies are found in celiac disease and systemic lupus erythematosus, which share the human lymphocyte HLA-B8 and HLA-DR3 histocompatibility antigens. This study examines the prevalence of celiac disease autoantibodies in systemic lupus erythematosus patients.

METHODS
Patients observed in the Department of Rheumatology at our institutions in San Antonio, Texas with known systemic lupus erythematosus were offered participation in the study. One hundred three of the 130 patients contacted agreed to participate. Patients were excluded if they were pregnant or medically unable to undergo endoscopy. All volunteers were tested for the serological presence of IgA and IgM antigliadin and IgA antiendomysial antibodies. Those with positive serology underwent esophagogastroduodenoscopy with duodenal mucosal biopsy.

RESULTS:Twenty-four of 103 (23.3%) systemic lupus erythematosus patients tested positive for either antigliadin antibody, whereas none of the 103 patients tested positive for antiendomysial antibody. None of the 24 antigliadin positive patients were found to have endoscopic or histological evidence of celiac disease, making the false positive rate of antigliadin antibody 23%.

CONCLUSION:The presence of false positive antigliadin antibodies in patients with systemic lupus erythematosus is common. Despite shared human lymphocyte antigen loci there does not seem to be an association between celiac disease and systemic lupus erythematosus.

False Positive Testing

10) devmnt2.path.uiowa.edu/home_net/house_staff/learning_resources/immunopathology/Bizarro_DigDisSci.pdf

IgA and IgG Tissue Transglutaminase Antibody Prevalence and Clinical Significance in Connective Tissue Diseases, Inflammatory Bowel Disease, and Primary Biliary Cirrhosis N. BIZZARO, MD,* D. VILLALTA, MD,y E. TONUTTI, MD,z A. DORIA, MD,x M. TAMPOIA, MD,{ D. BASSETTI, MD,** and R. TOZZOLI, MDyy

An association between celiac disease (CD) and other autoimmune diseases such as connective tissue diseases (CTD), inflammatory bowel diseases (IBD), and primary biliary cirrhosis (PBC) has been reported in several studies. However, a high rate of false positives in autoantibody testing was noted, especially when tissue transglutaminase (tTG) from guinea pig liver was used. Thus, the real prevalence of CD in CTD, IBD, and PBC is unclear.

In a case–control study, 400 patients with CTD, 170 with IBD, 48 with PBC, and 120 healthy subjects were investigated for CD by the analysis of IgA and IgG tTG antibodies using the more specific human recombinant tTG immunoenzymatic assay. Patients and controls with positive findings were further tested for antiendomysial antibodies by indirect immunofluorescence and HLA typing, and those found positive by either of these tests underwent duodenal biopsy to confirm a possible diagnosis of CD. Twelve patients were positive for IgA or IgG tTG antibodies, showing an overall prevalence of 1.9%. Only 1 healthy subject (0.8%) had a low level positive reaction for IgA anti-tTG. Among the 12 patients and the healthy subject, only 2 (1 SLE and 1 ulcerative colitis patient) were subsequently confirmed to be affected with CD by positive EMA, HLA, and small bowel biopsy findings. The highest rate of false positives was found in PBC patients (10.4%). For these reasons, serological screening testing for CD is not recommended in CTD patients or in subjects affected with IBD or PBC, unless there is a relevant clinical suspicion of CD.

11) www.ncbi.nlm.nih.gov/pmc/articles/PMC3088693/
Can J Gastroenterol. 2011 April; 25(4): 193–197. PMCID: PMC3088693

Testing for gluten-related disorders in clinical practice: The role of serology in managing the spectrum of gluten sensitivity David Armstrong, MA MB BChir FRCP(UK) FACG AGAF FRCPC,1 Andrew C Don-Wauchope, MD MBBCh FRCPE FRCPC FRCPath,2 and Elena F Verdu, MD PhD1

Other conditions reported to be associated with positive AGA serology: A higher prevalence of positive AGA serology has been reported in patients with RhA (30), Sjogren’s syndrome (31), systemic lupus erythematosus, sarcoidosis and type 1 diabetes (32–34). Dermatitis herpetiformis is a well-recognized, gluten-sensitive skin disorder associated with a positive tTG test. There have also been reports of an association between celiac markers and pemphigoid (35) and atopic eczema (36). IgA nephropathy has also been associated with positive AGA serology (37).

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Auto-Immune Disease Caused by Gluten and Triglycerides by Jonathan V Wright

12) www.faim.org/guestwriters/root-cause-autoimmune-disease.html
The Root Cause of Your Autoimmune Disease — and why treating it can be easier than you think by Dr. Jonathan V. Wright, Guest Writer

Low Triglyceride Level – a Sign of Gluten Sensitivity

13) www.faim.org/guestwriters/root-cause-autoimmune-disease.html

At Tahoma Clinic, our colleague Davis Lamson N.D. pointed out to the rest of the physicians that a fasting serum triglyceride measurement below 50 milligrams per deciliter (normal in most laboratories is said to be 50 to 150 milligrams per deciliter) means gluten sensitivity and gluten-induced malabsorption until proven otherwise. (In my experience, this has been true nearly 100 percent of the time.) Dr. Lamson also points out that any individual with both undiagnosed symptoms and health problems and a fasting serum triglyceride below 75 milligrams per deciliter should always be checked for gluten-gliadin sensitivity too, as the probability is high. Poor intestinal absorption is also to blame for abnormalities in two other tests commonly recommended by practitioners skilled and knowledgeable in natural medicine: the mineral analysis done with a hair specimen, and the fasting plasma essential amino acid determination. If either or both of these tests shows multiple low measurements (three or more of the essential amino acids, five or more of the essential minerals), I’ll recommend testing for gluten-gliadin sensitivity. Much more often than not, the test is positive.

Oral Triglyceride Loading Test

14) www.ncbi.nlm.nih.gov/pubmed/6853129

Isr J Med Sci. 1983 Apr;19(4):319-24.
Gluten-sensitive enteropathy: value of oral triglyceride loading test in the follow-up of patients on gluten challenge. Kleinberg-Zissin R, Avigad S, Yahav J, Jonas A.

Abstract Oral triglyceride (TG) loading tests were performed in 31 patients with gluten-sensitive enteropathy (GSE) upon gluten challenge, and the results were compared with the mucosal histology. Of 19 prechallenge tests, 16 were in the normal range previously established in this laboratory (2-h postcibal plasma TG rise greater than or equal to 55 mg/dl) although values were lower (76 +/- 38 mg/dl, mean +/- SD) than those of healthy age-matched controls (116 +/- 34 mg/dl). Postchallenge tests performed in 29 patients (both symptomatic and asymptomatic) were all pathologic (postcibal TG rise 9 +/- 18 mg/dl). Three tests performed in two patients in whom GSE was ultimately not confirmed remained normal (postcibal TG rise 82 +/- 21 mg/dl) during a 24-mo follow-up. A significant correlation was demonstrated between the TG loading test and the mucosal pathology. The test is useful in the follow-up of patients of gluten challenge and in directing the postchallenge biopsy.

Jonathan Wright MD,  Gluten and Systemic Lupus Question:

Can you provide any information on alternative treatments for lupus?

JVW: I have witnessed fantastic results after lupus patients eliminate all gluten-containing grains, milk, and other diary products from their diet. Although not a cure, remissions or great improvements are possible. I also recommend undergoing a comprehensive allergy testing and desensitization, and a gastric analysis. Plus, patients need to work with their physicians to develop an individual treatment plan, usually involving large amounts of omega-3 fatty acids, and many other oral and intravenous supplements. This may also entail hormone testing, and treatment with DHEA and testosterone.

15) www.faim.org/guestwriters/root-cause-autoimmune-disease.html

The Root Cause of Your Autoimmune Disease — and why treating it can be easier than you think by Dr. Jonathan V. Wright, Guest Writer Originally published in Nutrition & Healing newsletter; Vol. 8 Issue 12, February 2012.

The root cause of your autoimmune disease–and why treating it can be easier than you think

Gluten Sensitivity and Systemic Lupus Erythematosis- Jonathan Wright Newsletter

16) wrightnewsletter.com/files/2002/03/nah_0203.pdf

I first became aware of the wide reach of gluten sensitivity when I read the book Relatively Speaking, originally published in Australia and then re-published in the USA under the title Your Family Tree Connection. (This book is now out of print, but it can still be found on-line through used book sources.) The book, written by Dr. Christopher Reading and Ross Meillon, describes Dr. Reading’s detective work as he unravels the causes of many supposed “undiagnosable” symptoms by closely examining a family health history. Years later, during a trip to Australia in the 1980s, I got to visit Dr. Reading’s office in Sydney. On one wall was a chart that listed over 100 individuals who had initially consulted Dr. Reading about a common so-called “incurable” disease called lupus (systemic lupus erythematosis or SLE). All the patients on the list had suffered the symptoms (fever, joint pains, and skin rash are among the most common symptoms) and had tested positive for lupus in blood tests. However, everyone on this partic- ular list had been symptom free, with negative blood tests for five years or more! It’s true. Over 100 people were cured of socalled “incurable” lupus in the 1980s. Even today, in 2002, just about any “lupus specialist” in the United States will say that’s impossible…and then resume writing prescriptions for prednisone, the most commonly prescribed patent medication used to treat the disease. How did Dr. Reading do it?

Through complete elimination of all grains except rice and corn. (Note: His treatment also excluded milk and other dairy products from his recommended diet and included heavy nutritional supplementation, both orally and intravenously.) But celiac disease was known to be caused by an external phenomenon, gluten sensitivity to certain grains. The author asks: “Could this external agent, gluten sensitivity, also be involved in causing the rest of these diseases linked to HLA-B8?”

Autoimmune diseases linked to the genetic marker HLA-B8 include:

• Addison’s disease
• Autoimmune hemolytic anemia
• Celiac disease
• Childhood asthma
• Chronic autoimmune hepatitis
• Dermatitis herpetiformis
• Graves’ disease
• Insulin-dependent (type 1) diabetes mellitus
• Lupus erythematosis (systemic)
• Myasthenia gravis
• Pernicious anemia
• Polymyalgia rheumatica
• Scleroderma
• Sjogren’s syndrome
• Thyrotoxicosis
• Ulcerative colitis
• Vitiligo

Also recommended for the Lupus patient: “stop consuming milk and other dairy products.”

Gluten Sensitivity and Associated Disease:

Dr. Braly and Mr. Hoggan have compiled a list of 225 symptoms and disease conditions either linked to or caused by gluten sensitivity. The list includes symptoms and diseases in the following areas:

Gastroenterology: recurrent canker sores, chronic diarrhea, constipation, gas, bloating, abdominal pain, celiac disease, and ulcerative colitis

Hepatology (Liver disease): autoimmune hepatitis, gallbladder malfunction, primary biliary cirrhosis, and elevated liver function problems thought to be “of unknown cause”

Hematology (Blood diseases): iron and vitamin-deficiency anemias, vitamin K coagulation disorders, low white-blood cells (due to autoimmunity), and idiopathic thrombocytopenic purpura (ITP, a low platelet count again thought to be of “unknown origin”)

Internal medicine: unexplained weight loss, chronic fatigue syndrome, IgA nephropathy (an autoimmune kidney disease), kidney stones, and recurrent urinary tract infection

Pneumonology (Lung diseases): bronchiectasia (a disorder of small “bronchial tubes”)

Dermatology: vitiligo (an autoimmune depigmentation disorder), alopecia (“patchy” or complete hair loss), hives, and dermatomyositis

Obstetrics/Gynecology: infertility, amenorrhea (a lack of menstrual periods), recurrent spontaneous miscarriage, low birth weight, and vulvodynia (a painful vulva)

Rheumatology: rheumatoid arthritis in adults and children, Sjogren’s syndrome, autoimmune connective tissue disease, systemic lupus erythematosis (“lupus”), scleroderma, and polymyositis

Neurology: seizures accompanied by brain calcifications, cerebellar ataxia, brain atrophy, neuromuscular disorders, and peripheral neuropathy

Psychiatry: depression, schizophrenia, and autism Dentistry: defects in dental enamel Immunology: IgA deficiency (IgA is a specific immune globulin.)

Oncology (Cancer): cancers of the mouth, pharynx, and esophagus; intestinal lymphomas; other intestinal cancers; sarcoidosis; kidney adenocarcinoma; and rhabdomyosarcoma (a muscle cancer)

Orthopedics: “spontaneous” fractures, osteoporosis

Parasitology: relapsing giardiasis Infectious diseases: delayed recovery from infectious disease

Endocrinology: type 1 diabetes, autoimmune thyroiditis (Hashimoto’s), Addison’s disease (weak to very weak adrenal functioning), and Graves’ disease (another autoimmune thyroid problem)

Genetics: Down’s syndrome, Turner’s syndrome, and other chromosome problems

Jeffrey Dach MD
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