العربية
中国
Français
Deutsch
Ελληνική
हिन्दी
Italiano
日本語
Português
Русский
EspañolGLUTEN-SENSITIVE ENTEROPATHY ASSOCIATED CONDITIONS
GSE has a wide variety of associated condition(GSEA), however the key symptoms are typically
restricted to the bowel and associated tissues. These include irritable bowel disease,
eosinophilic gastroenteritis, villous atrophy(CD), crypt hyperplasia(CD), all of the common symptoms are discussed on the Coeliac Disease. The focus of this article
is on assorted autoimmunities[1] or allergic-like responses (IgE or IgA, IgG) markedly increased in GSE many which persist on a strict GF diet, and thus become indepedent of coeliac disease after triggering.
Ambiguities with other conditions has resulted because the clinical manifestations of celiac incidences that fall below clinical detection can still promote secondary allergic responses and secondary autoimmune diseases. The frequency in western societies is typically around 0.5 to 1%, but the detection rate are typically 10-fold lower. However, the association with other, secondary, diseases remains largely idiopathic and sporadic to coeliac disease. With such low co-occurrence frequencies, statisticians are unable to provide linkage. Overall, however, the incidence of
autoimmune diseases not directly linked to GSE in GSE patients is higher than the general population, thus these diseases deserve our attention.
GSEA blood disorders
Deficiencies
'Avitaminosis'. Maladsorption in GSE can results in decline of fat soluble vitamins and vitamin B, as well as maladsorption of essential fatty acids. This can cause a wide variety of secondary problems. hypocalcinemia is also associated with GSE. [2]. In treated GSE, the restrictions on diet as well as reduced absorption as a result of prolonged damage may result in post treatment deficiencies.[3]
★ Vitamin A - Poor adsorption of vitamin A has been seen in coeliac disease.[4] and it has been suggested that GSE associated cancers of the esophagus may be related to vitamin A deficiency [5][6]
★ 'Folic acid deficiency' - Folic acid deficiency is believe to be primary to the following secondary conditions:
★
★ Megaloblastic anemia
★
★ Calcification of brain channels - Epilepsy, Dementia, Visual Manifestations.
★ 'B-6' deficiency. Vitamin B-6 deficiency can result in neuropathies and increases in pain sensitivity.[7] may explain some of the peripheral neuropathies, pain and depression associated with GSE.[8]
★ 'B-12' deficiency
★
★ Megaloblastic anemia
★
★ Pernecious anemia
★ Vitamin D deficiency. Vitamin D deficiency can result in osteopenia and osteoporosis
★
★ Hypocalcemia[9]
★ 'Vitamin K' - Coeliac disease has been identified in patients with a pattern of bleeding which treatment of vitamin K increased levels of prothrombin.[10]
★ 'Vitamin E' - deficiency of vitamin E can lead to CNS problems [11] and possibly associated with myopathy[12]
'Mineral deficiencies'. GSE is associated with the following mineral deficiencies:
★ Calcium - Hypocalcemia causing Oesteopenia
★ Magnesisum - hypomagnesemia[13], may lead to parathyroid abnormalities.
★ Iron - Iron deficiency anemia
★ Phosphorous - hypophosphatemia [14], causing Oesteopenia
★ Zinc - Zinc deficiencies[15] are believed to be associated with increased risk of Esophagus Carcinoma
★ Copper - deficiency
★ Selenium - deficiency [16] - Selenium and Zinc deficiences may play a role increasing risk of cancer.[17]. Selenium deficinency may also be an aggrevating factor for autoimmune hyperthyroidism (Graves disease).[18]
'Blood factors'
★ Carnitine - deficiency.
★ Prolactin - deficiency (childhood). [19]
★ homocysteine - excess.[20]
Anemia
'Megaloblastic anemia' (MA) is associated with GSE and is believed to be the result of B-12 and folate deficiency. [21] In GSE, is appears to be associated with the IgA-less phenotype.[22]. Unlike other forms of megaloblastic anemia, GSEA MA is not a form of autoimmune gastritis.[23]
'Pernicious anemia'(PA). pernicious anemia is associated with GSE and is believed and results primarily from maladsorbtion phenomena.[21]
'Iron-deficiency anemia'. Iron-deficiency anemia (IDA) may be the only symptom for CD [25], detected in subclinical CD[26] and is accompanied by a decrease in serum ferritin levels.[27] This can cause addition problems (see: symptoms of IDA and certain conditions like such as Paterson-Brown Kelly (Plummer-Vinson). [28] Whereas IDA is corrected on GF diet, refractory disease or gluten-sensitive malignacies can cause persistent IDA.[29]
Clotting abnormalities
'Thromboembolism' is a well-described complication of IBD, with a clinical incidence of up to 6% and a three-fold higher risk of disease,[30][31] and the Factor V Leiden mutation further increases the risk of venus thrombosis[32]. Recent studies describe the co-occurrence between coeliac disease, in which IBD is common in venus thrombosis.[33][34]
GSEA Dermatitis
A study of patients with ''dermatitis herpetiformis'' or coeliac disease revealed significantly more
gluten in the blood than controls.[35] This increases the risk of asthma, anaphylaxis and dermatological conditions.
Dermatitis herpetiformis
''Triticeae'' glutens are the primary cause of ''dermatitis herpetiformis''(DH). Epidermal transglutaminase (eTG) is related to tTG and is the autoantigen of DH. It appears that all DH patients have or are susceptible on wheat ingestion to CD. Within CD DH is relatively rare or underdiagnosed with about 5% of patients having DH. Aphthous stomatitis is a common mouth lesion found with celiac disease.
Atopy, urticaria, eczema
Chronic ''urticaria'' has been seen in a few cases of CD.[36] and are likely the result of fortuitous allergies to wheat, or allergies secondary to GSE. Atopy disorders have been found to be more common in celiacs and in first degree relatives.[37]. Celiac disease is associated with a number of epidermal conditions including 'Psoriasis'[38][39]
Rare dermatitis
'''Prurigo nodularis'''. ''Prurigo nodularis'' has been identified with coeliac diease. [40][41]. 'Rothmund-Thomson syndrome'. Rothmund-Thomson syndrome, or poikiloderma congenitale, is a rare disorder, generally attributed to mutations of the RECQL4 helicase gene on 8q24 with features that include photosensitivity and poikilodermatous skin changes, etc and has been reported in one celiac patient.[42]
Alopecia areata
GSE has been found to be associated with ''alopecia areata'' (patchy baldness) [43] whereas regrowth did not necessarily occur on a gluten free diet. [44][45]
GSEA Endocrine disorders
Autoimmune thyroidosis
[Section under construction]
'Grave's Disease, Hashimoto's thyroiditis'. Grave's disease and Hashimoto's thryroiditis are greatly increased in patients with CD. [46] Grave's disease is an autoimmune hyperthyroidism, as GSE is a potentiator for autoimmune disease, but GD is more commonly found and avitaminosis of selenium and other minerals may be a factor in this increase.
Diabetes
'Type 1 (Juvenile onset)'. The incidence of juvenile Type 1 Diabetes (T1D) is about 1:500 in the U.S. population, and is the result of autoimmune damage to the Islets of Langerhans cells in the pancreas. The level of adult onset T1D plus ambiguous T1D/T2D is unknown. It is unclear how large a role ''Triticeae'' has in T1D which also shows stong linkage to DQ2.5 and DQ8. Childhood (male) Type 1 diabetes increases the risk for GSE and vice versa Antibodies to tissue transglutaminase C in type I diabetes., Lampasona V, Bonfanti R, Bazzigaluppi E, Venerando A, Chiumello G, Bosi E, Bonifacio E., , , Diabetologia., 1999 and it now appears that GSE precedes T1D in many cases[47] and an active search for coeliac disease in early juvenile diabetes patients revealed that GF diet resulted in some improvements.[48] A high frequency of diabetes patients have anti-transglutaminase antibodies One third of HLA DQ2 homozygous patients with type 1 diabetes express celiac disease-associated transglutaminase autoantibodies., Bao F, Yu L, Babu S, Wang T, Hoffenberg EJ, Rewers M, and Eisenbarth GS., , , J Autoimmun., 1999 along with increased levels of gluten specific T-cells in T1D patients. From an evolutionary point of view it is difficult to explain the high association of T1D and DQ2.5 given negatively selective nature of the disease in NW European population given the number of studies suggesting that the "Super B8" haplotypes has been under positive selection, and appears to be the most characteristic HLA type in NW Europeans indicating an advanced natural history of the haplotype. A ''T. aesitivum'' storage globulin, Glb-1 (locus), was identified that is similar to the hypersensitizing peanut protein Ara h 1 and other known plant hypersensitizing proteins. Antibodies to this protein correlated with levels of lymphocyte infiltration into Islet regions of the pancreas.[49] Gastrointestinal viruses may play a role.[50][51][52] [53]
Addison's disease
Studies from Sweden suggest that persons with Coeliac disease are 11 times more likely to have Addison's disease (primary adrenal insufficiency) relative to the normal population.[54]
Infertility
GSE can result in high risk pregnancies[55] and infertility. Some infertile women have GSE and iron deficiency anemia [56] others have zinc deficiency [57] and birth defects may be attributed to folic acid deficiencies.
It has also been found to be a rare cause of amenorrhea.[58]
GSEA Gastrointestinal diseases
Endoscopic image of peptic stricture, or narrowing of the esophagus near the junction with the stomach due to chronic gastroesophageal reflux. This is the most common cause of dysphagia, or difficulty swallowing, in scleroderma.
Irritable bowel (IBS)
In diarrhea dominant IB is a common symptom of GSE, increased celiac disease-associated serum IgG was found in treated and untreated CD patients. The IgG was most common in untreated patients with more active DQ2 expression which dropped on GF diet.[60]. Some irritable bowel can be the result of other food intolerances, such as casien intolerance, lactose intolerance, or intolerances to non-dextrose sugars in other foods. It can also be result of overgrowth of yeast or bacteria as a result of excesses of unadsorbed nutrients. IB may not resolve on GF diet and may become more severe in rare cases because it may not have initially been directly linked to gluten consumption.
Inflammatory bowel disease (IBD)
'Crohn's disease'.
'Ulcerative colitis'.
Gastroesophageal reflux disease
Gastroesophageal reflux disease (GERD) is the indirect result of many factors and some autoimmune diseases like schleroderma. GSE can cause inflammation and delayed gastric emptying, which can persist through most of the sleeping hours causing GERD. GSE is associated with an increase of food allergies, in some patients this can cause diarrhea, but in others constipation. In some patients, food allergies and GERD are an apparent symptom of GSE, but these allergies and GERD often persist on a GF diet. While GERD associated with GSE can be treated with acid blockers, it is most effectively treated with proper eating habits and elimination diet. The more powerful
acid blockers (omeprazole, esomeprezole) can interfere with calcium adsorption and can aggravated preexisting hypocalcaemia and Hypomagnesemia which are more common GSE[61]
Eosinophilic oesophagitis
A high proportion of children in Italy who were diagnose with eosinophilic oesophagitis were found to have coeliac disease. [62] All patients appeared
to improve on either a gluten-free or allergen free diet.
Diseases of the pancreas, gall bladder, bile duct
'Primary biliary cirrhosis'. CD is prevalent in primary biliary cirrhosis (PBC)[63][64]. In PBC anti-mitochondrial antibodies are directed toward 3 mitochondrial autoantigens (pyruvate dehydrogenase, oxoglutarate dehydrogenase,branched-chain alpha-keto acid dehydrogenase), 2 or more nuclear proteins (nucleoporin 210kDa, nucleoporin 62kDa, centromere protein, and sp100), and 57% of acute liver failure patients have anti-transglutaminase antibodies.
'cholangitis'. CD also found at higher than expected frequencies in autoimmune cholangitis and primary sclerosing cholangitis.. CD is frequently linked to pancreatitis but also to papillary stenosis[65] and, in India, tropical calcific pancreatitis appears also to be associated with CD.[66]
GSEA Neuropathies
Neuropathies tend to be associated with late onset celiac disease. Dementia and ataxia appear to be more common. A recent study of children with neuropathies revealed no increase of CD in early onset neuropathies.[67]. While there are many studies linking CD to various neuropathies such as migraine, encephalopathy, chorea, brain stem dysfunction, myelopathy, mononeuritis multiplex, Guillain-Barre-like syndrome, antiganglioside-positive neuropathy with antibodies. Strong associations remain largely unconfirmed in epidemiologic studies.[68] A recent study looking for changes in the physiology of the brain found regional cerebral hypoperfusion in 73% of untreated CD[69] The calcification of channels at the surface of the brain appear to be a leading
phenomena associated with Migrane, Visual, Auditory, Schizophrenia, Epilepsy, Dementia. The problem is that while these are found increased in GSE the cause of these calcifications
is unclear and this may extend beyond GSE to other immunological or allergic phenomena.
A recent study in Sweden of 14,000 GSE patients revealed 'no' association of CD with
multiple sclerosis, Parkinson's disease, Alzheimer's disease, hereditary ataxia, ataxia(the symptom), Huntington's disease, myasthenia gravis, or spinal muscular atrophy, but prior polyneuropathy was associated with subsequent CD.[70]
Peripheral neuropathies
Peripheral neuropathies are greatly increased in people who have GSE. In clinical CD there is on obvious reason, Avitaminosis and the inability to adsorb essential fatty acids and vitamins can lead to nervous system problems, including sensitivity of the peripheral nervous system. In addition to these problems there are a number or rare autoimmune conditions, secondary autoimmunities, such as fibromyalgia that are more frequent in GSE than in the normal population. Gulliane-Barre syndrome is associated with peripheral neuropathies, and it has been found that anti-ganglioside autoantibodies take part in the binding to axons and schwann cells. Antibodies to these gangliosides have been found elevated in coeliac disease[71]
Ataxia
A sizable fraction of individuals who have gluten-sensitive ataxia have signs of GSE (either CD or elevated intraepitheal lymphocytes) and ataxia is a common symptom in GSE.[72] Studies of clinically undefinable ataxia generally had higher proportion of late onset gait ataxia, mild upper limb symptoms, and evidence of peripheral neuropathy, questions were raised about the specificity of testing and false positives. Patients with ataxia and CD have antibodies that react with Purkinje fibers but is restricted to the anti-gliadin IgA/IgG.[73] A recent Swedish study of 14,000 registered celiacs showed no association of GSE with Ataxia.
Autism
Some cases of autism may be linked to cross-reactive allergic response to wheat but these primarily appear to be as a result of milk. A subset of wheat-sensitive autism and autistic spectrum disorders (ASD) appear to be linked to GSE. Some of the influences may be indirect. Pyridoxine (vitamin B6), Long-chain omega-3 fatty acids, magnesium, benefit large number of ASD cases. Vitamins A, B3, C, folic acid, calcium, zinc, cod-liver oil, and digestive enzymes, also offer some benefit.[74]. One of the core features of CD, to a lessor degree GSE, is malabsorption and the benefit of nutrient replacement (essential fatty acids, vitamins, minerals) parallels the above findings, suggesting a large link between autism and CD may be indirect result of malabsorption. However the methodological approach may show a benefit less than implied in these studies.[75]
Dementia, epilepsy
Epilepsy has been noticed in a sampling of Coeliac Disease patients.[76] One prime example is calcium channel obstruction in the brain and dementia.[77][78] There is a growing body of evidence suggesting that subclinical cases in older adults will typically progress toward dementia[79], a large number of studies in Italy and Spain have documented earlier onset cases, though the autoimmune condition is not known, folic acid malabsorption may be the cause.
Visual and Auditory disturbances
According to recent studies calcifications of channels seen in dementia can also occur in specific brain areas such as the visual complex in the occipital lobe. Such calcium channel blockages can cause visual problems or partial field hallucinations (Paroxysmal visual manifestations). [80]. Other papers show a link between migrane, visual aura and cerebral calcifications.[81] Disturbances may be followed by
convulsions and associated with gastrointestinal phenomena.
White matter leasions
Ten (of 75) young patients had neurologic findings such as febrile seizures, single generalized seizures, mild ataxia, and muscular hypotonia with retarded motor development, but magnetic resonance imaging detected unilateral and bilateral T2-hyperintensive white-matter lesions in 15 patients (20%)[82]
Depression
Depression in GSE has several causes, in the more severe CD depression can be the result of lower vitamin adsorption and essential fatty acid adsorption (see section on autism). Depression and Anger may also be the result of lower quality of life issues as a result of gluten-free diet.[83] Depression appears to persist on gluten free diet in a sizable fraction of GSE. [84]. Elevated anger has been noted also with GSE.
Anxiety
Anxiety is a common feature of GSE, treatment on a gluten-free diet is effective at reducing anxiety, some aspect of which may be do to maladsorption phenomena
and cytokine activity (i.e. constant stress). More resolution of anxiety is expected on gluten free diet.
Fibromyalgia
Fibromyalgia was found in 9% of adult patients relative to 0.03% in the general population with a link common to IBD.[85] Concurrent IBS is found in 30% to 70%. Small intestinal bacterial overgrowth is associated is common with a transient response to antimicrobial therapy.[86]
Chronic fatigue
Chronic fatigue associated with GSE is a systemic disorder, however there are neurological components that are especially manifest in blood deficiencies like avitaminosis, amineralosis and anemia. Reduced iron and the lack of vitamins folate, B6, B12 and maladsorption of essential fatty acids can cause depression and chronic fatigue.[87] Anti-gliadin antibodies correlate with higher risk for chronic-fatique when no clinical finding of CD is present.[88].
While fatigue is reduced on gluten-free diet, bouts of depression can become worse.
GSEA Connective tissue disorders
Arthritis
Some instance of arthritis with small bowel villous atrophy have been found to resolve
on gluten free diet[89], and anti-connective tissue antibodies have been found in increased levels in celiac disease.[90] Anti-rheumatoid factor antibodies are also increased.[91] In addition, cross-reactive anti-beef-collagen antibodies (IgG) may explain some ''rheumatoid arthritis'' (RA) incidences. Cross linking to tissue transglutaminase and collagen favours gliadin toxicity in coeliac disease., Dieterich W, Esslinger B, Trapp D, Hahn E, Huff T, Seilmeier W, Wieser H, and Schuppan D., , , Gut., 2006 Although the presence of anti-beef collagen antibodies does not necessarily lead to RA, the RA association with ''Triticeae'' consumption is secondary to GSE and involves DRB1
★ 0401/4 linkages to DQ8 A gut feeling for joint inflammation - using coeliac disease to understand rheumatoid arthritis., Molberg O, and Sollid LM., , , Trends Immunol., 2006 and is debatable. In one instance rhuematoid arthritis was tied directly to refractory disease.[92]
Still's disease
Still's disease (AOSD) is a rheumatic disorder of unknown etiology characterized by a triad of fever, polyarthritis and evanescent rash. An idiopathic case has been reported with celiac disease.[93]
GSEA Myositis
Some myopathies may be the indirect result of maladsorption of fat soluble vitamins such as vitamin E.[12]
Dermatomyositis
Dermatomyositis is associated with CD in children and more recently established in adults[95][96]
GSEA Nephritis
'glomerulonephritis'.Celiac disease is associated with immune complex glomerulonephritis. [97]
'IgA Nephropathy'. Anti-gliadin IgA antibodies are found also more commonly in patients
with IgA Nephropathy. The paper finds a link between GSE and IgA Nephropathy, but not between CD and Nephropathy.[98]
'Hyperoxaluria'. Calcium oxolate correlates with severity of fat maladsorption in celiac
disease.[99][100]
GSEA Cancers
There are two predominant cancers associated with coeliac disease. Cancer of the esophagus and lymphoproliferative diseases such as gluten-sensitive enteropathy associated T-cell lymphoma.[101]. For non-EATL cancers it is though the mineralemias such as zinc and selenium may play a role in increasing risk..
Precancerous states
CD is associated with two grades of disease linked precancerous states. This condition
is known as 'refractory celiac disease' ('RCD'), defined as malabsorption due to gluten-related enteropathy (villous atrophy or elevated intraepitheal lymphocytes) after initial or subsequent failure of a strict gluten-free diet (usually 1 year) and after exclusion of any disorder mimicking coeliac disease.[102][103]
★ 'RCD 1' involves precancerous tissues in which transformed T-cells continue to produce a response even though gluten is no longer present.[104] The stage is fairly treatable (azathioprine, prednisone) if caught early and infrequently produces lymphoma.. Elemental diet (proteins digested to amino acids) seems to be an effective alternative diet,[105] indicating other proteins are stimulating the IEL. 5 year viability is high when treate. DQ representation is similar to non-RCD celiacs.
★ 'RCD 2' involves neoplastic tissues that the lack of surface expression of usual T-cell markers.
★
★ Increased expression of:
★
★
★ Intracytoplasmic CD3e
★
★
★ Surface CD103
★
★ Decreased expression of:
★
★
★ CD8
★
★
★ CD4
★
★
★ TCR-alpha/beta
:Clonal T-cell expansion in RCD 2 is not managable with steroids (see: RCD 1) and sometimes managable with chemotherapuetic drugs,[106] however, more aggresive therapies seem more affective. A high percentage of RCD 2 patients spontaneously develope lymphoma, the 5 year survival rate is markedly lower than RCD1 but higher than lymphoma. DQ2.5/DQ2 individuals are more frequently found[107].
'Causes of RCD'.
★ Coeliac disease
★ Age at CD/GSE diagnosis - most people are over the age of 50 when first diagnosed at RCD
★ Length of latency - The length of time, often unknown in which the person is GSE+.
★ Severity - The severity of the microscopic destrustion appears to be a factor, and genetics appears now to play a role.[108]
★ Genetics - For RCD 2 and EATL, genetics plays large role DQ2.5/DQ2+ individuals are over-represented in the patient set.
GSEA Lymphoma
GSE increases the risk of cancers of specific types [109] Among these certain Enteropathy-Associated T-cell Lymphoma is the most common neoplasm[5] and cancers of the intestinal tract are of greatest risk, approximately 5 fold higher than normal. Sixty percent of individuals with gluten-sensitive enteropathy associated T-cell lymphoma were homozygotes for DQ2, whereas only 25% of celiac disease patients and 2.1% of controls are homozygotes for DQ2, these studies indicate that homozygotes of associated DQ types can increase the severity of the disease.[111] GS-EATL is always associated with clinical CD.
Esophageal cancer
Squamous carcinoma of the esophagus is more prevalent in coeliac disease [112]. The increased prevalence may be secondary to GERD that results from chronic delayed gastric emptying. Other studies implicate the maladsorption of vitamin A and zinc as a result of multi-vitamin and mineral deficiencies seen in Coeliac disease.
Adenocarcinoma
Adenocarinoma of the bowel has been associated with coeliac disease.[113]
=References=
1. Coeliac disease and immunological disorders, Cooper BT, Holmes GK, Cooke WT, , , British medical journal, 1978
2. Celiac disease as a cause of transient hypocalcemia and hypovitaminosis D in a 13 year-old girl, Rakover Y, Hager H, Nussinson E, Luboshitzky R, , , The Journal of pediatric endocrinology, 1994
3. Evidence of poor vitamin status in coeliac patients on a gluten-free diet for 10 years, Hallert C, Grant C, Grehn S, ''et al'', , , Aliment. Pharmacol. Ther., 2002
4. Evaluation of vitamin A absorption by using oil-soluble and water-miscible vitamin A preparations in normal adults and in patients with gastrointestinal disease, Johnson EJ, Krasinski SD, Howard LJ, Alger SA, Dutta SK, Russell RM, , , Am. J. Clin. Nutr., 1992
5. The major complications of coeliac disease, Wright DH, , , Baillieres Clin. Gastroenterol., 1995
6. Plasma zinc and vitamin A in human squamous carcinoma of the esophagus, Mellow MH, Layne EA, Lipman TO, Kaushik M, Hostetler C, Smith JC, , , Cancer, 1983
7. Vitamin B-6 absorption in children with acute celiac disease and in control subjects, Reinken L, Zieglauer H, , , J. Nutr., 1978
8. Reversal of psychopathology in adult coeliac disease with the aid of pyridoxine (vitamin B6), Hallert C, Aström J, Walan A, , , Scand. J. Gastroenterol., 1983
9. Hypocalcemia and skeletal disease as presenting features of celiac disease, Shaker JL, Brickner RC, Findling JW, ''et al'', , , Arch. Intern. Med., 1997
10. [Vitamin K deficiency bleeding as a leading symptom in celiac disease (author's transl)], Mitterstieler G, Zieglauer H, , , Pädiatrie und Pädologie, 1978
11. Cerebellar syndrome in adult celiac disease with vitamin E deficiency, Mauro A, Orsi L, Mortara P, Costa P, Schiffer D, , , Acta Neurol. Scand., 1991
12. Reversible inflammatory and vacuolar myopathy with vitamin E deficiency in celiac disease, Kleopa KA, Kyriacou K, Zamba-Papanicolaou E, Kyriakides T, , , Muscle Nerve, 2005
13. Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy, Rude RK, Olerich M, , , Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 1996
14. The watery diarrhea syndrome with hypercalcemia--a symptomatic response to phosphate buffer, Van Dyk D, Inbal A, Kraus L, Grifel B, Ravid M, , , Hepatogastroenterology, 1981
15. Zinc nutrition in celiac sprue, Solomons NW, Rosenberg IH, Sandstead HH, , , Am. J. Clin. Nutr., 1976
16. Serum carnitine and selenium levels in children with celiac disease, Yüce A, Demir H, Temizel IN, Koçak N, , , Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology, 2004
17. Body content of selenium in coeliac disease, Hinks LJ, Inwards KD, Lloyd B, Clayton BE, , , British medical journal (Clinical research ed.), 1984
18. Concentration of selenium in the whole blood and the thyroid tissue of patients with various thyroid diseases, Kucharzewski M, Braziewicz J, Majewska U, Góźdź S, , , Biological trace element research, 2002
19. Coeliac disease: always something to discover, Várkonyi A, Boda M, Endreffy E, Németh I, Timár E, , , Scand. J. Gastroenterol. Suppl., 1998
20. Celiac sprue, hyperhomocysteinemia, and MTHFR gene variants, Wilcox GM, Mattia AR, , , J. Clin. Gastroenterol., 2006
21. Diagnostic value of the serum folate assay, Forshaw J, Harwood L, , , J. Clin. Pathol., 1971
22. Selective IgA deficiency with multiple autoimmune disorders, Hauser GJ, Heiman I, Laurian L, Diamant S, Spirer Z, , , Journal of clinical & laboratory immunology, 1981
23. Low serum vitamin B12 is common in coeliac disease and is not due to autoimmune gastritis, Dickey W, , , European journal of gastroenterology & hepatology, 2002
24. Diagnostic value of the serum folate assay, Forshaw J, Harwood L, , , J. Clin. Pathol., 1971
25. Anemia: monosymptomatic celiac disease. A report of 3 cases, Depla AC, Bartelsman JF, Mulder CJ, Tytgat GN, , , Hepatogastroenterology, 1990
26. Subclinical coeliac disease is a frequent cause of iron-deficiency anaemia, Corazza GR, Valentini RA, Andreani ML, ''et al'', , , Scand. J. Gastroenterol., 1995
27. Iron deficiency in coeliac disease is mild and it is detected and corrected by gluten-free diet, Ståhlberg MR, Savilahti E, Siimes MA, , , Acta paediatrica Scandinavica, 1991
28. Celiac disease presenting as the Paterson-Brown Kelly (Plummer-Vinson) syndrome, Dickey W, McConnell B, , , Am. J. Gastroenterol., 1999
29. Metachronous small-bowel adenocarcinoma in coeliac disease: gluten-free diet is not protective, Kingham JG, Ramanaden D, Dawson A, , , Scand. J. Gastroenterol., 1998
30. Vascular complications of inflammatory bowel disease, Talbot RW, Heppell J, Dozois RR, Beart RW, , , Mayo Clin. Proc., 1986
31. Venous thrombosis in inflammatory bowel disease, Srirajaskanthan R, Winter M, Muller AF, , , European journal of gastroenterology & hepatology, 2005
32. The factor V Leiden mutation increases the risk of venous thrombosis in patients with inflammatory bowel disease, Liebman HA, Kashani N, Sutherland D, McGehee W, Kam AL, , , Gastroenterology, 1998
33. A rare association between ulcerative colitis (UC), celiac disease (CD), membranous glomerulonephritis, leg venous thrombosis, and heterozygosity for factor V Leiden, Casella G, Perego D, Baldini V, Monti C, Crippa S, Buda CA, , , J. Gastroenterol., 2002
34. Genetic association between factor V Leiden and coeliac disease, Mari T, Zullo A, Hassan C, Di Giulio L, Morini S, , , Gut, 2006
35. Detection of gluten in human sera by an enzyme immunoassay: comparison of dermatitis herpetiformis and celiac disease patients with normal controls, Lane AT, Huff JC, Weston WL, , , J. Invest. Dermatol., 1982
36. Chronic urticaria: a cutaneous manifestation of celiac disease, Haussmann J, Sekar A, , , Can. J. Gastroenterol., 2006
37. Atopic disorders and adult coeliac disease, Hodgson HJ, Davies RJ, Gent AE, , , Lancet, 1976
38. Celiac disease and skin: Psoriasis association, Abenavoli L, Leggio L, Gasbarrini G, Addolorato G, , , World J. Gastroenterol., 2007
39. Cutaneous manifestations in celiac disease, Abenavoli L, Proietti I, Leggio L, ''et al'', , , World J. Gastroenterol., 2006
40. Prurigo nodularis and gluten enteropathy, McKenzie AW, Stubbing DG, Elvy BL, , , Br. J. Dermatol., 1976
41. Prurigo nodularis (Hyde's prurigo) disclosing celiac disease, Francesco Stefanini G, Resta F, Marsigli L, ''et al'', , , Hepatogastroenterology, 1999
42. Rothmund-Thomson syndrome. The first case with plantar keratoderma and the second with coeliac disease, Popadić S, Nikolić M, Gajić-Veljić M, Bonaci-Nikolić B, , , Acta dermatovenerologica Alpina, Panonica, et Adriatica, 2006
43. Celiac disease and alopecia areata: report of a new association, Corazza GR, Andreani ML, Venturo N, Bernardi M, Tosti A, Gasbarrini G, , , Gastroenterology, 1995
44. Alopecia areata and coeliac disease: no effect of a gluten-free diet on hair growth, Bardella MT, Marino R, Barbareschi M, Bianchi F, Faglia G, Bianchi P, , , Dermatology (Basel), 2000
45. Failure of gluten-free diet in celiac disease-associated alopecia areata, Bondavalli P, Quadri G, Parodi A, Rebora A, , , Acta Derm. Venereol., 1998
46. Case report: idiopathic hypoparathyroidism co-existing with coeliac disease: immunologic studies, Wortsman J, Kumar V, , , Am. J. Med. Sci., 1994
47. Celiac disease and risk of subsequent type 1 diabetes: a general population cohort study of children and adolescents., Ludvigsson J, Ludvigsson J, Ekbom A, Montgomery S, , , Diabetes Care, 2006
48. Clinical benefit of a gluten-free diet in type 1 diabetic children with screening-detected celiac disease: a population-based screening study with 2 years' follow-up., Hansen D, Brock-Jacobsen B, Lund E, Bjørn C, Hansen L, Nielsen C, Fenger C, Lillevang S, Husby S, , , Diabetes Care, 2006
49. A type 1 diabetes-related protein from wheat (Triticum aestivum). cDNA clone of a wheat storage globulin, Glb1, linked to islet damage, MacFarlane AJ, Burghardt KM, Kelly J, ''et al'', , , J. Biol. Chem., 2003
50. Viral infections as potential triggers of type 1 diabetes, , , , Diabetes Metab Res Rev,
51. Rotavirus-specific T cell responses and cytokine mRNA expression in children with diabetes-associated autoantibodies and type 1 diabetes, Mäkelä M, Oling V, Marttila J, Waris M, Knip M, Simell O, Ilonen J, , , Clin Exp Immunol, 2006
52. Enteral virus infections in early childhood and an enhanced type 1 diabetes-associated antibody response to dietary insulin, Mäkelä M, Vaarala O, Hermann R, Salminen K, Vahlberg T, Veijola R, Hyöty H, Knip M, Simell O, Ilonen J, , , J Autoimmun, 2006
53. Coeliac disease--associated disorders and survival, Collin P, Reunala T, Pukkala E, Laippala P, Keyriläinen O, Pasternack A, , , Gut, 1994
54. Risk of primary adrenal insufficiency in patients with celiac disease, Elfström P, Montgomery SM, Kämpe O, Ekbom A, Ludvigsson JF, , , , 2007
55. Pregnancy in patients with coeliac disease, Ogborn AD, , , British journal of obstetrics and gynaecology, 1975
56. Infertility and coeliac disease, Collin P, Vilska S, Heinonen PK, Hällström O, Pikkarainen P, , , Gut, 1996
57. Zinc deficiency in malabsorption states: a cause of infertility?, Jameson S, , , Acta Med. Scand. Suppl., 1976
58. Celiac disease as a rare cause of primary amenorrhea: a case report, Pradhan M, Manisha, Singh R, Dhingra S, , , The Journal of reproductive medicine, 2007
59. Immunological abnormalities in coeliac disease and their response to dietary restriction. I. Serum immunoglobulins, antibodies and complement, Ratnaike RN, Wangel AG, , , Australian and New Zealand journal of medicine, 1977
60. Predictors of Clinical Response to Gluten-Free Diet in Patients Diagnosed With Diarrhea-Predominant Irritable Bowel Syndrome, Wahnschaffe U, Schulzke JD, Zeitz M, Ullrich R, , , , 2007
61. By the way, doctor. I heard that taking a proton-pump inhibitor could cause hip fractures. I've been taking 20 mg of Prilosec every day for a year. Should I be concerned?, Robb-Nicholson C, , , Harvard women's health watch, 2007
62. Eosinophilic oesophagitis and coeliac disease: is there an association?, Quaglietta L, Coccorullo P, Miele E, Pascarella F, Troncone R, Staiano A, , , , 2007
63. Primary biliary cirrhosis and coeliac disease: an association?, Logan RF, Ferguson A, Finlayson ND, Weir DG, , , Lancet, 1978
64. Celiac disease in autoimmune cholestatic liver disorders, Volta U, Rodrigo L, Granito A, ''et al'', , , Am. J. Gastroenterol., 2002
65. Celiac disease and recurrent pancreatitis, Patel RS, Johlin FC, Murray JA, , , Gastrointest. Endosc., 1999
66. Celiac disease and tropical calcific pancreatitis, Nanda R, Anand BS, , , Am. J. Gastroenterol., 1993
67. Prevalence of celiac antibodies in children with neurologic disorders, Lahat E, Broide E, Leshem M, Evans S, Scapa E, , , Pediatr. Neurol., 2000
68. Neurologic presentation of celiac disease, Bushara KO, , , Gastroenterology, 2005
69. Regional cerebral hypoperfusion in patients with celiac disease, Addolorato G, Di Giuda D, De Rossi G, ''et al'', , , Am. J. Med., 2004
70. A population-based study of coeliac disease, neurodegenerative and neuroinflammatory diseases, Ludvigsson JF, Olsson T, Ekbom A, Montgomery SM, , , Aliment. Pharmacol. Ther., 2007
71. Anti-ganglioside antibodies in coeliac disease with neurological disorders, Volta U, De Giorgio R, Granito A, ''et al'', , , Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver, 2006
72. Clinical, radiological, neurophysiological, and neuropathological characteristics of gluten ataxia, Hadjivassiliou M, Grünewald RA, Chattopadhyay AK, ''et al'', , , Lancet, 1998
73. The humoral response in the pathogenesis of gluten ataxia, Hadjivassiliou M, Boscolo S, Davies-Jones GA, ''et al'', , , Neurology, 2002
74. Autism, an extreme challenge to integrative medicine. Part 2: medical management, Kidd PM, , , Alternative medicine review : a journal of clinical therapeutic, 2002
75. Elimination diets in autism spectrum disorders: any wheat amidst the chaff?, Christison GW, Ivany K, , , Journal of developmental and behavioral pediatrics : JDBP, 2006
76. Increased prevalence of epilepsy in coeliac disease, Chapman RW, Laidlow JM, Colin-Jones D, Eade OE, Smith CL, , , British medical journal, 1978
77. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients, Molteni N, Bardella MT, Baldassarri AR, Bianchi PA, , , Am. J. Gastroenterol., 1988
78. Celiac disease, posterior cerebral calcifications and epilepsy, Gobbi G, Ambrosetto P, Zaniboni MG, Lambertini A, Ambrosioni G, Tassinari CA, , , Brain Dev., 1992
79. Cognitive impairment and celiac disease, Hu WT, Murray JA, Greenaway MC, Parisi JE, Josephs KA, , , Arch. Neurol., 2006
80. Visual disturbances representing occipital lobe epilepsy in patients with cerebral calcifications and coeliac disease: a case series, Pfaender M, D'Souza WJ, Trost N, Litewka L, Paine M, Cook M, , , J. Neurol. Neurosurg. Psychiatr., 2004
81. Migraine, celiac disease, and cerebral calcifications: a new case, D'Amico D, Rigamonti A, Spina L, Bianchi-Marzoli S, Vecchi M, Bussone G, , , Headache, 2005
82. Brain white-matter lesions in celiac disease: a prospective study of 75 diet-treated patients, Kieslich M, Errázuriz G, Posselt HG, Moeller-Hartmann W, Zanella F, Boehles H, , , Pediatrics, 2001
83. Psychological dimensions of celiac disease: toward an integrated approach, Ciacci C, Iavarone A, Siniscalchi M, Romano R, De Rosa A, , , Dig. Dis. Sci., 2002
84. Anxiety but not depression decreases in coeliac patients after one-year gluten-free diet: a longitudinal study, Addolorato G, Capristo E, Ghittoni G, ''et al'', , , Scand. J. Gastroenterol., 2001
85. Presentations of adult celiac disease in a nationwide patient support group, Zipser RD, Patel S, Yahya KZ, Baisch DW, Monarch E, , , Dig. Dis. Sci., 2003
86. Fibromyalgia: the gastrointestinal link, Wallace DJ, Hallegua DS, , , Current pain and headache reports, 2004
87. Fatigue in adult coeliac disease, Siniscalchi M, Iovino P, Tortora R, ''et al'', , , Aliment. Pharmacol. Ther., 2005
88. Do adults with high gliadin antibody concentrations have subclinical gluten intolerance?, Arnason JA, Gudjónsson H, Freysdóttir J, Jónsdóttir I, Valdimarsson H, , , Gut, 1992
89. Arthritis associated with gluten-sensitive enteropathy, Pinals RS, , , J. Rheumatol., 1986
90. Anticonnective tissue and other antitissue 'antibodies' in the sera of patients with coeliac disease compared with the findings in a mixed hospital population, Williamson N, Asquith P, Stokes L, Jowett W, Cooke WT, , , J. Clin. Pathol., 1976
91. Selective increase of IgA rheumatoid factor in patients with gluten sensitivity, Sökjer M, Jónsson T, Bödvarsson S, Jónsdóttir I, Valdimarsson H, , , Acta Derm. Venereol., 1995
92. Autoimmune enteropathy and rheumatoid arthritis: a new association in the field of autoimmunity, Volta U, De Angelis GL, Granito A, ''et al'', , , Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver, 2006
93. Celiac disease: Association with adult-onset Still's disease: Apropos of a clinical case, Kumar S, Gupta N, Jhamb R, Mishra D, , , Indian journal of medical sciences, 2007
94. Reversible inflammatory and vacuolar myopathy with vitamin E deficiency in celiac disease, Kleopa KA, Kyriacou K, Zamba-Papanicolaou E, Kyriakides T, , , Muscle Nerve, 2005
95. An uncommon association: celiac disease and dermatomyositis in adults, Marie I, Lecomte F, Hachulla E, ''et al'', , , Clin. Exp. Rheumatol., 2001
96. Dermatomyositis associated with celiac disease: response to a gluten-free diet, Song MS, Farber D, Bitton A, Jass J, Singer M, Karpati G, , , Can. J. Gastroenterol., 2006
97. Celiac disease associated with immune complex glomerulonephritis, Katz A, Dyck RF, Bear RA, , , Clin. Nephrol., 1979
98. Increased Prevalence of Anti-Gliadin IgA-Antibodies with Aberrant Duodenal Histopathological Findings in Patients with IgA-Nephropathy and Related Disorders, Almroth G, Axelsson T, Müssener E, Grodzinsky E, Midhagen G, Olcén P, , , Ups. J. Med. Sci., 2006
99. Hyperoxaluria correlates with fat malabsorption in patients with sprue, McDonald GB, Earnest DL, Admirand WH, , , Gut, 1977
100. Hyperoxaluria and intestinal disease. The role of steatorrhea and dietary calcium in regulating intestinal oxalate absorption, Stauffer JQ, , , The American journal of digestive diseases, 1977
101. Coeliac disease and malignancies, Ferguson A, Kingstone K, , , Acta paediatrica (Oslo, Norway : 1992). Supplement, 1996
102. Refractory coeliac disease, Daum S, Cellier C, Mulder CJ, , , Best practice & research. Clinical gastroenterology, 2005
103. Azathioprine and prednisone combination therapy in refractory coeliac disease, Goerres MS, Meijer JW, Wahab PJ, ''et al'', , , Aliment. Pharmacol. Ther., 2003
104. Update on the management of refractory coeliac disease, Al-Toma A, Verbeek WH, Mulder CJ, , , Journal of gastrointestinal and liver diseases : JGLD, 2007
105. Effect of elemental diet on mucosal immunopathology and clinical symptoms in type 1 refractory celiac disease, Olaussen RW, Løvik A, Tollefsen S, ''et al'', , , Clin. Gastroenterol. Hepatol., 2005
106. Cladribine therapy in refractory celiac disease with aberrant T cells, Al-Toma A, Goerres MS, Meijer JW, ''et al'', , , Clin. Gastroenterol. Hepatol., 2006
107. Human leukocyte antigen-DQ2 homozygosity and the development of refractory celiac disease and enteropathy-associated T-cell lymphoma, Al-Toma A, Goerres MS, Meijer JW, Peña AS, Crusius JB, Mulder CJ, , , Clin. Gastroenterol. Hepatol., 2006
108. HLA-DQB1
★ 0201 homozygosis predisposes to severe intestinal damage in celiac disease, Jores RD, Frau F, Cucca F, ''et al'', , , Scand. J. Gastroenterol., 2007
109. Coeliac disease, gluten-free diet, and malignancy, Holmes GK, Stokes PL, Sorahan TM, Prior P, Waterhouse JA, Cooke WT, , , Gut, 1976
110. The major complications of coeliac disease, Wright DH, , , Baillieres Clin. Gastroenterol., 1995
111. Survival in Refractory Coeliac Disease and Enteropathy associated T cell Lymphoma: Retrospective evaluation of single centre experience, Al-Toma A, Verbeek WH, Hadithi M, von Blomberg BM, Mulder CJ, , , , 2007
112. Malignancy in a 19-year experience of adult celiac disease, Selby WS, Gallagher ND, , , Dig. Dis. Sci., 1979
113. Adenocarcinoma of the jejunum associated with nontropical sprue, Petreshock EP, Pessah M, Menachemi E, , , The American journal of digestive diseases, 1975
This article provided by Wikipedia. To edit the contents of this article, click here for original source.
psst.. try this: add to faves
Featured Companies
| Vacation By V |
Newest Companies
Gluten-sensitive enteropathy associated conditions Travel Deals
