Celiac.com 01/20/2005 - A link between untreated celiac disease and a rare enteropathy-type T-cell lymphoma (ETTL) has been well established by several studies. According to Dr. Karin Ekstrom Smedby of the Karolinska Institute in Stockholm and colleagues, there is also an increase in the prevalence of other types of lymphomas in those with celiac disease, such as B cell and non-intestinal lymphomas. In their study the researchers reviewed and reclassified 56 cases of malignant lymphomas that occurred in 11,650 hospitalized celiac disease patients in Sweden. The observed numbers of lymphoma subtypes were compared with those expected in the Swedish population. The researchers discovered that a majority of the lymphomas were not intestinal T-cell lymphomas, but were B-cell non-Hodgkin lymphoma (NHL). In addition, 44% of the patients with B cell NHL had a history of other autoimmune/inflammatory diseases. As expected, the relative risks for T-cell NHL and primary gastrointestinal lymphomas were markedly increased. According to the researchers: "Most lymphomas complicating coeliac disease are indeed related to the disease and are not of the ETTL-type. There was a remarkable aggregation of autoimmune/inflammatory disorders, female sex, coeliac disease, and B cell lymphoma."
JAMA 2002;287:1413-1419. Celiac.com 04/12/2002 - According to a report published in the March 20th issue of the Journal of the American Medical Association, people with celiac disease are three times more likely to develop non-Hodgkin lymphoma (NHL) than the normal population. Dr. Carlo Catassi and colleagues from the University of Maryland in Baltimore compared the prevalence of celiac disease in 653 NHL patients with more than 5,000 healthy control subjects to determine the NHL-celiac disease occurrence rate. The results indicate that 1% of NHL patients also have celiac disease, in comparison with 0.42% of the healthy controls. Adjustments were made for age and sex, and the final results indicate that the odds ratios for a patient with celiac disease of developing NHL are: 3.1 for all types of NHL, 16.9 for gut NHL, and 19.2 for T-cell NHL. The overall risk, however, for someone with celiac disease developing NHL is only 0.63%. The researchers do not feel that their findings support mass screening for celiac disease, but they do feel that selected NHL patients should be screened for celiac disease. We would also like to add that these findings support the screening of people with celiac disease for NHL, which was not directly addressed by the report.
Celiac.com 08/14/2007 - It has long been documented that there is a connection between celiac disease and neoplasm. In fact, in the 1960s, a population-based study reported a 100-fold increase in risk of non-Hodgkins lymphoma in patients with celiac disease. It has also been shown that people with celiac disease are at greater risk for developing small bowel adenocarcinoma. Also, studies have shown an increased mortality rate from cancer among celiac patients, and there is mounting, but not conclusive evidence that a gluten-free diet provides a measure of protection against the development of malignancies. Strangely, several studies have documented a lower risk of breast cancer among celiac patients. However, to date, very little is known about the associated factors, particularly with regard to the development of gastrointestinal malignancies and their corresponding risk levels. A study recently published in BMC Gastroenterology documents the efforts of a team of Italian doctors to evaluate the risks of developing various types of gastrointestinal neoplasms associated with delayed diagnosis of celiac disease and the resulting consumption of gluten over time. The team was made up of doctors Marco Silano; Umberto Volta; Anna Maria Mecchia; Mariarita DessÃ¬; Rita Di Benedetto; and Massimo De Vincenzi. The team studied a group of 1,968 celiac patients from 20 GE referral centers between 01 January 1982 & 31 March 2005. Study Shows Higher Rates of Gastrointestinal Malignancy that Increase with Age in Patients with Delayed Diagnosis of Celiac Disease According to the results of the study celiac patients have an increased risk of developing cancer which corresponds directly with the age of diagnosis of celiac disease. This increased risk applies to gastro-intestinal malignancies. An accurate screening for tumors should be performed in patients diagnosed with celiac disease in adulthood. On average, the mean age of celiac patients who developed a neoplasm, either sooner or later, was 47.6 +/- 10.2 years, compared with 28.6 =/- 18.2 years in those did not develop neoplasm. BMC Gastroenterology 2007, 7:8 (9 March 2007) health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
Celiac.com 01/03/2008 - It’s pretty well documented that HLA-DQ2 and HLA-DQ8 sereotypes are closely associated with celiac disease. Patients who test positive for both sereotypes are at much greater risk for developing celiac disease. Celiac disease is closely associated with the presence of HLA-DQ2 and HLA-DQ8, and has also been tied to variations in the MY09B gene on the 19th chromosome.
Homozygosity is the condition of having two identical genes, of many possible combinations, on a single chromosome site.
HLA-DQ2 homozygosity means that a person has inherited the HLA-DQ2 gene from both parents.
In addition to having a much higher risk of developing celiac disease in general, people with HLA-DQ2 homozygosity have a much higher risk of developing refractory celiac disease type II, and enteropathy-associated T-cell lymphoma. Refractory celiac disease is a rare type of celiac disease in which a gluten-free diet fails to eliminate symptoms and to reverse celiac-associated damage. Eneteropathy-associated T-cell lymphoma is a type of cancer that often develops in people with advanced intestinal damage such as commonly found in celiac patients.
A team of Dutch doctors recently set out to determine if the presence of the MY09B gene carries an elevated risk of refractory celiac disease type II, and enteropathy-associated T-cell lymphoma.
The research team evaluated 62 people who were confirmed to have both refractory celiac disease type II and enteropathy-associated T-cell lymphoma. They also evaluated 421 people with simple celiac disease, along with a control group of 1624 people without celiac disease.
The team conducted genotyping of MY09B along with molecular HLA-DQ2 typing on all of the patients.
The tests showed that one nucleotide variation in MY09B was substantially different in the refractory celiac group than in either the simple celiac or the control group.
The allele in question is known as the rs7259292 T allele, and the results of the tests showed that it occurs far more frequently in patients with refractory celiac and enteropathy-associated T-cell lymphoma than in either the control group or the group with simple celiac disease. In fact, the halpotype that carries the rs7253292 T allele occurs in 11% of the patients with refractory celiac disease type II, and enteropathy-associated T-cell lymphoma compared with just 2% of the control group and 3% or patients with regular celiac disease.
Additionally, the results showed that patients who carry the MY09B rs7259292 allele or who showed HLA-DQ2 homozygosity faced similarly high risk levels for refractory celiac disease type II, and enteropathy-associated T-cell lymphoma compared to patients with simple celiac disease.
The results did not show any connection or interaction between the MY09B rs7259292 allele and HLA-DQ homozygosity.
Clinical Gastroenterology and Hepatology; 2007: 5(12): 1399-1405
Celiac.com 02/09/2009 - An extensive recent survey of the Swedish cancer registry reveals that people with celiac disease face a 5-fold increased risk of developing non-Hodgkin lymphoma, but that the risk has decreased by more than 50% over the last 40 years.
Researchers at the National Cancer Institute (NCI) in Bethesda, Maryland, and Sweden's Karolinska Institute recently undertook a review of more than 60,000 lymphoma cases diagnosed in Sweden between 1965 and 2004. They matched those cases to individual lymphoma-free controls with similar characteristics.
Dr. Ying Gao of the NCI and colleagues found 37,869 cases of non-Hodgkin's lymphoma, 8,323 cases of Hodgkin's lymphoma, 13,842 cases of chronic lymphocytic leukemia.
The researchers also enrolled 236,408 matched controls and 613,961 first-degree relatives. The team used hospital discharge information to identify people with a history of celiac disease.
The data revealed that people with a hospital discharge diagnosis of celiac disease faced a 5.35-fold increased risk of developing non-Hodgkin's lymphoma. The data also showed that risk of Hodgkin's lymphoma was mildly elevated, and thst celiac patients showed no elevated risk of developing chronic lymphocytic leukemia.
The data showed that from 1975-1984, patients with celiac disease faced a 13.2-fold greater risk of non-Hodgkin's lymphoma; from 1985-1994, that level fell to a 7.90-fold increased risk, and from 1995-2004 that risk fell again to 3.84-fold increased risk. Siblings of those affected with celiac disease also faced a 2.03-fold greater risk of non-Hodgkin's lymphoma.
At present, doctors do not clearly understand the causal link between the two. Earlier studies have indicated that the inflammation common to celiac disease leads drives lymphoma development.
According to the research team, the study carries two basic messages:
The first is that earlier detection of celiac disease is helping to lower the risk of developing lymphoma over time, so today, fewer people are detected in the late stages, when the risk of lymphoma is much greater.
The second message is that people with a family history of celiac disease have a greater chance of developing lymphoma. This family connection was shown to be separate from the personal celiac disease history of the individual.
Together, these revelations suggest that shared mechanisms might contribute to both celiac disease and lymphoma.
The full report appears in the medical journal Gastroenterology, January 2009.
Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
3 cups ripe fresh tomatoes, diced
1 cup shredded green cabbage
½ cup diced yellow onion
¼ cup chopped fresh cilantro
1 jalapeno, seeded
1 Serrano pepper, seeded
2 tablespoons lemon juice
2 tablespoons red wine vinegar
2 garlic cloves, minced
salt to taste
black pepper, to taste
Purée all ingredients together in a blender.
Cover and refrigerate for at least 1 hour.
Adjust seasoning with salt and pepper, as desired.
Serve is a bowl with tortilla chips and guacamole.
Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.
Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs).
However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease.
Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39).
They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature.
Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis.
Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023
Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients.
They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively.
After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
Alimentary Pharmacology & Therapeutics
Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination.
A team of researchers recently set out to develop a method to determine gluten intake and monitor gluten-free dietary compliance in patients with celiac disease, and to determine its correlation with mucosal damage. The research team included ML Moreno, Á Cebolla, A Muñoz-Suano, C Carrillo-Carrion, I Comino, Á Pizarro, F León, A Rodríguez-Herrera, and C Sousa. They are variously affiliated with Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain; Biomedal S.L., Sevilla, Spain; Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío, Sevilla, Spain; Celimmune, Bethesda, Maryland, USA; and the Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain.
For their study, the team collected urine samples from 76 healthy subjects and 58 patients with celiac disease subjected to different gluten dietary conditions. To quantify gluten immunogenic peptides in solid-phase extracted urines, the team used a lateral flow test (LFT) with the highly sensitive and specific G12 monoclonal antibody for the most dominant GIPs and an LFT reader.
They detected GIPs in concentrated urines from healthy individuals previously subjected to gluten-free diet as early as 4-6 h after single gluten intake, and for 1-2 days afterward. The urine test showed gluten ingestion in about 50% of patients. Biopsy analysis showed that nearly 9 out of 10 celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with quantifiable GIP in urine showed signs of gut damage.
The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development.
Gut. 2017 Feb;66(2):250-257. doi: 10.1136/gutjnl-2015-310148.
Your symptoms sounds like celiac disease to me. They could be something else I suppose but the testing should help determine that. The testing for celiac disease is a blood test to check for antibodies to gliaden, and then an endoscopy to take 4 to 6 biopsy samples of the lining of the small intestine. They check the biopsy for damage consistent with celiac disease. The antibodies are DGP IgA, DGP IgG, EMA, total IgA, Ttg-IgA. There is no medically accepted stool sample test for celiac disease.
There is a thread titled "Newbie 101" in the "Coping with Celiac" forum section with some good info on testing and getting started on the gluten-free diet.
Welcome to the forum!
Thank you, I have bouts of itchiness with no visible signs, irritability, I've lost 1 stone in weight, but find my appetite has increased since started folic acid supplements.
I am hoping the results of my tests will be back today.
Thank you all so much for your help and advice.
Not sure if I am replying to you or to myself as new to the site lol 😀😁