Celiac.com 02/28/2011 - Celiac disease is associated with an increased risk of lymphoma and small bowel malignancy. Colorectal cancer is the most common gastrointestinal cancers in the United States, but most studies have not found no higher rates of colorectal cancer for people with celiac disease, compared with rates in the general population.

The results of these studies might in fact be describing a true null relationship between celiac disease and colorectal cancers. However, the results may also be influenced by better health-care among patients with known celiac disease, particularly among those with gastroenterologists who are likely to perform screening colonoscopy.

Because colonoscopy can decrease the incidence of colorectal cancer via removal of precancerous adenomas during the procedure, and because gastroenterologists usually follow such patients, a possible underlying increased risk of colorectal cancer in patients with celiac disease may remain undetected.

The team of researchers sought to assess the underlying risk of colorectal cancer in patients with celiac disease by quantifying the relative prevalence of precancerous colorectal adenomas in these patients compared with patients without celiac disease in a cohort of individuals undergoing colonoscopy. The team included B. Lebwohl; E. Stavsky; A. I. Neugut; and P. H. R. Green.

To isolate the association of celiac disease with colorectal adenomas, the team controlled for three important predictors of adenoma detection on colonoscopy: endoscopist, patient age and patient gender.

They then identified all celiac disease patients who underwent colonoscopy at their institution during a 44-month period. They matched each celiac disease patient by age, gender and endoscopist, with non-celiac control subject.

The team then compared the adenoma rates between these groups, and used multivariate analysis to assess the independent association of celiac disease with adenomas.

The team isolated 180 patients with celiac disease and 346 control subjects. A total of 13% of celiac disease patients and 17% of controls (P = 0.20) showed at least one adenoma.

Multivariate analysis showed that age (OR per year 1.04, 95% CI 1.02–1.07) and male gender (OR 2.33, 95% CI 1.36–3.98) were both associated with higher rates of adenoma.

However, there were no higher adenoma rates among people with celiac disease (OR 0.75, 95% CI 0.41–1.34).

The study provides strong support for the notion that celiac disease is not associated with higher rates of colorectal cancer.

They conclude that the lack of increased rates of colorectal cancer is related to a true average risk of colorectal neoplasia, rather than reflecting higher colonoscopy and associated polyp removals among people with celiac disease.

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Celiac.com 12/29/2010 - A team of researchers recently conducted a prospective study the etiology of lymphocytic duodenosis. Among their findings are that sixteen percent of patients with lymphocytic duodenosis have celiac disease.

The research team was made up of I. Aziz, K. E. Evans, A. D. Hopper, D. M. Smillie, and D. S. Sanders. They are affiliated with the Department of Gastroenterology at Royal Hallamshire Hospital in Sheffield, UK.

The study came in response to earlier retrospective studies that have suggested different connections with lymphocytic duodenosis, indicating that patients with this condition should not be diagnosed with celiac disease, solely by histology.

Lymphocytic duodenosis is marked by normal villous architecture and less than 25 intraepithelial lymphocytes (IELs) per 100 enterocytes.

For their study, the team thoroughly evaluated one hundred patients with lymphocytic duodenosis for celiac disease and other aspects associatedwith lymphocytic duodenosis by using initial celiac blood screens, and excluding the presence of infection.

Of thirty-four patients with unexplained lymphocytic duodenosis, twenty-nine underwent repeat duodenal biopsies following a gluten challenge. Biopsy results showed that 16% of patients with lymphocytic duodenosis had celiac disease.

Once celiac disease was accounted for, the factors most commonly association with lymphocytic duodenosis were as follows: drugs were a factor in twenty-one percent of lymphocytic duodenosis patients; infection was a factor in nineteen percent, immune dysregulation was a factor in four percent, inflammatory bowel disease and microscopic colitis in two percent each, sarcoidosis and IgA deficiency in one percent of cases, respectively.

Of thirty-four patients with no known associations, eighteen showed symptoms of irritable bowel syndrome (IBS). Of twenty-nine patients examined with repeat duodenal biopsies, the IEL count returned to normal in twenty-two patients.

The study results show that known associations can be found in sixty-six percent of cases of lymphocytic duodenosis.

Importantly, sixteen percent will have celiac disease. In cases of lymphocytic duodenosis with no apparent cause, there may be a connection with IBS. In such cases the IEL count returns to normal on repeat biopsy in seventy-six percent.

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Celiac.com 09/17/2010 - People with celiac disease have higher risk for developing lymphoma and small bowel malignancy, though most studies have found no higher risk of colorectal cancer.

To compare rates of colorectal cancer in celiac disease patients with rates for non-celiac disease control subjects, Dr. Peter Greene and colleagues at Columbia University Medical Center conducted a study. The research team included B. Lebwohl, E. Stavsky, and A. I. Neugut.

For the study, the team reviewed case data for all celiac disease patients who underwent colonoscopy at Columbia Medical Center during a 44-month period. They matched each patient with non-coeliac disease controls according to age, gender and presiding endoscopist.

They then compared rates of colorectal adenoma between the groups, and used multivariate analysis to rate any independent association between celiac disease and cancers (adenomas).

The team found 180 patients with celiac disease and 346 controls. Thirteen percent of celiac patients and seventeen percent of control subjects showed at least one adenoma (P = 0.20).

Multivariate analysis showed that age and male gender were associated with adenomas in both groups, but showed no connection between celiac disease and adenomas.

More specifically, relative adenoma risk rose by 4% with each additional year of age, with men facing a 2.33-fold increased risk compared with women.

Their data showed clearly that celiac disease is not associated with an increased risk of colorectal neoplasia. They also note that the lack of increased risk of colorectal cancer seen in population studies reflects a genuine average risk of colorectal neoplasia, rather than an increase in colonoscopies and associated polypectomies in people with celiac disease.

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One possible trigger for Enteropathy-associated T cell lymphoma development is chronic exposure of intraepithelial lymphocytes (IELs) to strong anti-apoptotic signals, that is, signals that interfere in the normal mortality of the IEL cells. These signals are triggered by IL-15, a cytokine that is over-expressed in the enterocytes of people with celiac disease.

However, researchers have not yet fully mapped the signaling pathway by which IL-15 transmits these anti-apoptotic signals. Researchers consider type II refractory celiac disease (RCDII) to be a middle step between celiac disease and enteropathy-associated T cell lymphoma.

Eliminating abnormal IELs at the RCDII stage would likely block EATL development. So far, though, scientists have not found successful immunosuppressive and/or chemotherapeutic approaches able to accomplish this, and RCDII outcomes remain very poor.

A team of researchers recently set out to map the IL-15–driven survival pathway in human IELs, and to determine whether IL-15 triggered pathway in human intraepithelial lymphocytes represents a possible new target in type II refractory celiac disease and enteropathy-associated T cell lymphoma.

The research team was made up of Georgia Malamut, Raja El Machhour, Nicolas Montcuquet, Séverine Martin-Lannerée, Isabelle Dusanter-Fourt, Virginie Verkarre, Jean-Jacques Mention, Gabriel Rahmi, Hiroshi Kiyono, Eric A. Butz, Nicole Brousse, Christophe Cellier, Nadine Cerf-Bensussan, and Bertrand Meresse.

The are variously affiliated with INSERM U989, the Université Paris Descartes, Faculté de Médecine René Descartes, the Department of Gastroenterology, AP-HP, Hôpital Européen Georges Pompidou, the Institut Cochin, Université Paris Descartes, CNRS (UMR 8104), INSERM U1016, the Department of Pathology, AP-HP, of the Hôpital Necker-Enfants Malades in Paris, with the Division of Mucosal Immunology, Department of Microbiology and Immunology at the Institute of Medical Science at the University of Tokyo in Japan, and the Inflammation Department of AMGEN Inc., in Seattle, Washington, USA.

Their current findings reveal that the survival signals IL-15 directs to freshly isolated human IELs, and to human IEL cell lines derived from celiac disease patients with type II refractory celiac disease, depend on anti-apoptotic factors Bcl-2 and/or Bcl-xL.

The signals require IL-15Rβ, Jak3, and STAT5 for proper function, but functioned independently of PI3K, ERK, and STAT3. In support of these findings, the team recorded elevated levels of Bcl-xL, phospho-Jak3, and phospho-STAT5 in IELs from patients with active celiac disease and RCDII.

Moreover, by incubating patient duodenal biopsies with a fully humanized human IL-15–specific Ab, the team effectively blocked Jak3 and STAT5 phosphorylation.

Also, treatment with IL-15–specific Ab caused IEL cell mortality, and wiped out the massive IEL build-up in mice over-expressing human IL-15 in their gut epithelium.

The study marks the first successful mapping of the IL-15–driven survival pathway in human IELs, and demonstrates that IL-15 and its downstream effectors are meaningful therapeutic targets in RCDII.

These findings will likely help to pave the way for the development of successful immunosuppressive and/or chemotherapeutic treatments that destroy abnormal IELs at the RCDII stage and help to block EATL development, improving outcomes for RCDII patients.

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Celiac.com 05/18/2010 - A research team recently concluded a clinicopathologic and array comparative genomic hybridization study on enteropathy-associated T-cell lymphoma.

The team included Young Hyeh Ko MD, PhD; Sivasundaram Karnan; Kyeong Mee Kim MD, PhD; Cheol Keun Park MD, PhD; Eun Suk Kang MD, PhD; Young Ho Kim MD, PhD; Won Ki Kang MD, PhD; Seok Jin Kim MD, PhD; Won Seog Kim MD, PhD; Woo Yong Lee MD, PhD; Ho Kyung Chune; Masao Seto MD, PhD.

The are associated variously with the Department of Pathology, the Department of Laboratory Medicine, the Division of Gastroenterology, Hemato-oncology of Internal Medicine, the Department of General Surgery of Samsung Medical Center at Sungkyunkwan University in Seoul, Korea and the Division of Molecular Medicine of the Aichi Cancer Center Research Institute in Nagoya, Japan.

The latest World Health Organization classification system recognizes 2 types of enteropathy-associated T-cell lymphoma. The first, EATL type 1, is strongly associated with celiac disease, and makes up most EATL cases in Western countries. The second, EATL type 2 has no associations with celiac disease.

To properly classify enteropathy-associated T-cell lymphoma types in Korea, the team conducted clinicopathologic and immunophenotypic analyses of 8 Koreans with enteropathy-associated T-cell lymphoma, and investigated genomic profile via array comparative genomic hybridization.

Five patients presented tumors in the small intestine, while three presented tumors in the colorectum. Two patients carried an HLA DQB1âŽ0302 allele that corresponds to HLA DQ8. None of the patients suffered gluten-sensitive malabsorption syndrome.

The team found intraepithelial lymphocytosis in all patients. In seven patients showed small, or small-to-medium, tumor cells. One patient presented with a medium-to-large tumor. Tumor cell immunophenotypes were CD4−CD8+CD56+ in 4 cases, CD4−CD8+CD56− in 1 case, CD4−CD8−CD56+ in 2 cases, and CD4−CD8−CD56− in 1 case.

Using array comparative genomic hybridization analysis to spot recurring genomic alterations, the team found chromosome 9q33-q34.1 gain in four of five patients, chromosome 6p21.1-21.31 gain in three of five (60%), chromosome 6p21.1-21.31 gain in three of five (60%),  and chromosome 3p12.1-p12.2 and 3q26.31 loss in two out of five (40%).

These results show type 2 enteropathy-associated T-cell lymphoma to be the most prevalent type in this geographic region, and that associated genetic changes are similar to those in Western countries.

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F. Mühr-Wilkenshoff, M. Friedrich, H. D. Foss, M. Hummel, M. Zeitz, and S. Daum made up the research team. They are variously affiliated with the  Medical Clinic I, Gastroenterology, Rheumatology and Infectious Diseases, and with the Department of Pathology, Charité of the Campus Benjamin Franklin of University Medicine Berlin, Germany.

About 20–30% of all non-Hodgkin lymphomas (NHLs) are gastrointestinal in nature. Of these gastrointestinal lymphomas, about 20–30% occur in small intestine

The clinical team recently reported the case of a 72-year-old patient who had been diagnosed with celiac disease when he was 52-years old. The man had not followed a gluten-free diet, yet showed no evidence of enteropathy or celiac-associated antibodies, but still developed a jejunal T-cell lymphoma.

Doctors resected the lymphoma due to perforation and treated the patient with four courses of IMVP-16. The patient began and maintained a strict gluten-free diet.

Two years later, the patient appeared with weight loss and a clonally divergent refractory sprue type II with loss of antigen (CD8; T-cell receptor-) expression in intraepithelial lymphocytes.

At this time, he showed high titers of celiac-associated antibodies, although he was on a strict GFD.

The research team notes that the missing enteropathy under a gluten-containing diet supports the idea of immune suppression in malignant diseases, especially non-Hodgkin lymphoma.

They also note that the fact that, even while maintaining a strict gluten-free diet, the patient developed refractory sprue type II, an early form of another independent T-cell lymphoma, along with celiac-associated antibodies, suggests that clonal intraepithelial lymphocytes might be stimulating antibody production.

Thus, they conclude that isolated detection of celiac-associated antibodies in patients with celiac disease does not prove that patients have deviated from their gluten-free diets.

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Celiac disease (celiac disease) is the most common food intolerance disorder affecting Western civilization today. While most celiacs show an improvement in their health after  initiating a gluten free diet,  2-5%  of patients do not improve, and are thus considered to have refractory celiac disease (RCD).

RCD is further classified into two categories, Type 1 with intraepithelial lymphocytes of normal phenotype, or as type 2 with clonal expansion of intraepithelial lymphocytes with an aberrant phenotype. Type 2 patients are expected to have a five year overall survival rate (OS) of 50%-58%, and most Type 2 RCD  patients die from EATL.

EATL generally affects older patients in their 60's or 70's, with a history of celiac disease or RCD, and is most frequently presented in the form of malabsorption along with abdominal pain. However, EATL is not exclusive to patients with celiac disease or RCD and has also been found in patients without a history of either. Standard treatments until now have included surgical resection, with or without anthracycline-based chemotherapy, or high-dose chemotherapy with autologous stem cell transplant (ASCT). Results of these treatments have been dismal, with the patient typically dying from disease related complications.

Using a population-based setting, 26 EATL patients that qualified for intensive treatment were given the new aggressive treatment of, ifosfamide, vincristine, etoposide / methotrexate (IVE/MTX) &  ASCT, and their results were compared to that of the historical group. Statistically there was no difference between the groups; all groups had similar age, sex and features at initial evaluation. For all patients treated with the historical cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) therapy, the average PFS rate was approximately three months, and the average OS rate was about seven months. However,  the IVE/MTX - ASCT group showed a significantly higher five year PFS and OS compared to patients treated with the  historical CHOP therapy. Additionally, patients treated with IVE/MTX - ASCT showed improvement in their remission rates, and had profound reduction of death rates compared to the group treated with the historical CHOP chemotherapy. Of the patients that were solely treated with surgery, none survived.

While EATL has a somber outcome for most patients treated with conventional CHOP treatments, data collected from these tests reveal that the regime IVE/MTX – ASCT shows exceptional promise as a new treatment. It is recommended that EATL patients enter themselves into national studies like this one, to expand research data and to help explore potentially effective EATL treatment options.

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Previous studies done in the 1970s and 1980s indicated that patients with clinically recognized celiac disease face a higher risk for developing malignancies, Dr. Katri Kaukinen, of the University of Tampere, Finland, told reporters from Reuters Health. However, she explained, "it has not been known whether apparently clinically silent unrecognized cases also carry an increased risk of celiac disease-related complications, and thus whether the healthcare system should recognize and treat."

In an effort to answer that question, Dr. Kaukinen led team of researchers in assessing whether adults with previously unrecognized screening-identified evidence of celiac disease have an increased risk of malignancies.

Recent screening figures put the prevalence of celiac disease somewhere between 1% and 2% of the population, which means from 7 to 14 million Europeans with gluten intolerance. 75% to 90% of all the celiac disease remains undiagnosed due to absent or atypical symptoms.

The team examined data from a Finnish population-based adult-representative cohort of 8000 subjects compiled from 1978 to 1980. In 2001, the researchers screened blood samples of people with no history of celiac disease or any malignancy (n = 6849) for immunoglobulin A (IgA) class tissue transglutaminase antibodies. They further screened
positive samples for IgA class tissue transglutaminase antibodies (Celikey tTG) and for IgA endomysial antibodies (EMA).

The team analyzed a total of 6849 blood samples. 565 samples showed positive Eu-tTG results. 202 of these subjects showed positive Celikey tTG results ((2.9%) while 73 showed positive EMA screens (1.1%).

Just over 10% of the study subjects, a total of 694 participants, developed malignancies during the period of the study. Overall malignancy risk was no higher for celiac autoantibody-positive subjects. Adjusted for age and sex, the results showed that the relative risks were 0.91 for those who were Celikey tTG positive, and 0.67 and for those who were EMA positive.

According to Dr. Kaukinen, the results seem to support the current clinical approach, and suggests that "earlier diagnosis of the disease through serological mass screening would not be beneficial in improving the prognosis of celiac disease as regards malignancies."

However, before completely ruling out mass screening, Dr Kaukinen noted that it is important to pursue "further prognostic studies [on] mortality and fractures among earlier unrecognized celiac disease cases," as "[t]hese issues should be also addressed" before any official decisions are made regarding the use of mass blood screening for celiac disease.

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Quercetin is a tiny, but powerful compound that is easily absorbed from onions, peppers, tomatoes and most other common produce. According to Turner, nearly all plant-based foods offer "some level of quercetin," including "fun things like wine."

Previous laboratory research has shown quercetin to be effective in reducing rates of colon cancer, but Turner's study is the first to illuminate the mechanism by which quercetin works its magic.

These results offer researchers another line of inquiry into other inflammatory bowel diseases such as Crohn's and celiac disease, as it's quite likely that quercetin can offer some measure of protection against those conditions as well.

According to Turner, the levels of quercetin used in the study are comparable to those "achieved in diets around the world such as...the Mediterranean-style diets." As such, reaching such levels in American diets is "not an unachievable goal," she said.

In the study, Turner's research team observed the responses of rats to quercetin-supplemented diets. Some of the rats were in the early stages of colon cancer formation, while others were cancer-free. In people, as in animal models, early colonic lesions represent some of the very first pre-cancerous changes that can be seen visually. These so called  "aberrant crypts," are thought to mark or predict tumor formation.

Earlier studies have shown quercetin to reduce the number of these crypts, but Turner "wanted to know how it might be protecting."

Cancer is commonly understood as uncontrolled cell growth, but researchers are now realizing that the normal action of cell death, a process called "apoptosis," plays a crucial role in allowing cancer to develop. Healthy bodies generally maintain equilibrium between the generation of new cells and sloughing off cells that have completed their job. Quercetin seems to play a beneficial role in both cases. It decreases the number of cells being generated in the colon [and] increases the number of cells that were undergoing apoptosis. In all, quercetin helps to maintain a normal number of cells.

The research team then turned its attention to the relatively new discovery that inflammation is one of the prime instigators of colon cancer. The team focused on two enzymes, called Cox-1 and Cox-2. Cox-1 is a standard protein that the body usually exhibits. But Cox-2 has a potential role in a number of diseases. Turner explains that Cox-2 is an "inducible protein that is expressed in the body when there is some kind of external stimulus to a cell." Scientists consider high levels of Cox-2 "as being a bad thing."

Research shows that not only are elevated levels of Cox-2 present in colon cancer, but that the Cox-1 levels become elevated before Cox-2 levels rise. According to Turner, it seems that Cox-1 exerts some sort of influence over whether Cox-2 expression.

Both the control groups and the carcinogen-injected groups that consumed dietary quercetin had lower levels of both Cox-1 and Cox-2, suggests that there may be chance for quercetin to prevent tumor growth.

Clearly, further study is needed to better understand the links. But Turner encourages people to consume lots of fruits and vegetables. She points out that, in addition promising benefits for colon cancer, quercetin has demonstrated positive influence in fighting other chronic ailments such as cardiovascular disease.

*Turner's research was funded by the U.S. Department of Agriculture . Source: Open Original Shared Link

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.

There are two types of refractory celiac disease (RCD). In RCD type I,  immuno-phenotype of intraepithelial lymphocytes (IELs) are normal and polyclonal, while RCD) type II, is noted for the presence of an abnormal intraepithelial lymphocyte (IEL) population (CD7+ CD3− CD4/8-cytoplasmic CD3+). More than half of people with this condition develop enteropathy-associated T-cell lymphoma (EATL), a rare but virulent form of cancer with high mortality rates.

A team of doctors recently set out to examine the relationship between lymphoma development and intraepithelial gamma/delta T-lymphocytes in the small intestine of patients with all types of celiac disease, as compared to the general population.

The team was made up of Wieke H.M. Verbeek, M.D., B. Mary E. von Blomberg, Ph.D., Petra E.T. Scholten, B.Sc., D. Joop Kuik, M.Sc., Chris J.J. Mulder, M.D. Ph.D., and Marco W.J. Schreurs, Ph.D., all from Amsterdam’s VU University Medical Center.

A certain type of IELs called TCRγ/δ+ IELs may play an important role in repairing mucosa, maintaining homeostasis, and guarding against tumor development. TCRγ/δ+ IELs in the human intestine have recently shown promise in the regulation of uncomplicated celiac disease.

In the study, the research team wanted to see if patients with RCD II had fewer TCRγ/δ+ IELs than either RDC I, or celiac disease, an thus provide a possible explanation for ongoing mucosal damage and inflammation, and the development of abnormal T cells that tend to morph into EATL.

The team used a method called multi-parameter flow cytometric immuno-phenotyping on IELs obtained from recent small bowel biopsy specimens from a fairly large, distinct celiac disease and control groups (N = 87).

Patients with RCD II showed a much lower ratio of TCRγ δ+ IELs compared to either RCD I or celiac disease patients. Whereas, patients with uncomplicated celiac disease showed significantly higher numbers of TCRγ δ+ IELs than were found in the control group. The results showed the relationship between TCRγ δ+ IELs and aberrant IELs to be negative. It is interesting to note that TCRγ δ+ IELs numbers do rise in RCD II patients after effective treatment.

The negative relationship between TCRγ δ+ and abnormal IELs, together with their known role in regulating uncomplicated celiac disease, suggests that TCRγ δ+ IELs may play a crucial role in helping the body to repair mucosa, maintain homeostasis and possibly even guard against tumor development.

These cells may serve as important markers, along with the abnormal T cells, to help distinguish between types of celiac disease, and to gage the effectiveness of treatment efforts.

Am J Gastroenterol 2008;103:3152–3158

Recently though, a team of doctors at the National Cancer Institute in Bethesda, Md., led by Ying Gao, M.D., has discovered that siblings of celiac patients also face an increased risk of developing NHL. Results of the study appeared in the January issue of Gastroenterology.

The research team conducted a study using 37,869 patients with NHL, 8,323 with Hodgkin's lymphoma, and 13,842 with chronic lymphocytic leukemia who were diagnosed between 1965 and 2004. The study included 236,408 matched controls and 613,961 first-degree relatives.

The results indicated that people with celiac disease developed NHL at rates that were 5.35 times higher than non-celiacs, but that they faced no increased risk for developing Hodgkin’s lymphoma or chronic lymphocytic leukemia.

In some good news, the doctors found that the NHL risk level for people whose celiac disease was diagnosed between 1995 and 2004 dropped to just 3.86 times greater than for non-celiacs. This is a significant improvement over the 13.2 times greater risk of NHL faced by people diagnosed with celiac disease between 1975 and 1984.

However, the study also showed that siblings of celiac disease patients developed NHL at rates that were more than double those of the general population (2.03).

Clearly, as diagnosis and treatment of celiac disease has improved, the risk levels for NHL have decreased. The study underscores the need for greater vigilance on the part of both doctors and patients regarding NHL, and for greater understanding of the mechanisms that influence the development of NHL in both celiacs and non-celiacs.

As diagnosis and treatment and monitoring of celiac disease improves, and as understanding of NHL increases, it is likely that NHL risk levels for celiac patients will drop even further. Until then, celiac patients are encouraged to stay informed, stay vigilant, and to consult with a physician to keep on top of any developments that may influence risk levels for NHL.

Journal of Gastroenterology, January 2009; pp 91-98.