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    Collagenous Sprue Patients Achieving Relatively Good Clinical Outcomes


    Jefferson Adams

    Celiac.com 12/07/2009 - Collagenous sprue is associated with high morbidity, but the etiology of this condition is poorly understood. There is little data concerning the pathological and clinical manifestations of patients with collagenous sprue. The research team set out shed some light on the etiology, disease manifestations and outcomes of collagenous sprue.


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    A team of researchers recently undertook a clinico-pathological study of 19 patients with collagenous sprue and found that the condition does not always end badly for the patient.

    The research team was made up of Efsevia Vakiani, Carolina Arguelles-Grande, Mahesh M Mansukhani, Suzanne K Lewis, Heidrun Rotterdam, Peter H Green and Govind Bhagat. They are associated with either the Department of Pathology at New York's Memorial Sloan-Kettering Cancer Center, or with Columbia University's Department of Medicine or of Pathology.

    The team searched their departmental database covering the periods from 1999–2008 to identify cases of collagenous sprue and to gather clinical and lab data.

    The team evaluated small bowel histology, including thickness of sub-epithelial collagen, intra-epithelial lymphocyte phenotype and results of T-cell clonality assays.

    The found nineteen patients (15 women, 4 men, age 22–80 years, mean 57 years). Seventeen (89%) suffered from celiac disease and two from unclassified sprue. 9 of 17 (53%) celiac disease patients had refractory disease; 5 of 15 (33%) presented atypically without diarrhea, including 2 of 6 (33%) with active (untreated) celiac disease, and 3 of 9 (33%) with refractory celiac disease.

    They found autoimmune disorders in 12 of 19 (63%) patients and microscopic colitis (n¼7), lymphocytic gastritis (n¼2) or collagenous gastritis (n¼2) in nine patients.

    Thickness of subepithelial collagen increase varied from mild (n¼6), moderate (n¼10), or marked (n¼3), and
    villous atrophy from total (n¼13) to subtotal (n¼6).

    In no case did they find phenotypically aberrant intraepithelial lymphocytes. The only patient with refractory celiac disease type II showed a dominant T-cell clone with polymerase chain reaction analysis. 7 of 11 (64%) patients showed histological improvement.

    Overall, 8 of 19 (42%) responded favorably to a gluten-free diet, including 2 of 9 (22%) with refractory celiac disease. 10 of the 19 patients responded to immuno-modulatory therapy, including 6 of 9 (67%) with refractory celiac disease.  Only one patient died from the effects of refractory celiac disease. No patient developed lymphoma. The vast majority of patients with collagenous sprue did have celiac disease.

    Even though numerous patients required immuno-modulatory therapy to control symptoms, many responded to gluten-free diet alone.  The researchers conclude that most collagenous sprue patients have relatively good clinical outcomes.

    Source:
    Modern Pathology 23 October 2009; doi:10.1038/modpathol.2009.151

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    Guest Deborah

    Posted

    Collagenous sprue is defined as a condition in which extensive deposits of collagen are dumped into the intestine. Since animal products are the source of pre-formed collagen, it may be that people with this condition may require a vegan diet (plant foods only), as well as eating gluten-free.

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    Guest Harry Trent

    Posted

    I found the stats presented in paragraph 6 of this article impossible to understand.

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    my husband almost died from this disease, not many could or would help. he had to go to another state for treatment. still, we are still in the dark about what to expect and what and how do we deal with side affects? We used to hear the words deadly and fatal but they found another disease that makes too much iron in the blood. We hope one caused the other but any insight would be helpful.

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  • Related Articles

    Jefferson Adams
    Celiac.com 02/05/2010 - Collagenous sprue is classically understood as a disorder of the small intestinal mucosa marked by persistent diarrhea, severe malabsorption with multiple nutrient deficiencies, and progressive weight loss.
    H. J. Freeman of the Department of Medicine, University of British Columbia Hospital, Vancouver, BC, Canada offers an update on collagenous sprue.
    Patients with collagenous sprue typically show a severe to variably severe "flattened" mucosal biopsy lesion with distinctive sub-epithelial deposits in the lamina propria region.  These deposits contain collagens, as demonstrated by both histochemical stains and ultrastructural studies.
    Moreover, permanent disappearance of these deposits after resection of a localized colon cancer suggests that this disorder might actually involve a para-neoplastic morphologic marker of an occult malignancy.
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    A number of studies demonstrate gastric and/or colonic associations with the unusual inflammatory mucosal process in collagenous sprue, which suggests that the condition may be more complex and have more varied contributing causes than presently understood.
    Source: World Journal of Gastroenterology. 2010 Jan 21; 16(3):296-8
     


    Jefferson Adams
    Celiac.com 05/04/2010 - A team of clinicians recently set out to assess the effectiveness of treating collagenous sprue with a combination of gluten-free diet and steroids.
    The team was made up of Alberto Rubio-Tapia, Nicholas J. Talley, Suryakanth R. Gurudu, Tsung-Teh Wu, and Joseph A. Murray. They are affiliated variously with the Division of Gastroenterology and Hepatology of the Mayo Clinics in Scottsdale, Arizona, Jacksonville, Florida, and Rochester, Minnesota, and the Division of Anatomic Pathology in Rochester Mayo Clinic.
    Deposits of subepithelial collagen that form a distinctive band in the small bowel are one of the clinical hallmarks of collagenous sprue.
    For the study, the team evaluated clinical characteristics, treatments, and outcomes of patients with collagenous sprue. The team looked at medical records for thirty patients with collagenous sprue from the Mayo Clinics from Scottsdale, Jacksonville, and Rochester, for the periods covering 1993 and 2009.
    21 of the patients were female (70%), ranging in age from 53–91 years. The majority of patients suffered from severe diarrhea and weight loss.
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    Subjects showed subepithelial layers of collagen deposits in the small bowel ranging from 20 –56.5μm, and averaging 29 μm thickness. Eight patients showed subepithelial collagen deposits in the colon or stomach.
    24 patients (80%) showed a positive clinical response to treatment with a combination of a gluten-free diet and immunosuppressive drugs. Nine patients showed confirmed histologic improvement, while five patients experienced complete remission. Of two patients who died, one succumbed to complications from collagenous sprue, while one died of another illness.
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    Source:

     Clinical Gastroenterology and Hepatology 2010;8:344–349. doi:10.1016/j.cgh.2009.12.023

    Diana Gitig Ph.D.
    Celiac.com 05/27/2011 - Refractory Celiac Disease (RCD) is exactly what it sounds like: persistent malabsorption symptoms and intestinal villous atrophy even after following a gluten free diet. It is divided into two subtypes. RCDI has normal intraepithelial lymphocytes (IELs) while RCDII has abnormal IELs. RCDII is by far the more severe - there is no effective treatment, and it is often fatal within five years. Recent studies in Amsterdam and Paris have reported that RCDII can account for 28-75% of RCD patients. A group of researchers led by Ciaran Kelly at the Celiac Center at Beth Israel Deaconess Medical Center in Boston, the only specialized celiac center in New England, set out to determine if the same was true in the United States. They found a much lower incidence, 17%, of RCD patients with RCDII.
    An editorial by Malamut and Cellier accompanying Kelly's report in the American Journal of Gastroenterology suggests a number of factors that could account for the difference. Primary among them is the different methodology used to diagnose RCDII. In the US study only one method, immunohistochemistry, was used to ascertain whether the IELs were normal or not; in Europe they used three independent experimental techniques to confirm this data. The American researchers note that if they had in fact underdiagnosed RCDII they should have seen more severe cases of RCDI, and they did not. Malamut and Cellier point out that the Boston study may also have overdiagnosed RCDI by examining biopsy samples done only six months after institution of a gluten free diet, when villous atrophy may not have completely healed. An inflated number of RCDI cases would generate an erroneously low percentage of RCDII cases. But the Americans note that only four of the thirty-four cases of RCD they examined were from patients who had been on a gluten free diet for less than a year.
    Alternatively, the relative dearth of RCDII cases in the US as compared to Europe could be attributed to the different genetic backgrounds of the populations involved - the "melting pot" present in the US rather than the older stocks that may be in Europe. It has been reported that RCDII correlates with HLA-DQ2 homozygosity, and in fact, the HLA-DQ8 allele was found to be more common in celiac patients in New York than in those in Paris. It is also possible that an environmental factor, such as the amount or type of gluten consumed before diagnosis, could account for the discrepancy, but this remains to be investigated. Therapeutic options for the aggressive RCDII are still severely limited; research into it should certainly continue, on both continents.
    Sources:

    Roshan et al. The Incidence and Clinical Spectrum of Refractory Celiac Disease in a North American Referral Center. The American Journal of Gastroenterology 2011; 106: 923-928. Malamut and Cellier. Is Refractory Celiac Disease More Severe in Old Europe? The American Journal of Gastroenterology 2011; 106: 929-932.

    Jefferson Adams
    Celiac.com 09/21/2012 - Refractory celiac disease type II (RCDII) is a severe complication of celiac disease that occurs when symptoms and intestinal damage continue even when the patient adopt a gluten-free diet. Refractory celiac disease marked by abnormal intraepithelial lymphocytes (IELs) of unknown origin that display an atypical CD3(-)CD7(+)icCD3(+) phenotype. About 40% of patients with RCDII lymphocytes develop a dangerous and invasive lymphoma.
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    The team hypothesizes that the IL-15 cells are the counterpart of abnormal cells that are expanded in RCDII and transformed in RCDII-associated lymphoma.
    Source:
    Gut. 2012 Jul 6.

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    Dr. Ron Hoggan, Ed.D.
    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.
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    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.
    Sources:
    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.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    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.

    Jefferson Adams
    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). 
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    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. 
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    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. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023