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Crohn's, methotrexate and calprotectin test

I am 61 yrs old, have had pan Crohn's colitis for some 35 yrs. Breast cancer 3 yrs ago. Steroid dependent. My gasto prescribed self administered 12.5 mg injections of methotrexate weekly in Jan 06 but this was not keeping the morning diarrhea under control - I have lost some 22 lbs in the last year with no dieting - I weigh 110 lbs, 5'2". Recent small bowel follow through showed stricturing in the small bowel, which have not had before. Saw Gastro last week,  prescribed Cipro for 7 days, 3 weeks off, then another course. It has brought the D under control. I had full blood tests last week and a stool test for calprotectin, no results yet.  Had this done 3 yrs ago and it was elevated. One of the blood test forms said "Leukaemia?" which worries me as I had FEC chemo and rx for breast cancer.  How serious is this, and what does the test mean? He is very reluctant to increase the mtx or to prescribe more prednisone because of bone marrow, osteoporosis and post bc treatment risks. Every colonoscopy or examination I have had with him has shown active Crohn's. He said I have "empirical problems" and doesn't really know what to do. A second opinion is out of the question as he is the best gastro at my current hospital and being on socialised medicine cannot go out of area without a lot of hassle.  London, where there is a specialised hospital for IBD (St. Marks at Harrow, Middlesex) is some 280 miles away and would mean logistics/family problems as I have a disabled husband.
Do you have any advice as to my current situation and what I can do in the future regarding medications? I have tried azathioprine (sp?) and was violently allergic; flagyll makes me sick. Remicade is not indicated as I do not have fistulising disease and this is req'd under funding rules here in the UK for this drug.Any insight you have will be most appreciated.Thank you for your time.
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233190 tn?1278549801
MEDICAL PROFESSIONAL
A fecal calprotectin test is used to differentiate between inflammatory and non-inflammatory causes of chronic diarrhea.  However, this test is normally in the investigational stages.  

You are right that Remicade isn't first-line therpy in non-fistulizing disease.  However, if methotrexate and azathioprine are not options, then you can consider Remicade as a second or third-line therapy.  

Another option would be the use of chronic low-dose steroids, however this would be a last-resort option.

Discussion of these options should be made with your gastroenterologist.  

Followup with your personal physician is essential.

This answer is not intended as and does not substitute for medical advice - the information presented is for patient education only. Please see your personal physician for further evaluation of your individual case.

Kevin, M.D.
kevinmd_
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Avatar universal
Humira may work for you. Humira suppresses the immune system and is FDA-approved for treatment of rheumatoid arthritis. A study involved 13 patients with Crohn's disease. All had been taking Remicade, but were no longer getting any relief from it. In the six-month study, they got an initial 80-milligram injection of Humira, then 40-milligram injections every two weeks. Researchers tracked their symptom relief. Of the 13 patients, seven had complete symptom relief, four had partial relief, and two got no relief. Six of the patients required a boost in their dosage to maintain symptom relief. Almost three quarters of the patients (73%) were able to discontinue or significantly decrease their concurrent dose of steroids. All patients tolerated Humira without any allergic reactions; two patients had a skin reaction at the injection site. Overall, the study shows that Humira is a strong option for Crohn's disease patients.
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Avatar universal
Lizzie,

fecal calprotectin can be used to monitor disease activity.  here's the latest info.

CRP, Fecal Calprotectin Good Markers for IBD Diagnosis, Monitoring

NEW YORK (Reuters Health) Feb 27 - C-reactive protein (CRP) and fecal calprotectin are useful markers in the management of inflammatory bowel disease (IBD), but should be seen as an adjunct to rather than a replacement for clinical observation and physical examination, the authors of a new review conclude.

Evidence for the usefulness of other lab tests, such as erythrocyte sedimentation rate (ESR), as markers for IBD is lacking, they add, while none have been shown to be as effective as CRP.

There is currently no "gold standard" for diagnosing Crohn's disease (CD) or ulcerative colitis (UC), monitoring the effects of therapy, and determining prognosis, Dr. Severine Vermeire of the University Hospital Gasthuisberg in Leuven, Belgium and colleagues note in the March issue of Gut.

Lab tests have long been investigated as a means of objectively evaluating IBD patients, as well as an alternative to endoscopic procedures, the researchers add. But there is currently no single test that offers an ideal marker for IBD, meaning that it is simple, easy, minimally or non-invasive, cheap, fast and reproducible.

CRP, with its short half life of 19 hours, makes it effective for monitoring the onset and resolution of inflammation, the researchers note. It is the most extensively studied of all lab markers in IBD, and the most useful, but correlates more closely with disease activity in CD than in UC. It is also more specific for diagnosing CD than for UC.

A change in CRP levels is a good parameter for monitoring the effectiveness of treatment, the researchers note. Also, higher CRP levels predict a good response to anti-tumor necrosis factor treatment, while lower and normal levels are linked to a better response to placebo.

Studies have also shown that fecal calprotectin can be used to help diagnose both CD and UC, and is also an effective marker of disease activity in both conditions. Evidence suggests it is more effective in UC than in CD, the researchers note.

The use of lab and fecal markers to predict the course of IBD is less clear, especially for UC, they add.

"Whereas other acute phase reactants and markers of inflammation such as ESR also give reliable information on disease activity, their longer half life and interference with other factors make them less useful in clinical practice compared with CRP," the researchers write. They conclude that laboratory markers can indeed be useful, and should be a part of overall management of IBD patients.

Gut 2006;55:426-431.

and from Medscape:
Fecal Calprotectin and Prediction of IBD Relapse
Until recently, the utility of measuring intestinal inflammation directly as a means of predicting relapse has not been assessed. Indium leukocyte scanning and quantitative fecal 111indium-labeled leukocyte excretion have been used for localization of disease and assessment of disease severity, respectively, in patients with IBD.[17,18] However, the exposure to radiation and the 4-day collection of stools make it an unsuitable method for outpatient monitoring of mucosal inflammatory activity.
A recent study has demonstrated the usefulness of fecal calprotectin in predicting relapse of IBD.[19] Calprotectin, first isolated from granulocytes by Fagerhol and colleagues,[20] was initially termed "L1 protein," but subsequent to the identification of its calcium binding and antimicrobial properties, was renamed "calprotectin."[21] Within the neutrophil, calprotectin is found in the extra lysosomal cytosol, and constitutes up to 60% of the cytosolic protein fraction of these cells.[22] Calprotectin resists metabolic degradation by intestinal bacteria and is stable in stool for up to 1 week at room temperature.[23] Fecal calprotectin levels correlate significantly with histologic and endoscopic assessment of disease activity in ulcerative colitis (UC),[24] as well as with fecal alpha-1-antitrypsin levels and fecal excretion of 111indium-labeled white blood cells in patients with CD.[23, 25-27]

In patients with clinically quiescent IBD (UC and CD), it was shown that fecal calprotectin levels greater than 50 mg/L could be used to predict the likelihood of clinical relapse of disease within a few months, with over 80% sensitivity.[19] Most patients with quiescent IBD have low-grade inflammation,[28] and it is suggested that symptomatic relapse occurs only when the inflammatory process reaches a critical intensity. Furthermore, if inflammation is a continuous process, it may be that direct assessment of the level of inflammatory activity can provide a quantitative presymptomatic measure of imminent clinical disease relapse.

to see footnote references, go here:  http://www.medscape.com/viewarticle/407971

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