Reviews for Primary Care - Fall 2007 - (Page 26) Chronic Constipation and Functional Bowel Disorders continued As for insurance companies in the United States, this is an issue. You can get insurance companies to pay for biofeedback training if you are willing to write a standard letter that goes through the tests that were done, the assessment, and the diagnosis, as well as provide copies of all literature supporting its use. We have found that usually after this type of approach they will back down and actually will allow reimbursement for biofeedback training. Panel: Reimbursement with insurance is problematic everywhere. One approach that has been successful is to outsource the training to physical therapists who work with both urology and constipation patients. They bill it under muscle rehabilitation and do not use the word biofeedback because it is a red flag for many insurance companies. Honestly, now that we have 4 well-done studies by very good people all showing pretty much the same benefits of biofeedback, there should be a concerted effort from clinicians to make sure that the insurance companies now recognize biofeedback as a viable therapeutic option. Panel: One important thought to keep in mind as you attempt to utilize biofeedback and send studies off to insurance companies in support of it is that typically the patients in those studies already had failed first-line therapy. Biofeedback is not a first-line therapy. It is second- or third-line therapy. That is the key. Panel: There are certainly people out there who have dyssynergic defecation who respond to the laxatives, lubiprostone, and so forth. You cannot begin to identify those, but when they fail conventional therapy, then the stakes are higher, and only then do you do the studies. If you ultimately do the studies, you need to be ready to act on the results that you get. Do not do a study if you are not going to use the data meaningfully. So, when you commit to that study, you are going to commit to trying to do something based upon your findings, and in that small subgroup, we can make a very strong case for biofeedback now. Question: What is the role of impaired rectal sensation in the development of constipation? Is it cause or effect, or maybe both? Panel: The answer is we do not know. The researchers study large groups of patients who seem to have lower thresholds of sensation, but it would be very difficult to know which came first, the chicken or the egg, and it is not something to worry a lot about in terms of clinical practice. However, if megarectum or something of that order is present, it would be considered somewhat important in the development of constipation. Question: Could you please compare and contrast the mechanisms of action of misoprostol and lubiprostone? Panel: Misoprostol works through a prostaglandin receptor, so it has a number of effects, not only on chloride secretion but also on other things like motility.25 On the other hand, lubiprostone is an agent that is not absorbed, so in theory its action is topical.29 It acts specifically on ClC-2, which presumably would mean that it has fewer of the other side effects of misoprostol. Question: For slow-transit constipation, does one need to make the distinction between proximal versus distal slow transit? Does that distinction make any difference in treatment? Panel: You can certainly see regional transit differences on either scintigraphy or on colonic marker studies; however, the data overall suggest it does not really matter. Frankly, if you have to take the colon out, you take the whole colon out, which is actually part of the problem. If you are ever thinking about a colectomy in a patient, you need to do 3 things: • You should repeat the transit test. There have been reports of abnormal tests becoming normalized despite the fact that the patient is still constipated. • Pelvic floor disorders must be ruled out. This already has been emphasized. • Look for evidence of small intestinal abnormality because pseudo-obstruction is a disaster if you take the colon out. Question: Approximately 20% to 30% of patients taking lubiprostone in clinical trials report having nausea. Is this a realistic expectation in clinical practice, and is it persistent? Panel: Frankly, it is completely unknown. There is one theory espoused that the nausea caused by lubiprostone might be a result of small intestinal distention that causes the release of serotonin, which then is mediating some nausea in the central nervous system. On the other hand, for a “topical” agent to do this would be very unusual. Because lubiprostone is not systemically absorbed,25 it should rule out any normally suspected systemic cause. There does seem to be less nausea if you give the drug with food,25 and it appears in clinical practice to be present in young females more than in males and the elderly. Question: Is there any evidence for activation or modulation of the CFTR channel with lubiprostone, and why is the compound selective for ClC-2? Panel: At this point there is no evidence that lubiprostone activates the CFTR channel. It is also unlikely that 26 VOL. 1 NO. 1 2007 REVIEWS FOR PRIMARY CARE
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