Sphincter of Oddi function and dysfunction: TREATMENT OF SO DYSKINESIA
Sphincterotomy for patients with SO dyskinesia has been shown not to improve symptoms and cannot be recommended, especially in view of the increased risk of pancreatitis in patients with SO dysfunction. The role of pharmacotherapy is somewhat unclear because there are few well conducted studies using manometric criteria for the diagnosis of SO dysfunction. The main drawback is that there are no drugs that appear to be specific for the SO, are long acting and free of side effects. Nifedipine has been shown to reduce significantly SO basal pressure when given sublin- gually to patients with SO dyskinesia during SO manometry. Two studies have evaluated oral nifedipine for up to 12 weeks in patients with manometrically diagnosed ‘SO spasm’ and suspected type 2 SO dyskinesia (ie, no manometry). Both studies found that, compared with placebo, there was a significant decrease in pain episodes and pain scores. The therapy was well tolerated, but concerns still exist regarding the potential for systemic side effects of hypotension, flushing and headaches.
Glyceryl trinitrate given sublingually during SO manome- try has been shown to decrease SO basal pressure in patients with suspected pancreatobiliary disease. However, no long term study has been undertaken using nitrates in patients with SO dysfunction.
Intrasphincteric injection of botulinum toxin has been shown in animals to relax the SO. It has also been used in an attempt to predict which patients may respond to further treatment, either by repeat injections of botulinim toxin or other therapy. The two patients who were treated showed an objective decrease in SO pressure for up to four months, but clinical improvement was not evident. Given the lack of clinical response, the need for repeat injections and concerns regarding the risks that the injection process may induce pancreatitis, intrasphincteric injection of botulinum toxin cannot be recommended for clinical use.
It has taken over 100 years to provide the data to support Ru- gero Oddi’s original observations on the function and dysfunction of the SO. With our increased understanding of its normal physiology, we hope that it will not take as long to understand the mechanisms that control its motility and then malfunction to produce SO dysfunction. SO ma- nometry remains the ‘gold standard’ for correctly diagnosing and stratifying treatment for patients with SO dysfunction. Biliary scintigraphy shows promise as a nonin- vasive screening investigation for patients with suspected SO dysfunction. For patients with SO stenosis, sphincter- otomy is the treatment of choice. For patients with SO dyskinesia, pharmacotherapy may prove helpful in some patients, but systemic side effects may limit their use. Further studies into pharmacotherapeutic agents and botulinum toxin are needed.
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