by Brooke Keefer
A few years ago my doctor told me, “You know, they’ve discovered Sphincter of Oddi Dysfunction isn’t real.” He said this two months after my transduodenal sphincteroplasty, a major abdominal surgery in which my pancreatic and biliary sphincters controlling the flow of bile and pancreatic juices were sewn open. This surgery was my last ditch effort to regain my life and health from Sphincter of Oddi Dysfunction (SOD). I lost my career, could not parent, and spent my days vomiting, in severe pain, and on a feeding tube. I was 90 pounds and the emergency and hospital rooms became my second home.
After a pause of shock I responded, “I’ll have to disagree. How do you explain my sphincter pressures measured six times above the norm on the manometry scale? Also, since the surgery I no longer have 24/7 nausea and vomiting or the right upper quadrant and pancreatic pain.” In this doctor’s defense, he was always very supportive and compassionate. He witnessed firsthand the suffering I endured from SOD. I knew his statement did not come from a place of malice. He simply read or heard something and was repeating it to me.
Prior to my surgery, I traveled 1,200 miles to the University of Minnesota to put a name to the mystery condition slowly killing me. There, I had an endoscopic retrograde cholangiopancreatography (ERCP) with manometry—the gold standard diagnostic test for SOD. I was diagnosed with SOD Type 3. There are three SOD types. All require high pressure of the sphincter and pain as a symptom. Type 1 patients have a dilated common bile duct (CBD), abnormal liver function tests, and delayed biliary drainage. Type 2 patients have one or two of the Type 1 features. Type 3 patients present with a pain syndrome only and high pressures. I was actually a Type 2 as I had a dilated CBD but didn’t question the doctor.
Unfortunately, my doctor’s comment about SOD was not an isolated incident. I oversee The Sphincter of Oddi Dysfunction Awareness and Education (SODAE) Network website (www.sodae.org), Facebook page, and support group. As such, I read and listen to countless stories of doctors telling SOD patients that SOD (primarily SOD Type 3) does not exist. Most astounding is nearly all of these patients have been diagnosed with SOD by manometry. When some of our newest members ask their doctors to determine SOD as a diagnosis, they are told they do not have it and to move on. We are witnessing an epidemic in our community as too often those with SOD are abandoned by their doctors, and often told their symptoms are psychological or related to stress. This is of great concern since over 90% of SOD patients are women. Patients either exhaust their savings to travel far and wide to see a doctor who will help them (yes, there are some fantastic SOD doctors out there) or, those who cannot afford that option, are left with no treatment options and in time deteriorate physically and mentally.
Over the summer I happened to meet a gastroenterologist from Boston who repeated, almost verbatim, what my local doctor said--that SOD was not real! He heard this at a gastroenterology conference where the results of a National Institutes of Health study—The Evaluating Predictors and Interventions in Sphincter of Oddi Dysfunction (EPISOD) study—were discussed. I was a participant in the EPISOD study and can say I was never questioned about the validity of my diagnosis or the method used to diagnose my SOD. In fact, only those diagnosed with SOD could participate.
Even more alarming is a recent article published in the American Gastroenterological Association’s Gastroenterology journal titled, “Endoscopic Sphincterotomy for Sphincter of Oddi Dysfunction: Inefficacious Therapy for a Fictitious Disease”. This newfound opinion that SOD no longer exists is based on the fact the treatment at the center of the study did not relieve symptoms in all participants—not that SOD could not diagnostically be proven. That treatment was a sphincterotomy, where the sphincter is cut so it will provide greater access for fluids to flow rather than get backed up. Theoretically, if the treatment did not relieve the patient’s symptoms, then the problem could not originate in the sphincter. This makes absolutely no sense. Would we say other diseases measured by symptomology and/or diagnostic methods do not exist when a treatment is found to be ineffective, i.e. cancer, multiple sclerosis, Alzheimer’s, etc.? Researchers and medical professionals could instead postulate arguments for why this is happening. As we know, many diseases cause secondary conditions. It is quite possible SOD began as a primary condition, but as it precipitated (it often takes years to obtain a diagnosis), it spawned secondary issues like ductal spasms, nerve and/or visceral hypersensitivity, malnutrition, or gut dysmotility. The original disease did not change. It was always there. However, once the sphincters were cut, the body still had these secondary issues.
It is reckless to publish assumptions that SOD is fictitious and even more reckless for a medical professional to take it upon him- or herself to discredit decades of evidence-based research determining SOD as a very real disorder. Hundreds of these studies can be viewed on the NIH PubMed website. Moreover, within the past few years, research articles validate the diagnostic validity of SOD in such publications as The Journal of Gastrointestinal and Liver Disease, The Journal of Neurogastroenterology and Motility, The American Journal of Gastroenterology, and The Journal of Gastrointestinal Surgery.
Rather than spending valuable time slamming SOD, sufferers are in dire need for researchers, policymakers, and the medical profession to spearhead and fund research to identify the cause of this condition. By learning the exact nature and cause of SOD, we can then move on to identify and develop effective treatments and preventative measures. Of particular note is the need for investigating the possibility of a genetic and/or hormonal cause to SOD, since over 90% of sufferers are women. No such study has been initiated outside of a prairie dog study conducted in 1994 determining estrogen inhibited sphincter of oddi motility.
Sources and Links:
U.S. National Library of Medicine National Institutes of Health
Effect of Endoscopic Sphincterotomy for Suspected Sphincter of Oddi Dysfunction on Pain-Related Disability Following CholecystectomyThe EPISOD Randomized Clinical Trial
Estrogen Inhibits Sphincter of Oddi Motility