Category Archives: Gastroenterology

“If this was celiac, why didn’t it stop when she cut out gluten?”

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Here’s a link to a well-described case report. Her Searing Gut Pain Suggested Celiac Disease. Why Didn’t Cutting Out Gluten Help?

This 57 year old with ‘presumptive’ celiac disease did not improve with a gluten-free diet.  After an initial self-diagnosis and subsequently an endoscopy that also suggested celiac disease, she did not improve.  While the doctors involved in her care had labeled her ‘noncompliant,’ it turns out she did NOT have celiac disease and improved after the right diagnosis (diagnosis noted at bottom of this post).

My take: There are several entities that can mimic celiac disease (even histologically), including Crohn’s disease, Autoimmune enteropathy, CTLA4 deficiency, and Whipple’s disease (the diagnosis in this case).  When someone is not getting better, the diagnosis needs to be reconsidered.

Expert Advice on Bloating

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A recent article (AK Kamboj, AS Oxentenko. Clin Gastroenterol Hepatol 2018; 16; 1030-33) provides some useful guidance on bloating.

They describe bloating as an acronym:

  • Bowel disturbance (constipation, SIBO, celiac, IBD)
  • Liquid (ascites)
  • Obstruction
  • Adiposity
  • Thoracic (overexpansion, diaphragm contraction)
  • Increased sensitivity (functional bloating, IBS, dyspepsia)
  • Neuromuscular (gastroparesis, impaired accommodation, medications)
  • Gas (aerophagia, dietary sources, post-Nissen)

The diagnostic approach they recommend:

  • If bloating with diarrhea, evaluate diet, SIBO, celiac, IBD, IBS-D, and medications
  • If bloating with constipation, evaluate for constipation, pelvic floor dysfunction, IBS-C, and medications
  • If bloating and suspected mechanical disturbance, evaluate for gastric outlet obstruction/small bowel obstruction
  • If bloating without bowel disturbance, consider aerophagia, gastroparesis, and functional dyspepsia

Treatment:

  • Treat any underlying disorder
  • For mild symptoms, reassurance may be sufficient
  • Dietary modifications to avoid food triggers & reduce fermentable food products
  • Treating constipation when present
  • A large number of other treatments can be considered as well including antispasmotics, agents to help with visceral hyperalgesia, cognitive behavioral therapy

My take: I like BLOATING acronym, though the 5 Fs I learned a long time ago is a little easier for me to remember — which include flatus (gas), feces (constipation), fluid, fat, and fetus/masses. Flatus can be caused by swallowing air (aerophagia), malabsorption (celiac, lactose intolerance, parasites), muscular discoordination (abdominal phrenic dyssynergia), and motility problems.”

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Sunshine Meadows, Banff National Park

Clinical Practice Update: Extraesophageal Symptoms Attribute to Gastroesophageal Reflux Disease

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A recent practice update (MF Vaezi, D Katzka, F Zerbib. Clin Gastroenterol Hepatol 2018; 16: 1018-29) reviews the data and provides up-to-date recommendations for extraesophageal symptoms attributed to gastroesophageal reflux disease (GERD) in adults.

Extraesophageal symptoms attributed to GERD could include cough, asthma, hoarseness, sore throat, sinusitis, dental erosions, and ear pain.

Key recommendations:

  • Non-GI evaluations by ENT, pulmonary and/or allergy are essential and often should be performed initially in most patients.
  • “Abnormalities seen on endoscopy have poor predictive value for determination of GERD as the cause of extraesophageal symptoms”
  • “Ambulatory pH/impedance monitoring…have limited ability to establish GERD as the cause of an extraesophageal symptom.  The main role of testing is to document the absence of GERD.”
  • Empiric therapy with ‘aggressive’ acid suppression for 6-8 weeks can help in assessing association between reflux and extraesophageal symptoms.
  • Testing for reflux on therapy should be considered mainly in those with high probability of baseline reflux (eg. previous esophagitis, Barrett’s esophagus, or prior abnormal pH study).
  • Surgical treatment is discouraged in those with extraesophageal reflux symptoms unresponsive to aggressive PPI therapy

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Chronic Fatigue and Irritable Bowel Syndrome -10 years after Giardia Infection!

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A recent study (S Litleskare et al. Clin Gastroenterol Hepatol 2018; 16: 1064-72) involved prospective follow-up of 1252 laboratory-confirmed cases of giardiasis from a 2004 outbreak in Norway.

Key findings:

  • Prevalence of irritable bowel syndrome (IBS) was 43% 10 years after the outbreak among 576 exposed individuals compared with 14% among 685 controls. Thus, the odds ration of developing IBS was 4.74 following Giardia exposure.
  • Chronic fatigue at 10 years was higher as well, reported in 26% in the exposed group compared with 11% in the control group.
  • The authors note that the change in IBS between 6 years and 10 years following the infection was 40% and 43% respectively and the change in chronic fatigue was 31% at 6 years and 26% at 10 years.

My take: Don’t get Giardia!! It may cause chronic fatigue and IBS 10 years after acquisition of an infection.  This study reinforces other studies which have shown that numerous enteric pathogens can increase the risk of IBS.  These other studies reported lower rates of IBS following infections, between 7-36%.

Moraine Lake, Banff

Global Prevalence of Celiac Disease

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Briefly noted: P Singh et al. Clin Gastroenterol Hepatol 2018; 16: 823-36. After a systemic review which selected 96 articles from a pool of 3843 published between 1991 through 2016, the authors determined a pooled global prevalence of 1.4% in 275,818 individuals based on seroprevalence (positive TTG or EMA).  Biopsy-confirmed celiac disease was noted in 0.7% in 138,792 individuals.

In their study, biopsy-proven disease was most prevalent in Argentina, Egypt, Hungary, Finland, Sweden, New Zealand, and India.

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Clostridium difficile Guidelines

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Clinical Practice Guidelines for Clostridium difficile Infection in Adults and Children: 2017 Update by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA)

L Clifford McDonald Dale N Gerding Stuart Johnson Johan S BakkenKaren C Carroll Susan E Coffin Erik R Dubberke Kevin W Garey Carolyn V GouldCiaran Kelly … 
Clinical Infectious Diseases, Volume 66, Issue 7, 19 March 2018, Pages e1–e48,https://doi.org/10.1093/cid/cix1085

Summary from Infectious Disease Advisor: Updated C difficile Infection Clinical Guidance From IDSA/SHEA

The comprehensive clinical practice guideline …was endorsed by the Infectious Diseases Society of America (IDSA) and the Society for Healthcare Epidemiology of America (SHEA)…

Recommendations for treatment of CDI in adults… now favors a 10-day course of vancomycin or fidaxomicin rather than metronidazole for first-line therapy of mild/moderate CDI in adults… Fidaxomicin, also a newly recommended first-line therapy for mild/moderate CDI in adults, may reduce the risk for recurrent CDI because of its narrow spectrum compared with vancomycin.

Recommended treatment strategies for recurrent CDI, a complication that occurs in approximately 25% of patients, have also been revised…Following initial CDI treated with a 10-day course of vancomycin, either a several-week tapered and pulsed course of vancomycin or a 10-day course of fidaxomicin is recommended. For most patients, probiotics can be considered because of favorable cost and safety, although definitive efficacy data for probiotics to prevent recurrent CDI are still lacking. For multiply recurrent CDI (ie, at least 3 CDIs), correction of the patient’s underlying intestinal microbiota perturbation with fecal microbiota transplantation (FMT) should be strongly considered..

The diagnosis of CDI… Molecular tests (eg, nucleic acid amplification tests [NAATs], such as polymerase chain reaction), which do not differentiate colonization and infection, are now the most commonly used test for CDI among US hospitals. NAATs have the potential to misdiagnose patients with colonization as having CDI, particularly when used in patients with low likelihood of CDI. Thus, this guideline strongly reinforces the importance of practicing good diagnostic stewardship and limiting C difficile testing to patients with new-onset, unexplained, and clinically significant (ie, at least 3 unformed stools in a 24-hour period) diarrhea…formed stools should not be tested for C difficile, nor should patients be retested within 7 days of a previous negative C difficile test. In pediatric populations, because of the unclear role of C difficile as a cause of diarrhea in infants, children less than 12 months of age should not be tested…

If diagnostic stewardship is not an achievable goal, use of NAAT alone is likely to lead to frequent misdiagnosis of CDI among patients with C difficile colonization. In these cases, NAAT alone should be avoided and a multistep algorithm that incorporates toxin testing is recommended.

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Cumberland Island 2018

The Risk of Pancreatic Cancer After Acute Pancreatitis

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A recent study (J Kirkegard et al. Gastroenterol 2018; 154: 1729-36) determined that acute pancreatitis is associated with an increased risk of pancreatic cancer. This finding is based on a nationwide (Denmark), matched cohort study of all patients admitted with acute pancreatitis from 1980 to 2012.  This involved 41,669 patients with acute pancreatitis and 208,340 comparison subjects.

Key finding:

  • Five year pancreatic cancer risk was 0.87% compared to a risk of 0.13% in the comparison group (HR 2.02)

Limitations: While this study is based on a Danish registry, the authors note that the data had been prospectively entered and has a high validitiy.

My take: While I have not seen pancreatic cancer in the pediatric population, it is concerning that episodes of pancreatitis are likely to increase this risk for the children as well (over their lifetimes).

Mountain Laurel (?) -Pine Mountain Trail

PPIs NOT Linked to Cognitive Decline/Dementia & PPIs NOT Linked to Heart Attacks

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In a prospective study (M Wod et al. Clin Gastroenterol Hepatol 2018; 16: 681-89), data on middle-aged (n=2346, 46-67 yrs) and older individuals (n=2475) were collected in the Longitudinal Study of Aging Danish Twins.  This study showed that there was no difference in cognitive decline between PPI users and non-users.

The second study (SN Landi et al. Gastroenterol 2018; 154: 861-73) used a large administrative database and reviewed more than 5 million new  users of prescription PPIs and prescription H2RAs.  The authors found no significant difference in myocardial infarctions (MIs) between PPIs and H2RAs over a 12 month period.

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