Author Archives: gutsandgrowth

Unknown's avatar

About gutsandgrowth

I am a pediatric gastroenterologist at GI Care for Kids (previously called CCDHC) in Atlanta, Georgia. The goal of my blog is to share some of my reading in my field more broadly. In addition, I wanted to provide my voice to a wide range of topics that often have inaccurate or incomplete information. Before starting this blog in 2011, I would tear out articles from journals and/or keep notes in a palm pilot. This blog helps provide an updated source of information that is easy to access and search, along with links to useful multimedia sources. I was born and raised in Chattanooga. After graduating from the University of Virginia, I attended Baylor College of Medicine. I completed residency and fellowship training at the University of Cincinnati at the Children’s Hospital Medical Center. I received funding from the National Institutes of Health for molecular biology research of the gastrointestinal tract. During my fellowship, I had the opportunity to work with some of the most amazing pediatric gastroenterologists and mentors. Some of these individuals included Mitchell Cohen, William Balistreri, James Heubi, Jorge Bezerra, Colin Rudolph, John Bucuvalas, and Michael Farrell. I am grateful for their teaching and their friendship. During my training with their help, I received a nationwide award for the best research by a GI fellow. I have authored numerous publications/presentations including original research, case reports, review articles, and textbook chapters on various pediatric gastrointestinal problems. In addition, I have been recognized by Atlanta Magazine as a "Top Doctor" in my field multiple times. Currently, I am the vice chair of the section of nutrition for the Georgia Chapter of the American Academy of Pediatrics. In addition, I am an adjunct Associate Clinical Professor of Pediatrics at Emory University School of Medicine. Other society memberships have included the North American Society for Pediatric Gastroenterology Hepatology and Nutrition (NASPGHAN), American Academy of Pediatrics, the Food Allergy Network, the American Gastroenterology Association, the American Association for the Study of Liver Diseases, and the Crohn’s and Colitis Foundation. As part of a national pediatric GI organization called NASPGHAN (and its affiliated website GIKids), I have helped develop educational materials on a wide-range of gastrointestinal and liver diseases which are used across the country. Also, I have been an invited speaker for national campaigns to improve the evaluation and treatment of gastroesophageal reflux disease, celiac disease, eosinophilic esophagitis, hepatitis C, and inflammatory bowel disease (IBD). Some information on these topics has been posted at my work website, www.gicareforkids.com, which has links to multiple other useful resources. I am fortunate to work at GI Care For Kids. Our group has 17 terrific physicians with a wide range of subspecialization, including liver diseases, feeding disorders, eosinophilic diseases, inflammatory bowel disease, cystic fibrosis, DiGeorge/22q, celiac disease, and motility disorders. Many of our physicians are recognized nationally for their achievements. Our group of physicians have worked closely together for many years. None of the physicians in our group have ever left to join other groups. I have also worked with the same nurse (Bernadette) since I moved to Atlanta in 1997. For many families, more practical matters about our office include the following: – 14 office/satellite locations – physicians who speak Spanish – cutting edge research – on-site nutritionists – on-site psychology support for abdominal pain and feeding disorders – participation in ImproveCareNow to better the outcomes for children with inflammatory bowel disease – office endoscopy suite (lower costs and easier scheduling) – office infusion center (lower costs and easier for families) – easy access to nursing advice (each physician has at least one nurse) I am married and have two sons (both adults). I like to read, walk/hike, bike, swim, and play tennis with my free time. I do not have any financial relationships with pharmaceutical companies or other financial relationships to disclose. I have helped enroll patients in industry-sponsored research studies.

Casting a Wide Net: Whole-Exome Sequencing

Posted on by

A recent study shows that whole-exome sequencing can be used to diagnose genetic defects in patients with a range of phenotypes (NEJM 2013; 369: 1502-11).

In this study, the first 250 patients who had whole-exome sequencing performed at Baylor College of Medicine were studied.  80% had neurological problems and all had undergone previous extensive evaluation.

Results:

  • The authors identified “86 mutated alleles that were highly likely to be causative in 62 patients (25%)”
  • 83% of the autosomal dominant mutant alleles (n=33) and 40% of the X-linked mutant alleles (n=9) occurred de novo.
  • In four patients, the authors identified multiple causative genes.  This may lead to a paradigm shift from Occam’s razor towards more cases of “multiple hits.”
  • The authors speculate that the yield of this type of testing will improve as databases grow since many mutations at this time are of uncertain clinical significance

Bottomline: While this approach was used mainly in individuals with unexplained neurological problems, the use of whole-exome sequencing has broad potential.  In GI/Liver, the uses could include unexplained diarrheal disorders, metabolic/cholestatic liver disease, failure to thrive, inflammatory bowel disease, and many other conditions.

Related blog links:

Endoscopy Module -Postgraduate Course Notes

Posted on by

Advances in Hemostasis for Upper GI Bleeding —Brad Barth, MD, MPH  (page 77)

Upper GI Bleeding

Effect of IV PPI on patients with UGI bleeding PRIOR to EGD

  • 6 trials including 2223 patients
  • No significant difference in mortality, rebleeding or need for surgery compared to controls
  • DID significantly reduce rates of high risk stigmata identified on EGD
  • DID significantly decrease the need for endoscopic therapy
  • Reference: Sreedharan A, Martin J, Leontiadis G, et al. Proton pump inhibitor treatment initiated prior to endoscopic diagnosis in upper gastrointestinal bleeding. Cochrane Database of Systematic Reviews 2010

 

Upper GI Bleeding – Proton Pump Inhibitors/Prokinetics

  • Omeprazole 1 mg/kg q 12 hours  (Solana, et al. J Pediatr 2013:162:776-82)
  • Proposed PPI drip dose: 1 mg/kg bolus followed by 0.1 mg/kg/hour infusion
  • IV erythromycin or metoclopramide; infuse 20-120 minutes prior to endoscopy in patients with acute UGIB; decreased need for repeat endoscopy to determine cause and site of bleeding. Prokinetic did NOT affect transfusion requirements, duration of stay, need for surgery. Reference: Barkun et al. Prokinetics in acute upper GI bleeding:a metaanalysis. GIE 2010;17:126-132

Upper GI Bleeding —Other points:

  • Epinephrine alone is RARELY enough
  • Non bleeding adherent clot has 8-35% chance of rebleeding in adults. Consider removing it CAREFULLY!
  • A conservative transfusion strategy is usually appropriate

Useful References

Surveillance Endoscopies: The established, the debated, and the unknown –Mitchell Shub, M.D. (page 85)

“Beware of false knowledge; it is more dangerous than ignorance.” —George Bernard Shaw

Familial Adenomatous Polyposis

Surveillance protocol: Age of initial evaluation/Type of procedure/Frequency

  • Colon 10 – 12 y of age (Sooner: family h/o aggressive disease) -Flex sig or Colonoscopy, 1 – 2 y
  • Upper GI tract 20 – 25 y or at initial colonoscopy
  • EGD and side viewing scope, 1 – 3 y
  • Post-colectomy (pouch) 6 – 12 mo. after surgery, Flex sig 1 y (6 mo. If retained rectum)
  • Small bowel: capsule or MRI, frequency unknown

Peutz-Jeghers Syndrome: begin screening at age 8 years or when symptomatic with colonoscopy, EGD, and small bowel imaging (?capsule vs alternatives); then every 2-3 years

Juvenile Polyposis Syndrome: begin screening at age 10-15 years or when symptomatic with colonoscopy, EGD, and  possibly small bowel imaging (?capsule vs alternatives); then every 1-3 years

Discussed guidelines for IBD cancer surveillance and for Barrett’s esophagus

  • For UC, start surveillance 8-10 years after diagnosis.
  • For Crohn’s with ~1/2 colon (or more) involvement, follow same guidelines
  • For coexisting PSC, annual surveillance
  • Barrett’s esophagus in children: adenocarcinoma very rare, evidence lacking to develop surveillance schedule

Expanding the view: Update on Upper GI Strictures —Mark A. Gilger, M.D. (page 95)

Why balloons for kids (for dilatation)?

You can see what you’re doing

  • Blind pouches
  • Abnormal mucosa
  • Caustic injury
  • Epidermolysis bullosa
  • Already requires general anesthesia
  • Ability to wire through narrow strictures
  • Ability to use radiographic assistance

Tip: Can use vegetable spray (eg. Pam) to make advancement of balloon catheter easy

How to do balloon dilation

  • Inflate balloon to ½ desired initial atmospheres & re‐check placement
  • Begin dilation at to 1‐2 mm more than initial estimated stricture diameter
  • Hold for 1 minute/dilation
  • •ove balloon catheter in and out during dilation;  if balloon moves freely, increase diameter by 1mm.  If stricture moves with the balloon, hold x 1 minute, then done
  • Oh, oh, there’s blood! Good! No blood, no dilation.
  • After dilation, carefully advance endoscope through the stricture; if resistance stop, can try cork‐screw maneuver
  • Document everything; especially stricture location (CM from incisors), dilation diameters (to help you next time)

Adjunct therapy for recalcitrant strictures  –adjunct therapy to sustain dilation needs further study

  • Oral & intravenous corticosteriods
  • Injectable corticosteroids – Thins the mucosa, OK 1‐2 times, but not repeated
  • Mitomycin C
  • Acid reduction
  • Stents

Endoscopy in the high‐risk patient: Keeping your patient safe —Jenifer R. Lightdale, MD, MPH (page 63)

Safety of Pediatric GI Procedures

  • Peds‐CORI data from >10,000 procedures
  • Overall rate of complications 2.3%: risk of hypoxia 1.5%; risk of bleeding 0.3%

Examples of pediatric populations at increased risk for perforation

  • History of caustic ingestion
  • Esophageal atresia/tracheo‐esophageal fistula
  • Severe duodenitis
  • Severe ulcerative colitis
  • Patients with multiple co‐morbidities (i.e. Type I diabetes, cerbrovascular disease, peripheral vascular disease, renal insufficiency, liver disease)
  • Ehlers‐Danlos Syndrome (Vascular Type)

Pre‐procedure Assessment –lends itself to a checklist 

Thrombocytopenia -Current recommendations

  • EGD ok if platelets >20,000/mL
  • Biopsies ok if platelets >50,000/mL

Bleeding –discussed high risk conditions

Decreasing Risk of Perforation:

  • Avoiding excessive pressure
  • Avoiding premature cutting of a polyp – Coagulate before cutting
  • Avoiding blind intubation of the lumen

Decreasing Risks of Infection

  • SBE Prophylaxis– generally NOT indicated in diagnostic procedures. Congenital heart disease is complex & may be needed on a case‐by‐case basis
  • Single‐dose cephalexin has been shown to decrease peristomal infection during PEG placement
  • Prophylactic antibiotics recommended for cirrhotic patients admitted with GI hemorrhage

Postgraduate Course Syllabus (posted with permission) with complete slides of above lectures: PG Syllabus

Related blog references:

Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) and specific medical management interventions should be confirmed by prescribing physician.  Application of the information in a particular situation remains the professional responsibility of the practitioner.

Being Short -Not Pathologic

Posted on by

A recent retrospective review from Cincinnati Children’s showed a surprisingly low level of underlying disease in asymptomatic short children (J Pediatr 2013; 163: 1045-51).

The authors reviewed 1373 consecutive cases of short stature referrals (endocrinology) between 2008-2011.  In this cohort, there were 235 who met inclusion criteria as having height <3rd percentile and otherwise well.

Results:

  • “Nearly 99% of patients were diagnosed as possible variants of normal growth: 23% with familial short stature, 41% with constitutional delay…and 36% with idiopathic short stature”
  • New pathology: 1 patient with biopsy-proven celiac disease, 1 patient with unconfirmed celiac diease, and 1 patient with potential insulin-like growth factor I receptor defect.
  • Cost for each new diagnosis:  >$100,000

One important caveat from the study was the focus was not on those with growth failure –height velocity less than 5 cm/year; this study analyzed those with short stature only.  In all short (growth failure and isolated short stature) patients, previous studies have identified a much higher rate of organic pathology.  The authors also note that only 37% of their patients had appropriately maintained growth records forwarded (even after requests).  One other point that I found interesting: “Contrary to common belief, short stature has not been shown to result in impaired quality of life.”

Conclusions: “healthy short children do not warrant non directed, comprehensive screening.” The authors advocate for revision of pediatric endocrine guidelines for evaluation of these children. Reference: J Clin Endocrinol Metab 2008; 93: 4210-7.

These conclusions should be applied ONLY to those without symptoms and with normal exams (which should include a perianal examination).

Related blog posts:

Postgraduate Course Notes -Pancreatitis Module

Posted on by

When and how to assess pancreatic function: an update for clinicians –Sohail Z. Husain, MD (page 31)

Reviewed methods of detecting pancreatic insufficiency

Indirect (non-stimulatory) Methods

Stool:

  • Fecal Fat Analysis: Coefficient of fat absorption (CFA): (fat intake – fat in stool / fat intake) * 100
  • Normal > 93% (> 85% in less than 6 mo.
  • old)
  • 72 hr collection gold standard

ELASTASE-1: Stable, specific for human pancreas

  • Normal > 200 μg elastase/g stool
  • Particularly good for monitoring the development of PI in patients with CF
  • Low levels (false-positive) with diarrhea
  • Only detects severe PI

Other tests

  • Chymotrypsin: less sensitive; requires discontinuation of enzymes
  • Steatocrit: cheap; has low sensitivity
  • Serum
  • Breath
  • Direct (stimulatory)
  • Dreiling tube
  • Endoscopic pancreatic function testing (ePFT)
  • Secretin-enhanced MRCP (sMRCP)

Causes of Pancreatic Insufficiency

-85% of patients with Cystic Fibrosis have pancreatic insufficiency

Shwachman-Diamond Syndrome

  • Mutation in SBDS, found in ~90% of SDS patients
  • PI affects almost all SDS pts

Johanson-Blizzard syndrome (JBS): Key findings

  • PI
  • Severe developmental delay
  • Hypoplasia or aplasia of the nasal wings

Pearson marrow pancreas syndrome Key findings: Severe hypoplastic,macrocytic anemia,  Pancreatic insufficiency (due to pancreatic fibrosis)

Diagnosis: Clinical picture, High serum lactate/pyruvate,  Southern blot for mtDNA rearrangements

Other causes of pancreatic insufficiency

  • Chronic pancreatitis
  • Pancreatic obliteration after severe, acute pancreatitis
  • Pancreatic tumors
  • Celiac disease
  • Diabetes
  • IBD

Managing nutrition in cystic fibrosis: the role of the pediatric gastroenterologist — Sarah Jane Schwarzenberg, M.D. (page 41)

Good nutrition status correlates with better heights, better lung function, and better survival.  (Presentation did not delve into the issue of potential reverse causation.)

  • Patients with a Weight-for-Age percentile >50% at age 4 years reached a much higher height-for-age early in life and maintained this advantage into adulthood
  • Pulmonary function (FEV1%predicted) was much lower in CF patients with WAP<10% at age 4 years. This finding tracked through age 18 years.
  • Small bowel overgrowth is common in CF
  • Small bowel bacterial overgrowth contributes to poor nutritional intake and increased nutrient losses

Options to improve nutrition in CF

  • Review and optimize enzyme dose and adherence
  • Review patient’s diet with an experienced CF dietician
  • Consider adding a PPI to improve intestinal pH
  • Consider confounding disease
  • Evaluate for signs and symptoms of small bowel overgrowth and consider trial of metronidazole or rifaximin
  • Ask patient about abdominal pain
  • Evaluate for gastroparesis
  • Evaluate for DIOS
  • Consider non-CF gastrointestinal disease
  • Consider oral glucose tolerance test

Therapy to improve nutrition

  • Time-limited interventions
  • Behavior therapy to improve intake
  • Offer oral supplements
  • Consider cyproheptadine as an appetite stimulant
  • Consider a G-tube for nocturnal feeds
  • Consider Endocrinology consult

Beyond the Basics in the Management of Pancreatitis  –Aliye Uc, M.D. (page 51)

INSPPIRE To Study Acute Recurrent and Chronic Pancreatitis in Children-180 children from 14 centers enrolled to study the etiologies, epidemiology, natural history and outcome.

Pediatric Acute Recurrent and Chronic Pancreatitis-etiologies

  • Genetic (49%) (61 of 91 tested)
  • PRSS1-30%, CFTR-22%, SPINK1-14%, CTRC-3%
  • Obstructive (34%)
  • Idiopathic (20%)
  • Toxic-Metabolic (17%)
  • Autoimmune (3%)

Genetics of Pancreatitis:

1. PRSS1 (cationic trypsinogen): Autosomal dominant, 80% penetrance, Mutations are due to increased activation or decreased inactivation of trypsin (i.e. R122H, N29I).

2. SPINK1 (trypsin inhibitor): Autosomal recessive/complex inheritance, 2% have mutation, <1% have pancreatitis (i.e. N34S), Pancreatitis is dose-related (homozygous>>>het), Associated with other mutations (CFTR)

3. CFTR (>1700 mutations):

  • 2 Severe mutations = Cystic Fibrosis
  • 1 severe, 1 mild mutation = mild or atypical CF, ARP, CP
  • CF carriers = 3-4 fold increase risk in pancreatitis.
  • 1 any +SPINK1 = CFTR-associated pancreatitis
  • 1 any +divisum = CFTR-associated pancreatitis

4.New Modifier Genes in ARP and CP

  • CTRC (trypsin degrading enzyme)
  • CASR (a calcium-sensing receptor)
  • CLDN2 (tight junction protein on X chromosome)
  • CPA1 (Carboxypeptidase 1)  increased riskf for CP in younger patients

Management:

  • Unclear if antioxidants helpful for pain.
  • The role of pancreatic enzymes in CP is equivocal.

Diet

  • When to start feeds? depends on the severity of AP, OK to start early; correlate with clinical readiness, abd pain
  • What mode of nutrition? prefer enteral over TPN, NG vs. NJ
  • What to feed?  recent studies in adults with mild AP support full diet

(Moraes JM et al. J Clin Gastroenterol 2010 44:517)

No evidence that low-fat diet is helpful

IV Fluids: With acute presentation, Lactated Ringer’s preferred over Normal saline.

NG Suction

  • Not shown to decrease symptoms,mortality or hospital stay.
  • May be useful if: severe gastric distention, refractory nausea and vomiting, or obstruction seen on abdominal x-ray

IBD References 10/13

Posted on by

Recent useful references:

Inflamm Bowel Dis 2013; 19: 2490-2500.  “Endemic Fungal Infections in Inflammatory Bowel Disease Associated with Anti-TNF Antibody Therapy”

  • Reviews histoplasmosis, blastomycosis, & coccidioidomycosis. Provides endemic maps (which are available at CDC website), diagnostic tips, and treatment recommendations.  Of these three infections, blastomycosis is endemic in Northern Georgia.
  • Histoplasmosis can be diagnosed with urinary antigen, Blastomycosis is most commonly diagnosed with sputum cultures or bronchial washings for cytology, and coccidioidomycosis can be identified with serology (Coccidioides immittis)
  • Generally a good idea to get a chest radiograph in patients with respiratory symptoms, fever, chills, myalgias, and headaches.
  • CDC Fact Sheet – Centers for Disease Control and Prevention  Map for several endemic fungal diseases, including histoplasmosis and blastomycosis.
  • CDC Features – Valley Fever: Awareness is Key Map for endemic coccidiomycosis.

Inflamm Bowel Dis 2013; 19: 2457-2463. “Efficacy and Safety of Natalizumab in Crohn’s Disease Patients Treated at 6 Boston Academic Hospitals”

  • 44 of 64 with adequate evaluation had either a partial or complete clinical response.  In this select group of complicated patients, about one-third had clinical improvement for more than a year.
  • No cases of PML noted in this cohort.

Inflamm Bowel Dis 2013; 19: 2433-2439. “Serum IL-17A in Newly Diagnosed Treatment-Naive Patients with Ulcerative Colitis Reflects Clinical Disease Severity and Predicts the Course of Disease”

  • Mucosal mRNA expression of IL-17A was 99.8 times higher in ulcerative colitis patients compared to controls.
  • Serum IL-17A correlated with clinical disease severity and was a marker for disease course over the following 3 years.

Inflamm Bowel Dis 2013; 19: 2440-2443. “Assessment of the Relationship Between Quality of Sleep and Disease Activity in Inflammatory Bowel Disease Patients”

  • Data found an association between poor sleep quality and disease activity.  Furthermore, patients in clinical remission with abnormal sleep have a high likelihood of subclinical disease activity (another question for the EPIC smartform?).

Inflamm Bowel Dis 2013; 19: 2423-2432. “Nationwide Temporal Trends in Incidence of Hospitalization and Surgical Intestinal Resection in Pediatric Inflammatory Bowel Diseases in the United States from 1997-2009”

  • Annual percent increase (API) of 2.1% noted in incidence of intestinal resection for Crohn’s disease.  Stable colectomy rate for ulcerative colitis during this period.
  • Annual incidence of hospitalization was 5.7 per 100,000 for Crohn’s and 3.5 per 100,000 for ulcerative colitis; there was a significant increases during study period: 3.8% API for Crohn’s and 4.5% for ulcerative colitis.

Better HCV Treatments Approved

Posted on by

Both Simeprevir and Sofusbuvir have been approved unanimously by FDA panel.

Excerpt from AP report on simeprevir  (full link: ow.ly/qarKM from AGA twitter feed):

All 19 members of the Food and Drug Administration’s panel of virus experts voted in favor of approving J&J’s simeprevir, a daily pill designed to eliminate the most common form of hepatitis C.  The FDA is not required to follow the group’s recommendations, though it often does. A decision on the drug is expected next month.

Roughly 3.2 million people in the U.S. have hepatitis C, a blood-borne disease that causes liver damage and is blamed for 15,000 deaths a year…

New Brunswick, N.J.-based J&J is seeking approval to combine its pill with the long-established drug cocktail used to treat the most common form of the virus.

Despite the unanimous vote Thursday, the panel’s endorsement came with a number of conditions.

The panelists stressed that the drug is less effective in patients with a common genetic mutation called Q80K, and that people with the abnormality should be screened out so they can receive other drugs. The group also said the drug’s label should warn patients and doctors that sunburn is a common side effect. Finally, panelists said that the FDA should require J&J to conduct additional studies of the drug’s effectiveness in minorities, especially African-Americans who are disproportionately infected…

The FDA meeting comes as federal health officials urge all baby boomers to get tested for the virus…

J&J’s simeprevir appears to be slightly more effective than the standard of care, curing 80 percent of patients who had not previously been treated for the disease, according to studies submitted to the FDA. More significantly, the drug helped most patients cut the amount of time they had to take the traditional drug cocktail, with its unpleasant side effects, to six months rather than one year. Additionally, panelists said the drug’s once-a-day dosage should be far more manageable for patients than the current drugs from Merck and Vertex, which require taking 12 pills or six pills a day, respectively.

And for Sofusbuvir from Reuters (FDA panel backs Gilead hepatitis C drug sofosbuvir)

The FDA advisory panel voted 15 to 0 in favor of approval of the drug in patients with two variants of the liver-damaging disease – genotype 2 and genotype 3 – in combination with an existing treatment, ribavirin.

If approved, it will be the first all-oral treatment for genotypes 2 and 3, obviating the need for the injectable drug interferon, which can cause debilitating side effects. Panelists called the vote “historic” and a “game-changer.”

“Our patients have been waiting for this for a long time,” said Dr. Curt Hagedorn, chief of medicine service at the Central Arkansas Veterans Healthcare Service.

The panel also voted unanimously to approve the drug in patients with genotype 1 and genotype 4 variants in combination with ribavirin and interferon in patients who have not received prior therapy.

Related blog posts:

Quality care = Work Satisfaction for Physicians

Posted on by

From Atul Gawande’s twitter feed:

RAND study:

“Factors Affecting Physician Professional Satisfaction and Their Implications for Patient Care, Health Systems, and Health Policy” Full article: http://bit.ly/19vVAnK 

1) Best predictor of MD work satisfaction: how we rate system’s care quality.  Physicians who felt that they were working in an environment with high quality care had higher work satisfaction.

2) Bad EHRs are killing us.  (Related blog entry: Aptly titled “The Cost of Technology” | gutsandgrowth)

 

A C difficile two-fer

Posted on by

Two recent review articles on Clostridium difficile are quite useful:

  • Mezoff EA, Cohen MB. J Pediatr 2013; 163: 627-30.
  • Dupont HL. Clin Gastroenterol Hepatol 2013; 11: 1216-23.

The first publication reviews acid suppression and the risk of C difficile infection (CDI).  It starts off with  a terrific piece of advice from Sir William Osler: “One of the first duties of the physician is to educate the masses not to take medicine.”  The authors note that pH above 4 has been shown to increase bacterial survival, including  C perfringe spores in a mouse model.  In addition, the article notes that there have been concerns as early as 1982 that acid suppression could be a risk factor for CDI.  Several recent studies were summarized, including the following:

  • A recent meta-analysis (Kwok CS et al. Am J Gastroenterol 2012; 107: 1011-9) with 42 studies (N= 313,000 patients) “found an association between PPI use and risk of CDI (OR1.74, 05%CI 1.47-2.85).”
  • A review of the literature (Deshpande A et. Clin Gastroenterol Hepatol 2012; 10: 225-33) between 1990-2010 found an overall increase in CDI risk with PPIs to be OR 2.15 (95% CI 1.81-2.55). No prospective studies were identified.
  • In pediatrics, a study (Turco et al. Alimentary Pharmacol Therapeut 2010; 31: 754-9) with 910 children admitted for abdominal pain and diarrhea identified 68 with CDI.  Compared with control patients, use of PPIs was significantly higher in CDI patients (OR 4.52, 95% CI 1.4-14.4).

The FDA has stated that PPIs may be associated with an increased risk of CDI.  In addition, the use of antibiotics “appear to act synergistically with PPIs.”  Thus, the authors recommend stopping PPIs in those who do not need them.  Periodic ‘holidays’ or dosing step-downs may help assess continued need for PPIs.

The second publication succinctly reviews the diagnosis and management of CDI.  The various diagnostic methods are compared in Table 1.  Therapeutic options for 1st time infection are reviewed in Table 2.  For adults with mild-to-moderate infections, metronidazole (500 mg TID for 10 days) is preferred.  Vancomycin or Fidaxomicin are recommended for more severe infections.

Table 3 lists treatment options for recurrent CDI.  Repeat course of any of the 1st round treatments can be considered depending on patient’s illness severity.  In addition, other potential treatments included the following:

  • vancomycin tapered dose (week 1: 125 mg 4 times/day, week 2: 125 mg 2 times/day, week 3: 125 mg once/day, week 4: 125 mg every other day, week 5 & 6: 125 mg every third day)
  • rifaximin (550 mg BID x 20 days)
  • high-dose vancomycin (250-500 mg 4 times/day for 10 days) followed by S boulardii (2 capsules BID for 28 d)
  • fecal microbiota transfer (FMT) –“although family member stool donors have been used, the current movement is toward volunteer donor pools.”  [I do not think ‘current movement’ was intended as a pun by the authors.]  Volunteer donors could lower the screening costs.
  • intravenous immunoglobulin (small clinical trials have failed to show efficacy)
  • monoclonal antibodies to toxins A/B

Related blog posts:

Nutrition Module

Posted on by

More notes from this year’s postgraduate course:

Clinical issues in parenteral nutrition, Praveen S. Goday, MBBS, CNSC (page 105)

  • Fish‐oil vs minimizing soybean oil‐based lipid emulsions
  • Catheter‐related bloodstream infections (CRBSI): Ethanol locks “Humans like ethanol and bacterial don’t.”  Meta‐analysis:  In comparison with heparin locks, ETOH locks (various regimens) reduced the following: a) CRBSI‐rate per 1000 catheter days by 7.67 events (81% ↓)  b) catheter replacements by 5.07 (72% ↓), c) 108‐150 catheter days of ETOH lock exposure were necessary to prevent 1 CRBSI, d) Adverse events – rare and included thrombotic events.  Reference: Oliveira et al. Pediatrics 2012;129:318–329

Parenteral Drug Shortages: All PN products except dextrose and water have been in short supply at some point since spring 2010

Imported components from Europe (higher cost)

• Peditrace™ – zinc, copper, manganese, selenium, fluoride, and iodine

• Addamel N™ – zinc, copper, manganese, selenium, fluoride, and iodine, molybdenum, iron, and chromium

Summary / Take‐home points

  • Reduction in soybean oil emulsion or provision of fish oil emulsion results in improvement in cholestasis
  • Ethanol lock therapy decreases CRBSI in children on home PN
  • Significant PN shortages have affected our ability to care for our PN patients; thus need vigilance and good communication between physician, dietitian and pharmacist

Severe Obesity in Your Clinic: The disconnect between the epidemic and the intervention Sarah E. Barlow, MD, MPH (page 125)

What to do for obesity?

  • Behavior modification
  • Pharmacotherapy (and behavior modification)
  1. Orlistat (Xenical, Alli) -Enteric lipase inhibitor, FDA approved starting at age 12 years (OTC $200 per month)
  2. Approved for adults Lorcaserin (Belviq): 5-HT2C agonist
  3. Approved for adults: phentermine and topirimate (Qsymia)
  • Surgery (and behavior modification)
  • Meal replacement (and behavior modification)

Orlistat trial for adolescent obesity:

  • 54 week double-blind RCT
  • 539 subjects: 12 to 16 years of age, BMI 36 ±  4 kg/m2
  • BMI change kg/m2 (mean):  – .55  vs. + 0.31 for control
  • Fecal urgency (%) 20.7 (11.0 in controls)
  • Flatulence (%) 9.1 (4.4 in controls)
  • Fecal incontinence (%) 8.8 (0.6 in controls)
  • Reference: Chanoine et al. JAMA 2005;293:2873

Orlistat meta-analysis among adults :

  • -2.87 kg [95CI -3.21, -2.53] = placebo-subtracted change at 1 year
  • Reference  Rucker D. BMJ 2007;225:1194

Multiple potential medications are being studied

Selection criteria for adolescent bariatric surgery

  • Tanner stage IV or V
  • BMI ≥ 35 kg/m2 with severe
  • Comorbidity or BMI ≥ 40 kg/m2 with comorbidity
  • “Have failed” 6 month of organized attempts at weight loss
  • Committed to pre and post medical and psychological care
  • Supportive family
  • Able to give informed assent
  • Frequent barriers: Distance from center, Insurance, Age, Reluctance
  • Reference: Pratt Obesity 2009;17:901

Complications from Surgery

  • For all procedures: nutritional deficiencies, especially iron, vitamins B12, D, and thiamine
  • For gastric bypass: postprandial hypoglycemia in adults
  • For lap band: need for re-operation for slippage or erosion in adults and small adolescent study.
  • Also pouch dilatation
  • For sleeve gastrectomy: leak or bleeding along suture site

Summary

  1. 4% of children 6 to 19 are severely obese
  2. Severe obesity leads to high levels of cardiovascular disease risk factors, NAFLD, OSA, and pre-diabetes
  3. Behavior modification has modest efficacy, is a partner in all other intensive interventions, but is not readily available behavior modification is underutilized because it is time-intensive and resource-intensive.  It it is necessary even though it is not sufficient.
  4. Orlistat is the only medication currently available for adolescents.

 5 2 1 0

  • 5 servings of fruits and vegetables a day
  • 2 hours or less of screen time
  • 1 hour (60 minutes) or more of physical activity
  • 0 sugar-sweetened beverages

Postgraduate Course Syllabus (posted with permission): PG Syllabus

Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) and specific medical interventions should be confirmed by prescribing physician.  Application of the information in a particular situation remains the professional responsibility of the practitioner.