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.

Dollars for Doctors

A recent NPR report, Industry Payments To Doctors Are Ingrained, Federal Data Show, provides a link detailing payments by drug and device companies to U.S. doctors and teaching hospitals.  Doctors may be paid for promotional speaking, consulting, travel expenses, and meals.

If you want to see how much is reported for each doctor, check out the ProPublica Dollars for Doctors database.

Here’s a screenshot:

Screen Shot 2015-07-02 at 8.24.03 AM

The article notes that the a close relationship between doctors and pharmaceutical companies is important.  “Collaboration between physicians and biopharmaceutical professionals is critical to improving the health and quality of life of patients.”

Take-home point: Some financial relationships between doctors and pharmaceutical companies lead to important improvements in drug (or device) development; other relationships may alter prescribing habits without apparent patient benefit. Will this information empower patients to ask why their physicians has close ties to the pharmaceutical industry?

Related blog post:

Point of Care -Mobile, Anywhere, Cheap EKGs

Note:  This blog and author do not have any financial disclosures or receive any support from any companies.

Using a smartphone app, AliveCor has developed the technology to obtain a limited EKG (ECG) for a minimal cost; after an initial investment of $74.99, this technology can function similar to a standard EKG machine but only provides one lead (V1).

From the AliveCor website (thanks to Larry Saripkin for showing me this):

The FDA-cleared AliveCor Mobile ECG wirelessly communicates with the free AliveECG app, available in the U.S. App Store and Google Play Store. ECGs are stored in the app and on secure, encrypted servers that can be viewed anytime, anywhere. ECGs can also be printed or e-mailed directly from your smartphone or tablet, and you can grant access to your physician.

Do I have to attach the Mobile ECG to my smartphone or tablet? That is our recommendation, however, you may use the Mobile ECG within 12 inches of your smartphone or tablet if you’d like….

Simply rest it on your fingers or chest to record an ECG in just 30 seconds. Know right away when your ECG is normal and if atrial fibrillation is detected.

Potential Uses:

  • Detect atrial fibrillation
  • Correlate symptoms like palpitations and shortness of breath
  • Accurately assess heart rate
  • ?Assess for QT interval -this could be particularly useful to pediatric gastroenterologists

While many of the uses may be self-evident, the website offers ECG review by a U.S. board-certified Cardiologist, with an average turnaround time of 24 hours. The current price of this service is $12.

Bottomline: This is another example of how new technology improves clinical information and at the same time should be less expensive and more timely.

Related blog posts:

Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications/diets (along with potential adverse effects) and use of new technology should be confirmed by prescribing physician/nutritionist.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

Sign at Children's Healthcare of Atlanta

Sign at Children’s Healthcare of Atlanta

Generation R Study: Insights into the Effects of Anti-Tissue Transglutaminase Antibody Positivity

In a study from Rotterdam (Jansen MAE, et al. Clin Gastroenterol Hepatol 2015; 13: 913-20), the authors show that positivity for anti-tissue transglutaminase IgA antibodies (TTG) is associated with lower growth trajectories and bone mineral density.

This was a population-based prospective cohort study which examined children born from 2002-2006 (median age 6 years).  4249 children with TTG <7 U/mL were compared with 57 children with TTG >7 U/mL.  The authors specifically looked at those >70 U/mL as well. Children with a previous diagnosis of celiac disease were excluded.

Key findings:

  • Positive TTG serology was associated with reduced weight gain 0.05 standard deviation score (SDS) per year and less linear growth 0.02 SDS/year.
  • Children with positive TTG were shorter 0.29 SDS and weighed less 0.38 SDS.
  • Children with positive TTG had lower bone mineral density (BMD) 0.26 SDS less.
  • Children with positive TTG did not have increased gastrointestinal symptoms compared with control children.

The authors note that the majority of these effects (poor growth, shortness, lower BMD) were mostly present in children with TTG >10 times upper limit of normal.

Bottomline: Subclinical or potential celiac disease is associated with reduced growth and bone mineral density.

Briefly noted:  Emilsson L, et al. Clin Gastroenterol Hepatol 2015; 13: 921-27.  Using a Norwegian cohort study with 95,200 women and 114,500 children (199-2008), the authors showed that development of celiac disease was associated with maternal celiac disease and type 1 diabetes.  There was no significant association noted with intrauterine growth, or mode of delivery.

Related blog posts:

Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications/diets (along with potential adverse effects) should be confirmed by prescribing physician/nutritionist.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

Cumberland Island

Cumberland Island

 

Critique of the 21st Century Cures Act

The most compelling article (Avorn J, Kesselheim AS. NEJM 2015; 372: 2473-5) in a recent edition of the NEJM delved into the 21st Century Cures Act which was recently introduced in the U.S. House of Representatives; it was approved 51 to 0 in committee but continues to be debated.

One of the underlying premises of the bill is accelerate approval for new products. Key features:

  1. Increase in National Institutes of Health (NIH) of about 3% per year for 3 years. And, additional $2 billion per year for 5 years to create an “NIH Innovation Fund”
  2. Instructs FDA to consider nontraditional study designs for clinical trials.  This is aimed at shorter, smaller and less expensive studies.  This could allow FDA to rely on “observational studies” and “clinical experience.”
  3. The bill encourages the FDA to rely more on surrogate end points
  4. The bill would allow informed consent to be bypassed if the “proposed testing poses no more than minimal risk.”

Critiques for each point, point by point:

1. The funding increases largely counterbalance stagnating funds at the NIH secondary to sequestration and budget cuts.

2.  The premise that the FDA is inefficient is not accurate.

  • “A third of new drugs are currently approved on the basis of a single pivotal trial” with a median of 760 patients.
  • Most drugs are approved based on studies with a duration of 6 months or less, even medications taken for a lifetime.
  • Evaluation of nearly all new drug applications is completed within 6 to 10 months.

3.  Surrogate markers often overestimate the potential benefit of medications.  The FDA “already uses surrogate end points in about half of new drug approvals.” Specific examples:

  • Bevacizumab has been shown to delay tumor progression in breast cancer “but was shown not to benefit patients.
  • Rosiglitazone “lowered glycated hemoglobin levels in patients with diabetes even as it increased their risk of myocardial infarction.”
  • One new tuberculosis drug improved bacterial counts in the sputum but “the treatment group had a death rate four times that in the comparison group.”

4.  Informed consent has been “sacrosanct, with exceptions made only when consent is impossible or contrary to a patient’s best interests.”  With this new proposal, “it is not clear who gets to determine whether a given trial of a new drug poses “minimal risk.”

Bottomline (from authors): The 21st Century Cures Act’s call for increased NIH funding may prove to be its most useful component.  But political forces…could lead to the approval of drugs and devices that are less safe or effective than existing criteria would permit.”

Audio interview with Jerry Avorn: nej.md/1TPy6Ta

Some pictures from yesterday’s Peachtree Road Race:

Coveted T-shirt -2015 Edition

Coveted T-shirt -2015 Edition

Screen Shot 2015-07-04 at 6.34.03 PM

Rainy Day for a 10K

Largest 10K in U.S

Largest 10K in the World

Immune-Mediated Reactions to Anti-TNFs and What to Do About Them

Statue

A recent review article (Feuerstein JD et al. Inflamm Bowel Dis 2015; 21: 1176-86) serves as a useful reference regarding immune-mediated reactions to anti-tumor necrosis factor (anti-TNF) medications used in inflammatory bowel disease (IBD).

Background:

  • All anti-TNF agents induce antidrug antibodies (ADAs).
  • With regard to infliximab (IFX) which has the most literature, it is well-recognized that combination therapy with an immunomodulator reduces the risk of antibodies to infliximab (ATIs).  For example, in the SONIC study, ATIs were noted in 0.9% of those with combination therapy compared with 14.6% of those receiving monotherapy with IFX.  With the UC-SUCCESS, the rates were 19% and 3% respectively.

Acute Infusion Reactions -Key points:

  • Acute infusion reactions (IRs) are more common in patients with ADAs.  IRs can be categorized as acute (w/in 24h) and chronic (2-14 d after infusion).
  • Acute IRs can be mild (dizziness, flushing, nausea, palpitation), moderate (chest pain, hypertension [SBP increase of more than 20], hypotension, fevers urticaria, mild dyspnea, chills, rash) or severe (severe hypertensions [SBP increase of more than 40] , severe hypotension, significant dyspnea with brochospasm, stridor, and rigors)
  • The authors provide a treatment algorithm (Figure 1) based on severity of acute IR.  All reactions are initially treated by stopping infusion, but many can be restarted at a low rate after administration of acetaminophen (mild & moderate), normal saline (mild & moderate), diphenhydramine (moderate), and possibly hydrocortisone (if needed in moderate cases).  While the algorithm suggests the possibility of restarting infusion reaction in severe cases without anaphylaxis, if this is considered, it may be worthwhile to attempt in a hospital setting.
  • Typically if infusions are restarted, the rates are 10 mL/hr x 15 minutes –>20 mL/hr x 15 minutes–> 40 mL/hr x 15 minutes –>80 mL/hr x 15 minutes –>100 mL/hr x 15 minutes–>125 mL/hr until completion.
  • Following an IR, the authors recommend checking for ATIs and for IFX level.
  • Prophylaxis for mild IRs includes the use of acetaminophen and antihistamines (2nd generation antihistamine daily for 5 days prior or first generation antihistamine an hour prior to infusion).  In addition, the infusion should be started at 10 mL/hr
  • Prophylaxis for moderate IRs includes the use of acetaminophen and antihistamines and steroids (prednisone 50 mg q12 hr x 3 doses prior or hydrocortisone 100 mg (or equivalent) 20 minutes prior to infusion).  In addition, the infusion should be started at 10 mL/hr
  • The authors recommend against premedication in those who have not had IRs. Use of premedication may cause a paradoxical increase in IRs due to symptoms induced by the antihistamine.

Autoimmune Complications:

  • Autoantibodies: anti-nuclear antibody (ANA), anti-double-stranded DNA antibody (anti-dsDNA), anti-cardiolipin antibody, antihistone antibody
  • Drug-Induced Lupus Erythematosus (DILE) -“the most frequently presenting symptoms, seen in 90% of cases, is symmetric arthralgias.”  Systemic involvement of the kidneys or central nervous system is rare. Treatment is cessation of the offending medication.
  • Vasculitis -likely due to the development of circulating immune complexes that deposits into smaller capillaries–>result in a type III hypersensitivity reaction.  The most common manifestation would be palpable purpura due to a leukocytoclastic vasculitis.
  • While autoimmune complications can be a class effect, many patients have been able to switch to a different anti-TNF.

Dermatologic Complications:

The authors review both anti-TNF induced psoriasis and eczema.  Treatment should be in conjunction with dermatology.  For psoriasis that involves >5% of body surface area, this could require changing to a different anti-TNF or a different drug class.  For severe cases, “anti-TNF therapy should be discontinued.”

Related blog posts:

Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications/diets (along with potential adverse effects) should be confirmed by prescribing physician/nutritionist.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

Sunflowers

Stopping Infliximab –What Happens Next?

A recent retrospective single-center study (Papmichael K et al. Clin Gastroenterol Hepatol 2015; 13: 1103-10) of 100 patients with Crohn’s disease examined what happens to patients who discontinued infliximab therapy upon clinical remission.  The study used a medical database in Belgium.  The authors defined sustained clinical remission (SCR) as “maintenance of disease remission, without escalation in medical therapy or CD-related surgeries, until the end of the follow-up period, which was a median period of approximately 10 years.” 84 patients continued on immunomodulator therapy.

Key findings:

  • 52 (52%) had SCR.
  • Complete mucosal healing, lower infliximab trough concentrations, and serum positivity for vascular cell adhesion molecule-1 were factors associated with SCR.

Limitations: SCR was based on physician global assessment which may underestimate relapse rates and endoscopic data at the time of infliximab discontinuation was available in only a small subgroup.

Bottomline: In this small study, half of the patients did well clinically for a long time after stopping infliximab (most remained on immunomodulator therapy).  However, given the insidious nature of Crohn’s disease, careful monitoring before and after stopping infliximab is worthwhile.  In addition, other studies have demonstrated higher relapse rates.

Related blog posts:

 

Optimal Dose of Thiopurine When Used for Combination Therapy

To improve long-term outcomes and response in patients with inflammatory bowel disease, many experts advocate the use of combination therapy (thiopurine with anti-tumor necrosis factor).  Thiopurine cotherapy resulted in higher response rates in pivotal studies (eg. SONIC, UC Success), likely due to lower rates of antidrug antibody (ADA) and higher serum levels of biologic agents (e.g. infliximab).  To achieve these advantages, it is not clear whether a lower dose of a thiopurine may be similarly effective as a higher dose.  If a lower dose could result in a similar effect, it would likely result in fewer adverse effects.

A recent study (Yarur AJ, et al. Clin Gastroenterol Hepatol 2015; 13: 1118-24) provide some data to address the issue of optimal dosing of thiopurines.  The authors performed a cross-sectional study of 72 patients receiving infliximab (IFX) and a thiopurine.

Key findings:

  • The thiopurine metabolite 6-thioguanine (6-TG) that “best predicted a higher level of infliximab was 125 pmol/8 x 10 to the 8th RBCs.”
  • Only 8 patients (11%) had detectable antibodies to infliximab (ATI)
  • Patients with 6-TG <125 were more likely to have ATI (OR 1.3)
  • Higher 6-TG levels did not confer additional benefit

This study had many limitations including the small number of patients and the cross sectional design.  In addition, the patients may not be representative of typical patients; more than 50% were in endoscopic remission. A randomized controlled trial with larger number of patients is needed for a more definitive answer.

Take-home message: (from authors); “6-TGN metabolite levels rather than weight-based dosing may assist clinicians in optimizing treatment when using thiopurines in combination with IFX…lower target 6-TGN levels (125-176 pmol/8 x 10 to the 8th RBCs) may be adequate to maximize IFX levels and reduce immunogenicity while potentially minimizing toxicity.”

Briefly noted:

Ananthakrishnan AN et al. Clin Gastroenterol Hepatol 2015; 13: 1197-1200.  In this prospective study with 1659 patients with Crohn’s disease (CD) and 946 patients with ulcerative colitis, the authors found wide variation among the 7 participating academic centers, particularly with regard to CD treatment.  Comparing the site with the lowest usage to the highest usage, for CD:

  • Oral mesalamine 13% vs. 46%
  • Immunomodulator use 16% vs. 56%
  • Anti-TNF use 31% vs 60%
  • Combination therapy 8% vs 32%
  • Immunomodulator-naive anti-TNF use 10% vs. 17%
  • Surgery 32% vs 55%

Related blog posts:

Cumberland Island

Cumberland Island

New Target Drug Levels in Inflammatory Bowel Disease

According to a recent review (Vaughn BP, Sandborn WJ, Cheifetz AS. Inflamm Bowel Dis 2015; 21: 1435-42), higher target levels of infliximab should be considered.

After reviewing the relevant studies which are summarized in Table 1, the authors state that in their experience infliximab (IFX) levels of 5 to 10 mcg/mL are desirable.  Using this standard, they note in a retrospective review that proactive testing identifies only 29% of patients in this range.

Similarly, the TAXIT study (Casteele NV et al. Gastroenterol 2015; 148: 1320-29) identified 44% of patients with a trough concentration of 3-7 mcg/mL at baseline screening.  In this study, after achieving an adequate trough concentration, they found that patients had ~70% clinical remission at 1 year.  TAXIT acronym = the Trough Concentration Adapted Infliximab Treatment trial.  The TAXIT study was a 1-year randomized control trial with 263 adults (178 with CD and 85 with UC).

Recommendations from this review:

  • When therapeutic drug monitoring is used to react to symptomatic patients (Figure 1), if they test negative for antibodies to infliximab (ATIs) and have a low IFX level, then increasing the dose is recommended.  In those with therapeutic IFX and negative ATIs, then consider change in drug class or surgery (rather than dose escalation).
  • When therapeutic drug monitoring is used to react to symptomatic patients, if they test positive for ATIs, if there is a low level ATI (<15 mcg/mL for the referenced assay), then increasing the dose is recommended, otherwise consider change in drug class or surgery (rather than dose escalation).
  • For proactive monitoring, if negative ATI, and IFX trough level is >10 mcg/mL consider extending interval.  If the IFX level is low, increase dose.  If IFX is therapeutic, continue same dose and consider re-check in 6-12 months.
  • For proactive monitoring (Figure 3), if positive ATI, the authors recommend increasing dose if faced with low level ATI and consider change in drug class or surgery (rather than dose escalation). [If someone is doing well, I would not agree with this recommendation.  I would not stop a therapy based on a single blood test.]

One more useful point:

The authors note that combination therapy improves IFX levels and lessens the likelihood of ATIs.  “Current evidence suggests that combination of an anti-TNF with an immunomodulator is the most efficacious treatment for new-onset IBD.”  They speculate that proactive monitoring may allow IFX monotherapy without the need for combination therapy or allow de-escalation of combination therapy.

Bottomline: Consider a higher infliximab target level (5-10 mcg/mL) and using proactive monitoring to achieve higher remission rates.

Related blog posts:

Cumberland Island

Cumberland Island

Briefly noted:

Casen C, et al. Aliment Pharmacol There 2015; 42: 71-83. (Thanks to Ben Gold for this reference). After studying the stool of 165 healthy controls, the authors used 54 DNA probes targeting >300 bacteria.  This genetic analysis-map dysbiosis test, subsequently analyzed 330 more patients; it confirmed dysbiosis in 73% of IBS patients, 70% of treatment-naive IBD patients and 80% of IBD patients in remission compared with 16% of healthy individuals.  Take-home point: Ultimately stool analysis could lead to more accurate evaluation and monitoring of individuals with suspected IBS or IBD.

Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications/diets (along with potential adverse effects) should be confirmed by prescribing physician/nutritionist.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

 

What “Treat-to-Target” Could Look Like in Crohn’s Management

A recent study (treat to target full text -Bouguen G et al. Clin Gastroenterol Hepatol 2015; 13: 1042-50) proposes  a “new paradigm for the management of Crohn’s disease.”  The concept of treating-to-target has been discussed in several previous blogs:

The concern with the traditional management has been ongoing damage to the bowel in many patients and lack of optimizing long-term outcomes.  The authors in the report make the following points:

  • Only 10% of Crohn’s disease (CD) patients experience prolonged remission of symptoms
  • Even asymptomatic patients often have evidence of active inflammation on endoscopy
  • The majority of patients will require surgery
  • Two big obstacles: delay in initiation of highly effective therapy (eg. combined biologic/immunosuppressant) and underestimation of disease activity due to poor correlation of symptoms to actual disease activity

While the fact that the majority of patients are at risk, some populations are at increased risk including the following:

  • those who smoke cigarettes
  • patients younger than 40 years at diagnosis
  • stricturing or penetrating disease
  • need for surgery
  • inability to wean corticosteroids
  • deep ulcerations on endoscopy

However, the authors note that “the lack of adequate data in this area of research makes risk stratification very difficult in clinical practice.” The authors review several studies:

  • ACCENT-I
  • Step-Up Top-Down trial
  • IBSEN population-based cohort study
  • SONIC
  • The Leuven cohort study
  • EXTEND trial

The data from these studies is used to base their argument of pursuing mucosal healing/more aggressive treatment, though they acknowledge that one risk is potentially subjecting some patients to overtreatment.  The review indicates that mucosal healing (MH) is defined endoscopically as “the disappearance of ulceration” and that endoscopy is the tool for testing for MH for the near-term, but that other markers including MRE and surrogate biomarkers may be useful alternatives.

The authors’ Table 1 list their proposed recommendations for CD, modeled after similar recommendations for Rheumatoid Arthritis.  The Four Key points:

  1. The physician and patient need to agree on the treatment target strategy
  2. The primary target for treatment of CD should be absence of endoscopic ulceration
  3. The use of both clinical symptoms and objective measures of inflammation (endoscopic or imaging) is required in routine clinical practice to guide treatment decisions
  4. Until the desired treatment target is reached, MH should be assessed every 6 months until the disappearance of ulceration and every 1-2 years thereafter.  Drug therapy should be adjusted accordingly.

Limitations on this strategy:

  • Cost of assessment–both endoscopy and MRE are expensive
  • Cost of therapies
  • While MH can be achieved in a higher percentage of patients, there are some patients who will not respond to any of the currently available therapies
  • Risk of therapies.  Some patients will develop adverse effects from the available therapies which will limit their therapeutic options.
  • This proposed strategy has very limited data in clinical practice

Take-home message from the authors: The “natural history” is not likely to improve unless the overall, symptom-based, therapeutic strategy for CD is changed.

Atlanta Zoo, Wreathed Hornbill

Atlanta Zoo, Wreathed Hornbill

 

 

Iron Deficiency Common in Patients Requiring Long-Term Parenteral Nutrition

A recent study (JPEN J Parenter Enteral Nutr May 13, 2015 0148607115587329) demonstates a high rate of iron deficiency anemia in patients requiring home parenteral nutrition (Thanks to Kipp Ellsworth for reference).

From Abstract:

Methods: Medical records of patients receiving HPN at the Mayo Clinic from 1977 to 2010 were reviewed. Diagnoses, time to IDA development, and hemoglobin, ferritin, and mean corpuscular volume (MCV) values were extracted. Response of iron indices to intravenous iron replacement was investigated.

Results: Of 185 patients (122 women), 60 (32.4%) were iron deficient…Of 93 patients who had sufficient iron storage, 37 had IDA development after a mean of 27.2 months (range, 2–149 months) of therapy. Iron was replaced by adding maintenance iron dextran to PN or by therapeutic iron infusion. Patients with both replacement methods had significant improvement in iron status. With intravenous iron replacement, mean ferritin increased from 10.9 to 107.6 mcg/L (P < .0001); mean hemoglobin increased from 11.0 to 12.5 g/dL (P = .0001); and mean MCV increased from 84.5 to 89.0 fL (P = .007).

Conclusions: Patients receiving HPN are susceptible to IDA. Iron supplementation should be addressed for patients who rely on PN.

Zoo Atlanta

Zoo Atlanta