Pediatric pharmaceutical poisoning

Posted on by

Overdosing and taking a bad mix of medications is not just a problem in adults.  This remains a big problem in pediatrics (J Pediatr 2012; 160: 190-192, 265-70).  The study and accompanying editorial discuss the ongoing impact of pediatric pharmaceutical poisoning and what can be done to improve the situation.  This study involved 453,559 children (<5yrs) who had ingestion of a single product (55% prescription, 45% OTC).  Child self-exposure was responsible for 95%.  Between 2001-2008, these exposures led to 248,023 health care visits, 41,847 admissions, and 18,191 significant injuries.  This data likely underestimates the full extent as the data was collected ‘passively’ by the National Poison Data System (from the U.S. Poison Control Centers).

Although the number of ingestions has been increasing, the number of deaths declined marginally from 2001-2004 to 2005-2008, mainly due to a decline in pediatric acetaminophen deaths.  The authors conclude the problem is getting worse, not better.

What can be done to decrease this burden?

1. Packaging.  Since the poison prevention packaging act was passed in 1970, it has been recognized that the child-resistant closure (CRC) is not sufficient.  The main problem has been that once the vial is open, the entire contents of the vial are available for ingestion.

Options: insertion of needleless syringe for liquid medicines, requiring pressure to be applied to bottle to express medicine & blister packs (inside CRC container) for pills.

2. Targeting interventions for the highest risk medications.  Opioids, cardiovascular agents, and sedatives.

3. Healthy People 2020.  A collaborative approach to this problem is underway.

In our patient populations, we need to remember that the medications we prescribe may be inadvertently ingested by our patients (overdose) or by their siblings.  A word of precaution may save a life.

Additional references:

  • -Pediatrics 2011; 127: e1597-9. Preventing medication overdoses in young children.
  • -Ann Emerg Med 2009; 47: 348-54. Unrecognized toll of opioid abuse on young children.
  • -NEJM 2009; 361: 2105. Changes in FDA labeling of analgesics. ~30,000 hospitalizations  each year due to acetaminophen overdose in U.S. –1/2 inadvertent overdose.
  • -Hepatology 2007; 46: 966. AASLD public policy re: acetaminophen. It is leading cause of acute liver failure in U.S.  500 deaths annually. 10% of cases may occur in those receiving the proper doses.
  • -JAMA 2006; 296: 87-93. Prospective study of daily 4gm acetaminophen in healthy volunteers. (stayed at research facility). ALT >3 ULN in 38%. Resolved over 6 days.
  • http://www.healthypeople.gov/2020/topicsobjectives2020/objectiveslist.aspx?topicId+27

The undiscovered country

Posted on by

The title of this blog is derived from a Star Trek movie.  I think that when we see patients with eosinophilic esophagitis that we are often seeing something new and poorly characterized.

Despite so many unanswered questions, particularly on an individual basis, this topic has seen a lot of interest and there are many advances in both bedside and basic research.  The review article  (Allergy 2012; DOI: 10: 10.1111/j.1398-9995.2012.02787.x) focuses on many of the similarities and differences between pediatric and adult patients.  Is it the same disease? (Probably yes)

With regard to medical history, the article reminds clinicians to ask about coping strategies:

  • do you wash food down with liquid?
  • are you the last one to finish your food?
  • do you chew your food a long time?
  • do you avoid foods like meats or breads?

Clinical features –main difference is greater presentation variety in children.  Adults almost always have long-standing dysphagia.  In pediatrics, painful symptoms, reflux symptoms, and feeding refusal are often seen in early stages.  In both populations, other atopic diseases are very common.

Immunopathogenesis (same in pediatrics and adults):  Th2-type inflammatory response; not just eosinophils but also IL-5-expressing T-cells, B cells, and IgE-bearing mast cells.  A break-down of all the types of quantified cells from a large number of studies is detailed (Table 2).

Allergic profile –main difference is much higher aeroallergen sensitization in adolescent & adult patients than in pediatric patients.  In children, top four allergens: milk, wheat, egg, and soy.  In older patients/adults, nuts are frequent food allergens.

Treatment strategies –basic question of whether to treat for symptomatic relief or histologic response is still debated.  Three goals of treatment are the same:

  • improve quality of life
  • reduce the risk of severe esophageal injury
  • prevent esophageal damage

3 D’s of treatment drugs, diet, dilatation:

Drugs: topical steroids (fluticasone, budesonide) are effective in ~50% of children & these agents may reverse subepithelial fibrosis, PPIs -small percentage have EoE PPI-responsive disease, & systemic steroids.  Lower doses of budesonide may be effective as maintenance treatment (0.25mg BID).  Interestingly, infliximab has not been effective clinically or histologically despite the high amounts of TNF.  Azathioprine (or 6-MP) was effective in three steroid-dependent patients in a pilot study.

Diet –review does not cover new territory (see previous blog: Eosinophilic Esophagitis -Six Food Group Diet).  States that elemental diets are not practical in adults.  Discusses the fact that food allergy identification is difficult & remains a pressing research need.

Dilatation –can provide long-lasting symptom relief.  Dilatation is infrequently utilized in pediatrics and virtually never in absence of other therapies.

On a side note, in my training I was taught that there were 3D’s to treating every patient: diet, drugs, and demeanor — a good attitude goes a long way, particularly in an uncertain world.

Additional references:

  • -Gastroenterology 2011; 141: 1593.  anti-IL-5.  partially effective for EoE.
  • -JPGN 2010; 51: 723. n=91.  Incidental gastric eosinophils does not predict a worse response to fluticasone then isolated EoE.
  • -Clin Gastro & Hepatology 2011; 9: 400 (editorial 370). Budesonide at dose of 0.25mg BID was partially effective in adult cohort of n=28.
  • -Aceves SS et al. Allergy 2010; 65: 109-116. 3 month course of budesonide can lead to resolution of esophageal remodeling. Lamina propria fibrosis resolution correlates with response to topical steroids. Examined effect on lamina propria after 3 months of Rx.
  • -Gastroenterology 2010; 139: 1526. n=36. (summary pg 1429) 15 day course of budesonide (1mg BID). 13/18 in Rx group had improved dysphagia, 72% wiht histologic remission, 92% reduction in eosinophil count. Did not seem to matter if “allergic” or not. 3 pts developed mild candida.
  • -Gastroenterology 2010; 139: 418. Randomized placebo study showed effectiveness.n=15 Rx (n=9 placebo). 87% of Rx group responded.  2ml of water with 0.5gm pulmicort and mixed it with 4-5 packets of splenda.
  • -JPGN 2007; 45: 281/370/319. Review/research symposium/subepithelial fibrosis associated with EoE & dysphagia.
  • -JPGN 2007; 45: 22-31. Th2 Immunity w Eotaxin-3/ C-C chemokine receptor in EoE.
  • -Gastroenterology 2006; 131: 1381-1391. Randomized double-blind, placebo-controlled trial of fluticasone for EoE: 880mcg divided bid; n=21 Rx, n=15 placebo. 50% (vs 9% controls) achieved histologic remission; Rx more effective in those w/o detectable food allergies. 67% (vs. 27% controls) resolution of vomiting.
  • -Clin Gastro & Hep 2007; 5: xxiv. EoE causing Boerhaave’s syndrome (spontaneous rupture)
  • INCREASED FRAGILITY: -Gastrointest Endosc 2003; 57: 407-12. -Clin Gastro Hepatolo 2003; 1: 433-37.
  • -Clin Gastro & Hep 2006; 4: 1328. absolute eosinophilia (AEC 440 vs 140 controls), eosinophil-derived neurotoxin, and eotaxin-3 act as biomarkers of EE activity.
  • -Gastroenterology2006; 131: 2018 (-J Clin Invest 2006; 116: 536-547. ) Eostaxin-3/EcE transcript signature.
  • -J Pediatr 2005; 147: 540 Picture of ringed esophagitis.
  • -JPGN 2004; 39: S8 [abstract 0005]. CHOP experience in 250 pts. NG elemental diet was most effective. ~6% of pts presenting with GER. Strict avoidance of allergens needed.

One more cause of rectal bleeding

Posted on by

Two articles in this month’s JPGN, along with the editorials, make it clear that when patients are having rectal bleeding, we should ask if they are spending an inordinate amount of time straining on the toilet.  (JPGN 2012: 54: 263-65, 266-70, 167-68, 169-70).  This question may help uncover Solitary Rectal Ulcer Syndrome (SRUS).

This syndrome which is often a misnomer because many cases have erythema rather than ulcers; and, lesions can be ulcerative or polypoid.  They can be single or multiple involving the distal rectum.  SRUS often has a delayed diagnosis, 1.7 years and 3.2 years respectively in the two studies.  The differential diagnosis includes polyps, infections, IBD, abuse, and rectal manipulation.  Histology features include muscularinization of lamina propia, mixed inflammatory infiltrate, thickened muscularis mucosa, and epithelial hyperplastic changes.

Treatment includes avoidance of straining/behavior modification, use of laxatives, and perhaps topical mesalamine.

Additional references:

  • -Gastroenterol Clin North Am 2008; 37: 645-68. Rectal disorders/SRUS -review.
  • -Gastrointest Endosc 2005; 5: 755-62,
  • -Eur J Gastroenterol Hepatol 2008; 2: 89-92. SRUS in children.
  • -Gut 2004; 53: 368-70.  Biofeedback for SRUS.
  • -Pediatrics 2002; 110: e79.
  • -Clinical Perspectives in Gastroenterology 1999; 2: 190.

Protecting the most vulnerable

Posted on by

Although pediatric gastroenterologists are not on the front lines of the vaccine controversies, we should add our voices to support immunizations.  Some of our immunocompromised patients are among the most vulnerable and rely on herd immunity to lessen their chances of serious infection.  When healthy children and adults do not receive their immunizations, this does not only increase their risk of infections but the risk to others.

A perfect example of this is highlighted in NEJM 2012; 366: 391-92.  In 2010, California reported over 9000 cases of pertusis; of these cases, 89% occurred in infants less than 6 months.  This population is too young to be adequately immunized.  Ten of these infants died.

The author recommends trying to persuade those who are hesitant to proceed with immunizations.  Parents who are opposed based on personal beliefs will not be persuaded.

  • Remove socioeconomic barriers to vaccination
  • Enforce school entry requirements; it should not be easier to opt out of immunizations than to receive them
  • Aggressively address misinformation
  • Learn to use persuasion effectively: http://www.cdc.gov/vaccines/conversations

Additional references:

  • -NEJM 2011; 365: 1108. RV vaccine resulted in 64,000 less hospitalizations in US between 2007-2009.
  • -NEJM 2010; 362: 289, 299, & 358. Rotavirus vaccines lowering death rate in Africa & Mexico.
  • -NEJM 2011; 364: 2283. Rotavirus vaccine: risk of intussception ~1:50,000-1:70,000; thus could cause ~96 cases per year. Vaccine at same time prevented 80,000 hospitalizations & 1300 deaths in Brazil & Mexico.
  • -Gastroenterology 2007; 132: 1287. Two decades of HBV vaccination in Taiwan
  • -NEJM 2007; 16: 1275, 1278, 1281.  Medical evidence refuting Thimersol toxicity; yet many vaccine cases in litigation
  • -Liver Transplant 2008; 14: 1389.  Vaccine policies:  MMR/Varicella can be given as early as 6 months of age. Must give 3-4weeks before Tx. Can give inactivated ~6-12 mo p-OLT. Except for oral polio, good idea for contacts to get all their immunizations.
  • -Inflamm Bowel Dis 2009;15:1410–1416.  Vaccination Strategies for Patients with Inflammatory Bowel Disease on immunomodulators and biologics

Live Virus Vaccines, Generally Contraindicated in Patients Receiving Immune-Suppressive Therapy:

Anthrax vaccine
Intranasal influenza
Measles-mumps-rubella (MMR)
Polio live oral vaccine (OPV)
Rotavirus
Smallpox vaccine
Tuberculosis BCG vaccine
Typhoid live oral vaccine
Varicella
Yellow fever

Think twice about checking thyroid

Posted on by

Hypothyroidism is not a frequent cause of constipation in children (JPGN 2012; 54: 285-87).  According to this study, the yield on checking for hypothyroidism in pediatric patients with constipation is no greater than in the general population.

This retrospective study examined the records of 873 patients who underwent thyroid testing ordered by pediatric gastroenterology; 443 (51%) had isolated constipation.  In all, 56 had abnormal thyroid function testing though 40 were normal on repeat testing. Of these 16 remaining cases, 7 were known to have hypothyroidism.  Of the nine remaining “new” cases, 3 had slow growth (2 without constipation), 3 had trisomy 21, and 2 were taking medications which affect thyroid function.  This leaves only 1 patient who presented with constipation without a clear risk factor or other indication for testing.

The authors state that 1/443 (0.2%) is quite similar to background incidence of hypothyroidism (0.3%).  The costs of identifying this case would exceed $18,000 but could be considered much higher (~$200,000) when all of the costs of false-positives are considered (eg. endocrinology consultations, followup testing).  In patients with slow growth (with or without constipation), about 2.5% had hypothyroidism.

In short, think twice about checking thyroid status in patients with isolated constipation.

Additional references:

  • -JPGN 2011; 53: S2. 49, 55. ‘Rarely do children with constipation need w/u’–only if alarming features: Delayed meconium, bilious vomiting, bloody stools, fever, bladder disorders, poor growth, NO RESPONSE to conventional treatment, abnormal exam. 25% of functional constipation problems may persist into adulthood.
  • -JPGN 2010; 51: 155. Lack of utility of AXR -suggested only in uncooperative pts, concerns about abuse/concerns about psychologic impact of exam
  • -J Pediatr 2010; 156: 461-5. MRI in children with chronic constipation or not-retentive soiling (n=130, n=28) -MRI showed lumbar sacral abnormalities in 3% –none required neurosurgery (1 w spina bifida occulta, 3 w terminal filum lipomas). Prospective study.
  • JPGN 2006; 43: e1Ye13.  http://www.naspghan.org/user-assets/Documents/pdf/PositionPapers/constipation.guideline.2006.pdf  Guidelines suggest checking thyroid, calcium, celiac and lead if not responding to therapy.

Unexplained chest pain

Posted on by

Not surprisingly -unexplained pediatric chest pain has a high association with anxiety/psychiatric disorders (J Pediatr 2012; 160: 320).  In this study, the authors compared patients (8-17 years) with chest pain (n=100) to a cohort referred with innocent heart murmur (n=80).  In addition to cardiology evaluation, patients had a structured interview and a child health questionnaire to assess for psychiatric disorders; also, the investigators interviewed the parent(s).

Based on DSM-IV criteria, 70% of chest pain patients had an anxiety disorder and 9% had depression.  In contrast, 33% of heart murmur patients had an anxiety disorder and none were depressed.  Among the chest pain subjects, 26% had abdominal pain and 26% had headaches -both higher than the control group, 9% and 10% respectively.  Also, 90% of patients with chest pain had psychiatric disorders which preceded the chest pain.

For pediatric gastroenterologists, a take home message from this article is that chest pain is quite similar to abdominal pain (see references below); it might be interesting to discuss with cardiologists.

  • Do cardiologists experience the same reluctance from families to seek help from mental health?
  • How much testing is required before a functional diagnosis is accepted?
  • Do they follow patients with functional chest pain or send back promptly to primary care physician?

This article does not examine parental mental health issues.  This would be interesting.  In functional abdominal pain, maternal anxiety has been ascribed as the most consistent predictor of outcome (Acta Paediatr 2007; 96: 697-701).  Another factor that would be of interest would be level of activity; exercise helps reduce symptoms of irritable bowel/abdominal pain.

At the same time, the issue of reflux is not addressed by this article and not infrequently the issue of whether reflux is causing chest pain needs to be considered.  An article (Gut 2011; 60: 1473-78) regarding chest pain in adults indicates that patients with pH-probe (or endoscopic) proven GERD often respond partially (>50% reduction in symptoms) to PPI use.  This study reviewed RCTs involving chest pain and PPIs -six met inclusion criteria.  The RR of therapeutic gain for PPI usage was 4.3 for those with proven reflux and 0.4 for those with pH-probe (or endoscopic) negative chest pain.  Interestingly, in this study, heartburn was not predictive of whether chest pain was due to GERD on pH study.

Additional references:

  • -Pediatr Emerg Care 2010; 26: 830-6.  Psychopathology among children presenting to ER with unexplained chest pain.
  • -Clin Gastro 2008; 6: 329-32.  Depressive symptoms common in RAP -45%
  • -Pediatrics 2004; 113: 817.  Anxiety & depression commonly associated with RAP.  anxiety in ~79%, depression ~43%; anxiety often precedes RAP.
  • -JPGN 2011; 53: 200. n=98. 79% of FAP responded to low dose tricyclics
  • -Gastroenterology 2009; 137: 1261, 1207– Editorial.  Amitriptyline helped in 66% vs 58% with placebo. n=90. dose 10mg <35kg, 20mg >35kg. 89% had failed Rx prior to study. ‘Inability to use placebo.. in practice may justify amitriptyline’ Rx. Consider hypnotherapy/CBT first.
  • -Gut 2011; 60: 1473-78. PPI use in unexplained chest pain.
  • -Pain 2006; 122: 43-52. (Walker LS et al), J Pain 2006; 7: 319-26.  Distraction/ignoring important.
  • -J Pediatr 2009; 154: 313 (editorial), 322. Prospective school study. n=237. Weekly prevalence of abd pain was 38%. 18% with persistence for >12 weeks.
  • -Clin Gastro Hepatol 2008; 6: 329-32.  FAP persists into adulthood in 1/3 to 1/2 of cases.
  • -Gastroenterol 2006; 130: 1459-1465.  Functional esophageal d/o.
  • -Clin Gastro & Hep 2006; 4: 558. Review.
  • -Ann Heart J 2000; 40: 367-372.  Sertraline decreased chest pain independent of mood alteration/psychological scores.

Can I go?

Posted on by

How safe is it for IBD patients to travel?  A retrospective study from adult patients with IBD (n=222) compared with controls (n=224) indicates that the risk of travel for IBD patients is only a little more than the general population (Clin Gastroenterol Hepatol 2012; 10: 160-65).

IBD patients with an average age of 37 years had infections during 15% of trips compared with 11% for controls.  92% of infections were due to enteric disease. However, this increased risk was identified in travel to industrialized countries not to developing countries.  This likely indicates that much of the increase is due to IBD flares rather than increased susceptibility to infections.  Nearly half of patients in this study were receiving immunosuppression: immunomodulators 29%, biologics 5%, dual therapy 6%, or corticosteroids 4%.  Not surprisingly, patients with increased IBD flares (OR 1.9) and IBD-related hospitalizations (OR 3.5) represent a group with higher risk for illness.  Most illnesses were mild & self-resolving in a few days.  Only five IBD patients required hospitalization for the following: dehydration, perianal abscess, malaria, flare, & small bowel obstruction).

Additional references:

  • -Clin Gastro & Hep 2010; 8: 490. Review of traveler’s diarrhea. Recs pepto if emesis, rifaximin or cipro or azithromycin if watery diarrhea, azithromycin if bloody diarrhea
  • -Clin Gastro & Hep 2007; 5: 451. Use of rifaximin (200mg tid)-loperamide provided rapid improvement.
  • -NEJM 2006; 354; 119. Traveler’s diarrhea.
  • -NEJM 2002; 347: 505.  Illness after travel.
  • -www.cdc.gov/travel/index.htm

It’s worth the cost

Posted on by

Recently the cost of Sitzmarks® increased to $175 (for 12)–it’s worth the cost.  According to one study, the use of a transit study helps determine which patients will benefit from colonic manometry (JPGN 2012; 54: 258-62).  A retrospective review of 24 children showed that all five children with normal oral-anal transit (OTT) studies had normal colonic manometry.  In contrast, 9/19 (47%) with abnormal (slow OTT) had abnormal colonic manometry.

The authors define their approach to OTT which is helpful.

  • In patients with a fecal impaction, this was cleared prior to starting study
  • If patients had difficulty with capsule ingestion, markers were administered by embedding in part of a banana or mixed with applesauce
  • Stimulant laxatives withheld for 72hrs prior to study
  • AXR obtained on days 3 and 5
  • Slow OTT (abnormal) defined as >6 markers proximal to rectum on day 5

Of those with abnormal colonic manometry, two-thirds (6) were referred for surgical intervention; one patient with normal OTT had surgery.  Surgeries:  3 cecostomy, 4 subtotal colectomy.

Additional references:

  • -JPGN 2004; 38: 75. Colostomy in 10 children with intractable constipation.
  • -Arch Dis Child. 2004 Jan;89(1):13-6. Benninga MA, Voskuijl WP, Akkerhuis GW, Taminiau JA, Buller HA. Related Articles,  Colonic transit times and behaviour profiles in children with defecation disorders.
  • -J Pediatr Surg. 2004 Jan;39(1):73-7. Youssef NN, Pensabene L, Barksdale E Jr, Di Lorenzo C.  Is there a role for surgery beyond colonic aganglionosis and anorectal malformations in children with intractable constipation?
  • -Am J Gastroenterol. 2003 May;98(5):1052-7.  Pensabene L, Youssef NN, Griffiths JM, Di Lorenzo C. Related Articles, Colonic manometry in children with defecatory disorders. role in diagnosis and management.
  • -JPGN 2002 Jul;35(1):31-8. Gutierrez C, Marco A, Nogales A, Tebar R. Total and segmental colonic transit time and anorectal manometry in children with chronic idiopathic constipation.
  • -JPGN 2001 Nov;33(5):588-91.  Villarreal J, Sood M, Zangen T, Flores A, Michel R, Reddy N, Di Lorenzo C, Hyman PE.  Colonic diversion for intractable constipation in children: colonic manometry helps guide clinical decisions.
  • -http://www.sitzmarks.com/buyonline.aspx

Help with hepcidin

Posted on by

Over the past several years, the mechanisms involved in iron overload have been carefully examined and the genetic basis for most of these disorders is now understood.  Several review articles on these disorders have been published; the most recent with excellent diagrams is in last week’s NEJM (NEJM 2012; 366: 348-59 & NEJM 2012; 366: 376-77). Although the process is quite complicated, the most important aspect regarding iron homeostasis is a feedback loop involving hepcidin-ferroportin.  Hepcidin functions as a ‘hypoferremia hormone.’  It down regulates ferroportin release of iron into the circulation.  Hepcidin is also an acute-phase protein and inflammation affects its function.

Hepcidin levels fluctuate in response to the body’s iron needs: more hepcidin causes less iron absorption & less hepcidin causes more iron absorption.

  • Iron balance disorders can usually be attributed to altered hepcidin production.
  • Anemia of chronic disease, though multifactorial, is mostly due to increased hepcidin production in response to inflammation.
  • Hemochromatosis results from genetic mutations causing lack of normal hepcidin production.  The severity of these disorders correlates with hepcidin levels.
  • Hepcidin agonists could be used to treat hemochromatosis and other iron overload conditions (eg. thalassemia with transfusion therapy).  For hemochromatosis, phlebotomy will be less expensive.
  • Hepcidin antagonists could treat anemia of chronic disease

Additional references:

  • -Hepatology 2011; 54: 328.  Review.  Guidelines.
  • -Hepatology 2010; 52: 925.  HFE homozygotes, n=31,192 w low risk of clinical symptoms if ferritin <1000.
  • -Gastroenterology 2010; 139: 393. Review –pathogenesis/dx/Rx
  • -Hepatology 2009; 50: 94.  C282Y/H63D compound heterozygotes (n=180) are at low risk for hemochromatosis-related morbidity compared with control group.
  • -Hepatology 2008; 48: 991.  Review.
  • -Hepatology 2007; 46: 960, 1071.  Review of clinical phenotypes.  Of C282Y homozygotes, only 1-2% develop HCC, 6% cirrhosis, 25% liver fibrosis, 38% Fe overload, 61-75% develop raised serum iron indices.
  • -Hepatology 2007; 46: 1291. Review of hemochromatosis
  • -Hepatology 2007; 45: 253. Review of iron metabolism
  • -NEJM 2004; 350: 2383. Review.  Several genetic mutations associated with clinical phenotype.  type 1: Classic HFE, types 2A & 2B: (Juvenile type)  HJV & HAMP (gene products hemojuvelin & hepcidin), type 3:TFR2 (transferrin receptor 2), and type 4:SLC40A1
  • -NEJM 2005; 352: 1011. Algorithm.  If transferrin saturation <16%, check ferritin.  If ferritin less than 30, Fe-deficiency; if >100, anemia of chronic disease.  If 30-100, check soluble transferrin receptor (level of sTranReceptor/log ferritin less than 1 is c/w anemia of chronic disease whereas when this ratio is greater than 2, c/w combined Fe-def anemia and anemia of chronic disease).  Hepcidin is produced by hepatocytes and regulates iron homeostasis.  Hepcidin interacts with ferroportin, an iron export protein on enterocytes (& other cells), & facilitates internalization and degradation of ferroportin.  It may lead to decreased dietary iron absorption and to retention of iron body stores.  Hepcidin expression can be up-regulated by high iron levels or during acute phase inflammatory responses (thus can contribute to anemia of chronic disease).  Hereditary hemochromatosis associated with low hepcidin levels in the face of increased iron body stores.  Several genes can affect hepcidin loss of function, including HFE, hemojuvelin (HJV), and transferrin receptor 2 (TFR2).
  • -Gastroenterology 1996; 110: 1107.  Sentinel article discussing long-term survival in hemochromatosis and role of iron.

More on ethanol locks

Posted on by

In a post earlier this week (Four advances for intestinal failure), ethanol locks were discussed.  More on information this subject (Pediatrics 2012: 129: 318-29) comes in a meta-analysis.  These authors identified 4 retrospective studies in pediatric IF populations.  Ethanol locks reduced infections by 81% and line replacements by 72%.  The studies in this meta-analysis overlapped with the six studies cited in the previous post.  Adverse events were rare and included thrombotic events.

Additional reference:

  • -JPEN 2012; 36: 36S-42S