Anemia in IBD -NASPGHAN Position Paper

A Goyal et al. JPGN 2020; 71: 563-582 Full text (free). Anemia in Children With Inflammatory Bowel Disease: A Position Paper by the IBD Committee of the North American Society of Pediatric Gastroenterology, Hepatology and Nutrition.

Main Types of Anemia in Inflammatory Bowel Disease:

  • “IDA is the most common cause of anemia in children with IBD. True iron deficiency results from a number of factors, including chronic blood loss secondary to gastrointestinal bleeding, decreased iron absorption because of tissue or systemic inflammation and from reduced absorptive surface area. “
  • “Functional iron deficiency (FID) results from high levels of circulating hepcidin, which binds to and disables the iron transporter, ferroportin. Under the influence of hepcidin, ferroportin-mediated export of intracellular iron is stalled, leaving the iron trapped within the enterocytes and macrophages… the underlying inflammation, which induces hepcidin production can result in anemia secondary to FID.”
  • Anemia of chronic disease (ACD) “occurs from various downstream pathways secondary to inflammation.”

Table 4:

Recommended Testing

  • Screening Tests: “initially a complete blood count (CBC), CRP, and ferritin levels should be performed. If a patient is found to be anemic, then testing should include CBC with differential, including mean corpuscular volume (MCV), mean corpuscular Hgb concentration (MCHC), red cell distribution width (RDW), reticulocyte count, CRP, serum ferritin, and transferrin saturation (TSAT)”
  • Serum iron level … is … unreliable in the assessment of iron deficiency as the level fluctuates with several variables.
  • Transferrin saturation (TSAT) is a measure of the iron content in the circulating transferrin and reflects the availability of utilizable iron

Treatment of Anemia

  • In mild anemia (Hgb ≥10 g/dL) and/or quiescent disease, oral iron should be tried first.
  • Parenteral iron is indicated when oral iron is ineffective or poorly tolerated, in patients with moderate-severe anemia and/or with active inflammation.
  •  According to ECCO guidelines, an IV replacement goal of achieving of ferritin level of up to 400 μg/L is more likely to prevent recurrence of anemia…a transferrin saturation of 50% and serum ferritin of 800 μg/L should not be exceeded
  • Regarding iron effects on microbiome: studies indicate that dysbiosis at baseline worsens the unfavorable shifts in microbiome with oral iron therapy…Our position, however, is that further studies are required in humans before any reliable conclusions can be drawn. [My question: have the effects of oral iron supplementation on the microbiome been compared to IV iron supplementation on the microbiome?]
  • Table 6 lists various iron products including costs and dosing.
  • The hypersensitivity reactions to parenteral iron are mostly secondary to iron nanoparticles that trigger complement activation-related pseudo-allergy (CARPA)….It is important that parenteral iron be administered by trained personnel. Emergency medications and resuscitative equipment should be available during these infusions.

My take: This is a useful resource for a very common problem.

Related blog posts:

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Finding the Right Specialist

A recent clinical problem-solving case report highlights the fact that seeing the right specialist helps a great deal with pattern recognition (NEJM 2013; 368: 1345-51).  In this report, intriguingly titled “The Essential Element” the authors describe a 21-year-old who presented with refractory hemolytic anemia along with low albumin, low alkaline phosphatase, and elevated total & direct bilirubins.  Her course was somewhat protracted due to treatment of hemolytic anemia and lack of recognition of underlying hepatocellular disease.  After readmission three months later the diagnosis of Wilson’s disease was made and quickly she underwent orthotopic liver transplantation.

A couple of pointers from this article for me included the following:

  • Parenchymal injury from the oxidative effect of copper leads to the hepatocellular injury.  Release of copper also causes oxidative damage of erythroctye membranes.
  • The low alkaline phosphatase which is characteristic of Wilson’s is potentially due to the oxidative damage from free radicals or by competition at the active site of the alkaline phosphatase enzyme.
  • The combination of hemolysis with liver dysfunction should prompt consideration of Wilson’s.

Most hepatologists would quickly recognize the pattern presented in this case report.  Getting the patient to the right physician is the key.

Comprehensive review on Wilson’s:

Diagnosis and treatment of Wilson disease: An update – American …  AASLD Guidelines for Wilson disease.  This is an excellent resource for diagnosis and management.