Back at the VA, I inherited 3 patients. We are on call today (day 2), but given 3 patients I stretched rounds out for 100 minutes.
Internists can do that. I dissected each patient, made multiple teaching points, and just had a blast.
I have a dilemma that I uncovered.
The patient is in his early 50s, has had DM for around 10 years, and has a foot ulcer without osteomyelitis. Incidently, he has hepatitis C and may have early cirrhosis. The intern asked me about his anemia (Hgb <8).
We got into a long discussion of anemia. I asked about previous evaluation, and they could not recall details. We opened up the EMR and started searching.
B12 and folate are clearly normal (several times). Iron saturation is consistently low, but ferritin is always mildly elevated. His last retic count is 0.7 in the face of Hgb <10.
His creatinine now is 1.5 with eGFR of 49. His creatinine has been modestly elevated for the last year or two, although it fluctuates between 1.5 and 2.2.
We go to the bedside, and I explain several issues to the patient. I mention that we might want to do a bone marrow analysis, and he tells me that he had one last year.
We go back to the EMR and find the report – normal cellularity and normal iron stores.
How do you approach this problem? I made some decisions and will report back on those decisions.
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1 Response to 15 days at the VA – day 1
Stalwart Hospitalist
December 20th, 2009 at 6:29 pm
This patient has anemia secondary to chronic inflammation. Chronic active hepatitis C can be a chronically inflammatory condition (sometimes resulting in cryoglobulinemia, vasculitis, inflammatory arthritis, etc.).
Persistent inflammation, manifested by elevated levels of IL-6, result in higher levels of a short peptide called hepcidin. Hepcidin acts to sequester iron in the reticuloendothelial system (through downregulating ferroportin synthesis), making less iron available in the circulation and less iron mobilizable for erythrocytosis.
The typical iron studies and bone marrow evaluation in chronic inflammation anemia shows a low iron saturation (since iron is sequestered out of circulation), an elevated ferritin (as an acute phase reactant to inflammatory cytokines) and normal to high iron stores in the bone marrow (since hepcidin promotes iron storage rather than use).
Hepcidin is probably part of the innate immune system — sequestering iron was probably an evolutionary move to slow bacterial growth in bacteremia, since all organisms need iron to replicate and grow.
Treating this can be challenging — the body often has enough iron and erythropoietin, but the building blocks are prevented from being used. Hepcidin receptor antagonists and anti-hepcidin biologics are under investigation currently.