Severe Anemia in a Patient with Rheumatoid Arthritis: Differential Diagnosis and Hemolysis Workup

By SWA

This peripheral blood smear shows significant red blood cell abnormalities, and given the context of rheumatoid arthritis (RA) and severe anemia, several possibilities arise for diagnosis:

In this case of a rheumatoid arthritis (RA) patient presenting with severe anemia, a peripheral blood smear reveals several diagnostic clues, including the presence of schistocytes and possible bite cells. Given the patient's history and findings, the differential diagnosis includes Microangiopathic Hemolytic Anemia (MAHA), methotrexate-induced folate deficiency, and G6PD deficiency, with Large Granular Lymphocytic Leukemia (LGLL) considered due to the association with RA. Further diagnostic testing including hemolysis labs and G6PD activity is crucial for accurate diagnosis.

  1. Rheumatoid Arthritis with Anemia: RA is commonly associated with anemia of chronic disease, which usually presents with normocytic, normochromic anemia. However, given the severe anemia and additional findings, more specific causes need to be considered.

  2. Large Granular Lymphocytic Leukemia (LGLL): As you mentioned, LGLL can be associated with RA and anemia. LGLL typically shows large granular lymphocytes, which may not be seen in this image. Absence of granularity in the cells makes LGLL less likely at this stage, but it is still worth considering if there are other clinical signs or peripheral lymphocytosis.

  3. Folate Deficiency: Methotrexate (MTX), often used in RA treatment, can lead to folate deficiency, which causes megaloblastic anemia. However, the smear does not show hypersegmented neutrophils, which are characteristic of folate deficiency, making it less likely as a primary cause in this case.

  4. Microangiopathic Hemolytic Anemia (MAHA): The presence of schistocytes (fragmented red blood cells) on the smear suggests the possibility of a hemolytic process such as MAHA. Causes include thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), or disseminated intravascular coagulation (DIC). MAHA should be considered, and appropriate labs (LDH, haptoglobin, bilirubin, and a Coombs test) should be done to evaluate hemolysis. The lack of platelets is concerning and suggests thrombocytopenia, which could be related to MAHA or another process.

  5. G6PD Deficiency: The possible bite cell you mention could indicate oxidative damage, which might suggest G6PD deficiency, especially if the patient has been exposed to oxidative stressors (drugs, infections). This should be reviewed by checking the patient’s medication history and testing for G6PD activity.

  6. Other Considerations: If hemolysis is confirmed, other causes of hemolytic anemia such as autoimmune hemolytic anemia (AIHA) should be evaluated. RA patients are also at risk for AIHA, especially if on immunosuppressive therapy.

Suggested Next Steps:

  • Perform hemolysis labs: LDH, haptoglobin, reticulocyte count, indirect bilirubin, and Coombs test to rule out hemolysis.
  • Investigate for MAHA: Check for schistocytes, and evaluate for TTP, HUS, or DIC.
  • Consider G6PD testing if oxidative stress from medications is suspected (especially in the context of bite cells).
  • Folate/B12 levels, especially given MTX use.

In summary, based on the smear and clinical context, you should focus on ruling out hemolytic anemia (MAHA) and medication-induced causes like G6PD deficiency and folate deficiency, given the patient's RA and treatment history.

Reference:

Image
© 2000-2025 Sieglinde W. Alexander. All writings by Sieglinde W. Alexander have a fife year copy right.
Library of Congress Card Number: LCN 00-192742
ISBN: 0-9703195-0-9

Comments

Post a Comment

Popular posts from this blog

Toxic Skin Condition Post-mRNA COVID-19 Vaccination

By SWA
Image
Identifying Severe Skin Conditions Post-Vaccination Following administration of the BioNTech mRNA vaccine, a small subset of individuals may develop severe and complex reactions. These reactions are often misdiagnosed or misunderstood due to their rarity and diverse presentation. This essay examines a case characterized by severe skin conditions, systemic symptoms, and complications such as hypercalcemia and crystal formation. It highlights the need for accurate diagnosis, holistic management, and increased awareness of these rare but significant vaccine-related adverse events. Initial Symptoms and Misdiagnoses Severe symptoms began shortly after the first dose of the BioNTech vaccine, initially presenting as petechiae, diagnosed by a rheumatologist. However, following the second dose, symptoms rapidly escalated, resulting in intense burning pain and thinning of the skin. The skin on the legs and thighs became paper-thin and could tear with the slightest touch, with the affected area e...
Read more

Dysferlin Protein: Key Roles, Genetic Locations

By SWA
Image
The purpose of this article is to share and discuss the details of a new discovery, which is highlighted within: CRISPR-Cas9: A Breakthrough Tool to Repair the DYSF Gene The dysferlin protein plays an essential role in maintaining the integrity of muscle cell membranes, particularly in tissues that endure significant mechanical stress, such as skeletal and cardiac muscles . Encoded by the DYSF gene , dysferlin is indispensable for repairing damaged cell membranes after injury caused by muscle contraction or external forces. This article explores the main locations where dysferlin is produced, its role in muscle repair, and supportive nutritional and therapeutic strategies for individuals with dysferlin deficiency, such as those affected by dysferlinopathies (e.g., Limb-Girdle Muscular Dystrophy Type 2B or Miyoshi Myopathy). Currently, there is no definitive answer as to why the severity of dysferlin protein expression or depletion varies. Do pathogens play a role in the methylation o...
Read more

Is ME CFS connected to Spinal Muscular Atrophy (SMA) or Post Polio?

By SWA
Image
Today, I understand why Spinal Muscular Atrophy (SMA) received little attention, particularly in the mid-50s. This complex and debilitating genetic illness was poorly understood, and patients' symptoms were often minimized or even dismissed. For more information, please visit the Spinal Muscular Atrophy (SMA) page on MalaCards . Even now, many neurologists lack detailed knowledge of SMA, and comprehensive examinations mentioned in research are rarely pursued. In 2008, while investigating permanent adrenal insufficiency, an MRI ordered by my endocrinologist unexpectedly revealed Chiari Malformation II. However, surgery in 2009 brought no improvement. In 2010, a DNA test showed a genetic marker in the ACTN3 gene: https://www.malacards.org/search/results?q=ACTN3%20gene%20and%20Spinal%20Muscular%20Atrophy%20(SMA) A 2015 MRI revealed ankylosing spondylitis, multiple Tarlov cysts, stenosis at L4 and L5, spinal canal narrowing, and widespread degenerative changes. Surgery on L4 and L5 ...
Read more