# Lead Toxicity Masquerading as Autoimmune Haemolytic Anaemia: A Diagnostic Pitfall in Unexplained Anaemia

**Authors:** John Ee Chew, Nathan Klose

PMC · DOI: 10.7759/cureus.102622 · Cureus · 2026-01-30

## TL;DR

A case of lead poisoning mistaken for autoimmune anemia shows the importance of checking for toxic exposure in unexplained blood disorders.

## Contribution

Highlights lead toxicity as an under-recognized cause of unexplained anemia mimicking autoimmune haemolytic anaemia.

## Key findings

- Lead toxicity can mimic autoimmune haemolytic anaemia with similar hematological features.
- Peripheral blood morphology and exposure history are crucial for accurate diagnosis.
- Chelation therapy improved clinical and hematological outcomes in this case.

## Abstract

Lead toxicity is an uncommon but clinically important cause of unexplained anaemia. Its heterogeneous haematological manifestations can mimic autoimmune haemolytic anaemia, resulting in diagnostic uncertainty and delayed recognition.

A 49-year-old woman presented with a three-week history of worsening abdominal pain and lethargy. She had a background of inclusion body myositis treated with long-term intravenous immunoglobulin and recent initiation of mycophenolate mofetil. Initial investigations demonstrated severe anaemia with reticulocytosis but minimal biochemical evidence of haemolysis. A weakly positive direct antiglobulin test (IgG 1+, C3d negative) raised suspicion for autoimmune haemolysis. The initial peripheral blood film was reported as showing marked red cell agglutination without additional abnormalities. Progressive anaemia prompted extensive investigations, including infectious, immunological, and haematological workups, all of which were unremarkable. Bone marrow aspirate demonstrated atypical plasma cells, prompting re-examination of the peripheral blood film, which revealed Pappenheimer bodies and basophilic stippling. Further history identified ingestion of an unlabelled health supplement, and toxicology testing confirmed markedly elevated blood lead levels. Chelation therapy with succimer led to clinical and haematological improvement. Public health investigation subsequently confirmed the supplement as the source of lead and mercury exposure.

This case highlights lead toxicity as an important but under-recognised mimic of autoimmune haemolytic anaemia. Careful review of peripheral blood morphology and a thorough exposure history are essential when evaluating unexplained anaemia with an inconclusive haemolysis workup.

## Linked entities

- **Chemicals:** lead (PubChem CID 5352425), mercury (PubChem CID 23931), succimer (PubChem CID 2724354)
- **Diseases:** inclusion body myositis (MONDO:0007827)

## Full-text entities

- **Genes:** CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, GGTLC5P (gamma-glutamyltransferase light chain 5 pseudogene) [NCBI Gene 653590] {aka GGT}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, TF (transferrin) [NCBI Gene 7018] {aka HEL-S-71p, PRO1557, PRO2086, TFQTL1}, FECH (ferrochelatase) [NCBI Gene 2235] {aka EPP, EPP1, FCE}, ERVK-13 (endogenous retrovirus group K member 13) [NCBI Gene 100861467] {aka c3_D}, GGT1 (gamma-glutamyltransferase 1) [NCBI Gene 2678] {aka CD224, D22S672, D22S732, GGT, GGT 1, GGTD}, ALPP (alkaline phosphatase, placental) [NCBI Gene 250] {aka ALP, PALP, PLAP, PLAP-1}, HP (haptoglobin) [NCBI Gene 3240] {aka HP2ALPHA2, HPA1S}, ALAD (aminolevulinate dehydratase) [NCBI Gene 210] {aka ALADH, PBGS}, CMPK1 (cytidine/uridine monophosphate kinase 1) [NCBI Gene 51727] {aka CK, CMK, CMPK, UMK, UMP-CMPK, UMPK}
- **Diseases:** infection (MESH:D007239), haemolytic (MESH:D006463), impaired (MESH:D060825), neuropsychiatric symptoms (MESH:D001523), Toxicity (MESH:D064420), lethargy (MESH:D053609), abdominal pain (MESH:D015746), AIHA (MESH:D000744), Lead poisoning (MESH:D007855), haematologic abnormalities (MESH:D006402), reticulocytosis (MESH:D045262), erythroid hyperplasia (MESH:D006965), saturnine colic (MESH:D003085), autoimmune haemolysis (MESH:D006461), gastrointestinal bleeding (MESH:D006471), haematologic, renal, and neurologic toxicity (MESH:D007674), autoimmune (MESH:D001327), ring sideroblasts (MESH:D012303), constipation (MESH:D003248), inclusion body myositis (MESH:D018979), myositis (MESH:D009220), Anaemia (MESH:D000743)
- **Chemicals:** haem (MESH:D006418), EDTA (MESH:D004492), bilirubin (MESH:D001663), dimercaprol (MESH:D004112), Lead Toxicity (-), mycophenolate mofetil (MESH:D009173), mercury (MESH:D008628), arsenic (MESH:D001151), Lead (MESH:D007854), heavy metals (MESH:D019216), Folate (MESH:D005492), DMSA (MESH:D004113), B12 (MESH:C034730), Iron (MESH:D007501)
- **Species:** Mycoplasmoides pneumoniae (Filterable agent of primary atypical pneumonia, species) [taxon 2104], human gammaherpesvirus 4 (Epstein Barr virus, no rank) [taxon 10376], Homo sapiens (human, species) [taxon 9606]
- **Mutations:** L, H

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12949993/full.md

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12949993/full.md

## References

10 references — full list in the complete paper: https://tomesphere.com/paper/PMC12949993/full.md

---
Source: https://tomesphere.com/paper/PMC12949993