# Use of Human Intravenous Immunoglobulin Therapy in Two Dogs with Non-Neoplastic Bone Marrow Disorders Refractory to Immunosuppressive Therapy

**Authors:** Eun-Ji Kim, Hyun-Jung Han

PMC · DOI: 10.3390/vetsci13020145 · Veterinary Sciences · 2026-02-03

## TL;DR

Human intravenous immunoglobulin improved anemia in two dogs with non-cancerous bone marrow disorders that did not respond to standard treatments.

## Contribution

This is the first report showing human intravenous immunoglobulin can be an effective adjunct therapy for refractory canine non-neoplastic bone marrow disorders.

## Key findings

- Reticulocyte production index increased significantly in both dogs after hIVIG treatment.
- Transfusion intervals were prolonged, reducing the need for blood transfusions.
- Hematocrit levels remained normal for extended periods following treatment.

## Abstract

Immune-mediated non-neoplastic bone marrow disorders in dogs are uncommon conditions characterized by impaired erythropoiesis and resultant non-regenerative anemia. Affected dogs develop severe anemia and require repeated blood transfusions, and they may not improve with commonly used immunosuppressive medications. Human intravenous immunoglobulin, a concentrated preparation of antibodies collected from healthy people, has been used in human medicine to regulate the immune system in refractory immune disorders. This case report describes two dogs with chronic, non-regenerative anemia associated with non-neoplastic bone marrow disorders that did not improve despite multiple transfusions and immunosuppressive treatment. Both dogs received several doses of human intravenous immunoglobulin over four months. After treatment, erythroid regeneration improved, with the reticulocyte production index increasing from 0.42 to 3.81 in case 1 and from 0.27 to 1.34 in case 2. The average transfusion interval was prolonged (10.3 to 20.9 weeks in case 1; 11.6 to 31.7 weeks in case 2), and the duration of maintaining a normal hematocrit increased. These findings suggest that human intravenous immunoglobulin may represent adjunctive therapy for dogs with non-neoplastic bone marrow disorders refractory to standard immunosuppressive treatment, improving hematologic parameters and reducing transfusion requirements.

Immune-mediated non-neoplastic bone marrow disorders (NNBMD), including precursor-targeted immune-mediated anemia (PIMA) and myelodysplastic syndrome (MDS), can cause non-regenerative anemia in dogs and often fail to respond to immunosuppressive treatment. Human intravenous immunoglobulin (hIVIG) has been proposed as an immunomodulatory therapy for refractory hematologic disease in humans, but evidence in veterinary patients remains limited. This case report describes the adjunctive use of hIVIG and the associated clinical responses observed in two dogs with refractory NNBMD. A 10-year-old (3.2 kg) spayed female Maltese (case 1) showed persistent non-regenerative anemia, with hematocrit (HCT) 15.6–20.2% and reticulocyte production index (RPI) 0.12–0.69, requiring four transfusions over 10 months, and was diagnosed with PIMA based on bone marrow cytology demonstrating destruction of erythroid precursors. A 7-year-old (9.3 kg) intact female Dachshund (case 2) had sustained non-regenerative anemia (HCT 10.8–20.9%, RPI 0.12–0.40) necessitating eight transfusions over 20 months and was diagnosed with MDS characterized by dyserythropoiesis. Human intravenous immunoglobulin (0.5 g/kg over 6 h) was administered six times in case 1 and seven times in case 2 over a four-month period. After initiating hIVIG therapy, RPI increased (0→1.80 and 0.25→2.10 in cases 1 and 2), and HCT remained above 20% without further transfusions. To our knowledge, this is the first clinical report demonstrating the adjunctive use of hIVIG and associated hematologic improvement in canine NNBMD.

## Linked entities

- **Diseases:** myelodysplastic syndrome (MONDO:0018881)
- **Species:** Canis lupus familiaris (taxon 9615)

## Full-text entities

- **Genes:** CRP (C-reactive protein) [NCBI Gene 488629], EPO (erythropoietin) [NCBI Gene 404002], EPO (erythropoietin) [NCBI Gene 2056] {aka DBAL, ECYT5, EP, MVCD2}, JAK1 (Janus kinase 1) [NCBI Gene 442952], FASLG (Fas ligand) [NCBI Gene 356] {aka ALPS1B, APT1LG1, APTL, CD178, CD95-L, CD95L}
- **Diseases:** lethargy (MESH:D053609), erythroid disorder (MESH:D029503), Evans syndrome (MESH:C536380), Bone Marrow Disorders (MESH:D001855), thrombocytopenia (MESH:D013921), immune (MESH:D007154), hypothyroidism (MESH:D007037), hematologic disease (MESH:D006402), leukemia (MESH:D007938), autoimmune hemolytic anemia (MESH:D000744), collapse (MESH:D001261), -mediated anemia (MESH:D000740), flushing (MESH:D005483), thrombotic (MESH:D013927), bleeding diathesis (MESH:D006474), intra-abdominal hemorrhage (MESH:D000082122), hematochezia (MESH:D006471), pulmonary hypertension (MESH:D006976), refractory anemia (MESH:D000753), myasthenia gravis (MESH:D009157), pemphigus foliaceus (MESH:D010392), erythroid hyperplasia (MESH:D006965), -mediated non-neoplastic bone marrow disorders (MESH:D019046), thromboembolic (MESH:D013923), aplastic processes (MESH:D000741), Kawasaki disease (MESH:D009080), hemolytic anemia (MESH:D000743), hypersensitivity (MESH:D004342), lymphoma (MESH:D008223), macrocytic hypochromic anemia (MESH:D000748), tricuspid regurgitation (MESH:D014262), essential thrombocytosis (MESH:D013922), immune thrombocytopenia (MESH:D016553), cardiopulmonary disease (MESH:D006323), facial edema (MESH:D004487), erythroid aplasia (MESH:C536482), congenital dysmyelopoiesis (MESH:D008209), neoplasia (MESH:D009369), pancytopenia (MESH:D010198), dysplasia (MESH:D015792), dyserythropoiesis (MESH:C566368), inflammation (MESH:D007249), gastrointestinal symptoms (MESH:D012817), injury to (MESH:D014947), chronic inflammatory demyelinating polyneuropathy (MESH:D020277), syncope (MESH:D013575), morphological abnormalities (MESH:D000013), bone marrow failure (MESH:D000080983), dysplastic (MESH:D004416), vomiting (MESH:D014839), iron deficiency (MESH:D000090463), anaphylaxis (MESH:D000707), hemolysis (MESH:D006461), non (MESH:C580335), myelodysplasia (MESH:D009436), acute myeloid leukemia (MESH:D015470), hypotension (MESH:D007022), MDS (MESH:D009190), -mediated hemolytic anemia (MESH:C567355), diarrhea (MESH:D003967)
- **Chemicals:** leflunomide (MESH:D000077339), aclarubicin (MESH:D015250), omeprazole (MESH:D009853), homocysteine (MESH:D006710), Sildenafil (MESH:D000068677), Cyclosporine (MESH:D016572), DEA 1 (-), clopidogrel (MESH:D000077144), T4 (MESH:D013974), prednisolone (MESH:D011239), azacitidine (MESH:D001374), folate (MESH:D005492), cobalamin (MESH:D014805), prednisone (MESH:D011241), azathioprine (MESH:D001379), triglyceride (MESH:D014280), methylmalonic acid (MESH:D008764), lactate (MESH:D019344), mycophenolate mofetil (MESH:D009173), histamine (MESH:D006632), decitabine (MESH:D000077209), oclacitinib (MESH:C588062), chlorpheniramine (MESH:D002744), iron (MESH:D007501)
- **Species:** Homo sapiens (human, species) [taxon 9606], Canis lupus familiaris (dog, subspecies) [taxon 9615], Babesia (genus) [taxon 5864]

## Full text

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## References

28 references — full list in the complete paper: https://tomesphere.com/paper/PMC12945045/full.md

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Source: https://tomesphere.com/paper/PMC12945045