Concurrent immune thrombocytopenia and amyotrophic lateral sclerosis with transient improvement in both conditions following efgartigimod: a case report
Case Report

Concurrent immune thrombocytopenia and amyotrophic lateral sclerosis with transient improvement in both conditions following efgartigimod: a case report

Kazuto Togitani1 ORCID logo, Ryosuke Oki2, Daisuke Kuzume3, Yoshiki Uemura1

1Department of Hematology, Chikamori Hospital, Kochi, Japan; 2Department of Neurology, Tonan Hospital, Kochi, Japan; 3Department of Neurology, Chikamori Hospital, Kochi, Japan

Contributions: (I) Conception and design: K Togitani; (II) Administrative support: None; (III) Provision of study materials or patients: All authors; (IV) Collection and assembly of data: K Togitani; (V) Data analysis and interpretation: K Togitani; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Kazuto Togitani, MD. Department of Hematology, Chikamori Hospital, 1-1-16 Okawasuzi, Kochi-shi, Kochi 780-8522, Japan. Email: togitani@outlook.jp.

Background: Immune thrombocytopenia (ITP) is an acquired autoimmune disorder characterized by isolated thrombocytopenia, most commonly mediated by pathogenic immunoglobulin G (IgG) autoantibodies. Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease with incompletely understood etiology, in which immune dysregulation has been implicated. Efgartigimod, the neonatal Fc receptor (FcRn) inhibitor approved for chronic/persistent ITP, accelerates IgG degradation by blocking IgG recycling via FcRn. We describe a patient with ITP and comorbid ALS in whom FcRn inhibition was temporally associated with transient improvement in both conditions.

Case Description: A 66-year-old Japanese man with ALS diagnosed in March 2023 developed severe thrombocytopenia in September 2024, with a platelet count of 1.0×109/L and an elevated immature platelet fraction (18.1%). After differential diagnosis, ITP was diagnosed. Prednisolone and eltrombopag were ineffective. Intravenous efgartigimod (10 mg/kg) was initiated in October 2024 (day 0), resulting in a prompt platelet increase. Total IgG decreased from 1,643 to 858 mg/dL, and platelet-associated IgG normalized. During efgartigimod therapy, the revised ALS Functional Rating Scale (ALSFRS-R) score showed a subtle increase from 40 to 41 in January 2025 (day 83). After nine doses, efgartigimod was discontinued in January 2025 (day 91) and romiplostim was titrated with the goal of treatment cessation, but platelet counts remained unstable without remission. Unexpectedly, vital capacity increased from 81% to 93.9% in February 2025 (day 109). Thereafter ALS progressed and frequent clinic visits became difficult, romiplostim was replaced with eltrombopag and fostamatinib was added in June 2025 (day 238), resulting in stable platelet counts. In December 2025 (day 422, eleven months after efgartigimod discontinuation) total IgG increased to 1,499 mg/dL; platelet-associated IgG remained normal, however, ALSFRS-R declined to 31 and gastrostomy was required.

Conclusions: This case documents concurrent ITP and ALS with transient improvement in platelet counts and ALS functional measures during FcRn inhibition with efgartigimod, followed by deterioration after discontinuation. Although causality cannot be inferred from a single case and neurologic changes may be coincidental, the temporal association raises the possibility that IgG-mediated immune mechanisms contribute to disease activity in a subset of ALS patients with autoimmune comorbidities. Further clinical and translational studies are warranted.

Keywords: Immune thrombocytopenia (ITP); amyotrophic lateral sclerosis (ALS); efgartigimod; revised ALS Functional Rating Scale (ALSFRS-R); case report

Received: 28 December 2025; Accepted: 26 February 2026; Published online: 24 March 2026.

doi: 10.21037/aob-2025-1-59

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Key findings

• This case report describes a patient with concurrent immune thrombocytopenia (ITP) and amyotrophic lateral sclerosis (ALS) who showed transient clinical improvement in both conditions following treatment with the neonatal Fc receptor (FcRn) inhibitor efgartigimod. Rapid recovery of platelet counts was accompanied by temporary stabilization of neurologic function, which deteriorated after discontinuation of efgartigimod.

What is known and what is new?

• ITP is primarily mediated by pathogenic immunoglobulin G (IgG) autoantibodies, and FcRn inhibition with efgartigimod increases platelet counts in patients with chronic ITP. ALS is a heterogeneous neurodegenerative disease in which immune dysregulation and autoantibodies have been implicated, although immunomodulatory therapies have generally not demonstrated clinical benefit.

• To our knowledge, this is the first report of concurrent ITP and ALS in which both hematologic and neurologic manifestations improved temporally with FcRn inhibition. The parallel and reversible responses in this patient suggest a potential involvement of IgG-mediated immune mechanisms in a subset of ALS patients with autoimmune comorbidities.

What is the implication, and what should change now?

• Clinicians should consider immune-mediated mechanisms in ALS patients who are present with concomitant autoimmune disease. Longitudinal assessment of neurologic function during IgG-targeted therapy may provide clues to potential effects beyond the primary indication. From a research perspective, studies evaluating FcRn inhibition in ALS and identification of immunologic biomarkers predictive of response are needed.

Introduction

Primary immune thrombocytopenia (ITP) is an acquired autoimmune disorder characterized by isolated thrombocytopenia (platelet count <100×109/L) without an identifiable secondary cause (1). Secondary ITP may occur in association with connective tissue diseases (e.g., systemic lupus erythematosus, mixed connective tissue disease, Sjögren’s syndrome), lymphoproliferative disorders, and infections [e.g., chronic hepatitis, human immunodeficiency virus (HIV) infection, Helicobacter pylori] (2). In Japan, the annual incidence of primary ITP is estimated at 2.16 per 100,000 population, with higher incidence in young children, women aged 20–34 years, and older adults (3). In contrast, the annual incidence of amyotrophic lateral sclerosis (ALS) in Japan is approximately 2.2 per 100,000 population, with the highest incidence in individuals aged 70–79 years and a male-to-female ratio of approximately 1.5 (4). To date, concurrent ALS and ITP has not been reported.

The pathogenesis of ITP is primarily driven by autoantibodies (5), predominantly of the immunoglobulin G (IgG) class, directed against platelet surface glycoproteins. These autoantibodies lead to accelerated platelet clearance and can also impair platelet production (6,7). Although other immune mechanisms, including T-cell-mediated cytotoxicity, are involved (8), the central role of pathogenic IgG is well-established (9). As ITP lacks a single diagnostic biomarker, it remains a diagnosis of exclusion, often supported by response to therapy (10).

Therapeutic options for ITP include corticosteroids, intravenous immunoglobulin (IVIG), thrombopoietin receptor agonists (e.g., eltrombopag, romiplostim, avatrombopag), rituximab, fostamatinib, and splenectomy (11). Although splenectomy yields high rates of sustained remission off therapy, its use has declined due to thromboembolic and infectious risks and the availability of additional medical therapies. Efgartigimod is an engineered human IgG1 Fc fragment that blocks IgG binding to the neonatal Fc receptor (FcRn), thereby inhibiting IgG recycling and lowering serum concentrations of total IgG, including pathogenic IgG autoantibodies (12). Clinical trials have demonstrated that efgartigimod produces rapid IgG reduction with clinically meaningful platelet responses in chronic/persistent ITP (13,14). In Japan, efgartigimod was approved on March 26, 2024, for persistent and chronic ITP.

ALS is a progressive neurodegenerative disorder characterized by motor neuron loss leading to weakness and respiratory failure (15). Proposed mechanisms include genetic susceptibility, oxidative stress, excitotoxicity, mitochondrial and proteasomal dysfunction, altered synaptic function, impaired axonal transport, and neuroinflammation (15).

Herein, we report the first known case of concurrent ITP and ALS. The objective of this report is to describe the clinical course of this patient, in whom treatment with the FcRn inhibitor efgartigimod led to a transient improvement in both thrombocytopenia and ALS functional measures. Through this case, we aim to explore the hypothesis that pathogenic IgG autoantibodies may contribute to the pathogenesis of not only ITP but also certain forms of ALS, suggesting a potential shared immunologic mechanism. We present this article in accordance with the CARE reporting checklist (available at https://aob.amegroups.com/article/view/10.21037/aob-2025-1-59/rc).

Case presentation

A 66-year-old Japanese man was diagnosed with ALS in March 2023 after developing dysarthria and gait difficulty. Riluzole, and edaravone were started. In August 2024, he remained independently ambulatory, and his revised ALS Functional Rating Scale (ALSFRS-R) score was 40. Platelet counts were stable at 170–180 ×109/L through August 2024 but decreased to 97×109/L at a routine visit in September 2024. He subsequently developed facial and scalp ecchymoses after a fall.

In October 2024, he was referred to our hospital for severe thrombocytopenia (platelet count 1.0×109/L) with cutaneous bleeding. There was no family history of bleeding disorders or neuromuscular disease. His medications included irbesartan/amlodipine, febuxostat, vonoprazan, dextromethorphan hydrobromide hydrate, mosapride, and ambroxol for hypertension, hyperuricemia, reflux esophagitis, and chronic bronchitis. Because several drugs were potentially associated with thrombocytopenia, all medications except irbesartan/amlodipine were discontinued, including riluzole and edaravone.

Physical examination showed petechiae of oral mucosa and lower extremities. A peripheral blood smear confirmed marked thrombocytopenia with an elevated immature platelet fraction (18.1%). Bone marrow aspiration revealed increased megakaryocytes and normal cytogenetics. Viral serologies and antinuclear antibody testing were negative. Platelet-associated IgG (PAIgG) was elevated at 236 ng/107 cells (reference range, 25–46 /107 cells). With alternative causes excluded, ITP was diagnosed (the clinical course is shown in Figure 1).

Figure 1 Clinical course: the top panel shows ITP therapies. The middle panel depicts platelet count, IgG, PAIgG, ALSFRS-R and %VC. %VC, percent predicted vital capacity; ALS, amyotrophic lateral sclerosis; ALSFRS-R, revised ALS Functional Rating Scale; EFGART, efgartigimod; ELT, eltrombopag; FOS, fostamatinib; IgG, immunoglobulin G; ITP, immune thrombocytopenia; PAIgG, platelet-associated IgG; Plt, platelet count; PRED, prednisolone; ROM, romiplostim.

Prednisolone did not increase the platelet count, and eltrombopag was initiated one week later. The platelet counts transiently increased to 55×109/L but then fell to 4×109/L. To obtain a rapid platelet response and reduce the risk of trauma-related bleeding given ALS-associated motor impairment, intravenous efgartigimod (10 mg/kg) was started ten days after start of predonisolone (we define the start date of Efgartigimod administration as day 0). Platelet counts increased to 43×109/L one week after starting efgartigimod, 74×109/L two weeks later, and 103×109/L three weeks later. No treatment-emergent adverse events were observed. The patient was subsequently discharged, and treatment with riluzole and edaravone was resumed.

In the fifth week after starting efgartigimod, eltrombopag was replaced with romiplostim with the intent of inducing immune tolerance (16). Efgartigimod and romiplostim were administered intermittently according to platelet counts (maximum 440×109/L, minimum 24×109/L). After efgartigimod exposure, total IgG decreased from 1,643 to 858 mg/dL and PAIgG normalized to 29 ng/107 cells. During efgartigimod therapy the revised ALS Functional Rating Scale (ALSFRS-R) score showed a subtle increase from 40 to 41 in January 2025 (day 83). After nine doses, efgartigimod was discontinued in January 2025 (day 91), and romiplostim was titrated with the goal of achieving treatment-free remission (17,18). However, platelet counts continued to fluctuate markedly, and sustained remission was not achieved. Unexpectedly, an increase in vital capacity (VC) from 81% to 93.9% was observed in February 2025 (day 109).

Because self-injection of romiplostim is not approved in Japan and frequent hospital visits became increasingly difficult as ALS progressed, therapy was changed from romiplostim to eltrombopag, and fostamatinib was added. Platelet counts subsequently stabilized. In December 2025 (day 422, eleven months after efgartigimod discontinuation) total IgG increased to 1,499 mg/dL, while PAIgG remained normal, however, ALSFRS-R declined to 31 and a gastrostomy tube was required. The patient reported being satisfied that oral therapy eliminated the need for frequent visits for ITP treatment, as their daily activities had declined due to ALS. Therefore, the patient did not wish to resume efgartigimod. Management strategies for future respiratory decline are being discussed. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent for publication of this case report was obtained from the patient. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Humoral mechanisms in ITP were historically suggested by neonatal purpura in infants born to mothers with chronic ITP and by Harrington’s classic transfusion experiment (5). Subsequent studies demonstrated antiplatelet antibodies directed against platelet membrane glycoproteins IIb/IIIa, Ib/IX, or V in many patients; these antibodies are predominantly IgG and contribute to both accelerated platelet destruction and impaired platelet production (6,7). Autoantibodies can opsonize platelets for clearance by splenic macrophages, induce platelet apoptosis, activate complement, promote platelet desialylation with hepatic clearance, and participate in Fc-independent pathways (9). In addition, T-cell-mediated cytotoxicity also contributes to ITP pathogenesis (8). Because ITP is heterogeneous and lacks a single diagnostic biomarker, it remains a diagnosis of exclusion, and response to therapy is often used to support the diagnosis (10).

Corticosteroids are recommended as first-line therapy for patients who are H. pylori negative or unresponsive to eradication and who have severe thrombocytopenia (e.g., <20,000/µL) or clinically significant bleeding (2). Although this patient did not have major bleeding, the profoundly low platelet count prompted steroid therapy, which was ineffective; eltrombopag also failed to achieve a sustained response.

According to the American Society of Hematology guideline (1), IVIG is recommended for patients who require a rapid platelet increase. In retrospect, IVIG could have been administered at the time of steroid refractoriness. IVIG may act through multiple immunomodulatory mechanisms, including anti-idiotypic neutralization of antiplatelet antibodies, increased expression of inhibitory Fc gamma receptor IIB, and inhibition of Fc receptor–mediated platelet destruction. Emerging evidence suggests that competitive inhibition of FcRn and accelerated elimination of pathogenic IgG may contribute substantially to IVIG efficacy (19,20). IVIG might therefore have produced a rapid platelet increase similar to efgartigimod; however, IVIG has not demonstrated benefit in ALS (21).

Efgartigimod is an engineered human IgG1 Fc fragment with increased affinity for FcRn. By competing with endogenous IgG for FcRn binding, it promotes lysosomal degradation of IgG and reduces the IgG half-life from approximately 21 days to roughly 7 days, depending on dose, with an average IgG reduction of about 60%. In ITP, reducing total IgG is expected to decrease opsonization and destruction mediated by pathogenic antiplatelet autoantibodies. Nevertheless, analyses of antigen-specific antiplatelet autoantibodies in clinical trials are limited by assay sensitivity and low baseline positivity rates (14). In Japan, the PAIgG test is reimbursed but has low specificity and limited diagnostic value (22). Changes in PAIgG can reflect platelet count rather than disease activity (23). Therefore, despite the recovery of total IgG to baseline (1,499 mg/dL) following discontinuation of efgartigimod, the persistent low levels of PAIgG are thought to be solely due to platelet counts being maintained by eltrombopag and fostamatinib.

We attempted romiplostim monotherapy with the goal of sustained remission off treatment but were unable to achieve it, with persistent, marked platelet fluctuations. Such variability may reflect incomplete establishment of immune tolerance (17). As ALS progressed, frequent clinic visits for romiplostim injections became increasingly burdensome, and treatment was transitioned to oral eltrombopag plus fostamatinib, resulting in stable platelet counts. Notably, ALS continued to worsen after efgartigimod discontinuation.

Although an improvement of ALSFRS-R Scale from 40 to 41 is minimal and could fall within measurement variability or a placebo effect, the increase of VC from 81% to 93.9% is more substantial and clinically significant. Thus, the temporal improvement in these ALS functional measures during and shortly after discontinuation of efgartigimod exposure raises the possibility that IgG-mediated immune mechanisms contributed to neurologic disease activity in this patient. Autoantibodies have been reported in serum and cerebrospinal fluid of ALS patients, and some have been associated with disease progression (24). However, prior trials of immunomodulatory therapies—including plasma exchange, corticosteroids, azathioprine, cyclophosphamide, interferon-α, and cyclosporine—have not shown clinical benefit in ALS (25). Fc receptors, including FcRn, contribute to antibody-dependent effector mechanisms. In this case, the temporal association with efgartigimod and the lack of apparent neurologic benefit after introduction of fostamatinib (a Syk inhibitor that reduces Fc receptor-mediated phagocytosis) may suggest that FcRn-mediated IgG homeostasis might be central rather than downstream phagocytosis alone. In this regard, FcRn may be involved in IgG transport across the blood-brain barrier and into the central nervous system, potentially relating to ALS pathology (26); however, this inference is speculative and requires mechanistic investigation. Efgartigimod is approved for myasthenia gravis, a prototypic IgG-mediated autoimmune disease (27). While the evidence for autoantibodies in ALS is less direct than in myasthenia gravis, this case supports further exploration of FcRn inhibition in carefully selected ALS populations.

This report has important limitations. First, it describes a single patient; therefore, causal relationships cannot be established. Second, ALS is heterogeneous with variable progression, and spontaneous fluctuation or temporary stabilization cannot be excluded. Third, IVIG was not administered at the time of steroid refractoriness, deviating from guideline-based practice and limiting direct comparison with standard therapy. Fourth, detailed immunologic analyses, including serial measurements of antigen-specific autoantibodies and cerebrospinal fluid biomarkers, were not performed; thus, the immunopathologic mechanisms underlying the parallel hematologic and neurologic changes remain speculative. Finally, efgartigimod is not approved for ALS, limiting immediate clinical applicability.

Conclusions

We report a patient with concurrent ITP and ALS who experienced rapid platelet recovery and transient improvement in ALS functional measures during FcRn inhibition with efgartigimod, followed by neurologic decline after discontinuation. Although the neurologic changes may be coincidental, the temporal association raises the possibility that IgG-mediated immune mechanisms contribute to disease activity in a subset of ALS patients with autoimmune comorbidities. Further clinical and translational studies are warranted to clarify the role of FcRn inhibition in ALS and to identify biomarkers that may predict responsiveness to IgG-depleting therapies.

Acknowledgments

An abstract of this case was presented at the 134th Shikoku Regional Meeting of the Japanese Society of Internal Medicine.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://aob.amegroups.com/article/view/10.21037/aob-2025-1-59/rc

Peer Review File: Available at https://aob.amegroups.com/article/view/10.21037/aob-2025-1-59/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://aob.amegroups.com/article/view/10.21037/aob-2025-1-59/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent for publication of this case report was obtained from the patient. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

  1. Neunert C, Terrell DR, Arnold DM, et al. American Society of Hematology 2019 guidelines for immune thrombocytopenia. Blood Adv 2019;3:3829-66. [Crossref] [PubMed]
  2. Kashiwagi H, Kuwana M, Hato T, et al. Reference guide for management of adult immune thrombocytopenia in Japan: 2019 Revision. Int J Hematol 2020;111:329-51. [Crossref] [PubMed]
  3. Kurata Y, Fujimura K, Kuwana M, et al. Epidemiology of primary immune thrombocytopenia in children and adults in Japan: a population-based study and literature review. Int J Hematol 2011;93:329-35. [Crossref] [PubMed]
  4. Doi Y, Atsuta N, Sobue G, et al. Prevalence and incidence of amyotrophic lateral sclerosis in Japan. J Epidemiol 2014;24:494-9. [Crossref] [PubMed]
  5. Harrington WJ, Minnich V, Hollingsworth JW, et al. Demonstration of a thrombocytopenic factor in the blood of patients with thrombocytopenic purpura. J Lab Clin Med 1951;38:1-10.
  6. Al-Samkari H, Rosovsky RP, Karp Leaf RS, et al. A modern reassessment of glycoprotein-specific direct platelet autoantibody testing in immune thrombocytopenia. Blood Adv 2020;4:9-18. [Crossref] [PubMed]
  7. Porcelijn L, Schmidt DE, Oldert G, et al. Evolution and Utility of Antiplatelet Autoantibody Testing in Patients with Immune Thrombocytopenia. Transfus Med Rev 2020;34:258-69. [Crossref] [PubMed]
  8. Olsson B, Andersson PO, Jernås M, et al. T-cell-mediated cytotoxicity toward platelets in chronic idiopathic thrombocytopenic purpura. Nat Med 2003;9:1123-4. [Crossref] [PubMed]
  9. Martínez-Carballeira D, Bernardo Á, Caro A, et al. Pathophysiology, Clinical Manifestations and Diagnosis of Immune Thrombocytopenia: Contextualization from a Historical Perspective. Hematol Rep 2024;16:204-19. [Crossref] [PubMed]
  10. Miltiadous O, Hou M, Bussel JB. Identifying and treating refractory ITP: difficulty in diagnosis and role of combination treatment. Blood 2020;135:472-90. [Crossref] [PubMed]
  11. Provan D, Arnold DM, Bussel JB, et al. Updated international consensus report on the investigation and management of primary immune thrombocytopenia. Blood Adv 2019;3:3780-817. [Crossref] [PubMed]
  12. Broome C. Efgartigimod alfa for the treatment of primary immune thrombocytopenia. Ther Adv Hematol 2023;14:20406207231172831. [Crossref] [PubMed]
  13. Broome CM, McDonald V, Miyakawa Y, et al. Efficacy and safety of the neonatal Fc receptor inhibitor efgartigimod in adults with primary immune thrombocytopenia (ADVANCE IV): a multicentre, randomised, placebo-controlled, phase 3 trial. Lancet 2023;402:1648-59. [Crossref] [PubMed]
  14. Newland AC, Sánchez-González B, Rejtő L, et al. Phase 2 study of efgartigimod, a novel FcRn antagonist, in adult patients with primary immune thrombocytopenia. Am J Hematol 2020;95:178-87. [Crossref] [PubMed]
  15. Brotman RG, Moreno-Escobar MC, Joseph J, et al. Amyotrophic lateral sclerosis. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan.
  16. Carpenedo M, Zappaterra A, Ferrari B, et al. Sequential Use of Efgartigimod and Romiplostim Restored Platelet Response in Two Multi-Refractory Thrombocytopenic Patients, Previously Treated with Thrombopoietin Receptor Agonists. Mediterr J Hematol Infect Dis 2023;15:e2023021. [Crossref] [PubMed]
  17. Schifferli A, Rüfer A, Rovo A, et al. Immunomodulation with romiplostim as a second-line strategy in primary immune thrombocytopenia: The iROM study. Br J Haematol 2023;203:119-30. [Crossref] [PubMed]
  18. Schifferli A, Nimmerjahn F, Kühne T. Immunomodulation in Primary Immune Thrombocytopenia: A Possible Role of the Fc Fragment of Romiplostim? Front Immunol 2019;10:1196. [Crossref] [PubMed]
  19. Jin F, Balthasar JP. Mechanisms of intravenous immunoglobulin action in immune thrombocytopenic purpura. Hum Immunol 2005;66:403-10. [Crossref] [PubMed]
  20. Yu Z, Lennon VA. Mechanism of intravenous immune globulin therapy in antibody-mediated autoimmune diseases. N Engl J Med 1999;340:227-8. [Crossref] [PubMed]
  21. Mimic S, Aru B, Pehlivanoğlu C, et al. Immunology of amyotrophic lateral sclerosis - role of the innate and adaptive immunity. Front Neurosci 2023;17:1277399. [Crossref] [PubMed]
  22. Kelton JG, Murphy WG, Lucarelli A, et al. A prospective comparison of four techniques for measuring platelet-associated IgG. Br J Haematol 1989;71:97-105. [Crossref] [PubMed]
  23. Kashiwagi H, Kuwana M, Murata M, et al. Reference guide for the diagnosis of adult primary immune thrombocytopenia, 2023 edition. Int J Hematol 2024;119:1-13. [Crossref] [PubMed]
  24. Liu S, Hong Y, Wang BR, et al. The presence and clinical significance of autoantibodies in amyotrophic lateral sclerosis: a narrative review. Neurol Sci 2024;45:4133-49. [Crossref] [PubMed]
  25. Dalakas MC, Stein DP, Otero C, et al. Effect of high-dose intravenous immunoglobulin on amyotrophic lateral sclerosis and multifocal motor neuropathy. Arch Neurol 1994;51:861-4. [Crossref] [PubMed]
  26. Lafrance-Vanasse J, Sadekar SS, Yang Y, et al. Leveraging neonatal Fc receptor (FcRn) to enhance antibody transport across the blood brain barrier. Nat Commun 2025;16:4143. [Crossref] [PubMed]
  27. Bhandari V, Bril V. FcRN receptor antagonists in the management of myasthenia gravis. Front Neurol 2023;14:1229112. [Crossref] [PubMed]
doi: 10.21037/aob-2025-1-59
Cite this article as: Togitani K, Oki R, Kuzume D, Uemura Y. Concurrent immune thrombocytopenia and amyotrophic lateral sclerosis with transient improvement in both conditions following efgartigimod: a case report. Ann Blood 2026;11:5.

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