Abstract
Background
Anti-myelin-associated glycoprotein (MAG) neuropathy is an uncommon IgM-mediated autoimmune demyelinating peripheral neuropathy, which is prone to misdiagnosis due to overlapping clinical manifestations with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Serum anti-MAG IgM ≥ 1:1000 is widely accepted as the standard diagnostic cut-off value clinically, while cases with low-titer positive results remain poorly summarized. We report one low-titer MAG-antibody-positive case receiving individualized low-dose rituximab to supplement clinical evidence for this disease.
Case presentation
A 65-year-old male patient presented with progressive numbness and limb unsteadiness lasting for 5 months. Neurological examination identified predominantly distal lower limb weakness and prominent deep sensory ataxia. Pre-treatment INCAT disability score was 4 and decreased to 2 one month after intervention. Serum anti-MAG IgM was positive at 1:320; all nodal/paranodal antibodies including NF155, CNTN1, Caspr1 and pan-neurofascin tested negative. Immunofixation electrophoresis demonstrated an IgM-λ monoclonal gammopathy, with serum free κ/λ light chain within normal reference ranges. Cerebrospinal fluid (CSF) protein was markedly elevated. Nerve conduction study (NCS) performed prior to medication revealed diffuse distal-predominant demyelination combined with axonal injury. The patient failed high-dose methylprednisolone pulse therapy, then received split low-dose rituximab (100 mg on Day 1, 500 mg on Day 2). One-month follow-up showed antibody titer dropped to 1:100 and obvious clinical improvement; incident hyperthyroidism was detected during hospitalization. Bone marrow biopsy excluded B-cell proliferative disorders.
Conclusions
Low-titer anti-MAG IgM combined with typical clinical, electrophysiological and serological findings can confirm MAG neuropathy. Individualized low-dose rituximab achieves satisfactory efficacy for elderly patients complicated with underlying cerebrovascular disorders in early disease stage. Concurrent new-onset autoimmune hyperthyroidism is a rare clinical coincidence in this disease, requiring long-term follow-up observation.
Keywords: Anti-MAG neuropathy, Rituximab, Distal-predominant demyelination, Monoclonal gammopathy of undetermined significance, Case report
Background
Anti-myelin-associated glycoprotein (MAG) neuropathy refers to an autoimmune demyelinating peripheral neuropathy triggered by IgM-type monoclonal autoantibodies targeting peripheral nerve MAG antigen [1]. Its overall population prevalence is approximately 1/100 000, mostly affecting middle-aged and elderly males [1]. The disorder manifests as chronically progressive length-dependent peripheral nerve damage dominated by sensory ataxia and late-onset distal limb weakness, and is frequently misdiagnosed as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) [1]. The disease occurs either sporadically or secondary to monoclonal gammopathy of undetermined significance (MGUS) or Waldenström macroglobulinemia and other B-cell proliferative disorders [1]. Diagnosis mainly relies on serum anti-MAG antibody assay plus immunofixation electrophoresis, and characteristic distal demyelination can be identified via neurophysiological testing [1].
Conventional glucocorticoids and intravenous immunoglobulin (IVIG) show limited therapeutic efficacy. Rituximab serves as the most investigated targeted agent; available randomized controlled trials failed to reach primary endpoints, but meta-analyses verified favorable clinical benefits via standardized administration [2]. Evidence supporting Bruton’s tyrosine kinase (BTK) inhibitors in anti-MAG neuropathy extends beyond isolated case reports [3]: a multicenter Korean cohort (n = 68) reported a 50% response rate to zanubrutinib, exceeding that of rituximab (36.4%) [4]; in the phase 3 ASPEN trial post-hoc analysis of Waldenström macroglobulinemia–associated peripheral neuropathy (n = 49), zanubrutinib and ibrutinib were associated with 71.4% neuropathy symptom resolution, with greater improvement in patients with lower baseline anti-MAG antibody titers [5]; real-world data also document ibrutinib or zanubrutinib use in IgM-gammopathy neuropathies (n = 24) [6], and second-generation BTK inhibitors such as tirabrutinib have shown symptomatic and serological benefit in rituximab-refractory cases [7, 8].
Herein we describe a corticosteroid-resistant early MAG neuropathy patient treated with low-dose rituximab, and review relevant literature to elaborate diagnostic and therapeutic considerations of this disease.
Case presentation
Clinical features
A 65-year-old male was admitted on December 23, 2025 due to insidious progressive numbness and limb unsteadiness for 5 months. Numbness initially arose in the right distal lower limb, then gradually involved the left distal lower limb, and was followed by gait unsteadiness. Paresthesia with a cotton-wool sensation extended proximally to involve both upper extremities over the disease course; no syncope, episodes of leg giving way, bladder/bowel dysfunction or cranial nerve complaints were documented. Past medical history included glaucoma surgery, cervical disc stenosis and untreated hypertension, without known drug or food allergy.
Vital signs were stable on admission. Cranial nerve examination was unremarkable. Upper limb muscle strength and tone were normal, and no weakness of intrinsic hand muscles was detected on examination. In the lower limbs, proximal muscle strength was grade 5, while distal muscles were selectively impaired: ankle dorsiflexion and toe grip strength were grade 4+, and bilateral toe-standing could not be completed. Ataxia tests (finger-nose, rapid alternating movement, heel-knee-shin) were clumsy, which was attributed to impaired proprioception rather than polyminimyoclonus or muscle weakness; Romberg sign was positive. The patient presented with a wide-based staggering gait and could not perform tandem walking. Distal-predominant impairment of proprioception and vibration sense was noted in all four limbs, while superficial pain/temperature sensation remained intact. Bilateral deep tendon reflexes were diminished, with absent Achilles reflexes. INCAT disability score was 4 at baseline before rituximab treatment, and decreased to 2 at one-month follow-up.
Auxiliary examinations
1. Serum and CSF tests (December 24, 2025): CSF protein 2269.85 mg/L (reference range: 150–450 mg/L), glucose 3.54 mmol/L, white blood cell count 1.7×10⁶/L, red blood cell count 0.488×10⁹/L. The marked CSF protein elevation, though seemingly disproportionate to the distal-predominant clinical phenotype, is consistent with published features of anti-MAG neuropathy: subclinical antibody deposition at proximal spinal nerve roots disrupts the blood-nerve barrier, leading to serum protein leakage into the CSF [9].
Serum anti-MAG IgM titre 1:320, anti-sulfatide antibody weakly positive; the full panel of nodal/paranodal antibodies (NF155, CNTN1, Caspr1, pan-neurofascin) were all negative. Free κ light chain 8.47 mg/L, free λ light chain 18.59 mg/L, κ/λ ratio 0.46 (reference intervals: κ 3.3–19.4 mg/L, λ 5.7–26.3 mg/L, κ/λ 0.26–1.65). Urine Bence Jones protein negative. Immunofixation electrophoresis confirmed an IgM-λ monoclonal band.
Connective tissue disease screening: antinuclear antibody (ANA) 1.20 U/L; anti-Jo-1, anti-Scl-70, anti-SSB, anti-SM, anti-U1-snRNP, anti-AHA, anti-AnuA, anti-P protein, anti-Ro60kD, anti-Ro52kD, anti-CenpB and anti-dsDNA antibodies were all negative. Antineutrophil cytoplasmic antibody (ANCA) was not tested. Paraneoplastic antibody panel (including anti-Hu, SOX-1) was all negative.
2. Bone marrow aspiration was arranged after positive MAG antibody confirmation: no clonal B-cell proliferation was detected, consistent with MGUS-associated laboratory features.
3. Imaging: Cervical spine MRI showed no obvious intramedullary abnormalities; coronal sections for evaluation of nerve root enlargement were not available. Carotid ultrasound demonstrated intima-media thickening; chest and abdominal CT revealed incidental pulmonary nodule and left renal calculus, none correlating with peripheral neuropathy.
4. Nerve conduction studies (December 26, 2025, performed prior to rituximab infusion): diffuse distal demyelination combined with mild axonal damage was found in all tested nerves; prominent prolongation of distal motor latency was observed, consistent with the typical pattern of reduced terminal latency index (TLI) in anti-MAG neuropathy. Exact TLI numerical values cannot be calculated because distal nerve segment lengths were not recorded during routine EMG testing. Detailed motor nerve conduction data are summarized in Table 1; corresponding sensory nerve conduction parameters are presented in (Table 2).
Table 1.
Motor nerve conduction parameters Abbreviations: ADM, abductor digiti minimi; APB, abductor pollicis brevis; EDB, extensor digitorum brevis; Rec1, recording site 1 over the extensor digitorum muscle; TLI, terminal latency index (calculated value unavailable, distal nerve segment lengths not recorded in routine EMG); ND, no definable waveform
| Nerve & stimulation site | Distal latency (ms) | Compound muscle action potential (mV) | Motor conduction velocity (m/s) | F-wave latency (ms) | F-wave occurrence rate (%) | TLI | Conduction abnormality/temporal dispersion |
|---|---|---|---|---|---|---|---|
| Right ulnar (wrist→ADM) | 5.69 | 5.5 | – | – | – | Not calculated (distal nerve length unrecorded) | None |
| Right ulnar (below elbow→wrist) | 10.2 | 4.4 | 44.3 | – | – | Not calculated (distal nerve length unrecorded) | None |
| Right ulnar (above elbow→below elbow) | 13.9 | 4.0 | 28.4 | – | – | Not calculated (distal nerve length unrecorded) | Mild dispersion |
| Left ulnar (wrist→ADM) | 5.12 | 6.3 | – | – | – | Not calculated (distal nerve length unrecorded) | None |
| Left ulnar (below elbow→wrist) | 9.01 | 5.1 | 56.6 | – | – | Not calculated (distal nerve length unrecorded) | None |
| Left ulnar (above elbow→below elbow) | 11.7 | 5.1 | 37.2 | – | – | Not calculated (distal nerve length unrecorded) | Mild dispersion |
| Right radial (elbow→Rec1) | 5.11 | 4.2 | – | – | – | Not calculated (distal nerve length unrecorded) | None |
| Right radial (radial groove→elbow) | 6.97 | 3.8 | 67.2 | – | – | Not calculated (distal nerve length unrecorded) | None |
| Left radial (elbow→Rec1) | 9.45 | 4.7 | – | – | – | Not calculated (distal nerve length unrecorded) | None |
| Left radial (radial groove→elbow) | 12.5 | 4.1 | 39.3 | – | – | Not calculated (distal nerve length unrecorded) | Mild dispersion |
| Right median (wrist→APB) | 14.3 | 2.8 | – | 43.2 | 100 | Not calculated (distal nerve length unrecorded) | Distal latency prolongation |
| Right median (elbow→wrist) | 19.4 | 2.7 | 48.0 | – | – | Not calculated (distal nerve length unrecorded) | None |
| Left median (wrist→APB) | 10.5 | 3.9 | – | 40.4 | 85.0 | Not calculated (distal nerve length unrecorded) | Distal latency prolongation |
| Left median (elbow→wrist) | 15.8 | 2.8 | 41.5 | – | – | Not calculated (distal nerve length unrecorded) | None |
| Right tibial (ankle→AH) | 17.3 | 0.24 | – | ND | ND | ND: no definable waveform, TLI uncalculable | Distal latency prolongation |
| Right tibial (popliteal→ankle) | 34.2 | 0.28 | 23.4 | ND | ND | ND: no definable waveform, TLI uncalculable | Mild dispersion |
| Left tibial (ankle→AH) | 17.2 | 0.54 | – | ND | ND | ND: no definable waveform, TLI uncalculable | Distal latency prolongation |
| Left tibial (popliteal→ankle) | 29.7 | 0.56 | 30.8 | ND | ND | ND: no definable waveform, TLI uncalculable | Mild dispersion |
| Right peroneal (ankle→EDB) | ND | ND | ND | ND | ND | ND: no definable waveform, TLI uncalculable | No recordable response |
| Right peroneal (knee→ankle) | ND | ND | ND | ND | ND | ND: no definable waveform, TLI uncalculable | No recordable response |
| Left peroneal (ankle→EDB) | 12.2 | 0.34 | – | ND | ND | Not calculated (distal nerve length unrecorded) | Distal latency prolongation |
| Left peroneal (knee→ankle) | 27.8 | 0.15 | 20.8 | ND | ND | Not calculated (distal nerve length unrecorded) | Mild dispersion |
Table 2.
Sensory nerve conduction parameters of the patient Abbreviations: EPL, extensor pollicis longus; ND, no definable waveform
| Nerve & stimulation site | Distal latency (ms) | Sensory amplitude (µV) | Sensory conduction velocity (m/s) |
|---|---|---|---|
| Right ulnar (digit V→wrist) | 6.92 | 1.11 | 18.1 |
| Left ulnar (digit V→wrist) | ND | ND | ND |
| Right radial (EPL tendon→wrist) | ND | ND | ND |
| Left radial (EPL tendon→wrist) | ND | ND | ND |
| Right median (digit III→wrist) | 6.78 | 1.24 | 21.4 |
| Left median (digit III→wrist) | 5.54 | 5.70 | 26.2 |
| Right sural (mid-calf→lateral malleolus) | 3.74 | 2.90 | 32.1 |
| Left sural (mid-calf→lateral malleolus) | 3.59 | 4.00 | 33.4 |
| Right medial plantar (sole→med malleolus) | ND | ND | ND |
| Left medial plantar (sole→med malleolus) | ND | ND | ND |
5. Post-treatment peripheral lymphocyte test (performed 7 days after the second rituximab infusion): CD19⁺/CD20⁺ B lymphocyte percentage dropped to 0%.
Clinical management
Initial tentative diagnosis was CIDP, and 3 consecutive days of high-dose methylprednisolone (1000 mg/d) intravenous pulse was prescribed alongside neuroprotective adjuvants (mecobalamin tablets, compound vitamin B tablets) and basic antihypertensive treatment (irbesartan/hydrochlorothiazide tablets) for his long-standing untreated hypertension, but clinical symptoms did not improve. After serological confirmation of MAG neuropathy, an individualized split-dose rituximab regimen was administered: 100 mg on December 31, 2025, followed by 500 mg on January 1, 2026, with routine premedication for hypersensitivity prophylaxis.
Dosing rationale: The patient was 65 years old with hypertension and cerebrovascular comorbidities, carrying elevated risk of infusion reactions, IgM flare and cardiovascular events under the standard 375 mg/m² weekly × 4 induction regimen. The 100 mg starting dose was designed to test infusion tolerance and mitigate the risk of abrupt IgM release secondary to rapid B-cell lysis; after uneventful administration, the remaining 500 mg was given on the following day, with a total induction dose of 600 mg.
Evidence from other antibody-mediated autoimmune diseases supports the feasibility of dose-tailored rituximab regimens. In a 52-week clinical trial comparing three rituximab dosing schedules in pemphigus vulgaris/foliaceus, ultra-low-dose (100 mg days 0 and 14), low-dose (500 mg days 0 and 14) and standard-dose (1000 mg days 0 and 14) all achieved complete CD20⁺ B-cell depletion by week 2, with comparable remission rates and fewer adverse events in lower-dose groups [10]. In corticosteroid-resistant immune thrombocytopenia, low-dose rituximab (100 mg weekly × 4) yielded overall response rates of 59%–80% [11]. A Cochrane systematic review of rituximab for myasthenia gravis also noted that the optimal dose remains undefined, with low-dose regimens showing benefit in newly diagnosed generalized disease [12]. Collectively, these data support individualized dose reduction in elderly patients with comorbidities to achieve adequate B-cell depletion while minimizing safety risks.
The patient tolerated the whole infusion course without allergic or febrile adverse events.
One-month recheck (Jan 31, 2026): anti-MAG IgM decreased to 1:100 (68% reduction), CSF protein slightly declined to 2168.50 mg/L; the patient could walk continuously for over one hour. Incidental elevated FT3 and suppressed TSH confirmed hyperthyroidism, treated with methimazole for symptomatic control.
Final discharge diagnoses:
(1) Anti-MAG-associated neuropathy; (2) New-onset hyperthyroidism; (3) History of glaucoma surgery; (4) Cervical disc herniation with spinal stenosis; (5) Left renal calculus; (6) Pulmonary small nodule.
Discussion
Anti-MAG neuropathy is an IgM-mediated autoimmune demyelinating peripheral neuropathy caused by MAG-targeted autoantibodies, with clinical features easily overlapping with CIDP and leading to frequent misdiagnosis [1]. In this case, initial steroid monotherapy failed to achieve clinical improvement, and definitive diagnosis was established only after targeted antibody testing, highlighting the importance of routine MAG antibody screening in steroid-refractory chronic sensorimotor neuropathy with monoclonal gammopathy.
This case carries notable clinical value in three aspects.
First, it supplements the evidence for low-titer anti-MAG antibody in disease diagnosis. A Bühlmann ELISA titer ≥ 10 000 BTU or indirect immunofluorescence titer ≥ 1:1000 is widely accepted as the classical diagnostic cutoff [1]. However, a large French cohort (n = 202) documented low-titer positivity in 11% of confirmed cases, with indistinguishable clinical phenotype, electrophysiological features and IgM paraprotein association compared with medium- or high-titer cases [13]. Our patient presented with a titer of 1:320, but had typical length-dependent sensory ataxia, distal-predominant demyelination on NCS, IgM-λ monoclonal gammopathy and steroid refractoriness, which together supported a definitive diagnosis. This case underscores that anti-MAG neuropathy should not be excluded solely on the basis of antibody titer, and integrated clinico-serological phenotyping is essential.
Second, this case provides real-world evidence for low-dose rituximab in elderly patients with comorbidities. Standard rituximab regimens yield favorable clinical benefits in anti-MAG neuropathy, but carry higher risks of infusion reactions, infection and IgM flare in elderly populations with cardiovascular comorbidities [2, 14]. Our patient achieved complete B-cell depletion and significant clinical improvement with a total dose of 600 mg split over 2 days, with no adverse events. The favorable response aligns with evidence from other autoimmune neurological and dermatological diseases supporting reduced-dose rituximab efficacy [10–12], suggesting that individualized dose adjustment is a reasonable option for early mild disease in elderly patients with comorbidities. Of note, short-term serological and clinical improvement does not equate to long-term sustained response, and regular follow-up is required.
Third, the concurrent new-onset hyperthyroidism represents a rare autoimmune comorbidity. Anti-MAG neuropathy is associated with B-cell dysregulation, and coexistence with other autoimmune endocrinopathies has rarely been reported. Whether the two conditions share a common immunopathogenic basis, and whether rituximab has a simultaneous therapeutic effect on both, requires long-term sequential follow-up to clarify.
Regarding the marked CSF protein elevation in this case, previous studies have demonstrated that anti-MAG antibody deposition at proximal spinal nerve roots and cauda equina can disrupt the blood-nerve barrier, leading to albuminocytologic dissociation, even when clinical manifestations are dominated by distal symptoms [9]. This finding is consistent with our observation and does not contradict the diagnosis of distal-predominant neuropathy.
Differential diagnosis mainly includes CIDP and subacute combined degeneration. CIDP typically presents with multifocal conduction block on NCS and favorable response to steroids and IVIG, with negative anti-MAG antibodies [15]. Subacute combined degeneration is associated with vitamin B12 deficiency and characteristic posterior column signal changes on spinal MRI [15]. In contrast, our patient showed exclusive distal latency prolongation without conduction block, positive anti-MAG antibody and normal cervical spinal MRI, which supported the diagnosis of anti-MAG neuropathy.
BTK inhibitors have emerged as a promising therapeutic option for anti-MAG neuropathy, especially in cases associated with Waldenström macroglobulinemia. Evidence from multicenter cohorts and clinical trial post-hoc analyses has shown favorable response rates for zanubrutinib, ibrutinib and second-generation agents such as tirabrutinib [4–8], which may become an alternative for rituximab-refractory cases in the future.
Study limitations
Anti-MAG testing was not reported in standardized Bühlmann units, limiting direct cross-study comparison.
Follow-up duration is short; 6-month CD19⁺ B-cell count, long-term electrophysiological and serological sequential data are not yet available.
No peripheral nerve biopsy was performed to obtain pathological confirmation of demyelination.
Only post-treatment B-cell count was available, lacking baseline pre-treatment lymphocyte data.
Serum TRAb and TPOAb were not tested during inpatient stay, and are scheduled for outpatient follow-up.
Cervical spine MRI coronal sections for nerve root evaluation were not available.
ANCA screening for connective tissue disease was not performed.
Conclusions
We report an MGUS-related MAG neuropathy case with low-titer anti-MAG positivity refractory to high-dose steroid but responsive to early split low-dose rituximab. Simultaneous de novo hyperthyroidism represents an uncommon autoimmune comorbidity. Three key clinical takeaways: First, subthreshold anti-MAG titre combined with typical phenotype and paraprotein can establish diagnosis; second, low-dose individualized rituximab is a safe preferred option for elderly patients complicated with cardiovascular comorbidities at early disease stage; third, serial monitoring of autoimmunity-associated complications is necessary throughout long-term follow-up of MAG neuropathy.
Acknowledgements
Not applicable.
Abbreviations
- ADM
Abductor digiti minimi
- APB
Abductor pollicis brevis
- CIDP
Chronic inflammatory demyelinating polyradiculoneuropathy
- CSF
Cerebrospinal fluid
- EDB
Extensor digitorum brevis
- EPL
Extensor pollicis longus
- IVIG
Intravenous immunoglobulin
- MAG
Myelin-associated glycoprotein
- MGUS
Monoclonal gammopathy of undetermined significance
- ND
No definable waveform
- NCS
Nerve conduction study
- TLI
Terminal latency index
- TRAb
Thyroid-stimulating hormone receptor antibody
- TPOAb
Thyroid peroxidase antibody
Authors’ contributions
Dachuan Chang: clinical data collection and manuscript drafting; Xufang Bao: literature sorting and table compilation; Yuhua Li: study design, revision and correspondence management.
Funding
Not applicable.
Data availability
All raw clinical, laboratory and electrophysiology data supporting the findings are available within the article, including Tables 1 and 2. No extra unpublished datasets were produced in this study.
Declarations
Ethics approval and consent to participate
This research was approved by the ethics committee of the First Naval Hospital of Southern Theatre Command, and all procedures complied with the Declaration of Helsinki.
Consent for publication
Written informed consent was obtained from the patient for publication of clinical data and electrophysiological findings.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
References
- 1.Min YG, Visentin A, Briani C, et al. Neuropathy with anti-myelin-associated glycoprotein antibodies: update on diagnosis, pathophysiology and management. J Neurol Neurosurg Psychiatry. 2025;96(4):340–9. [DOI] [PubMed] [Google Scholar]
- 2.Siconolfi G, Vitali F, Sciarrino MA, et al. IgM Flare in Anti-MAG neuropathy post rituximab treatment: a clinical case and a systematic review of the literature. Brain Sci. 2024;14(12):1294. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Pein R, Steinberg A. Treatment of Anti-Myelin-Associated Glycoprotein (MAG) Antibody Neuropathy Using Zanubrutinib in a Patient With Waldenström Macroglobulinemia: A Clinical Vignette. Cureus. 2025;17(4):e81946. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Min YG, Han HJ, Shin HY, et al. Therapeutic Outcomes and Electrophysiological Biomarkers in Anti-Myelin-Associated Glycoprotein Neuropathy: A Multicenter Cohort Study in South Korea. J Clin Neurol. 2024;20(1):50–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Heyman BM, Opat SS, Wahlin BE, et al. Peripheral neuropathy in the phase 3 ASPEN study of Bruton tyrosine kinase inhibitors for Waldenström macroglobulinemia. Blood Adv. 2025;9(4):722–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Klein CJ, Triplett JD, Murray DL, et al. Optimizing anti-myelin-associated glycoprotein and IgM-gammopathy testing for neuropathy treatment evaluation. Neurology. 2024;103(11):e210000. [DOI] [PubMed] [Google Scholar]
- 7.Yuzawa C, Tajiri M, Usuda M, et al. Treatment of Anti-myelin-associated glycoprotein neuropathy with tirabrutinib and a 3-year follow-up. Intern Med. 2025;64(20):3039–43. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Yasuda H, Tomizawa Y, Harada S, et al. Anti-myelin-associated-glycoprotein neuropathy successfully treated with tirabrutinib. Heliyon. 2022;8(10):e10928. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Ruiz M, Puthenparampil M, Campagnolo M, et al. Oligoclonal IgG bands in chronic inflammatory polyradiculoneuropathies. J Neurol Neurosurg Psychiatry. 2021;92(9):969–74. [DOI] [PubMed] [Google Scholar]
- 10.Cao S, Yang B, Wang Z, et al. Efficacy, safety, and B-cell depletion capacity of 3 rituximab dosing regimens in the treatment of moderate-to-severe pemphigus vulgaris and pemphigus foliaceus: A 52-week clinical trial. J Am Acad Dermatol. 2025;93(3):634–43. [DOI] [PubMed] [Google Scholar]
- 11.Wu YJ, Liu H, Zeng QZ, et al. All-trans retinoic acid plus low-dose rituximab vs low-dose rituximab in corticosteroid-resistant or relapsed ITP. Blood. 2022;139(3):333–42. [DOI] [PubMed] [Google Scholar]
- 12.Dodd KC, Clay FJ, Forbes AM, et al. Rituximab for myasthenia gravis. Cochrane Database Syst Rev. 2025;7(7):CD014574. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Svahn J, Petiot P, Antoine JC, et al. Francophone anti-MAG cohort Group. Anti-MAG antibodies in 202 patients: clinicopathological and therapeutic features. J Neurol Neurosurg Psychiatry. 2018;89(5):499–505. [DOI] [PubMed] [Google Scholar]
- 14.Mak G, Bennett D, Phan C, et al. Reversible rituximab demyelination in anti-MAG polyneuropathy: A role for IVIG? J Neuroimmunol. 2025;400:578436. [DOI] [PubMed] [Google Scholar]
- 15.Kuwabara S. Updated diagnosis and treatment for chronic inflammatory demyelinating polyradiculoneuropathy based on the EAN/PNS guideline 2021. Brain Nerve. 2025;77:29–34. [DOI] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
All raw clinical, laboratory and electrophysiology data supporting the findings are available within the article, including Tables 1 and 2. No extra unpublished datasets were produced in this study.