Фульминантный внематочный рецидив множественной миэломы с редким сердцем, сосудистым и многовизорным участием: отчет о деле.

Introduction

Multiple myeloma (MM) is a genetically heterogeneous hematological malignancy characterized by the clonal proliferation of malignant plasma cells within the bone marrow. While MM typically follows a protracted and indolent clinical course, the emergence of extramedullary disease (EMD) signifies a transition to a more aggressive and treatment-resistant phenotype. 1 , 2 EMD is defined by the ability of plasma cells to grow independently of the bone marrow microenvironment, occurring in approximately 7% to 18% of patients at initial diagnosis and up to 20% during disease progression.
3
Traditionally, EMD manifests as soft tissue masses or skin involvement; however, systemic multivisceral infiltration—particularly involving the heart and major vasculature—remains an exceptionally rare and catastrophic clinical event.
1

The biological underpinnings of EMD are closely linked to high-risk cytogenetic abnormalities. Genomic aberrations, such as 1q21 amplification and t 4 , 5 (IGH/FGFR3), are known to promote cell adhesion-mediated drug resistance 4 , 6 and facilitate the “escape” of plasma cells from the medullary cavity.
7
A particularly challenging clinical phenomenon associated with these high-risk features is medullary-extramedullary dissociation, where patients exhibit explosive systemic EMD despite having a minimal tumor burden within the bone marrow.
8
This discordance often renders standard response assessments inadequate and complicates the selection of salvage therapies.

Despite the advent of proteasome inhibitors, immunomodulatory drugs, and monoclonal antibodies, the prognosis for patients with relapsed/refractory MM (RRMM) presenting with widespread EMD remains dismal, with an average overall survival of less than 12 months. 9 , 10 Cases involving fulminant infiltration of the cardiovascular system and multiple solid organs are rarely documented in the medical literature, and a standardized therapeutic approach has yet to be established.

Herein, we report a unique case of a 65-year-old female with genetically high-risk RRMM who exhibited a rapid and fatal progression characterized by extensive infiltration of the heart, major blood vessels, liver, spleen, and lungs, occurring in the absence of significant bone marrow involvement. Through this case report and a comprehensive review of the literature, we aim to delineate the clinical characteristics of this rare EMD phenotype and discuss the diagnostic challenges and therapeutic limitations in the management of fulminant extramedullary relapse.

Case presentation

This case report was prepared in accordance with the CARE (CAse REport) guidelines.
11
The completed checklist is provided in the Supplementary Material.

A 64-year-old woman presented in February 2024 with a 2-month history of left chest wall mass and pain. Her medical history was notable for hypertension. Physical examination revealed a palpable mass measuring approximately 4.0 × 3.0 cm in the left chest wall. Initial laboratory findings included anemia (hemoglobin 105 g/L), hypoalbuminemia (27.9 g/L), hyperglobulinemia (99.8 g/L), elevated beta2-microglobulin (4.31 mg/L), markedly elevated IgG (>30.00 g/L), and decreased IgA and IgM. Serum free light chain assay showed a markedly elevated lambda light chain level (798.82 mg/L) with a severely inverted kappa/lambda ratio (0.0114), suggesting a plasma cell neoplasm.

Subsequent abdominal magnetic resonance imaging (MRI) revealed a round-like mass with long T1 and long T2 abnormal signal in the left chest wall, measuring approximately 4.4 × 7.0 cm, with high signal on diffusion-weighted imaging (DWI) and markedly reduced signal on the apparent diffusion coefficient (ADC) map (Figure 1 (a)–(d)). Thoracolumbar MRI demonstrated multiple slightly long T1 and slightly long T2 abnormal signals involving several thoracic and lumbar vertebral bodies, spinous processes, manubrium sterni, and sternal body (Figure 1 (e)–(h)). Contrast-enhanced chest computed tomography (CT) showed osteolytic destruction with inhomogeneous bone density in the right third rib and left sixth–seventh ribs, with surrounding soft tissue masses exhibiting marked heterogeneous enhancement (Figure 1 (i)–(j)). CT-guided percutaneous needle biopsy was performed. Hematoxylin and eosin (HE) staining revealed diffuse infiltration of plasmacytoid tumor cells with eccentric nuclei and abundant eosinophilic cytoplasm (Figure 2 (a)). Immunohistochemistry demonstrated tumor cells positive for CD38, CD138, CD56, and lambda light chain (Figure 2 (b)–(e)). Cyclin D1 showed partial positivity (Figure 2 (f)), kappa light chain was negative (Figure 2 (g)), and the Ki-67 proliferation index was approximately 60% (Figure 2 (h)). These findings confirmed a monoclonal plasma cell proliferative disorder. Bone marrow cytology showed 32% plasmacytoid tumor cells (Figure 2 (i)–(j)). Immunophenotyping detected 18.56% abnormal plasma cells. Fluorescence in situ hybridization (FISH) detected 1q21 amplification (Figure 2 (k)) and IGH-FGFR3 fusion (Figure 2 (l)), indicating high-risk cytogenetic abnormalities. The patient was diagnosed with multiple myeloma (IgG lambda type, revised ISS stage II, mSMART high-risk group) with multiple bone destructions and extramedullary soft tissue infiltration. Figure 1. Imaging findings at initial diagnosis. (A–D) Abdominal MRI revealed a rounded mass with abnormal signal intensity in the left chest wall, measuring approximately 4.4 cm × 7.0 cm. The lesion exhibited prolonged T1 (A) and T2 (B) signals. Diffusion-weighted imaging (DWI) demonstrated high signal intensity (C), with a corresponding marked signal reduction on the apparent diffusion coefficient (ADC) map (D). (E–H) Thoracolumbar MRI: Sagittal T1-weighted (E) and T2 fat-suppressed (T2FS) (F) images of the lumbar spine, along with sagittal T1-weighted (G) and T2FS (H) images of the thoracic spine, revealed multiple lesions with mildly prolonged T1 and T2 signals. (I–J) Contrast-enhanced chest CT demonstrated osteolytic destruction and inhomogeneous bone density in the right 3rd anterior rib (I) and the left 6th and 7th anterior ribs (J). The surrounding soft tissue masses exhibited marked, heterogeneous enhancement. Red arrows indicate the lesions. Figure 2. Histopathological, immunohistochemical, bone marrow cytology, and cytogenetic findings at initial diagnosis. (A) Hematoxylin and eosin (H&E) staining demonstrated diffuse infiltration of plasmacytoid tumor cells characterized by eccentric nuclei and abundant eosinophilic cytoplasm (original magnification, ×100). (B–H) Immunohistochemical staining revealed positive expression for CD38 (B), CD138 (C), CD56 (D), and lambda light chain (G), with a Ki-67 proliferation index of approximately 60% (E). Cyclin D1 exhibited partial positivity (F), whereas kappa light chain expression was negative (H). All immunohistochemical images are shown at an original magnification of ×200. (I–J) Bone marrow smears confirmed the presence of 32% plasmacytoid tumor cells (original magnification, ×100). (K–L) Fluorescence in situ hybridization (FISH) analysis detected 1q21 amplification (K) and an IGH-FGFR3 fusion (L).

Imaging findings at initial diagnosis. (A–D) Abdominal MRI revealed a rounded mass with abnormal signal intensity in the left chest wall, measuring approximately 4.4 cm × 7.0 cm. The lesion exhibited prolonged T1 (A) and T2 (B) signals. Diffusion-weighted imaging (DWI) demonstrated high signal intensity (C), with a corresponding marked signal reduction on the apparent diffusion coefficient (ADC) map (D). (E–H) Thoracolumbar MRI: Sagittal T1-weighted (E) and T2 fat-suppressed (T2FS) (F) images of the lumbar spine, along with sagittal T1-weighted (G) and T2FS (H) images of the thoracic spine, revealed multiple lesions with mildly prolonged T1 and T2 signals. (I–J) Contrast-enhanced chest CT demonstrated osteolytic destruction and inhomogeneous bone density in the right 3rd anterior rib (I) and the left 6th and 7th anterior ribs (J). The surrounding soft tissue masses exhibited marked, heterogeneous enhancement. Red arrows indicate the lesions.

Histopathological, immunohistochemical, bone marrow cytology, and cytogenetic findings at initial diagnosis. (A) Hematoxylin and eosin (H&E) staining demonstrated diffuse infiltration of plasmacytoid tumor cells characterized by eccentric nuclei and abundant eosinophilic cytoplasm (original magnification, ×100). (B–H) Immunohistochemical staining revealed positive expression for CD38 (B), CD138 (C), CD56 (D), and lambda light chain (G), with a Ki-67 proliferation index of approximately 60% (E). Cyclin D1 exhibited partial positivity (F), whereas kappa light chain expression was negative (H). All immunohistochemical images are shown at an original magnification of ×200. (I–J) Bone marrow smears confirmed the presence of 32% plasmacytoid tumor cells (original magnification, ×100). (K–L) Fluorescence in situ hybridization (FISH) analysis detected 1q21 amplification (K) and an IGH-FGFR3 fusion (L).

From March 2024 to January 2025, the patient received 12 cycles of VCD induction chemotherapy (bortezomib 2.08 mg, cyclophosphamide 480 mg, and dexamethasone 40 mg). After one cycle, the chest wall mass decreased significantly with notable pain relief. Sequential bone marrow assessments revealed a steady decline in plasma cell burden, dropping from 32% at diagnosis to 1% by May 2024, and further to 0.5% by October 2024. Correspondingly, multiparameter flow cytometry-based minimal residual disease (MRD) assessment (sensitivity 10 -5 ) detected 0.06% abnormal plasma cells in May 2024, which became completely undetectable by October 2024. Serum free light chains (sFLC) normalized concomitantly (longitudinal trends are illustrated in Figure S2C ). Despite these hematological improvements, a chest CT performed on January 3, 2025 (following cycle 11 of VCD) revealed residual soft-tissue masses adjacent to the left sixth and seventh ribs. Consequently, local radiotherapy was administered at a total dose of 30 Gy in 10 fractions ( Figure S1A–D ). Following the completion of 12 VCD cycles and radiotherapy, a bone marrow assessment on January 24, 2025, confirmed sustained MRD negativity ( Figure S2A–B ). Notably, post-radiotherapy imaging was not performed to evaluate the extramedullary response. In February 2025, the patient commenced maintenance therapy with bortezomib. Due to treatment-induced diarrhea, the regimen was switched to oral ixazomib (3 mg once weekly) in April 2025. No further imaging surveillance was conducted during the maintenance phase prior to the patient’s fulminant relapse.

In late May 2025, a rapidly enlarging abdominal wall mass was discovered, accompanied by decreased appetite, occasional cough, and approximately 7 kg of weight loss. Readmission in June 2025 revealed a firm abdominal wall mass measuring 2.0 × 2.5 cm. Laboratory studies showed anemia (hemoglobin 110 g/L), thrombocytopenia (89 × 10 9 /L), renal impairment (creatinine 170.2 μmol/L, estimated glomerular filtration rate 27.7 mL/min/1.73 m 2 ), hyperuricemia (819 μmol/L), elevated C-reactive protein (16.88 mg/L), beta2-microglobulin >10.0 mg/L, and hyperglobulinemia. Urinalysis demonstrated elevated microalbuminuria (>0.15 g/L). Bone marrow examination showed only 1% plasma cells with no evidence of bone marrow infiltration at this stage (Figure 3 (a)), highlighting a marked dissociation between systemic extramedullary disease and medullary involvement. Serum free light chain assay, serum protein electrophoresis, and immunofixation electrophoresis confirmed a monoclonal IgG component with elevated lambda globulin (>8.000 g/L) and an M protein level of 49.5% (52.19 g/L) (Figure 3 (b)–(c)), a level not seen in healthy individuals. 18F -FDG PET-CT revealed widespread hypermetabolic foci involving the heart, liver, spleen, major blood vessels, lungs, and multiple soft tissue sites (Figure 3 (d)–(h)), indicating relapsed refractory multiple myeloma with multifocal extramedullary disease involving the chest wall, abdominal wall, lungs, liver, spleen, heart, blood vessels, and soft tissues. In June 2025, salvage chemotherapy with the KDD regimen (carfilzomib 20 mg, liposomal doxorubicin 32 mg, and dexamethasone 20 mg) was initiated. The patient developed severe hepatic enzyme elevation, electrolyte disturbances (hypocalcemia, hypophosphatemia, hypomagnesemia, and critical hypokalemia), and chemotherapy-induced myelosuppression. Despite aggressive supportive care, the abdominal wall mass showed no response, and the patient’s general condition deteriorated. The patient was discharged upon request and died shortly thereafter. The integrated timeline of diagnosis and treatment is illustrated in Figure 4 . Figure 3. Bone marrow cytology, serum protein electrophoresis (SPEP), immunofixation electrophoresis (IFE), and PET/CT findings at relapse. (A) Bone marrow smears demonstrated 1% plasma cells (original magnification, ×100). (B–C) SPEP and IFE identified a monoclonal IgG-λ M-protein. (D–H) PET/CT revealed multifocal extramedullary disease at the time of relapse. (D) Coronal PET/CT imaging displayed multiple hypermetabolic lesions involving the heart, liver, and spleen. (E) Axial abdominal imaging showed hypermetabolic lesions within the liver and spleen. (F) Axial thoracic imaging detected hypermetabolic foci surrounding major blood vessels and within the lungs. (G) Axial pelvic imaging revealed hypermetabolic lesions in the subcutaneous soft tissues and pelvic cavity. (H) Axial thoracic imaging highlighted hypermetabolic foci in the heart. White arrows indicate the lesions. Figure 4. Timeline of diagnosis and treatment. (Created with Figdraw.)

Bone marrow cytology, serum protein electrophoresis (SPEP), immunofixation electrophoresis (IFE), and PET/CT findings at relapse. (A) Bone marrow smears demonstrated 1% plasma cells (original magnification, ×100). (B–C) SPEP and IFE identified a monoclonal IgG-λ M-protein. (D–H) PET/CT revealed multifocal extramedullary disease at the time of relapse. (D) Coronal PET/CT imaging displayed multiple hypermetabolic lesions involving the heart, liver, and spleen. (E) Axial abdominal imaging showed hypermetabolic lesions within the liver and spleen. (F) Axial thoracic imaging detected hypermetabolic foci surrounding major blood vessels and within the lungs. (G) Axial pelvic imaging revealed hypermetabolic lesions in the subcutaneous soft tissues and pelvic cavity. (H) Axial thoracic imaging highlighted hypermetabolic foci in the heart. White arrows indicate the lesions.

Timeline of diagnosis and treatment. (Created with Figdraw.)

Discussion

In this report, we describe a rare manifestation of relapsed/refractory multiple myeloma (RRMM) characterized by explosive multivisceral extramedullary disease (EMD) involving the heart, vasculature, liver, spleen, lungs, and soft tissues, along with a marked medullary–extramedullary dissociation. Whereas EMD typically presents as localized soft tissue or cutaneous lesions, simultaneous involvement of major organs represents an exceptionally rare and catastrophic event. Although multivisceral EMD has been documented in the literature, cardiac and great vessel involvement in multiple myeloma remains exceedingly rare, with only five comparable cases reported in the past decade ( Table 1 ). 5 , 12 – 15 These limited reports highlight the therapeutic challenges of this manifestation; our patient, presenting with the most extensive multivisceral involvement reported to date, underscores the aggressive potential of this rare EMD phenotype. Table 1. Reported cases of multiple myeloma with cardiac and great vessel involvement (2015–2025). ​ Age (yrs)/Sex Symptoms Sites of extramedullary metastasis Treatment Survival Present Case 65/F Abdominal mass Heart, Liver, Spleen, Lungs Chemotherapy, radiotherapy Died Xuan Guan
12
44/F Chest pain LV,pulmonary artery, aortic arch,brachiocephalic artery Chemotherapy, ASCT Alive at 7 mo Shuzhen Wang
13
57/M Dyspnea, facial and bilateral upper limb swelling RA; endocardium; SVC Chemotherapy, surgery Alive at 7 mo Ling Peng
14
67/M exertional dyspnea and fatigue RA; SVC; IVC Chemotherapy, surgery Alive at 7 mo Aliki Tsagkridi
5
50/M Right chest pain; subcutaneous nodules the atria, inter-atrial septum, the vena cava, and pulmonary artery Radiotherapy; chemotherapy Died at 6 wk Jeet Ram Kashyap
15
64/M Progressive dyspnea Atrium; pericardium; SVC Chemotherapy; corticosteroids Died at 18 wk

Table 1. Reported cases of multiple myeloma with cardiac and great vessel involvement (2015–2025). ​ Age (yrs)/Sex Symptoms Sites of extramedullary metastasis Treatment Survival Present Case 65/F Abdominal mass Heart, Liver, Spleen, Lungs Chemotherapy, radiotherapy Died Xuan Guan
12
44/F Chest pain LV,pulmonary artery, aortic arch,brachiocephalic artery Chemotherapy, ASCT Alive at 7 mo Shuzhen Wang
13
57/M Dyspnea, facial and bilateral upper limb swelling RA; endocardium; SVC Chemotherapy, surgery Alive at 7 mo Ling Peng
14
67/M exertional dyspnea and fatigue RA; SVC; IVC Chemotherapy, surgery Alive at 7 mo Aliki Tsagkridi
5
50/M Right chest pain; subcutaneous nodules the atria, inter-atrial septum, the vena cava, and pulmonary artery Radiotherapy; chemotherapy Died at 6 wk Jeet Ram Kashyap
15
64/M Progressive dyspnea Atrium; pericardium; SVC Chemotherapy; corticosteroids Died at 18 wk

Reported cases of multiple myeloma with cardiac and great vessel involvement (2015–2025).

The biological foundation of this fulminant presentation is likely multifactorial and closely associated with the patient’s high-risk cytogenetic profile, specifically the concurrent 1q21 amplification and the IGH/FGFR3 fusion. Amplification of 1q21, observed in approximately 30% of MM cases, drives the overexpression of genes that promote tumor proliferation, immune evasion, and cell adhesion-mediated drug resistance, serving as a critical driver of disease progression. 16 – 18 Concurrently, the IGH/FGFR3 translocation constitutively activates the RAS-MAPK and PI3K-AKT signaling pathways, conferring a profound survival advantage to malignant plasma cells.
19
The synergistic effect of these dual high-risk aberrations may have facilitated rapid clonal evolution, enabling the malignant cells to escape the bone marrow microenvironment and may have been one of the contributing factors to the catastrophic multi-organ extramedullary relapse observed in this patient.

Furthermore, at initial diagnosis, the patient presented with soft-tissue extramedullary disease (EMD) of the chest wall and a high Ki-67 proliferation index of approximately 60%. Baseline EMD is an established independent risk factor for a poor prognosis; it is associated with rapid disease progression and shorter survival, even in the modern treatment era.
20
Similarly, an elevated Ki-67 index is a well-recognized marker of tumor proliferative activity, further indicating disease aggressiveness and unfavorable outcomes.
21
The coexistence of these clinical features, alongside 1q21 amplification and an IGH/FGFR3 fusion, constituted a highly proliferative and aggressive baseline biological profile. This profile perfectly aligns with the patient’s clinical course of a deep medullary remission followed by early, widespread extramedullary relapse. Ultimately, this suggests the patient harbored a biological predisposition for rapid extramedullary progression from the time of diagnosis, underscoring the critical need for heightened vigilance and enhanced systemic monitoring throughout treatment.

Another notable feature of this case was the marked medullary–extramedullary dissociation. Although VCD therapy achieved a deep medullary remission, persistent extramedullary residual disease limited the overall depth of response. According to the 2016 International Myeloma Working Group (IMWG) criteria, a complete response requires the radiographically confirmed disappearance of all soft-tissue plasmacytomas.
22
In this patient, a chest CT following cycle 11 of VCD revealed residual soft-tissue masses adjacent to the left sixth and seventh ribs; consequently, the overall response was assessed as a partial response (PR). We acknowledge that the lack of post-radiotherapy imaging to evaluate the extramedullary response represents an important limitation of this report. At relapse, the stark contrast between extensive extramedullary disease and a bone marrow plasma cell burden of only 1% underscored a critical clinical caveat: bone marrow MRD and serological markers primarily reflect intramedullary tumor burden and cannot substitute for the adequate radiological evaluation of extramedullary lesions.

Bortezomib-lenalidomide-dexamethasone (VRd) is widely utilized as induction therapy in multiple myeloma.
23
For high-risk patients, the addition of daratumumab to VRd (D-VRd) has demonstrated superior efficacy,
24
and has become the standard of care for transplant-eligible newly diagnosed multiple myeloma (NDMM).
25
Given the patient’s high-risk baseline profile described above, D-VRd would theoretically have been the optimal initial regimen. However, two primary factors precluded the use of D-VRd or VRd in this case. First, based on our long-term institutional experience regarding the adverse effects associated with locally available generic lenalidomide, tolerability concerns prompted the selection of a lenalidomide-free regimen (VCD). Second, daratumumab was not covered by the patient’s medical insurance, and financial constraints precluded its out-of-pocket use. Autologous stem cell transplantation (ASCT) was also deferred due to similar economic limitations. Consequently, in the absence of both anti-CD38 immunotherapy and transplant consolidation, VCD therapy was extended to 12 cycles to maintain disease control.

Managing RRMM with extensive EMD remains a formidable clinical challenge. Although second-generation proteasome inhibitors (PIs) like carfilzomib exhibit superior antineoplastic activity and lower neurotoxicity compared to first-generation PIs, significantly improving survival in standard RRMM, 26 – 28 their efficacy in widespread EMD is often severely limited. Clinical data indicate that the median overall survival (OS) for RRMM patients with EMD is historically poor, often less than 9.3 months.
29
Carfilzomib in combination with dexamethasone (Kd) is the standard second-line therapy for relapsed/refractory multiple myeloma at our institution. However, given the multifocal vital organ involvement observed during this patient’s relapse, liposomal doxorubicin was incorporated to formulate the KDD regimen. This strategy was selected to achieve rapid cytoreduction of the extramedullary disease burden while maintaining systemic clonal control. In our case, despite initiating a salvage regimen comprising carfilzomib, liposomal doxorubicin, and dexamethasone, the patient exhibited an abysmal response and rapid deterioration. This highlights that EMD clones, particularly those driven by high-risk genetics, possess intrinsic resistance mechanisms that render conventional PI-based salvage therapies insufficient to halt disease progression. Furthermore, the soft tissue invasion already present at initial diagnosis in this patient is also one of the high-risk factors for subsequent rapid multi-organ metastasis.

For high-risk MM patients, early autologous hematopoietic stem cell transplantation (ASCT) remains a cornerstone of upfront consolidation, capable of overcoming certain genetic high-risk features and significantly prolonging progression-free survival.
30
A study by Gagelmann et al. demonstrated that ASCT confers survival benefits even in MM patients with concurrent EMD,
31
and its early application is critical for modifying the disease course in genetically high-risk populations.
32
The patient was clinically transplant-eligible at diagnosis based on age (64 years), acceptable performance status (ECOG 1), and absence of severe comorbidities. Unfortunately, financial constraints precluded ASCT in our patient, which may have allowed the early and unchecked emergence of the aggressive EMD clone. In the modern therapeutic era, novel immunotherapies—such as anti-CD38 monoclonal antibodies (e.g., daratumumab), CAR-T cell therapies, and bispecific T-cell engagers (BiTEs)—are shifting the treatment paradigm and have demonstrated promising efficacy for relapsed/refractory EMD. 33 , 34 While our patient’s rapid clinical decline prevented the initiation of these advanced therapies, their incorporation into earlier lines of treatment may represent the most viable strategy for preventing or managing fulminant multi-organ EMD.

The findings of this report should be interpreted in the context of several limitations. First, as a single-case report, the clinical trajectory described herein may not represent the general pathological patterns of all EMD presentations. Second, due to financial constraints, the patient did not receive ASCT or novel immunotherapies (e.g., anti-CD38 monoclonal antibodies). Consequently, we were unable to assess the potential efficacy of these cutting-edge approaches in reversing this specific multi-organ EMD phenotype. Third, the lack of a repeat biopsy and genetic sequencing upon relapse prevented us from determining the molecular basis of the rapid disease progression, thereby hindering the selection of customized and potent salvage therapies. Fourth, the lack of serial imaging surveillance during the post-radiotherapy and maintenance phases precluded an adequate assessment of the extramedullary response. This is a critical limitation, as EMD can progress independently of bone marrow parameters. Fifth, the absence of longitudinal M protein quantification via serum protein electrophoresis (SPEP) required us to rely on limited serum free light chain (sFLC) data to evaluate serological trends.

Conclusion

In conclusion, we present an exceptionally rare and catastrophic case of relapsed multiple myeloma featuring explosive multivisceral and cardiovascular extramedullary infiltration, notably occurring with minimal bone marrow involvement. This case starkly illustrates the aggressive clonal evolution and profound treatment refractoriness driven by concurrent high-risk genetic aberrations, specifically 1q21 amplification and the t 4 , 5 translocation. The patient’s rapid and fatal trajectory, despite conventional PI-based salvage therapy, underscores the critical inadequacy of current standard regimens for this unique and aggressive EMD phenotype. Continuous exploration of tailored, biology-driven therapeutic algorithms is urgently required to improve the dismal prognosis associated with multi-organ EMD in multiple myeloma.

Supplemental material

Supplemental material - Fulminant extramedullary relapse of multiple myeloma with rare cardiac, vascular, and multivisceral involvement: A case report

Supplemental material for Fulminant extramedullary relapse of multiple myeloma with rare cardiac, vascular, and multivisceral involvement: A case report by Yuhui Wei, Xuejiao Yang, Yulan Zheng, and Dongdong Zhang in Therapeutic Advances in Hematology.