Evaluation of the Cytogenetic Aberration Pattern in AL Amyloidosis Compared to Monoclonal Gammopathies Not Requiring Treatment: Translocation t(11;14) Is More Frequent in AL Amyloidosis.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2500-2500 ◽  
Author(s):  
Tilmann Bochtler ◽  
Stefan O. Schonland ◽  
Anna Jauch ◽  
Christiane Heiss ◽  
Axel Benner ◽  
...  
Keyword(s):  
Plasma Cell ◽  
Monoclonal Gammopathy ◽  
Control Group ◽  
Al Amyloidosis ◽  
Fish Analysis ◽  
Cell Content ◽  
Cytogenetic Aberration ◽  
Cytogenetic Aberrations ◽  
Plasma Cell Disorders ◽  
Unknown Significance

Abstract Introduction: Cytogenetic aberrations (CA) have emerged as important pathogenetic and prognostic factors in plasma cell disorders. However, in AL amyloidosis (AL) only a few reports with small numbers of patients have been published. Methods: Using interphase FISH analysis in CD138+ cells, we evaluated the role of CA in a series of 85 AL patients as compared to 146 patients with a monoclonal gammopathy without treatment requirement in a prospective manner. Our panel included IgH translocations t(11;14), t(4;14), t(14;16) and translocation of 14q32 with an unidentified partner, gains of 1q21, 11q23 and 19q13 as well as deletions of 8p21, 13q14 and 17p13. Using these probes we could detect at least one of these aberrations in 95% of AL and in 88% of the control group. Age, gender and plasma cell content were statistically equally distributed among both groups. Results: The most frequent aberration in AL was t(11;14), which was detected in 45% of AL patients as compared to 26% of the control group (p=0,056). It was strongly associated with the lack of an intact immunoglobulin (p<0,001), thus accounting for the frequent light chain only subtype in AL. Markedly, t(11;14) was more frequently found in combination with gain 11q23 in AL than in the control group (20% versus 6%, p = 0.005). Other frequent aberrations in AL included deletion 13q14 (32%) and gain 1q21 (21%), which were observed in the control group at comparable frequencies (34% and 20%). The overlapping character of the underlying plasma cell disorder in both disease entities was also emphasized by the similarities of branching patterns of the five major CA in cluster analysis applied in 169 patients (figure 1). The relation of clinical parameters and chromosomal aberrations was also evaluated. The analyzed CA had no impact on the organ involvement pattern in AL patients. Conclusions: We observed a high frequency for t(11;14) in AL. Apart from this finding, the cytogenetic patterns known in monoclonal gammopathy of unknown significance and multiple myeloma were widely shared by AL amyloidosis. Figure Figure

Evaluation of the cytogenetic aberration pattern in amyloid light chain amyloidosis as compared with monoclonal gammopathy of undetermined significance reveals common pathways of karyotypic instability

Blood ◽  
2008 ◽  
Vol 111 (9) ◽  
pp. 4700-4705 ◽  
Author(s):  
Tilmann Bochtler ◽  
Ute Hegenbart ◽  
Friedrich W. Cremer ◽  
Christiane Heiss ◽  
Axel Benner ◽  
...  
Keyword(s):  
Plasma Cell ◽  
Light Chain ◽  
Monoclonal Gammopathy ◽  
Common Mechanism ◽  
Fish Analysis ◽  
Tree Model ◽  
Light Chain Amyloidosis ◽  
Plasma Cell Disorders ◽  
Karyotypic Instability ◽  
Amyloid Light Chain

AbstractChromosomal aberrations (CAs) have emerged as important pathogenetic and prognostic factors in plasma cell disorders. Using interphase fluorescence in situ hybridization (FISH) analysis, we evaluated CAs in a series of 75 patients with amyloid light chain amyloidosis (AL) as compared with 127 patients with monoclonal gammopathy of unknown significance (MGUS). We investigated IgH translocations t(11;14), t(4;14), and t(14;16) as well as gains of 1q21, 11q23, and 19q13 and deletions of 8p21, 13q14, and 17p13, detecting at least one CA in 89% of the patients. Translocation t(11;14) was the most frequent aberration in AL, with 47% versus 26% in MGUS (P = .03), and was strongly associated with the lack of an intact immunoglobulin (P < .001), thus contributing to the frequent light chain subtype in AL. Other frequent aberrations in AL included deletion of 13q14 and gain of 1q21, which were shared by MGUS at comparable frequencies. The progression to multiple myeloma (MM) stage I was paralleled by an increased frequency of gain of 1q21 (P = .001) in both groups. Similar branching patterns were observed in an oncogenetic tree model, indicating a common mechanism of underlying karyotypic instability in these plasma cell disorders.

Exome Sequencing To Define A Genetic Signature Of Plasma Cells In Systemic AL Amyloidosis

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 3098-3098 ◽  
Author(s):  
Brian A Walker ◽  
Dorota Rowczienio ◽  
Eileen M Boyle ◽  
Christopher P Wardell ◽  
Sajitha Sachchithanantham ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Exome Sequencing ◽  
Plasma Cell ◽  
Copy Number ◽  
Monoclonal Gammopathy ◽  
Plasma Cells ◽  
Chromosomal Abnormalities ◽  
Light Chains ◽  
Al Amyloidosis ◽  
Plasma Cell Disorders

Abstract Systemic amyloid light chain amyloidosis (AL) is characterized by the deposition of immunoglobulin light chains as amyloid fibrils in different organs, where they form toxic protein aggregates. Most AL patients have relatively low levels of circulating free light chains and bone marrow plasmacytosis. The underlying disease is a plasma cell disorder, likely a monoclonal gammopathy, but limited data are available on the biology of the plasma cell clone underlying AL and existing studies have concentrated on chromosomal abnormalities. Many of the chromosomal abnormalities identified in AL are also seen in other plasma cell disorders, such as monoclonal gammopathy of undetermined significance (MGUS) and myeloma. These abnormalities include translocations involving the IGH locus, gains of 1q and deletions of 13q and 17p. Fluorescence in situhybridization studies have identified the translocation t(11;14) to be more frequent in AL and hyperdiploidy to be rare. The causal link between genetic changes in plasma cells and light chain instability remains unknown and progression to symptomatic myeloma is rare. We report the initial findings of the first exome sequencing to define the plasma cell signature in AL and compared this to MGUS and myeloma. CD138+ cells were selected using either EasySep (Stem Cell Technologies) or MACSort (Miltenyi) from the bone marrow of 18 AL patients and 5 MGUS patients. DNA was extracted from the CD138+ cells using the AllPrep kit (Qiagen). Non-involved DNA was isolated from peripheral white blood cells using the Flexigene kit (Qiagen). 200 ng DNA was subjected to exome sequencing using NEBNext kit (NEB) and SureSelect Human All Exon kit v5 and sequenced using 76-bp paired end reads. Fastq files were aligned to the reference genome using BWA and Stampy aligners. BAM files were recalibrated using the GATK and deduplicated using Picard. Paired tumour/normal BAMs were realigned together using the GATK indel realigner and SNVs were called using Mutect. Copy number data were estimated using the R package ExomeCNV. The median depth across all samples was 42x with 97% of the exome covered at 1x and 72% covered at 20x. Exome data to determine the cytogenetic groups of AL samples identified 42% hyperdiploid and 21% with t(11;14). The AL samples with t(11;14) did not contain any other copy number abnormalities. Exome sequencing on samples from patients with MGUS and myeloma was also performed to compare the genetic makeup and mutation spectrum of these well characterised plasma cell neoplasias with AL samples. MGUS samples had a median of 30 acquired nonsynonymous variants (range 24-189) and AL amyloidosis samples had a median of 17 acquired nonsynonymous variants (range 4-44). The AL samples had four recurrent mutations in PCMTD1 (n=3; L267F, P266S and M187I), C21orf33 (n=2; E72K), NLRP12 (n=2; L1018P, W959* ) and NRAS (n=2; Q61R, Q61H). In this small dataset, only 5 genes were mutated in both the MGUS and AL samples (DNMBP, FRG1, HIST1H1B, KRTAP4-11 and MCCC1). In order to assess the similarity (or differences) of plasma cells in AL to malignant plasma cells in general, we compared them to a random sampling of 20 multiple myeloma samples which had also been exome sequenced (median number of acquired nonsynonymous variants = 39 vs. 17 in AL samples). This revealed that the AL contained 21 mutated genes in common with the myeloma cohort, including DIS3 and NRAS. There were two DIS3 mutations in one AL sample at c.379D>E (p.D479E) and c.1999A>T (p.M667L), both of which were in the Ribonuclease II/R catalytic domain. Data on correlation of gene mutations and organ involvement in AL amyloidosis will be presented. We conclude that exome sequencing identifies a genetic signature of AL amyloidosis which is similar to other plasma cell disorders. This not only includes copy number abnormalities and translocations but also a similar number of nonsynonymous mutations to MGUS and fewer than the advanced myeloma samples. Study of further samples is in progress. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Treatment in AL Amyloidosis: Moving towards Individualized and Clone-Directed Therapy

Hemato ◽  
2021 ◽  
Vol 2 (4) ◽  
pp. 739-747
Author(s):  
Ute Hegenbart ◽  
Marc S. Raab ◽  
Stefan O. Schönland
Keyword(s):  
B Cell ◽  
Plasma Cell ◽  
Cell Clone ◽  
Secretory Activity ◽  
Underlying Disease ◽  
Al Amyloidosis ◽  
Cytogenetic Aberrations ◽  
Plasma Cell Disorders ◽  
Amyloid Light Chain ◽  
Underlying Diseases

Systemic amyloid light chain (AL) amyloidosis is a rare protein deposition disease caused by a clonal B cell disorder of the bone marrow. The underlying diseases can be plasma cell disorders (monoclonal gammopathy of clinical significance, smoldering or symptomatic myeloma) or B cell non-Hodgkin’s lymphoma (e.g., Waldenstrom’s disease or marginal zone lymphoma) with secretory activity. It is crucial to characterize the underlying disease very precisely as the treatment of AL amyloidosis is directed against the (often small) B cell clone. Finally, the detection of cytogenetic aberrations of the plasma cell clone will likely play an important role for choosing an effective drug in the near future.

Hyperdiploidy is less frequent in AL amyloidosis compared with monoclonal gammopathy of undetermined significance and inversely associated with translocation t(11;14)

Blood ◽  
2011 ◽  
Vol 117 (14) ◽  
pp. 3809-3815 ◽  
Author(s):  
Tilmann Bochtler ◽  
Ute Hegenbart ◽  
Christiane Heiss ◽  
Axel Benner ◽  
Marion Moos ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Fluorescence In Situ Hybridization ◽  
Monoclonal Gammopathy ◽  
Early Stage ◽  
Al Amyloidosis ◽  
Tree Model ◽  
Cytogenetic Aberrations ◽  
Plasma Cell Disorders ◽  
Undetermined Significance

Abstract In multiple myeloma (MM) pathogenesis, hyperdiploidy and nonhyperdiploidy are recognized as 2 major cytogenetic pathways. Here, we assessed the role of hyperdiploidy in 426 patients with monoclonal plasma cell disorders, among them 246 patients with AL amyloidosis (AL), by interphase fluorescence in situ hybridization. Hyperdiploidy was defined by a well-established score requiring trisomies for at least 2 of the 3 chromosomes 5, 9, and 15. The hyperdiploidy frequency in AL was a mere 11% compared with 30% in monoclonal gammopathy of undetermined significance (P < .001) and 46% in AL with concomitant MM I (P < .001). Overall, hyperdiploidy was associated with an intact immunoglobulin, κ light chain restriction, higher age, and bone marrow plasmacytosis, but was unrelated to the organ involvement pattern in AL. Clustering of 6 major cytogenetic aberrations in AL by an oncogenetic tree model showed that hyperdiploidy and t(11;14) were almost mutually exclusive, whereas gain of 1q21 favored hyperdiploidy. Deletion 13q14 and secondary IgH translocations were equally distributed between ploidy groups. We conclude that the interphase fluorescence in situ hybridization–based hyperdiploidy score is also a feasible tool to delineate hyperdiploid patients in early-stage monoclonal gammopathies and that the cytogenetic pathogenetic concepts developed in MM are transferable to AL.

scholarly journals Differential diagnosis of monoclonal gammopathy of undetermined significance

Hematology ◽  
2012 ◽  
Vol 2012 (1) ◽  
pp. 595-603 ◽  
Author(s):  
Giampaolo Merlini ◽  
Giovanni Palladini
Keyword(s):  
Differential Diagnosis ◽  
Plasma Cell ◽  
Monoclonal Gammopathy ◽  
Cell Clone ◽  
Organ Damage ◽  
Organ Injury ◽  
Al Amyloidosis ◽  
Monoclonal Protein ◽  
Undetermined Significance

Abstract Monoclonal gammopathy of undetermined significance (MGUS) is an asymptomatic plasma cell disorder occurring in 4.2% of adults > 50 years of age, which can progress into symptomatic diseases either through proliferation of the plasma cell clone, giving rise to multiple myeloma and other lymphoplasmacellular neoplasms, or through organ damage caused by the monoclonal protein, as seen in light-chain amyloidosis and related conditions. Differential diagnosis of asymptomatic and symptomatic monoclonal gammopathies is the determinant for starting therapy. The criteria for determining end-organ damage should include markers of organ injury caused by the monoclonal protein. Patient assessment and optimal follow-up are now performed using risk stratification models that should also take into account the risk of developing AL amyloidosis. Patients with low-risk MGUS (approximately 40% of all MGUS patients) need limited assessment and very infrequent follow-up. The ongoing development of novel molecular biomarkers and advanced imaging techniques will improve the identification of high-risk patients who may benefit from early therapeutic intervention through innovative clinical trials.

scholarly journals Follow-up Care of Monoclonal Gammopathy of Undetermined Significance: A Guide for Primary Care Physicians

2021 ◽  
Vol 8 (5) ◽  
Author(s):  
Hammad Z ◽  
◽  
Hernandez E ◽  
Tate S ◽  
◽  
...  
Keyword(s):  
Plasma Cell ◽  
Primary Care Physicians ◽  
Monoclonal Gammopathy ◽  
Plasma Cells ◽  
Organ Damage ◽  
M Protein ◽  
Bone Lesions ◽  
Al Amyloidosis ◽  
End Organ Damage ◽  
Undetermined Significance

Monoclonal Gammopathy of Undetermined Significance (MGUS) is a condition in which M protein, an abnormal monoclonal immunoglobulin, is present in the blood at a nonmalignant level. Specifically, it is defined by: blood serum M protein concentration <3 g/dL (<30 g/L), <10% plasma cells in the bone marrow, and no evidence of end organ damage [1,2]. Evidence of end organ damage includes hypercalcemia, renal insufficiency, anemia, and bone lesions. These are indicative of MGUS progression and which can be attributed to the monoclonal plasma cell proliferative process [3]. MGUS occurs in 3% of the general population older than 50 years. Incidence increases with age and varies with sex with higher rates observered in males than females [1,4]. MGUS is the most common plasma cell disorder, with 60% of patients that present to the Mayo Clinic with a monoclonal gammopathy being diagnosed with MGUS [3]. While it is typically an asymptomatic condition, it is premalignant disorder to other monoclonal gammopathies. Multiple Myeloma (MM) is almost always preceded by MGUS and the majority of patients will have detectable levels of M protein for at least 5 years prior to MM diagnosis [5,6]. MGUS also precedes immunoglobulin light chain (AL) amyloidosis and Waldenstrom Macroglobulinemia (WM) and tends to progress to disorders at a fixed but unrelenting rate of 1% per year [4].

T Cell Large Granular Lymphocytic Leukemia and Co-Existing Plasma Cell Disorders

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5368-5368
Author(s):  
M Hasib Sidiqi ◽  
Mohammed A Aljama ◽  
David S. Viswanatha ◽  
David Dingli
Keyword(s):  
Multiple Myeloma ◽  
Plasma Cell ◽  
Mayo Clinic ◽  
Monoclonal Gammopathy ◽  
Specific Therapy ◽  
Plasma Cell Disorders ◽  
Plasma Cell Disorder ◽  
Cell Disorder ◽  
Lgl Leukemia

Abstract T cell large granular lymphocytic (T-LGL) leukemia has been reported to occur in patients with plasma cell disorders (PCD). We conducted a retrospective review of patients diagnosed with T-LGL leukemia and a PCD at the Mayo Clinic. 22 patients were identified with T-LGL leukemia and a plasma cell disorder. The T-LGL leukemia preceded the PCD in 18% (n=4), was synchronous in 50% (n=11) and diagnosed post plasma cell disorder in 32% (n=7) of patients. The PCD diagnosis varied and included monoclonal gammopathy of undetermined significance (MGUS, n=13), multiple myeloma (MM, n=5), smoldering multiple myeloma (SMM. N=2), lymphoplasmacytic lymphoma (LPL, n=1) and monoclonal gammopathy of renal significance (MGRS, n=1). 5 patients developed T-LGL leukemia after treatment for a PCD (4 with MM and 1 with LPL). 4 patients with MGUS progressed to a more aggressive disease, 3 to MM and 1 to LPL. Neutropenia (76%) and anemia (70%) were the most common clinical presentation. None of the patients had rheumatoid arthritis. Treatment for the TLGL was variable with a number of different agents used listed in Table 1. 45% (n=10) of patients had an indolent course and did not receive specific therapy for TLGL. 6 patients responded to a single line of therapy, all of whom received either cyclophosphamide or methotrexate based regimens. The remainder had a relapsing course with multiple lines of therapy including 2 patients that received splenectomy. Nine patients were identified as having symptomatic multiple myeloma and TLGL, Table 2. Four patients had progressed from a preexisting plasma cell disorder, 3 with MGUS and 1 with SMM. The diagnosis of TLGL preceded myeloma in 1 patient was concurrent in 4 and post myeloma diagnosis in 4 patients. Time to diagnosis of TLGL post myeloma ranged from 10 to 63 months. At time of LGL diagnosis neutropenia was present in 7/9 patients and anemia in 6/8 (data unavailable for 1 patient). Cytogenetics data was available in 7 patients. Hyperdiploidy was the most common abnormality (3/7) followed by deletion 13q (2/7), t(14;16) in 1 patient and 1q amplification in 1 patient. The majority of patients were treated with novel agents with 7 receiving bortezomib based therapy. 3 patients underwent autologous stem cell transplantation. Therapy directed at the TLGL was given to 4/9 patients. This consisted of a combination of cyclophosphamide and prednisone in 3/4 patients all of whom responded to therapy with resolution of cytopenias. One patient had TLGL with multiple relapses and required multiple lines of therapy including eventual splenectomy. 3 patients with TLGL diagnosed after the diagnosis of myeloma did not receive specific therapy directed at the TLGL. The clinical course of the TLGL in these 3 patients was indolent and did not appear to be affected by therapy for multiple myeloma. At last follow up 5 patients have died. After a median follow up of 76 months post TLGL diagnosis the median overall survival (OS) post TLGL diagnosis was not reached for the entire cohort. In the cohort of patients with multiple myeloma, median OS from time of myeloma diagnosis was 71 months. Median OS from time of TLGL diagnosis was not reached. T-LGL leukemia can present in patients with a variety of plasma cell disorders and occur at any stage of the disease process. It is an important differential to consider in patients with unexplained cytopenias that are incongruent with the activity of the plasma cell disorder. Disclosures Dingli: Millennium Takeda: Research Funding; Alexion Pharmaceuticals, Inc.: Other: Participates in the International PNH Registry (for Mayo Clinic, Rochester) for Alexion Pharmaceuticals, Inc.; Alexion Pharmaceuticals, Inc.: Other: Participates in the International PNH Registry (for Mayo Clinic, Rochester) for Alexion Pharmaceuticals, Inc.; Millennium Takeda: Research Funding.

Expression of CD126 (IL-R alpha) on Plasma Cells in Monoclonal Gammopathies.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 5066-5066
Author(s):  
Syed T. Mahmood ◽  
Shaji Kumar ◽  
Teresa K. Kimlinger ◽  
Jessica L. Haug ◽  
Michael Timm ◽  
...  
Keyword(s):  
Plasma Cell ◽  
Monoclonal Gammopathy ◽  
Plasma Cells ◽  
Cell Subset ◽  
Primary Amyloidosis ◽  
Normal Plasma ◽  
Plasma Cell Disorders ◽  
Plasma Cell Disorder ◽  
Cell Disorder

Abstract Background: IL-6 is important for proliferation and inhibition of apoptosis in malignant plasma cells. Understanding the role of IL-6 receptor alpha chain (CD126) in the pathogenesis of plasma cell disorders may help in developing future treatment therapies for these diseases. A previous study has shown that CD126 (alpha subunit of IL-6 receptor) is expressed distinctly in myeloma, monoclonal gammopathy of unknown significance (MGUS), and plasmacytomas when compared to normal. We performed this study in order to confirm and describe the expression of CD126 in different plasma cell disorders. Design and Methods: Using flow cytometry we assessed CD126 expression on clonal plasma cells from patients with Primary Amyloidosis (n=7), monoclonal gammopathy of undetermined significance (MGUS) (n=13), smoldering Myeloma (SMM) (n=19) and active Myeloma (n=22), as well as normal plasma cells (n=9). Plasma cells were identified by their characteristic CD38/45 expression. The expression of CD126 was separately analyzed on the CD45 positive and negative plasma cells. CD 126 expression was considered significant when more than 20% of the cells had expression. Results: CD126 expression was seen distinctly in plasma cell disorder plasma cells and not in normal plasma cells when all plasma cells were studied together. The highest expression percentages were found in Amyloid (28%) followed closely by MGUS 29(%), then SMM (23%), and Myeloma (12%) cells. The CD45 neg subset was similarly positive in the plasma cell disorder group. In this group, MGUS showed the highest expression percentage followed distantly by Amyloid, Myeloma, and SMM. The CD45 pos subset was uniformly positive in expression of CD126. If was found that this subset expressed higher levels of CD126 in all the studied plasma cell disorders and normal plasma cells when compared to the CD45 neg subset. Conclusion: The findings of this study confirm the increased expression of CD126 in plasma cell disorders when compared to normal plasma cells. The higher expression of CD126 in the CD45 pos plasma cell subset has not been previously described. In addition, the CD45 pos subset expressed higher levels of CD126 in all study groups when compared to the CD45 pos subset. This data contributes to the understanding of IL-6 receptor physiology and confirms the important role of the CD45 pos subset in the proliferation of neoplastic plasma cells. The findings are in accordance with the increased proliferative rates seen in the CD45 fraction of malignant plasma cells.

scholarly journals Incidentally Detected Amyloid Light-Chain Amyloidosis Caused by Monoclonal Gammopathy of Undetermined Significance: Possible Time-Dependent Change in Colonic Findings

2018 ◽  
Vol 12 (3) ◽  
pp. 737-746
Author(s):  
Toshiro Fukui ◽  
Yuji Tanimura ◽  
Yasushi Matsumoto ◽  
Shunsuke Horitani ◽  
Takashi Tomiyama ◽  
...  
Keyword(s):  
Plasma Cell ◽  
Light Chain ◽  
Monoclonal Gammopathy ◽  
Amyloid Deposition ◽  
Fecal Occult Blood ◽  
Al Amyloidosis ◽  
Plasma Cell Disorder ◽  
Amyloid Light Chain ◽  
Cell Disorder ◽  
Undetermined Significance

Amyloid light-chain (AL) amyloidosis is associated with plasma cell disorder and monoclonal light chains. This type of amyloidosis is the prominent type involving the gastrointestinal tract. Monoclonal gammopathy of undetermined significance (MGUS) is the most common plasma cell disorder and a known precursor of more serious diseases. A 72-year-old male was treated for high blood pressure, diabetes, and gout at the clinic of a private physician. Due to a positive fecal occult blood test discovered during colon cancer screening, he underwent colonoscopy and was diagnosed with adenomatous polyps by biopsies. Two months later, he was referred to our hospital for endoscopic resection of the polyps. Although the polyps were successfully removed, a colonoscopy revealed two types of ulcerative lesions. Immunohistopathological evaluations obtained from these lesions and polyps confirmed amyloid deposition. Although esophagogastroduodenoscopy results were normal, a biopsy specimen from the patient’s stomach showed the same type of amyloid deposition. Immunoelectrophoresis showed M-proteins for anti-IgG-λ in the serum and λ type Bence-Jones protein in the urine. His blood, bone marrow, and urine test results led to a diagnosis of MGUS. A coronary angiography revealed multivessel stenosis, and the patient’s cardiac function improved after coronary artery stenting. Hereafter, a combination therapy with bortezomib, lenalidomide, and dexamethasone is planned. This is a case report of systemic AL amyloidosis caused by MGUS, which was incidentally detected by colonoscopy.

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