Clinical Characteristics and Outcome of Primary AL Amyloidosis in Greece.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4729-4729
Author(s):  
Michalis Michail ◽  
Efstathios Kastritis ◽  
Sossana Delimpassi ◽  
Marie Christine Kyrtsonis ◽  
Evridiki Michali ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Autonomic Neuropathy ◽  
Congo Red ◽  
Plasma Cells ◽  
Primary Treatment ◽  
Response To Treatment ◽  
Light Chains ◽  
High Dose ◽  
Al Amyloidosis ◽  
Heart Involvement

Abstract Introduction: Primary systemic amyloidosis (AL) is a clonal plasma cells disorder characterized by deposition of amyloid fibrils derived from abnormal light chains, leading to multiorgan involvement and failure. There is no information regarding the clinical, laboratory, treatment characteristics and outcome of such patients in Greece. We performed a retrospective analysis in order to clarify these issues. Patients and Methods: Diagnosis of primary AL amyloidosis was based on positive Congo red staining, immunohistochemistry and the presence of typical clinical and laboratory features. Definition of organ involvement and treatment response was based on established criteria (Gertz et al Am J Hematol 2005). Results: between 1995 and 2007, we identified 109 patients with previously untreated systemic AL amyloidosis. Median age was 66.3 years; 51% were males and lambda-light chain was involved in 74% of patients. Bone marrow biopsy stained positive for Congo-red in 56.5%, immunohistochemical staining was performed in 80 cases: 63 (78.75%) stained positive for λ and 17 for κ light chains. A monoclonal protein by immunofixation was found in the serum and/or urine of 97 (87%) patients. More than 10% bone marrow plasma cells were found in 65%. B2microglobulin was elevated in 36% of patients (median value 2.8 mg/l). The most frequent symptoms at presentation were fatigue and weakness (81%). Heart was involved in 66 (59%), kidney in 79 (71%), liver in 21(19%), GI tract in 17 (16%) and soft tissue in 35 (32%) patients respectively. Symptoms of peripheral and/or autonomic neuropathy were present in 38 (35%) patients. More than two organs were involved in 50 patients (45%). Primary treatment with high-dose dexamethasone based regimens (VAD or pulse Dexamethasone) was used in 45% while 37% of patients were treated with melphalan and prednisone. Six patients (5%) were treated upfront with high dose melphalan and ASCT while another 6 patients were transplanted at a later stage of their disease. Hematologic response was achieved in 50 (46%) including 16 (14.5%) patients who achieved a CR. Organ responses were seen in 32 (29%) patients: 4 had cardiac, 21 renal and 7 liver response respectively while 11 patients had subjective improvement of peripheral or autonomic neuropathy. Median survival from initiation of treatment was 61 months and the 5 year-survival was 44%. Patients with heart involvement or with more than 2 affected organs had a worse prognosis. Survival was significantly longer for patients who responded to primary treatment than for those who did not (p=0.018). Conclusions: Greek patients with AL amyloidosis share the same characteristics with that of patients from other reported studies. Hematologic responses were noted in one-half and organ responses in one-third of patients. Prognosis depended primarily on the presence of heart involvement and on the lack of response to treatment.

High Dose Melphalan with Autologous Stem Cell Transplantation Overcomes Poor Prognosis of Primary Amyloidosis

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1350-1350
Author(s):  
Simrit Parmar ◽  
Mubeen Khan ◽  
Gabriela Rondon ◽  
Nina Shah ◽  
Qaiser Bashir ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Plasma Cells ◽  
High Dose ◽  
Al Amyloidosis ◽  
Hematologic Response ◽  
Bone Marrow Plasma ◽  
Organ Response ◽  
High Dose Melphalan

Abstract Abstract 1350 Background: Systemic Primary AL Amyloidosis is a rare but potentially fatal disease resulting from tissue deposits of amyloid fibrils derived from monoclonal immunoglobulin light chains. High-dose melphalan followed by autologous hematopoietic stem cell transplant (auto HCT) is associated with hematologic and organ responses and improved survival. Methods: In this retrospective analysis we identified 46 patients with primary AL amyloidosis who received auto HCT between 01/1998 to 05/2010 at MDACC. Organ responses were determined using Amyloidosis Consensus Criteria. Results: The median age at auto HSCT was 56 years (34-74) where 61% were males and 35% were older than 60 years of age. 61% had lambda light chain restriction and only 4% had cytogenetic abnormalities. Disease characteristics are summarized in Table 1. The median time from diagnosis to auto HCT was 6.6 months (2.2-29.4 months). 22 pts (47.8%) had one organ, 19 pts (41.3%) had 2 organ and 4 pts (8.7%) had 3 organ involvement. 11 pts (23.9%) had heart and 35 pts (76.1%) had kidney involvement. The median follow up from the time of diagnosis was 22.4 months and from time of auto HCT was 16.7 months. High dose Melphalan dose was 200mg/m2 in 24 pts (52%) and 140mg/m2 in 22 (47.8%). There were 4 early deaths and 4 pts whose follow up was less than 3 months and their response was not assessed. Out of the 38 evaluable patients, the post-transplant organ responses were as follows ≥PR 25(66%), ≥stable disease 35(92%) (Table2). The hematologic responses were: CR=5 (13%), ≥VGPR=10(26%), ≥PR=26 (68%), ≥SD=37(97%). One patient had progressive disease. There was a correlation between organ response and hematologic response (chi square;p<10-3). The day-100 treatment related mortality (TRM) was 8.7% and 1-yr TRM was 13%. The median progression-free (PFS) and overall survival (OS) from auto HCT was 73.8 months and not reached (from transplant). The median PFS and OS from diagnosis were 93 months and 59.8 months respectively. In multivariate analysis, heart involvement (p=0.01), female sex (p=0.011), age ≥60 years (p=0.002), bone marrow plasma cells≥10% (p=0.043) and Beta-2 microglobulin>3.5mg/l (p=0.02) were associated with poor OS. Improved OS correlated with organ response (52.6 vs 11.4 months; p=0.01) and hematologic response (52.6 vs.6.1months; p=0.002). Hemoglobin <10 g/dl (p=0.047), bone marrow plasma cells≥10% (p=0.043) and age≥60 years (p=0.075) were associated with shorter PFS. Hematologc response (p=0.48) and organ response (p=0.12) were not associated with improved PFS. Conclusion: In this analysis the outcome of patients with primary systemic AL amyloidosis was durable with auto HCT with acceptable mortality risk and improved survival. Disclosures: No relevant conflicts of interest to declare.

MR-Proanp and VEGF As Markers of Response to MEL-DEX Treatment in Systemic AL Amyloidosis

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 4970-4970
Author(s):  
Alessandro Moscetti ◽  
Giusy Antolino ◽  
Federica Resci ◽  
Daniela De Benedittis ◽  
Virginia Naso ◽  
...  
Keyword(s):  
Stress Responses ◽  
Plasma Cells ◽  
Disease Risk ◽  
Conflicts Of Interest ◽  
Serum Levels ◽  
Response To Treatment ◽  
Al Amyloidosis ◽  
Significant Independent Predictor ◽  
Heart Involvement ◽  
Cell Mitogen

Abstract Abstract 4970 Background. The natriuretic peptides are a family of different biomarkers including NT-proBNP and MR-proANP. As recommended by guidelines, they are important in heart failure diagnosis and monitoring. MR-proANP (1–98) is the mid-regional portion of the active atrial natriuretic peptide prohormone (99–126) and is considered a significant independent predictor of death, adding prognostic value to NT-proBNP. Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen with angiogenic and nonangiogenic role in several disorders including cardiovascular ones. Moreover, it regulates multiple cellular stress responses, including survival, proliferation, migration and differentiation. Systemic AL amyloidosis represents a peculiar disease with a clinical heart involvement that needs of a specific monitoring in order to avoid poor outcome. Aims and Methods. The study was devoted to evaluate treatment related changes in cardiovascular activity by MR-proANP and VEGF serum levels in systemic AL amyloidosis. Blood samples were collected from 8 patients with systemic AL amyloidosis (median age 72. 8 yrs) admitted to our Unit and analyzed for serum MR-proANP (mean±SD) and VEGF levels (Kits Brahms MR-proANP Kryptor and Randox Evidence Biochips Arrays). According to age and disease risk stratification all patients were treated with upfront oral Mel-Dex association (Melphalan 9 mg/sm, Dexamethasone 20mg day 1–4 q28). From each patient 2 samples of peripheral blood were performed (T0: at exordium of disease and T1: at conclusion of the first course of treatment). The sera were frozen to −80°C until their use. The results were analyzed by paired t test and Person correlation, p values ≤ 0. 05 were considered statistically significant. Results. VEGF serum levels were significantly (p=0. 01) reduced at the end of the first course of treatment (M±SD: T0: 282. 3 ± 86. 23 pg/mL vs. T1: 189. 7 ± 64. 24 pg/mL). Also MR-proANP serum levels were significantly decreased (M±SD: T0: 204. 4 ± 28. 82 pmol/L vs. T1: 160. 2 ± 21. 05 pmol/L, p=0. 008; see figure). The decreases of VEGF and MR-proANP were significantly (r =0. 79; p=0. 02) related. Conclusions. MR-proANP serum levels reduction could be hypothized as related to the decrease of inflammatory activity of disease, including heart involvement and a consequent reduced probability of fatal events. Our hypothesis seems to be confirmed by VEGF serum level reduction suggesting an inhibition of new angiogenesis with reduced interactions between neoplastic plasma cells and bone marrow microenvironment. The effective role of treatment in reducing the disease activity is demonstrated by the significant correlation between VEGF and MR-proANP level decreases. MR-proANP and VEGF could be used to evaluate and select systemic AL amyloidosis patients with an early good response to treatment. Disclosures: No relevant conflicts of interest to declare.

A patient with AL amyloidosis with negative free light chain results

2016 ◽  
Vol 54 (6) ◽  
Author(s):  
Paolo Milani ◽  
Veronica Valentini ◽  
Giovanni Ferraro ◽  
Marco Basset ◽  
Francesca Russo ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Biopsy ◽  
Light Chain ◽  
Left Ventricular ◽  
Free Light Chain ◽  
Response To Treatment ◽  
Light Chains ◽  
Al Amyloidosis ◽  
Light Chain Restriction ◽  
Serum And Urine

AbstractThe detection and quantification of amyloidogenic monoclonal light chains are necessary for the diagnosis and evaluation of response to treatment in AL amyloidosis. However, the amyloid clone is often small and difficult to detect. We report the case of a 68-year-old man who was referred to our Center in April 2013 after syncope and the identification of left ventricular hypertrophy at echocardiography, suspected for amyloidosis. A commercial agarose gel electrophoresis immunofixation (IFE) did not reveal monoclonal components in serum and urine. The κ serum free light chain (FLC) concentration was 21.5 mg/L, λ 33 mg/L (κ/λ ratio 0.65), NT-proBNP 9074 ng/L (u.r.l. <332 ng/L) and an echocardiogram confirmed characteristic features of amyloidosis. The abdominal fat aspiration was positive and the amyloid typing by immune-electron microscopy revealed λ light chains deposits. A high-resolution (hr) IFE of serum and urine showed a faint monoclonal λ component in the urine. A bone marrow biopsy showed 8% plasma cells (BMPC) and a kappa/lambda light-chain restriction with λ light chain on immunofluorescence. The diagnosis of AL (λ) amyloidosis with cardiac involvement was made. In May 2013, patient was started on cyclophosphamide, bortezomib and dexamethasone. After six cycles, serum and urine hr-IFE were negative, the bone marrow biopsy showed 3% BMPC without light chain restriction by immunofluorescence, and a decrease of NT-proBNP was observed (5802 ng/L).Thus, treatment was discontinued. In this patient the amyloid clone could be detected only by in house hr-IFE of urine and bone marrow examination. The detection of the small dangerous amyloidogenic clone should be pursued with a combination of high-sensitivity techniques, including assessment of BMPC clonality. Studies of novel tools, such as mass spectrometry on serum and next-generation flow cytometry analysis of the bone marrow, for detecting plasma cell clones in AL amyloidosis and other monoclonal light chain-related disorders are warranted.

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 Long-term Follow-up of Plasma Cells in Bone Marrow and Serum Free Light Chains in Primary Systemic AL Amyloidosis

2008 ◽  
Vol 47 (20) ◽  
pp. 1783-1790 ◽  
Author(s):  
Takuhiro Yoshida ◽  
Masayuki Matsuda ◽  
Nagaaki Katoh ◽  
Ko-ichi Tazawa ◽  
Yasuhiro Shimojima ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Plasma Cells ◽  
Light Chains ◽  
Al Amyloidosis ◽  
Free Light Chains ◽  
Serum Free ◽  
Long Term Follow Up ◽  
Serum Free Light Chains

scholarly journals Splenic plasma cells can serve as a source of amyloidogenic light chains

Blood ◽  
2009 ◽  
Vol 113 (7) ◽  
pp. 1501-1503 ◽  
Author(s):  
Alan Solomon ◽  
Sallie D. Macy ◽  
Craig Wooliver ◽  
Deborah T. Weiss ◽  
Per Westermark
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Monoclonal Antibodies ◽  
Light Chain ◽  
Plasma Cells ◽  
The Body ◽  
Light Chains ◽  
Al Amyloidosis ◽  
Hematopoietic Organ ◽  
Significant Evidence

Abstract Bone marrow-derived clonal plasma cells, as found in systemic amyloidogenic light chain–associated (AL) amyloidosis, are presumed to be the source of light chains that deposit as fibrils in tissues throughout the body. Paradoxically, people with this disorder, in contrast to multiple myeloma, often have a low percentage of such cells, and it is unknown whether this relatively sparse number can synthesize enough amyloidogenic precursor to form the extensive pathology that occurs. To investigate whether another hematopoietic organ, the spleen, also contains monoclonal light chain–producing plasma cells, we have immunostained such tissue from 26 AL patients with the use of antiplasma cell, antifree κ and λ, and anti-VL subgroup-specific monoclonal antibodies (mAbs). In 12 cases, there was statistically significant evidence of a monoclonal population bearing the same κ or λ isotype as that within the bone marrow and identical to the amyloid. Our studies have shown that the spleen may be another source of amyloidogenic light chains.

Bone disease as the first manifestation of systemic AL-amyloidosis

2020 ◽  
Vol 92 (7) ◽  
pp. 85-89
Author(s):  
L. P. Mendeleeva ◽  
I. G. Rekhtina ◽  
A. M. Kovrigina ◽  
I. E. Kostina ◽  
V. A. Khyshova ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Bone Disease ◽  
Plasma Cells ◽  
Interventricular Septum ◽  
Bone Destruction ◽  
Amyloid Deposition ◽  
Bone Lesions ◽  
Al Amyloidosis ◽  
Linear Type

Our case demonstrates severe bone disease in primary AL-amyloidosis without concomitant multiple myeloma. A 30-year-old man had spontaneous vertebral fracture Th8. A computed tomography scan suggested multiple foci of lesions in all the bones. In bone marrow and resected rib werent detected any tumor cells. After 15 years from the beginning of the disease, nephrotic syndrome developed. Based on the kidney biopsy, AL-amyloidosis was confirmed. Amyloid was also detected in the bowel and bone marrow. On the indirect signs (thickening of the interventricular septum 16 mm and increased NT-proBNP 2200 pg/ml), a cardial involvement was confirmed. In the bone marrow (from three sites) was found 2.85% clonal plasma cells with immunophenotype СD138+, СD38dim, СD19-, СD117+, СD81-, СD27-, СD56-. FISH method revealed polysomy 5,9,15 in 3% of the nuclei. Serum free light chain Kappa 575 mg/l (/44.9) was detected. Multiple foci of destruction with increased metabolic activity (SUVmax 3.6) were visualized on PET-CT, and an surgical intervention biopsy was performed from two foci. The number of plasma cells from the destruction foci was 2.5%, and massive amyloid deposition was detected. On CT scan foci of lesions differed from bone lesions at multiple myeloma. Bone fragments of point and linear type (button sequestration) were visualized in most of the destruction foci. The content of the lesion was low density. There was no extraossal spread from large zones of destruction. There was also spontaneous scarring of the some lesions (without therapy). Thus, the diagnosis of multiple myeloma was excluded on the basis based on x-ray signs, of the duration of osteodestructive syndrome (15 years), the absence of plasma infiltration in the bone marrow, including from foci of bone destruction by open biopsy. This observation proves the possibility of damage to the skeleton due to amyloid deposition and justifies the need to include AL-amyloidosis in the spectrum of differential diagnosis of diseases that occur with osteodestructive syndrome.

scholarly journals Chronic lymphocytic leukemia (CLL) terminating in multiple myeloma: report of two cases

Blood ◽  
1978 ◽  
Vol 52 (3) ◽  
pp. 532-536 ◽  
Author(s):  
RH Kough ◽  
AZ Makary
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Chronic Lymphocytic Leukemia ◽  
Plasma Cells ◽  
Medical Center ◽  
White Male ◽  
Lymphocytic Leukemia ◽  
Light Chains ◽  
White Female ◽  
Pathologic Fractures

Abstract Two cases of multiple myeloma (MM) developed late in the course of chronic lymphocytic leukemia (CLL). An 81-yr-old white female developed, after 6 yr of CLL, IgAk MM with sheets of plasma cells abutting sheets of lymphocytes in the bone marrow, multiple pathologic fractures, and 0.26 g/24 free k light chains in the urine. A 74-yr-old white male developed, after 16 yr of CLL, k light chain MM with 20% plasma cells in the bone marrow, multiple panthologic fractures, and 3.7 g/24 hr free k light chains in the urine. In both cases the CLL had responded well to intermittent low-dose chlorambucil therapy, but the MM failed to respond to cyclic melphalanprednisone therapy. A review of 105 cases of CLL seen at the Geisinger Medical Center failed to turn up any other cases of MM developing during the course of CLL. The suggestion that there is an increased prevalence of MM in CLL is an attractive one because both diseases are B cell neoplasms and because of the increased frequency of asymptomatic monoclonal gammopathies in CLL found by others.

scholarly journals Silver Nanoparticle-Based Assay for the Detection of Immunoglobulin Free Light Chains

Materials ◽  
2019 ◽  
Vol 12 (18) ◽  
pp. 2981 ◽  
Author(s):  
Anna Lizoń ◽  
Magdalena Wytrwal-Sarna ◽  
Marta Gajewska ◽  
Ryszard Drożdż
Keyword(s):  
Light Scattering ◽  
Silver Nanoparticle ◽  
Plasma Cells ◽  
Wide Spectrum ◽  
Metal Nanoparticle ◽  
Light Chains ◽  
Hydrodynamic Diameter ◽  
Al Amyloidosis ◽  
Free Light Chains ◽  
Optimal Test

There is a wide spectrum of malignant diseases that are connected with the clonal proliferation of plasma cells, which cause the production of complete immunoglobulins or their fragments (heavy or light immunoglobulin chains). These proteins may accumulate in tissues, leading to end organ damage. The quantitative determination of immunoglobulin free light chains (FLCs) is considered to be the gold standard in the detection and treatment of multiple myeloma (MM) and amyloid light-chain (AL) amyloidosis. In this study, a silver nanoparticle-based diagnostic tool for the quantitation of FLCs is presented. The optimal test conditions were achieved when a metal nanoparticle (MNP) was covered with 10 particles of an antibody and conjugated by 5–50 protein antigen particles (FLCs). The formation of the second antigen protein corona was accompanied by noticeable changes in the surface plasmon resonance spectra of the silver nanoparticles (AgNPs), which coincided with an increase of the hydrodynamic diameter and increase in the zeta potential, as demonstrated by dynamic light scattering (DLS). A decrease of repulsion forces and the formation of antigen–antibody bridges resulted in the agglutination of AgNPs, as demonstrated by transmission electron microscopy and the direct formation of AgNP aggregates. Antigen-conjugated AgNPs clusters were also found by direct observation using green laser light scattering. The parameters of the specific immunochemical aggregation process consistent with the sizes of AgNPs and the protein particles that coat them were confirmed by four physical methods, yielding complementary data concerning a clinically useful AgNPs aggregation test.

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