**Author Listing - Lead/ Submitting Author (we will be communicating with this individual): Name, Institution, City and State where the work was done. Co-authors will be added in a separate section.**
Takeshi Kuroda, Division of Clinical Nephrology and Rheumatology, Niigata University, Niigata, Japan

**Main Body of the Abstract**
BACKGROUND: AA amyloid deposits consist mainly of serum amyloid A (SAA) derivatives and minor components such as apolipoprotein E (apoE). Although an association between gene polymorphism of SAA4 or apoE and amyloidogenesis has been reported, evaluation of the clinical data remains insufficient. Here, we investigated the SAA isotype present in these deposits, and considered the clinical implications of the data in relation to apoE4 polymorphism.
MATERIALS & METHODS:Thirty-seven patients with rheumatoid arthritis in whom AA amyloidosis had been confirmed by gastrointestinal biopsy were included. The biopsy specimens were subjected to LC-MS/MS for analysis of SAA derivatives. Phenotyping of apoE was performed using a commercially available kit. Clinical data were assessed by reference to patient records at the time of amyloidosis diagnosis.
RESULTS: LC-MS/MS revealed SAA 1.1 derivatives in 8 patients (21.6%), 1.2/1.5 in 37, 1.3 in 30 (81.1%), and 1.4 in 27 (73.0%). Among 26 patients, the E2/3 apoE phenotype was detected in 2 patients (7.7%), E3/3 in 17 (65.4%), and E3/4 in 7 (26.9%). Patients with SAA1.1 derivatives showed a significantly shorter period from the onset of RA to amyloid detection than patients without SAA1.1. Additionally, patients with SAA1.3 had significantly lower levels of C3 and C4 than patients without SAA1.3. Moreover, in patients with apoE4, the ESR level was significantly higher than in patients without apoE4.
CONCLUSION: Polymorphism of both SAA and apoE may contribute to some features of AA amyloidosis.



**Author Listing - Lead/ Submitting Author (we will be communicating with this individual): Name, Institution, City and State where the work was done. Co-authors will be added in a separate section.**
Takeshi Kuroda, Division of Clinical Nephrology and Rheumatology, Niigata University, Niigata, Japan

**Main Body of the Abstract**
**BACKGROUND:** AA amyloid deposits consist mainly of serum amyloid A (SAA) derivatives and minor components such as apolipoprotein E (apoE). Although an association between gene polymorphism of SAA4 or apoE and amyloidogenesis has been reported, evaluation of the clinical data remains insufficient. Here, we investigated the SAA isotype present in these deposits, and considered the clinical implications of the data in relation to apoE4 polymorphism.
**MATERIALS & METHODS:**Thirty-seven patients with rheumatoid arthritis in whom AA amyloidosis had been confirmed by gastrointestinal biopsy were included. The biopsy specimens were subjected to LC-MS/MS for analysis of SAA derivatives. Phenotyping of apoE was performed using a commercially available kit. Clinical data were assessed by reference to patient records at the time of amyloidosis diagnosis.
**RESULTS:** LC-MS/MS revealed SAA 1.1 derivatives in 8 patients (21.6%), 1.2/1.5 in 37, 1.3 in 30 (81.1%), and 1.4 in 27 (73.0%). Among 26 patients, the E2/3 apoE phenotype was detected in 2 patients (7.7%), E3/3 in 17 (65.4%), and E3/4 in 7 (26.9%). Patients with SAA1.1 derivatives showed a significantly shorter period from the onset of RA to amyloid detection than patients without SAA1.1. Additionally, patients with SAA1.3 had significantly lower levels of C3 and C4 than patients without SAA1.3. Moreover, in patients with apoE4, the ESR level was significantly higher than in patients without apoE4.
**CONCLUSION:** Polymorphism of both SAA and apoE may contribute to some features of AA amyloidosis.



Implication of serum amyloid A and apolipoprotein E polymorphism in AA amyloidosis secondary to rheumatoid arthritis OC21 (#83)

We invite you to attend the XIX International Symposium on Amyloidosis to be held in Rochester, MN.

This symposium is organized as a hybrid meeting (with the focus on in-person) held from Sunday, May 26 through Thursday, May 30, 2024.

Together with the ISA Board and members of Mayo Clinic, a very attractive scientific hybrid program is being planned. The program will cover a variety of types of systemic amyloidosis: ATTR (hereditary and wild-type), AL (light-chain), AA and less frequent forms. There will be key lectures, specific symposia including those company sponsored, oral presentations and poster sessions of accepted abstracts.

COURSE DESCRIPTION
This program will provide a comprehensive review of state-of-the-art education in systemic amyloidosis: basic science, pathophysiology, diagnosis, current and emerging treatments. Scientific presentations will include competitive oral and poster abstracts. The rapid evolution of scientific discovery and expanding treatment options has created tremendous interest in the field and this meeting will fill and important gap in educating scientists and clinicians.