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.
Melissa Rudie DO
OhioHealth
Columbus, OH United States

Main Body of the Abstract
Background
Transthyretin amyloidosis (ATTR) is an underdiagnosed and underestimated cause of heart failure and polyneuropathy. ATTR can be familial (ATTRm) caused by misfolding of mutated transthyretin or wild type (ATTRw) caused by misaggreation of genetically normal transthyretin. ATTRw is most often found to be concentrated in the heart, however, patient presentations can mimic ATTRm. We present three unique cases that demonstrate unusual deposition of ATTRw.

Case Presentations
Case one: 72-year-old female with polyneuropathy was referred for leukopenia and anemia. Bone marrow biopsy was negative for light chain plasma cells, mass spectrometry identified ATTR (Fig 1a). Cardiac nuclear PYP grade 0.

Case two: 83-year-old male with bilateral carpal tunnel referred for gross hematuria. Found to have a bladder mass, biopsy followed by mass spectrometry positive for ATTR (Fig 1b). Cardiac PYP grade 3.

Case three: 66-year-old male with chronic atrial fibrillation was referred for progressive bilateral lower extremity weakness. Muscle biopsy followed by mass spectrometry was positive for ATTR. Cardiac PYP grade 2.

Genetic testing revealed normal transthyretin in all three cases leading to a diagnosis of wild type transthyretin amyloidosis.
Conclusion
These cases highlight the variability of ATTRw tissue deposition leading to a variety of clinical presentations and diagnostic challenges.

**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.**
Melissa Rudie DO
OhioHealth
Columbus, OH United States

**Main Body of the Abstract**
**Background**
Transthyretin amyloidosis (ATTR) is an underdiagnosed and underestimated cause of heart failure and polyneuropathy. ATTR can be familial (ATTRm) caused by misfolding of mutated transthyretin or wild type (ATTRw) caused by misaggreation of genetically normal transthyretin. ATTRw is most often found to be concentrated in the heart, however, patient presentations can mimic ATTRm. We present three unique cases that demonstrate unusual deposition of ATTRw.

**Case Presentations**
Case one: 72-year-old female with polyneuropathy was referred for leukopenia and anemia. Bone marrow biopsy was negative for light chain plasma cells, mass spectrometry identified ATTR (Fig 1a). Cardiac nuclear PYP grade 0.

Case two: 83-year-old male with bilateral carpal tunnel referred for gross hematuria. Found to have a bladder mass, biopsy followed by mass spectrometry positive for ATTR (Fig 1b). Cardiac PYP grade 3.

Case three: 66-year-old male with chronic atrial fibrillation was referred for progressive bilateral lower extremity weakness. Muscle biopsy followed by mass spectrometry was positive for ATTR. Cardiac PYP grade 2.

Genetic testing revealed normal transthyretin in all three cases leading to a diagnosis of wild type transthyretin amyloidosis.
**Conclusion**
These cases highlight the variability of ATTRw tissue deposition leading to a variety of clinical presentations and diagnostic challenges.

Unusual location and presentation of wild type Transthyretin Amyloidosis: A case series PB71 (#223)

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.