Rika Terashima

All Publications

• Prevalence of Human Leukocyte Antigen (HLA)-B*58:01 and Allopurinol-Induced Adverse Reactions in Filipino Patients in Hawai'i: Implications for Genotyping. International journal of rheumatic diseases Terashima, R., Medina, A. J., Del Mundo, H. J., Briones, R. S., Aquino, J. A., Quiminiano, E. M., Sin, Y. M., Bautista, R. A., Sonido, C. Y., Yamada, S. 2025; 28 (2): e70127

  Abstract

  Allopurinol, a first-line treatment for gout and hyperuricemia, is associated with severe cutaneous adverse reactions (SCAR) in individuals carrying the HLA-B*58:01 allele. Genotyping is conditionally recommended in Han Chinese, Korean, and Thai populations with an allele prevalence of 7.4%, and in African Americans at 3.8%. The prevalence in Filipino patients has not been studied. We investigate the prevalence of HLA-B*58:01 among Filipino patients in Hawai'i and evaluate the incidence of allopurinol-induced adverse reactions following genotyping.We conducted a retrospective chart review of 312 patients who underwent HLA-B*58:01 genotyping at a primary care clinic in Hawai'i between November 2021 and July 2024. After excluding patients with missing ethnicity data, non-Filipino ethnicity, or prior allopurinol use, 237 Filipino patients were included in the analysis. The prevalence of the HLA-B*58:01 allele and the incidence of allopurinol-induced adverse reactions were calculated.Among the 237 Filipino patients, 17 (7.2%) were HLA-B*58:01 positive. A total of 97 patients were started on allopurinol after genotyping and 1 (1.0%) developed mild cutaneous reactions, 0 (0%) developed SCAR, and 2 (2.1%) experienced gastrointestinal symptoms (nausea and diarrhea).The high prevalence of HLA-B*58:01 allele among Filipino patients in Hawai'i suggests that genotyping may be considered before initiating allopurinol treatment. Given no instances of SCAR were observed in patients who were administered allopurinol after undergoing HLA-B*58:01 genotyping, genotyping may play a crucial role in reducing the risk of allopurinol-induced SCAR in this population. Further studies with larger cohorts are suggested to confirm our findings and assess broader clinical utility of genotyping.

  View details for DOI 10.1111/1756-185X.70127

  View details for PubMedID 39929784

• Left atrial intramural haematoma: a fatal complication of cardiac amyloidosis-a case report. European heart journal. Case reports Terashima, R., Nakagawa, T., Hara, H., Hiroi, Y. 2023; 7 (3): ytad116

  Abstract

  Spontaneous left atrial intramural hematoma (LAIH) is extremely rare and there are only two cases of spontaneous LAIH involving cardiac amyloidosis (CA) reported in literature. In both cases, LAIH rapidly compromised hemodynamic stability proving to be a rare yet fatal complication.An 83-year-old man presented with cardiogenic shock. Electrocardiogram showed complete atrioventricular block, and echocardiogram revealed severe hypokinesis and left ventricular hypertrophy. Coronary angiography revealed no significant coronary stenosis and tissue biopsy was taken from the left ventricle. The patient was intubated, placed on extracorporeal membrane oxygenation with intra-aortic balloon pump and temporary pacemaker, and admitted to ICU. Day 6 of admission, he became hemodynamically unstable, and presented with atrial fibrillation. Transesophageal echocardiography showed a newly formed large mass in the left atrium. Day 11 of admission, the patient passed away. Autopsy revealed cardiac amyloidosis and showed the mass to be a left atrial intramural hematoma. Diffuse amyloid deposits were found in the myocardium as well as the blood vessel walls of the region surrounding the LAIH.LAIH is a rare yet fatal complication of CA. Autopsy revealed diffuse amyloid deposits within the left atrium may lead to left atrial fragility and contribute to development of LAIH. LAIH should be considered as an important differential diagnosis in the setting of a rapidly growing left atrial mass, and in hemodynamic instability in patients with CA.

  View details for DOI 10.1093/ehjcr/ytad116

  View details for PubMedID 36969510

  View details for PubMedCentralID PMC10035636