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Article detail · 2020

A Monogenic Disease with a Variety of Phenotypes: Deficiency of Adenosine Deaminase 2

Journal

Journal of Rheumatology

ISSN 0315-162X

YÖKSİS OpenAlex SJR Q1 JCR Q2 Citations 102 Top 10% Percentile 96.1% FWCI 4.67
Year
2020
Type
article

Data source split

  • YÖKSİS YÖKSİS article record
  • YÖKSİS venue JOURNAL OF RHEUMATOLOGY
  • Catalog match (ISSN) Journal of Rheumatology
  • OpenAlex OpenAlex enrichment (abstract, citations, topics)

Abstract

OpenAlex · English

Objective. Deficiency of adenosine deaminase 2 (DADA2) is an autosomal recessive autoinflammatory disorder associated with ADA2 mutations. We aimed to investigate the characteristics and ADA2 enzyme activities of patients with DADA2 compared to non-DADA2 patients. Methods. This is a descriptive study of 24 patients with DADA2 who were admitted to the Adult and Pediatric Rheumatology, Pediatric Haematology, and Pediatric Immunology Departments of Hacettepe University. All ADA2 exons were screened by Sanger sequencing. Serum ADA2 enzyme activity was measured by modified spectrophotometric method. Results. Twenty-four patients with DADA2 were included: 14 with polyarteritis nodosa (PAN)-like phenotype (Group 1); 9 with Diamond-Blackfan anemia (DBA)-like features, and 1 with immunodeficiency (Group 2). Fourteen PAN-like DADA2 patients did not have the typical thrombocytosis seen in classic PAN. Inflammatory attacks were evident only in Group 1 patients. Serum ADA2 activity was low in all patients with DADA2 except one, who was tested after hematopoietic stem cell transplantation. There was no significant difference in ADA2 activities between PAN-like and DBA-like patients. In DADA2 patients with one ADA2 mutation, serum ADA2 activities were as low as those of patients with homozygote DADA2. ADA2 activities were normal in non-DADA2 patients. ADA2 mutations were affecting the dimerization domain in Group 1 patients and the catalytic domain in Group 2 patients. Conclusion. We suggest assessing ADA2 activity along with genetic analysis because there are patients with one ADA2 mutation and absent enzyme activity. Our data suggest a possible genotype–phenotype correlation in which dimerization domain mutations are associated with PAN-like phenotype, and catalytic domain mutations are associated with hematological manifestations.

Topics

Citations

OpenAlex cited_by_count. Not a WoS or Scopus citation count; those sources have no separate column here.

102 citations

OpenAlex cited_by_count (cache / database)

Authors

  1. Seza Ozen
  2. EZGİ DENİZ BATU AKAL HACETTEPE ÜNİVERSİTESİ
  3. Ekim Z. Taskiran
  4. Hatice Asuman Ozkara
  5. Sule Unal
  6. Naz Guleray
  7. Abdulsamet Erden
  8. ÖMER KARADAĞ
  9. Fatma Gumruk
  10. Mualla Cetin
  11. HAFİZE EMİNE SÖNMEZ
  12. Yelda Bilginer
  13. DENİZ NAZİRE ÇAĞDAŞ AYVAZ HACETTEPE ÜNİVERSİTESİ
  14. Ilhan Tezcan