Serum leptin levels in patients with childhood immune thrombocytopenic purpura


Kose M., Ozdemir M. A., Gumus H., Karakukcu M., Akcakus M.

JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY, cilt.29, sa.1, ss.23-26, 2007 (SCI-Expanded, Scopus) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 29 Sayı: 1
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1097/mph.0b013e318030ac0e
  • Dergi Adı: JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.23-26
  • Anahtar Kelimeler: immune thrombocytopenic purpura, leptin, autoimmunity, pathophysiology
  • Erciyes Üniversitesi Adresli: Evet

Özet

Acute immune thrombocytopenic purpura (ITP) induces thrombocytopenia by means of an autoimmune mechanism. Recent studies suggested that T helper immune response is responsible for the pathogenesis of chronic ITP. Despite several studies that were carried out, we do not have a clue as to what triggers the autoimmunity. Leptin is a 16-kd protein secreted from the adipose tissue. Leptin is structurally similar to interleukin (IL)-2, IL-6, and IL-15. The structural similarities between leptin receptor and hernatopoietic cytokine receptors suggested that leptin could play a role in hematopoiesis and immune function. Recent studies suggested that leptin could play an important role in autoimmunity. We made a prospective analysis of a series of 39 newly diagnosed acute childhood ITP in a year period. Serum leptin levels were obtained after diagnosis and before treatment and all patients were followed up at least 6 months to designate acute or chronic event. We conclude that in childhood acute ITP, leptin did not play a role in the pathophysiology of the disease. Further investigations are needed to examine what triggers T cells and how the autoimmune disease became.