Abnormalities in thrombin-antithrombin pathway in AL amyloidosis

G. Gamba, N. Montani, E. Anesi, G. Palladini, F. Lorenzutti, V. Perfetti, G. Merlini

Research output: Contribution to journalArticlepeer-review


Various pathogenic factors have been proposed to explain the abnormal hemostasis observed in AL amyloidosis. Since imbalance between clotting factors and inhibitors could play a pathogenic role in both hemorrhagic and thrombotic manifestations, we investigated the thrombin-antithrombin pathway in 35 patients with AL amyloidosis. Ten patients suffered from bleeding while 3 patients experienced deep venous thrombosis. Thrombin time was prolonged in 29 subjects, the mean values of antithrombin III activity (ATIII Act) were significantly lower than those of antithrombin III antigen (ATIII Ag) with loss of relationship between these two different techniques of ATIII detection, normally observed in healthy controls. In 19 patients increased levels of thrombin-antithrombin (TAT) complexes were present. Crossed immunoelectrophoresis of ATIII, performed in presence of heparin, evidenced ATIII forms with reduced binding capacity to heparin and TAT complexes of various electrophoretic mobilities. In conclusion, the impairment of the thrombin-antithrombin pathway, in association with the low ATIII biological activity, might play a pathogenic role in the hypercoagulable state reported in AL amyloidosis, despite the higher frequency of bleeding manifestations.

Original languageEnglish
Pages (from-to)273-277
Number of pages5
Issue number4
Publication statusPublished - 1999


  • AL amyloidosis
  • Antithrombin III
  • Clotting abnormalities
  • Hemostasis
  • Protease inhibitors
  • Thrombin-antithrombin complexes

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Medicine(all)


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