Abstract
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 language | English |
|---|---|
| Pages (from-to) | 273-277 |
| Number of pages | 5 |
| Journal | Amyloid |
| Volume | 6 |
| Issue number | 4 |
| Publication status | Published - 1999 |
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Keywords
- AL amyloidosis
- Antithrombin III
- Clotting abnormalities
- Hemostasis
- Protease inhibitors
- Thrombin-antithrombin complexes
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Medicine(all)
Cite this
Abnormalities in thrombin-antithrombin pathway in AL amyloidosis. / Gamba, G.; Montani, N.; Anesi, E.; Palladini, G.; Lorenzutti, F.; Perfetti, V.; Merlini, G.
In: Amyloid, Vol. 6, No. 4, 1999, p. 273-277.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Abnormalities in thrombin-antithrombin pathway in AL amyloidosis
AU - Gamba, G.
AU - Montani, N.
AU - Anesi, E.
AU - Palladini, G.
AU - Lorenzutti, F.
AU - Perfetti, V.
AU - Merlini, G.
PY - 1999
Y1 - 1999
N2 - 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.
AB - 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.
KW - AL amyloidosis
KW - Antithrombin III
KW - Clotting abnormalities
KW - Hemostasis
KW - Protease inhibitors
KW - Thrombin-antithrombin complexes
UR - http://www.scopus.com/inward/record.url?scp=0033405473&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033405473&partnerID=8YFLogxK
M3 - Article
C2 - 10611948
AN - SCOPUS:0033405473
VL - 6
SP - 273
EP - 277
JO - Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
JF - Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
SN - 1350-6129
IS - 4
ER -