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PubMed · 3603427

Fibronectin during thyroid hormone replacement therapy.

H Watzke·H P Schwarz·M Weissel
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Abstract

Hemostasis may be affected by thyroid function in various ways. We studied plasma concentration of Fibronectin in 13 untreated patients after total thyroidectomy due to thyroid carcinoma. Fibronectin levels were significantly decreased compared to an equal numbered group of healthy volunteers (p 0.0005). The same patients were studied again after an oral thyroid replacement of 200 micrograms L-thyroxine/d over at least six weeks. Fibronectin had increased significantly, compared to untreated patients and controls resp. Furthermore, a significant positive correlation was found between plasma concentrations of Fibronectin and total T4 (r = 0.92; y = 6.617 + 0.52x). In contrast Factor V activity was low in untreated patients but normal during high dose replacement therapy. No correlation was found between Factor V and thyroid hormone concentrations. We discuss the relation between fibronectin plasma levels and thyroid hormones.

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Factor VFemaleFibronectinsHemostasisHumansHyperthyroidismHypothyroidismLiverMaleThyroid HormonesThyroid NeoplasmsThyroidectomyThyroxineJournal Article

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H Watzke, H P Schwarz, M Weissel. 1987-04-15. Fibronectin during thyroid hormone replacement therapy.. https://doi.org/10.1016/0049-3848(87)90296-9

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No interaction between factor V Leiden and hyperhomocysteinemia or MTHFR 677TT genotype in venous thrombosis. Results of a meta-analysis of published studies and a large case-only study.

Homocysteine may have a thrombogenic effect through inhibition of inactivation of factor Va by activated protein C. Because factor V Leiden also leads to resistance of factor V to activated protein C, it would be possible that both factors show interaction for the risk of venous thrombosis. This has been reported in some studies, but not in others. We performed a metaanalysis to investigate a possible interaction between factor V Leiden and hyperhomocysteinemia, including 825 subjects with venous thrombosis and 2,109 controls, for the risk of venous thrombosis. In addition, we assessed a possible interaction between factor V Leiden and MTHFR 677TT genotype (the most common genetic determinant of homocysteine levels), including 2,547 subjects with venous thrombosis and 4,327 controls. We also investigated the interaction effect of factor V Leiden and hyperhomocysteinemia in a large case-only study using data of the VITRO study, including 2,077 subjects with first-time venous thrombosis. The meta-analysis yielded no evidence for additive or multiplicative interaction between factor V Leiden and hyperhomocysteinemia [relative excess risk due to interaction (RERI) -1.77 (95%CI -8.61 to 5.08) and multiplicative interaction term 0.86 (95%CI 0.35 to 2.14)]. The case-only study also showed no interaction effect [0.58 (95%CI 0.29 to 1.16)]. Also the metaanalysis on factor V Leiden and MTHFR 677TT yielded no evidence of interaction; RERI 0.13 (95%CI -3.60 to 3.86) and multiplicative interaction term 1.23 (95%CI 0.72 to 2.11). Both the meta-analyses of published studies and a large case-only study did not show evidence for interaction between factor V Leiden and hyperhomocysteinemia for risk of venous thrombosis.

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