Table 1.

Studies investigating the effect of PTH on markers of coagulation and fibrinolysis.

Author, year	Study design	Sample	Increased levels	No association	Conclusion
Erem et al. (6)	Cohort	Cases: 23 patients with primary HPT	Platelet count, FVII, FX and d-dimer	Fibrinogen, FV, FVIII, FIX, vWF, AT, protein C, protein S, t-PA, PAI-1	Results suggest a potential hypercoagulable state
		Controls: 20 age-matched healthy controls
Erem et al. (7)	Cohort	Cases: 24 patients with primary HPT	t-PA, PAI-1, and PAI-1/t-PA ratios	–	Represents a potential hypercoagulable and hypofibrinolytic state
		Controls: 20 age-, sex-, and weight-matched healthy controls	TFPI levels decreased
Chertok-Shacham et al. (8)	Cohort	Cases: 35 patients with primary HPT	PAI-1	Fibrinogen and d-dimer	Hypercoagulability may be involved in the pathogenesis of CVD in these patients
		Controls: 25, age and weight-matched controls
Farahnak et al. (5)	Case-control	Cases: 49 patients with primary HPT	–	PAI-1, vWF, before and after PTX in comparison with controls	No differences as regards biomarkers predicting CVD
		Controls: 49 healthy matched controls
Jorde et al. (9)	Cohort	Cases: 206 healthy subjects	–	t-PA, PAI-1, prothrombin fragment 1+2, FVII	No significant relations between any of the haemostatic factors tested and serum PTH

HPT, hyperparathyroidism; F, factor; vWF, von Willebrand Factor; AT, antithrombin; t-PA, tissue-type plasminogen activator; PAI-1, plasminogen activator inhibitor-1; TFPI, tissue factor pathway inhibitor; CVD, cardiovascular disease; PTX, parathyroidectomy; PTH, parathyroid hormone.