E-Poster 63rd Endocrine Society of Australia Annual Scientific Meeting 2020

Clotting factors & its associations in patients with hyperparathyroidism – Evidence from a systematic review & meta-analysis. (#96)

Kavindra N Ratnaweera 1 , Alexander J Rodriguez 2 3
  1. School of Medicine, Griffith University, Southport, QLD, Australia
  2. Bone and Muscle Health Research Group, School of Clinical Sciences, Faculty of Medicine, Nursing and Health Sciences, Monash University, Melbourne, Victoria, Australia
  3. Disorders of Mineralisation Research Group, School of Medical and Health Sciences, Edith Cowan University, Perth, Western Australia, Australia

Calcium is critical in coagulation. Parathyroid hormone (PTH) maintains calcium homeostasis. Elevated PTH increases cardiovascular risk, but it is unclear if these patients are predisposed to thrombosis possibly related to PTH action on calcium. We aimed to determine if PTH was associated with increased clots or markers of coagulation in a systematic review. We searched MEDLINE and EMBASE (29 March, 2020) for studies that were non-randomized; directly measured PTH levels or specifically enrolled patients with hyper/hypo-parathyroidism; measured any clotting factor; or reported thromboembolic or haemorrhagic events. We excluded interventional studies, case reports, studies of surgical correction of hyperparathyroidism or therapies that interfere with mineral metabolism or haemostasis. Primary outcome was the association between PTH and clotting factors and the association of PTH with the incidence of thromboembolic or haemorrhagic events. Continuous data were meta-analysed if reported in at least 100 patients in more than one study. Random-effects models were fitted and reported as standardized mean difference (SMD) with 95% confidence intervals (95%CI). Heterogeneity was determined by the I2 statistic. All data were computed using R (4.0.0). 2404 records were screened. Eight were eligible for inclusion. Seven studies were cross-sectional analyses of patients with primary (PHPT) or secondary (SHPT) hyperparathyroidism compared to controls. Study quality was poor. In pooled analyses comparing PHPT to controls, there was no statistical difference in fibrinogen [SMD=0.01 (-0.92–0.94); k=3 trials; n=133 patients; I2=86%]; D-dimer [0.46 (0.03–0.97); 3; 133; 52]; PAI [0.01 (-0.54–0.57); 3; 181; 69]. Other outcomes were reported in less than 100 patients as were outcomes in studies involving SHPT patients. There was little evidence to support an association between PTH and increased coagulation. Prospective data are needed to understand what role if any, PTH plays in coagulation and if patients with elevated or reduced PTH are predisposed to clots or bleeds.