PE and GDM have similar risk factor profiles, particularly high BMI, which is thought to increase the risk of PE directly as well as indirectly through its association with GDM, which itself predisposes to PE.3-5 Both PE and GDM are associated with elevated uric acid levels. 6,7
PE and GDM result in similar changes in a number of adipokines that regulate metabolic and vascular function.8
Maternal insulin resistance is associated with PE and PE-associated inflammation.9,10 Both PE and GDM increase the risk of subsequent type-2 diabetes.11,12
Women with preexisting type-1 diabetes are at increased risk for PE.13,14
A previous study demonstrated that treatment of GDM reduced the rate of PE by 30%, and the recent recommendation of low-dose aspirin (LDA) for PE prevention may be translatable to GDM based upon the promising effects of salicylates on glycemic control in type-2 diabetes.15-18
GlyFn, a metabolic biomarker for detection of GDM and PE, provides efficient identification of patients whose chances for successful pregnancy outcomes can be facilitated by cost-effective, standard interventions such as LDA and nutritional counseling that can also reduce future healthcare expenses.
Fibronectin is known to regulate blood vessel organization, so that increased maternal serum levels may contribute directly to PE development.19
Recent studies indicate that a particular glycosylated version of fibronectin (GlyFn) is specifically associated with the risk of developing severe PE. Determination of GlyFn levels in maternal blood represents an improved method for detecting and monitoring PE.20
GlyFn is a pregnancy-specific biomarker for early identification of women at risk for GDM as early as the first trimester of pregnancy.23
The relative change in GlyFn concentrations in GDM is greater than the changes in HbA1c, CRP and adiponectin, although all these biomarkers are associated with GDM status.*
* HbA1c used to identify existing type 1/2 diabetes.
In addition to GlyFn, the PE test panel includes pregnancy associated plasma protein PAPPA-2, placental lactogen, and uric acid, and employs an algorithm to estimate the risk of PE and potential adverse outcomes.
Placental lactogen is produced by the placenta, and maternal serum levels are decreased in PE, while PAPPA-2 and uric acid levels are increased.21,22
Our PE test is recommended for pregnant patients who may have one or more of the following:
Clinical assessment of increased risk for PE
Family history of or previous hypertension PE-Family history of or preexisting type-1 or type-2 diabetes
Clinically evaluated obesity
Initial: 17-36 weeks
Follow up: 20-36 weeks
The PMP PE test provides the biochemical confirmation of PE.
The test should be used in assessment of subjects suspected of PE, borderline blood pressure and proteinuria changes. The test is positive 2-4 weeks before the onset of symptoms.
In addition to GlyFn, the GDM test panel includes hemoglobin HbA1c, C-reactive protein (CRP) and adiponectin, and employs an algorithm to estimate the risk of GDM and potential adverse outcomes.
Maternal serum HbA1c levels indicate potential hyperglycemia often seen in GDM.
Elevated CRP and placental lactogen levels are associated with GDM, as are decreased adiponectin levels.24-27
Our GDM test is recommended for pregnant patients who may have one or more of the following:
Clinical assessment of increased risk for GDM
Family history of or preexisting type-1 or type-2 diabetes
History of GDM
Presence of glycosuria
History of abnormal glucose tolerance
Overweight or obese prior to pregnancy
The PMP GDM test performed in the first trimester is more sensitive than the Glucose Challenge Test in predicting GDM.
90% of subjects with a positive PMP GDM test in the first trimester will test positive with the Oral Glucose Tolerance Test (OGTT) at 24-28 weeks gestation.