To study the prevalence of spontaneous abortions in pregnant women with hypothyroidism in the tertiary referral centre

Faisal, Shameel; Tibrewala, Satish; Afreen, Sana; Shetty, Raksha

doi:10.18203/2320-1770.ijrcog20161894

Cited by 1 publication

(1 citation statement)

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“…The effect of thyroid disease and autoimmunity on adverse pregnancy outcome, such as decreased LBR, premature delivery, miscarriage and first-trimester RPL, has been pointed out by many authors (van den Boogaard et al, 2011;Thangaratinam et al, 2011;Mannisto et al, 2013;Dhanwai Kumar et al, 2016), but is also under debate. Hypothyroidism and subclinical hypothyroidism (SCH), defined as elevated serum thyroid stimulating hormone (TSH) with normal serum free thyroxine (free T4) levels (Vissenberg et al, 2012;van Dijk et al, 2016), are regarded as causes of adverse pregnancy outcome (Chan et al, 2015;Faisal et al, 2016). The effect of SCH in women with miscarriage is unclear.…”

Section: General Aspectsmentioning

confidence: 99%

Platelet aggregation in healthy women during normal pregnancy - a longitudinal study

et al. 2018

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Increased platelet activation is involved in obstetric complications such as preeclampsia and intrauterine growth retardation. It is of interest to study platelet aggregation during pregnancy, since increased aggregation theoretically could be a mechanism associated with placenta-mediated complications, which possibly could be prevented by drugs inhibiting platelet aggregation. There are, however, few robust studies describing platelet aggregation during normal pregnancy. The present longitudinal study was performed in order to study platelet aggregation during normal pregnancy resulting in a healthy child, during the puerperium and in nonpregnant, fertile women. Healthy, nonsmoking, pregnant women (n = 104), aged under 39 years and with BMI < 35, were followed during pregnancy and postpartum. Twenty-seven nonpregnant, non-puerperal, fertile women were studied for comparison. Platelet aggregation was determined with multiple electrode impedance aggregometry and analyzed at inclusion, 4 times during pregnancy and after at least 3 months postpartum. Platelet aggregation postpartum was compared with gestational weeks 8-15 and 37-40, respectively, and with nonpregnant, fertile women. Hemoglobin, leucocyte count, platelet count, prothrombin time, and activated partial thromboplastin time were determined at inclusion in order to verify normal hemostasis. Activation of platelets by arachidonic acid, adenosine diphosphate (ADP), and thrombin receptor activating peptide (trap-6) resulted in less aggregation during pregnancy, compared with postpartum (p < 0.03-< 0.001). Platelet aggregation following activation by collagen was unchanged. A minor increase in aggregation as pregnancy continued was found related to ADP (p < 0.021). Positive correlations were found between platelet counts and platelet aggregation. Postpartum platelet aggregation after activation with arachidonic acid, collagen, and trap-6 was lower than in the non-puerperal fertile state. Other hemostatic analyses were normal. In conclusion, there is a minor decrease in platelet aggregation after activation with arachidonic acid, trap-6, and ADP, measured with multiple electrode impedance aggregometry during normal pregnancy resulting in healthy babies, compared with the postpartum period. The small changes in platelet aggregation may be a consequence of a minor decrease in platelet count and probably lack clinical significance under normal conditions. Interindividual variations at certain time-points are substantial, which limits the usefulness of the multiple electrode impedance aggregometry for determining minor changes in platelet function.

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