الفهرس 
Hypertensive Disorders with PregnancyOnly 14 pages are availabe for public view
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Abstract
Preeclampsia is one of the most common cause of maternal mortality worldwide. In addition, preeclampsia frequently coexists with intrauterine growth restriction, placental abruption, and the need for iatrogenic preterm delivery, which are other major causes of adverse perinatal outcome.
The severity of this condition and its consequences have demanded a focus on markers capable of predicting preeclampsia. Early detection of this condition allows for planning the appropriate monitoring, management, and early identification of complications. Although trials of prophylactic intervention for preeclampsia from mid gestation have been largely unsuccessful, it has been suggested that first-trimester prediction may make early prophylactic strategies feasible.
No single screening test in the prediction of this condition has gained widespread adoption into clinical practice.
Despite these uncertainties, the relationship between inflammation and pre-eclampsia has prompted the search for markers of inflammation Increased serum amyloid protein A (SAA), like CRP, has also been shown to reflect systemic inflammation. CRP and SAA are inflammation markers synthesized by hepatocyte upon stimulation by interleukin-6 (IL-6) and tumor necrosis factor; however, both serum levels of SAA and CRP can be increased to about 1,000- fold in response to inflammation
We conducted this case control study on women with Preeclampsia to estimate serum amyloid A in pregnant women with preeclampsia. Members of the control group are healthy, non-smoker pregnant women who had an uncomplicated antenatal course and all arterial blood pressure measurements were normal.
All cases in the groups were subjected to Full history taking including personal history to exclude smoking, medical history to exclude preexisting disease such as diabetes, hypertension and drug history, Body weight, height and BMI, General and abdominal examination (Vital signs &Abdominal examination to exclude multiple pregnancy), Gestational age calculation & Ultrasound to exclude multiple pregnancy, polyhydramnios and fetal abnormality.
In currant study, the mean value of age among cases of preeclampsia without severe features was (26.09±4.30), and cases of preeclampsia with severe features was (26.64±4.48), BMI was (28.23±4.20) and (27.84±3.21) respectively, while range of gestational age was (30+3 – 38+2) and (23+4 - 39+2) respectively. On other hands; we found the mean value of age in control group was (26.68±3.83), gestational age range was (35+3 – 40+1), and BMI mean was (28.19±2.37). With no statistically significant difference between cases and control as regard age (p value 0.87) and BMI (p-value =0.90).
No significant differences were found between the women of the three groups regarding age and BMI. Gestational age differed significantly between the three groups, being significantly higher in the control group compared to both preeclampsia groups; whereas no statistically significant differences were found between the two preeclampsia groups.
Among our cases of preeclampsia without severe features and preeclampsia with severe features, the range of albumin urea was (2-4) and (3-3) respectively and the mean of platelet count of both group was (261.76±75.18) and (218.287±94.73) respectively and serum creatinine of both group mean (0.67±014) and (0.86±0.38) respectively, Hb mean of both group was (11.20±1.20) and (10.58±1.16) respectively, ALT range of both group was (7.0-33.0) and (7.0-167.0) respectively and AST range of both group was (6.0-39.0) and (15.0-120.0) respectively and serum amyloid A of both group was (4.0-34.0) and (11.0-40.0) respectively, while in the control group no albuminuria was found, platelet count mean was (273.04±91.56), creatinine mean was (0.59±0.15), Hb mean was (11.22±0.93), ALT range was (6.0-30.0), AST range was (9.0-34.0) and the range of amyloid A was (2.5-5.0). No statistically significant differences were found between the three groups regarding hemoglobin concentration or platelet counts. Serum AST, ALT and creatinine levels were statistically significantly higher in the preeclampsia with severe features group compared to those without severe features or control women; whereas no statistically significant differences were found between the latter two groups. Albuminuria varied significantly between the three groups, being significantly lower in the control group compared to both preeclampsia groups; whereas no statistically significant differences were found between the latter two groups.
We found that there was highly statistically significant difference between control, mild and severe pre-eclampsia groups in SBP and DBP (p-value < 0.001 for all).
Serum amyloid A level (SAA) varied significantly between the three groups; being higher in the preeclampsia with severe features group (range of serum amyloid A was 11.0-40), compared to the other two groups and also higher in the preeclampsia without severe features group compared to the control group (p value < 0.001).
This study was one of the first studies that correlated between amyloid A and different demographic data in preeclamptic women. In currant study among cases group, we found non-significant correlation between Amyloid A and age (r = 0.05 & p=0.66) and there was non-significant correlation between Amyloid A and BMI (r= -0.001 & p=0. 66), hemoglobin concentration (r= - 0.08 & p=0. 47) or platelet count (r= - 0.17 & p=0. 12). Overall, statistically significant positive correlation was found between serum amyloid A level and most of the indices of severity of preeclampsia. A statistically significant correlation was found between serum amyloid A and systolic blood pressure measurements (r = 0.82 & p < 0.001) and diastolic blood pressure measurements (r = 0.82 & p < 0.001), ALT (r = 0.64 & p < 0.001), AST (r = 0.45 & p < 0.001) serum creatinine (r = 0.26 & p =0.02) and albuminuria (r = 0.73 & p < 0.001) and we think that this is a matter of association rather than causation
Our data sustain the limited number of studies investigating the SAA levels in both preeclamptic and healthy pregnant women, in which it was hard to reach a consensus regarding the association between SAA levels and preeclampsia. Taken in consideration that an elevated plasma level of SAA in preeclamptic women should be considered pathologic, we believe that the response of relationship between the preeclampsia and SAA levels could be caused by an inflammatory condition associated with preeclampsia.