Conclusions and recommendations - Complexity of perceptions of fairness within appeals (Parent

Vignette 3: Complexity of perceptions of fairness within appeals (Parent 5).

7. Conclusions and recommendations

Data was analyzed using SPSS 16 (Statistical Program for Social Science) statistical package. The mean, standard deviations and range were calculated for quantitative variables. Qualitative variables were expressed in numbers and percentages. Univariate analysis for categorical variables was performed using Chi-square. Bi-variate test analysis was also done and two-tailed t-test was used to compare means where applicable. Test of significance was based on 95% confidence interval with P value <0.05 taken as being significant. Tables, charts, graphs were drawn using Microsoft Excel 2007.

CALCULATION OF CUT OFF PONTS FOR α- FETOPROTEIN AND β- HCG LEVELS In order to determine what proportion of the population were beyond the 95% confidence interval of the values for α- fetoprotein and β- HCG, the mean levels of α- fetoprotein and β- HCG for the control population were first of all calculated assuming a normal distribution (Z) in the control group of the study.

Determination of cut off values for levels above the 95^th percentile which were considered as elevated was calculated thus:

The means and standard deviation for α- fetoprotein and β- HCG levels were calculated respectively for the control using statistical package for social sciences SPSS Version 16.0.

Cut off points were calculated by adding 2 standard deviation to the mean values (corresponding to 95% confidence interval). Values ≤ +2 S.D were taken as normal values while values >2 S.D were considered to be elevated levels of α- fetoprotein and β- HCG levels respectively.

For α- fetoprotein:

Mean= 158.56

Standard deviation, S.D= 92.71.

+2 S.D from the mean = 158.56 + (2 × 92.71) = 343.98ng/ml Normal α- fetoprotein level ≤ 343.98ng/ml

Elevated α- fetoprotein level > 343.98ng/ml

47 For β- HCG:

Mean = 5989.65

Standard deviation, S.D = 6449.67

+2 S.D from the mean =5989.65 + (2 × 6449.67) = 18,888.99mIU/ml.

Normal β- HCG levels ≤ 18,888.99mIU/ml Elevated β- HCG levels > 18,888.99mIU/ml

RESULT PRESENTATION

Table 1: COMPARISON OF SOCIODEMOGRAPHIC CHARACTERISTICS BETWEEN CASE AND CONTROL GROUPS

VARIABLES CASE(N=94) CONTROL(N=94) SIG

AGE (years)

% %

16-20 2(2.1) 2(2.1)

χ²=0.74 p=0.946 df=4

21-25 20(21.3) 20(21.3)

26-30 41(43.6) 41(43.6)

31-35 29(30.9) 27(28.7)

36-40 2(2.1) 4(4.3)

Mean Age (years) 28.70 ± 0.485 29.01 ± 0.490

PARITY NULLIPARA 40(42.6) 40(42.6) χ²=0.08

PRIMIPARA 20(21.3) 20(21.3) p=0.994

df=3

MULTIPARA 26(27.7) 26(27.7)

GRANDMULTIPARA 8(8.5) 8(8.5)

BOOKING STATUS BOOKED 23(25.5) 94(100) χ²=114.09

p<0.0001 df=1

UNBOOKED 71(74.5) 0(0.0)

MARITAL STATUS SINGLE 2(2.1) 1(1.1) χ²=0.34

p=0.561 df=1

MARRIED 92(97.9) 93(98.9)

OCCUPATION SKILLED 29(30.9) 53(56.4) χ²=16.66

p<0.001 df=2

UNSKILLED 50(53.2) 38(40.0)

UNEMPLOYED 15(16) 3(3.2)

LEVEL OF

EDUCATION

PRIMARY 7(7.4) 8(8.5) χ²=8.88

p=0.012 df=2

SECONDARY 40(42.6) 21(22.3)

TERTIARY 47(50.0) 65(69.1)

TRIBE

ESAN 49(52.1) 55(58.5) χ²=0.90

p=0.825 df=3

IGBO 13(13.8) 10(10.6)

YORUBA 3(3.2) 3(3.2)

OTHERS 29(30.9) 26(27.7)

AWARENESS OF DISEASE

NO 79(84.0) 60(63.8) χ²=9.96

p=0.002 df=1

YES 15(16) 34(36.2)

There was a statistically significant relationship in comparison between booking status in case and control groups (p<0.0001). The statistical relationships between occupation, level of education and awareness of disease as compared between case and control groups were also significant (p<0.001; p=0.012 and p=0.002 respectively).

Table 2: COMPARISON OF RISK FACTORS FOR PREECLAMPSIA BETWEEN CASE AND CONTROL GROUPS

VARIABLES CASE(N=94) CONTROL(N=94) SIG

PREVIOUS HX OF PREECLAMPSIA

% %

χ²=0.09 p=0.956 df=2

NO 51(54.2) 49(52.1)

YES 4(4.3) 4(4.3)

NOT APPLICABLE 39(41.5) 41(43.6)

AGE

% %

16-20 2(2.1) 2(2.1)

χ²=0.74 p=0.946 df=4

21-25 20(21.3) 20(21.3)

26-30 41(43.6) 41(43.6)

31-35 29(30.9) 27(28.7)

36-40 2(2.1) 4(4.3)

PARITY

% %

NULLIPARA 40(42.6) 40(42.6) χ²=0.08

p=0.994 df=3

PRIMIPARA 20(21.3) 20(21.3)

MULTIPARA 26(27.7) 26(27.7)

GRANDMULTIPARA 8(8.5) 8(8.5)

% %

BMI NORMAL 47(50.0) 48(51.1) χ²=5.79

p=0.122 df=3

MILD 28(29.8) 27(28.7)

MODERATE 14(14.9) 19(20.2)

SEVERE 5(5.3) 0(0.0)

FAMILY HISTORY OF PREECLAMPSIA

% %

χ²=0.21 p=0.650 df=1

NO 91(96.8) 92(97.9)

YES 3(3.2) 2(2.1)

PERSONAL HX OF HTN

% %

χ²=0.34 p=0.561 df=1

NO 92(97.9) 93(98.9)

YES 2(2.1) 1(1.1)

PRIMIPATERNITY

% %

χ²=4.01 p=0.135 df=2

NO 66(70.2) 54(57.5)

YES 0(0.0) 1(1.1)

NOT APPLICABLE 28(37.8) 39(41.4)

There was no statistically significant relationship between the risk factors for preeclampsia as compared between cases and control groups.

50 Table 3: CLINICAL DIAGNOSTIC CRITERIA FOR PREECLAMPSIA

CASE CONTROL SIG.

SYSTOLIC BLOOD PRESSURE LEVEL

MEAN 179.04 108.30 P<0.0001

t=29.96

S.E OF MEAN 2.10 1.08

STD. DEVIATION 20.32 10.44

DIASTOLIC BLOOD

PRESSURE LEVEL

MEAN 113.40 67.77 P<0.0001

t=30.87

S.E OF MEAN 1.23 0.82

STD. DEVIATION 11.87 7.92

MEAN ARTERIAL BLOOD PRESSURE LEVELS

MEAN 135.28 81.20 P<0.0001

t=35.621

S.E OF MEAN 1.32 0.75

STD. DEVIATION 12.79 7.30

PROTEINURIA AT DIAGNOSIS (dipstick)

0 0(0.0) 91(96.8) χ²=178.12

P<0.001 df=4

1+ 14(14.9) 3(3.2)

2+ 26(27.7) 0(0.0)

3+ 23(24.5) 0(0.0)

4+ 31(33.0) 0(0.0)

There was a statistically significant difference in the mean values of systolic, diastolic, and mean arterial blood pressures of cases vs. control respectively (all P values <0.0001). A statistically significant relationship was found in proteinuria assessed by dipstick urinalysis between cases and control (P<0.001)

Table 4: RELATIONSHIP BETWEEN BIOCHEMICAL MARKERS OF DISEASE SEVERITY IN CASE AND CONTROL GROUPS

CASE CONTROL SIG.

ASPARTATE TRANSAMINASE

LEVEL

MEAN 16.44 8.97 P<0.0001

t=8.627

S.E OF MEAN 0.84 0.21

STD. DEVIATION 8.14 2.06

51 ALANINE

TRANSAMINASE LEVEL

MEAN 9.58 3.69 P<0.0001

t=12.765

S.E OF MEAN 0.40 0.23

STD. DEVIATION 3.87 2.28

URIC ACID LEVEL MEAN 6.12 4.23 P<0.0001

t=7.159

S.E OF MEAN 0.24 0.11

STD. DEVIATION 2.35 1.05

CREATININE LEVEL MEAN 0.84 0.66 P<0.0001

t=6.364

S.E OF MEAN 0.02 0.02

STD. DEVIATION 0.23 0.22

PLATELET LEVEL MEAN 186506.38 238734.04 P<0.0001

t=6.652

S.E OF MEAN 6725.51 4050.67

STD. DEVIATION 65206.24 39272.74

There was a statistically significant difference between the means of biochemical markers of disease severity (AST, ALT, Uric acid , Creatinine and platelet levels) in patients with preeclampsia compared to those in the control arm of the study (all with P<0.0001).

Figure 1: DISTRIBUTION OF PATIENTS WITH PREECLAMPSIA ACCORDING TO DISEASE SEVERITY

Of 94 patients with preeclampsia in the study, 86 (91%) had severe preeclampsia while 8 (9%) had mild preeclampsia

Table 5: DISTRIBUTION OF α-FETOPROTEIN AND β-HCG IN PATIENTS WITH MILD AND SEVERE PREECLAMPSIA

SEVERITY OF PRE-ECLAMPSIA SIGNIFICANCE TEST

MILD SEVERE TOTAL

α-FETOPROTEIN LEVEL

ELEVATED 0 (0.0) 21(100) 21(100) ^χ²^=2.52 p=0.113 NORMAL 8 (11.0) 65 (89.0) 73(100) df=1

TOTAL 8 (8.5) 86 (91.5) 94(100)

SEVERITY OF PRE-ECLAMPSIA SIGNIFICANCE TEST

MILD SEVERE TOTAL

β-HCG LEVEL ELEVATED 1(3.0) 32 (97.0) 33(100) ^χ²^=1.96 p=0.161 NORMAL 7 (11.5) 54 (88.5) 61(100) df=1

TOTAL 8 (8.5) 86 (91.5) 94(100)

There was no statistically significant relationship in the distribution of elevated α-fetoprotein and β-HCG between mild and severe cases of preeclampsia with P values of 0.113 and 0.161 respectively.

Table 6: COMPARISON OF MEAN VALUES OF α- FETOPROTEIN AND β - HCG LEVELS AS MARKERS OF DISEASE SEVERITY BETWEEN MILD AND SEVERE CASES OF PREECLAMPSIA

MILD PREECLAMPSIA

SEVERE PREECLAMPSIA

SIG.

α- FETOPROTEIN LEVEL

MEAN 148.62 262.08 P=0.171

t=1.380

S.E OF MEAN 40.45 24.7

STD. DEVIATION 114.41 22.9

β - HCG LEVEL MEAN 9470.00 10912.00 P=0.557

S.E OF MEAN 126.70 741.37 t=0.591

STD. DEVIATION 3583.71 6875.22

There was no statistically significant difference in the means of α- fetoprotein (P=0.171) and β - HCG levels (0.557) in patients with mild and severe preeclampsia respectively

Figure 2: RELATIONSHIP BETWEEN MATERNAL GROUPS AND α- FETOPROTEIN LEVELS

Mean AFP level plots in maternal groups show a slight decline in levels between control and mild cases of preeclampsia. There was however a steep rise between mild and severe cases of preeclampsia.

Figure 3: RELATIONSHIP BETWEEN MATERNAL GROUPS AND β- HCG LEVELS

Mean plots of β- HCG LEVELS showed rising levels from control to mild preeclampsia and between mild and severe preeclampsia

Table 7: RELATIONSHIP BETWEEN α- FETOPROTEIN LEVELS IN PATIENTS WITH PREECLAMPSIA AND CLINICAL CRITERIA FOR DISEASE SEVERITY

SYSTOLIC BLOOD PRESSURE

ELEVATED NORMAL TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 21(100)

% 0(0)

% 21(100)

N.A*

NORMAL 73(100) 0(0) 73(100)

TOTAL 94(100) 0(0) 94(100)

57 DIASTOLIC BLOOD PRESSURE

ELEVATED NORMAL TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 21(100)

% 0(0)

21(100) N.A*

NORMAL 73(100) 0(0) 73(100)

TOTAL 94(100) 0(0) 94(100)

HEADACHE

NO YES TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 7(33.3)

% 14(66.7)

% 21(100)

χ²=1.15 p=0.284 df=1

NORMAL 16(22.0) 57(78.0) 73(100)

TOTAL 23(24.5) 71(75.5) 94(100)

VISUAL DISTURBANCE

NO YES TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 11(52.4)

% 10(47.6)

% 21(100)

χ²=0.48 p=0.488 df=1

NORMAL 32(43.8) 41(56.2) 73(100)

TOTAL 43(45.7) 51(54.3) 94(100)

NAUSEA/VOMITING

NO YES TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 15(71.4)

% 6(28.6)

% 21(100)

χ²=0.87 p=0.351 df=1

NORMAL 44(60.3) 29(39.7) 73(100)

TOTAL 59(62.5) 35(37.2) 94(100)

*N.A- Chi Square tests not applicable.

Comparison could not be performed between α-fetoprotein levels and systolic and diastolic blood pressures. The relationship between α- fetoprotein levels amongst patients with preeclampsia and clinical criteria for disease severity was not statistically significant

Table 7 (CONTINUED): RELATIONSHIP BETWEEN α- FETOPROTEIN LEVELS IN PATIENTS WITH PREECLAMPSIA AND CLINICAL CRITERIA FOR DISEASE SEVERITY

UPPER ABDOMINAL PAIN

NO YES TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 17(81.0)

% 4(19.0)

% 21(100)

χ²=0.96 p=0.328 df=1

NORMAL 65(89.0) 8(11.0) 73(100)

TOTAL 82(87.2) 12(12.8) 94(100)

58 OLIGURIA

NO YES TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 21(100)

% 0(0.0)

% 21(100)

χ²=0.89 p=0.345 df=1

NORMAL 70(95.9) 3(4.1) 73(100)

TOTAL 91(96.8) 3(3.2) 94(100)

HYPERREFLEXIA/CLONUS

NO YES TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 20(95.2)

% 1(4.8)

% 21(100)

χ²=1.87 p=0.172 df=1

NORMAL 61(83.6) 12(16.4) 73(100)

TOTAL 81(86.2) 13(13.8) 94(100)

PEDAL OEDEMA

NO YES TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 3(14.3)

% 18(85.7)

% 21(100)

χ²=1.87 p=0.172 df=1

NORMAL 35(47.9) 38(52.1) 73(100)

TOTAL 38(40.4) 56(59.6) 94(100)

CONVULSION

NO YES TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 21(100)

% 0(0)

% 21(100)

χ²=0.29 p=0.599 df=1

NORMAL 72(98.6) 1(1.4) 73(100)

TOTAL 93(99.0) 1(1.1) 94(100)

There was no statistically significant relationship between α-fetoprotein levels and clinical criteria for disease severity

Table 8: RELATIONSHIP BETWEEN α -FETOPROTEIN LEVELS IN PATIENTS WITH PREECLAMPSIA AND BIOCHEMICAL CRITERIA FOR DISEASE SEVERITY

DIP STICK URINALYSIS

+ ++ +++ ++++ TOTAL SIG.

α-

FETOPROTEIN LEVELS

ELEVATED

% 3(14.3)

% 12(5.7)

21(100) χ²=7.689 p=0.053 df=3

NORMAL 11(15.1) 23(31.5) 20(27.4) 19(26.0) 73(100)

TOTAL 14(14.9) 26(27.7) 23(24.5) 31(33.0) 94(100)

24HR URINARY PROTEIN ESTIMATE

NOT DONE ELEVATED

MARKEDLY

ELEVATED TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 2(9.5)

% 9(42.9)

% 10(47.6)

21(100) χ²=4.177 p=0.124 df=2

NORMAL 5(6.9) 49(67.1) 19(26.0) 73(100)

TOTAL 7(7.4) 58(61.7) 29(30.9) 94(100)

PLATELET LEVELS

NORMAL MILD

THROMB.

MODERATE THROMB.

TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 13(62.0)

% 4(19.0)

21(100) χ²=2.747 p=0.253 df=2

NORMAL 58(79.0) 7(10.0) 8(11.0) 73(100)

TOTAL 71(75.5) 11(11.7) 2(21.3) 94(100)

ASPARTATE TRANSAMINASE LEVELS

NORMAL ELEVATED TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 6(28.6)

% 15(71.4)

21(100) χ²=0.36 p=0.548 df=1

NORMAL 26(35.6) 47(64.4) 73(100)

TOTAL 32(34.0) 62(66.0) 94(100)

ALANINE TRANSAMINASE LEVELS

NORMAL ELEVATED TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 17(81.0)

% 4(19.0)

% 21(100)

χ²=0.19 p=0.661 df=1

NORMAL 62(84.9) 11(15.1) 73(100)

TOTAL 79(84.0) 15(16.0) 94(100)

*Chi square test not applicable.

There was no statistically significant relationship between α-fetoprotein levels and biochemical criteria for disease severity

Table 8 (CONTINUED): RELATIONSHIP BETWEEN α -FETOPROTEIN LEVELS IN PATIENTS WITH PREECLAMPSIA AND BIOCHEMICAL CRITERIA FOR DISEASE SEVERITY

URIC ACID LEVELS

NORMAL ELEVATED TOTAL SIG.

α-fetoprotein levels

ELEVATED 6(28.6) 15(71.4) 21(100) χ²=2.84 p=0.092 df=1

NORMAL 36(49.3) 37(50.7) 73(100)

TOTAL 42(44.7) 52(55.3) 94(100)

60 CREATININE LEVELS

NORMAL ELEVATED TOTAL SIG.

α-fetoprotein levels

ELEVATED 21(100) 0(0.0) 21(100)

N.A*

NORMAL 73(100) 0(0.0) 73(100)

TOTAL 94(100) 0(0.0) 94(100)

*Chi square test not applicable

There was no statistically significant relationship between α-fetoprotein levels and biochemical criteria for disease severity

Table 9: RELATIONSHIP BETWEEN β - HCG LEVELS IN PATIENTS WITH PREECLAMPSIA AND CLINICAL CRITERIA FOR DISEASE SEVERITY

SYSTOLIC BLOOD PRESSURE

ELEVATED NORMAL TOTAL SIG.

β - HCG LEVEL ELEVATED

% 33(100)

% 0(0.0)

33(100) N.A*

NORMAL 61(100) 0(0.0) 61(100)

TOTAL 94(100) 0(0.0) 94(100)

DIASTOLIC BLOOD PRESSURE

ELEVATED NORMAL TOTAL SIG.

% % %

β - HCG LEVEL ELEVATED 33(100) 0(0.0) 33(100) N.A*

NORMAL 61(100) 0(0.0) 61(100)

TOTAL 94(100) 0(0.0) 94(100)

HEADACHE

NO YES TOTAL SIG.

β - HCG LEVEL

ELEVATED

% 5(15.2)

% 28(84.8)

33(100) χ²=2.39 p=0.122 df=1

NORMAL 18(29.5) 43(70.5) 61(100)

TOTAL 23(24.5) 71(75.5) 94(100)

VISUAL DISTURBANCE

NO YES TOTAL SIG.

β - HCG LEVEL

ELEVATED

% 13(39.4)

% 20(60.6)

33(100) χ²=0.83 p=0.363 df=1

NORMAL 30(49.2) 31(50.8) 61(100)

TOTAL 43(45.7) 51(54.3) 94(100)

NAUSEA/VOMITING

NO YES TOTAL SIG.

β - HCG LEVEL

ELEVATED

% 20(60.6)

% 13(39.4)

% 33(100)

χ²=0.10 p=0.750 df=1

NORMAL 39(63.9) 22(36.1) 61(100)

TOTAL 59(62.8) 35(37.2) 94(100)

*Chi square test not applicable

There was no statistically significant relationship between β-HCG levels and clinical criteria for disease severity

Table 9 (CONTINUED): RELATIONSHIP BETWEEN β - HCG LEVELS IN PATIENTS WITH PREECLAMPSIA AND CLINICAL CRITERIA FOR DISEASE SEVERITY

UPPER ABDOMINAL PAIN

NO YES TOTAL SIG.

β - HCG LEVEL ELEVATED

% 28(84.8)

% 5(15.2)

33(100) χ²=0.26 P=0.610 df=1

NORMAL 54(88.5) 7(11.5) 61(100)

TOTAL 82(87.2) 12(12.8) 94(100)

OLIGURIA

NO YES TOTAL SIG.

62 β - HCG LEVEL ELEVATED

% 32(96.9)

% 1(3.1)

33(100) χ²=0.00 P=0.948 df=1

NORMAL 59(96.7) 2(3.3) 61(100)

TOTAL 91(96.8) 3(3.2) 94(100)

HYPERREFLEXIA/CLONUS

NO YES TOTAL SIG.

β - HCG LEVEL ELEVATED

% 24(72.7)

% 9(27.3)

33(100) χ²=7.71 P=0.005 df=1

NORMAL 57(93.4) 4(6.6) 61(100)

TOTAL 81(86.2) 13(13.8) 94(100)

PEDAL OEDEMA

NO YES TOTAL SIG.

β - HCG LEVEL ELEVATED 13(39.4) 20(60.6) 33(100) χ²=0.02 P=0.881 df=1

NORMAL 25(41.0) 36(59.0) 61(100)

TOTAL 38(40.4) 56(59.6) 94(100)

There was a statistically significant relationship between β - HCG levels and hyperreflexia (P=0.005)

Table 10: RELATIONSHIP BETWEEN β - HCG LEVELS IN PATIENTS WITH PREECLAMPSIA AND BIOCHEMICAL CRITERIA FOR DISEASE SEVERITY

DIP STICK PROTEINURIA

+ ++ +++ ++++ TOTAL SIG.

Β- HCG LEVELS ELEVATED

% 0(0.0)

% 8(24.2)

% 9(27.3)

% 16(48.5)

33(100) χ²=11.659 P=0.009 df=3

NORMAL 14(23.0) 18(29.5) 14(23.0) 15(24.6) 61(100)

TOTAL 14(14.9) 26(27.7) 23(24.5) 31(33.0) 94(100)

24HR URINARY PROTEIN ESTIMATE

NOT DONE ELEVATED

MARKEDLY

ELEVATED TOTAL SIG.

β - HCG ELEVATED

% 2(6.1)

% 17(51.5)

% 14(42.4)

33(100) χ²=3.194

LEVEL NORMAL 5(8.2) 41(67.2) 15(24.6) 61(100) P=0.202

df=2

TOTAL 7(7.4) 58(61.7) 29(30.9) 94(100)

PLATELET LEVELS

NORMAL MILD

THROMB.

MODERATE THROMB.

TOTAL SIG.

β - HCG LEVEL

ELEVATED

% 26(78.8)

% 4(12.1)

% 3(9.1)

33(100) χ²=0.617 P=0.735 df=2

NORMAL 45(73.8) 7(11.5) 9(14.8) 61(100)

TOTAL 71(75.5) 11(11.7) 12(12.8) 94(100)

ALANINE TRANSAMINASE LEVELS

NORMAL ELEVATED TOTAL SIG.

β - HCG LEVEL

ELEVATED

% 28(84.8)

% 5(15.2)

33(100) χ²=0.02 P=0.875 df=1

NORMAL 51(83.6) 10(16.4) 61(100)

TOTAL 79(84.0) 15(16.0) 94(100)

ASPARTATE TRANSAMINASE LEVEL

NORMAL ELEVATED TOTAL SIG.

β - HCG LEVEL

ELEVATED

% 9(27.3)

% 24(72.7)

% 33(100)

χ²=1.04 P=0.308 df=1

NORMAL 23(37.7) 38(62.3) 61(100)

TOTAL 32(34.0) 62(66.0) 94(100)

There was a statistically significant relationship between β – HCG levels and Dipstick urinalysis (P=0.009)

Table 10 (CONTUNUED): RELATIONSHIP BETWEEN β - HCG LEVELS IN PATIENTS WITH PREECLAMPSIA AND BIOCHEMICAL CRITERIA FOR DISEASE SEVERITY

URIC ACID LEVELS

NORMAL ELEVATED TOTAL SIG.

β - HCG LEVEL

ELEVATED

% 16(48.5)

% 17(51.5)

33(100) χ²=0.30 p=0.585 df=1

NORMAL 26(42.6) 35(57.4) 61(100)

TOTAL 42(44.7) 52(55.3) 94(100)

CREATININE LEVELS

NORMAL ELEVATED TOTAL SIG.

β - HCG LEVEL

ELEVATED

% 33(100)

% 0(0.0)

33(100) N.A*

NORMAL 61(100) 0(0.0) 61(100)

TOTAL 94(100) 0(0.0) 94(100)

*Chi square test not applicable.

There was no statistically significant relationship between β – HCG and uric acid levels (P=0.585)

Table 11: RELATIONSHIP BETWEEN α- FETOPROTEIN AND β- HCG LEVELS IN PATIENTS WITH PREECLAMPSIA β- HCG LEVELS

ELEVATED NORMAL TOTAL SIG.

α-

FETOPROTEIN LEVELS

ELEVATED 8(38.1) 13(61.9) 21(100) χ²=0.11

P=0.745 df=1

NORMAL 25(34.2) 48(65.8) 73(100)

TOTAL 33(35.1) 61(64.9) 94(100)

There was no statistically significant relationship between α- fetoprotein levels and β- HCG levels (P=0.745)

Table 12: CORRELATION OF α- FETOPROTEIN LEVELS AND Β - HCG LEVELS IN PATIENTS WITH PREECLAMPSIA

β- HCG LEVELS α-FP LEVELS

CORELLATION BETWEEN CASES

β- HCG LEVELS

PEARSON CORRELATION 1 -0.046

SIG. (2-tailed) 0.659

N 94 94

α-FP LEVELS

PEARSON CORRELATION -0.046 1

SIG. (2-tailed) 0.659

N 94 94

The correlation between β- HCG level and α-FP level

 β- HCG had perfect correlation of 1

 α-FP levels had a poor correlation of -0.046

 2-tailed t tests were not significant

Figure 4: MATERNAL GROUPS AND MEAN PLOTS OF SOME CLINICAL AND BIOCHEMICAL MARKERS OF DISEASE SEVERITY

MABP- mean arterial blood pressure; SBP- systolic blood pressure; DBP- diastolic blood pressure; ALT- alanine transaminase; AST- aspartate transaminase; HCG- human chorionic gonadotrophin; AFP- alpha feto protein.

Mean plots of clinical and biochemical markers in relation to cases and control groups showed similar patterns for all but the alpha fetoprotein mean level. The mean platelet levels showed a slight increasing pattern from that of the control to mild cases of preeclampsia. Meanwhile there is a fall in mean platelet level as disease progressed towards severe preeclampsia.

Table 13: α- FETOPROTEIN LEVELS/ β - HCG LEVELS AND PERIOD OF ONSET OF DISEASE GESTATIONAL AGE AT ONSET OF DISEASE

EARLY ONSET (<34 WEEKS)

LATE ONSET

(>34 WEEKS) TOTAL SIG.

α-fetoprotein levels

ELEVATED

% 6(28.6)

% 15(71.4)

21(100) χ²=1.86 p=0.173

NORMAL 33(45.2) 40(54.8) 73(100)

TOTAL 39(41.5) 55(58.5) 94(100) df=1

ONSET OF DISEASE USING G.A AT DIAGNOSIS

EARLY ONSET (<34 WEEKS)

LATE ONSET

(>34 WEEKS) TOTAL SIG.

β - HCG LEVEL ELEVATED

% 16(48.5)

% 17(51.5)

% 33(100)

χ²=1.03 p=0.311 df=1

NORMAL 23(37.7) 38(62.3) 61(100)

TOTAL 39(41.5) 55(58.5) 94(100)

The statistical relationship between α-fetoprotein and β – HCG levels and gestational age at onset of disease was not significant as P values for α-fetoprotein and β – HCG were 0.173 and 0.311 respectively.

DISCUSSION

This study showed that preeclampsia occurred most commonly in nulliparous women (42.6%). Also most of the women who had this disorder where unbooked (74.5%) and of unskilled employ (53.5%). These have also been reported as risk factors of preeclampsia.^33-37 The mean age for patients with preeclampsia in this study was 28.7 years which is similar to that reported by Conde-Agudelo et al³⁴ in a study amongst Latin American and Caribbean women. Also in this study preeclampsia occurred most commonly (43.6%) in women between the ages of 26 – 30 years. Conde-Agudelo et al similarly reported highest frequency of

preeclampsia in women aged between 20 – 34 years. This is in contrast to the finding in the study by Omole-Ohonsi et al³⁷ in which preeclampsia occurred most frequently in the 10-19 age group in Northern Nigeria. The peculiarity of relatively early marriages and consequent early pregnancy may account for this difference observed in Northern Nigeria.

In this study, the mean levels of maternal serum α-fetoprotein and β-HCG were markedly elevated in severe preeclampsia compared to mean levels in women in the normal population.

This finding indicates that an abnormal placental secretory function exists in patients with severe preeclampsia. Placental pathologic examinations have revealed focal cellular necrosis in the syncytiotrophoblast and increased mitotic activity with cellular proliferation in the cytotrophoblast.⁷²These changes result from vasospasm which causes vascular damage and local hypoxia. This in turn results in hyperplasia of the cytotrophoblastic cells, increased secretion and leakage of these placental peptides into the maternal circulation. The degree of leakage of these placental markers is expected to parallel the severity of the disease. This was however not demonstrated in my study as the mean value of α-fetoprotein observed in patients with mild preeclampsia was less than that observed in normal pregnant women. The mean level of α-fetoprotein in this study for patients with mild preeclampsia was 148.62 ± 40.45ng/ml, which was lower than that of normal patients which was 158.56 ± 9.56ng/ml.

There was however a marked increase in the mean of those with severe preeclampsia (262.08

± 24.7ng/ml). Of note in my study is the fact that, only patients with severe preeclampsia had elevated levels of α-fetoprotein. Also, the difference in mean levels of α-fetoprotein between mild and severe preeclampsia was not statistically significant (P = 0.171).

Davidson et al in a study which aimed at evaluating the role of α-fetoprotein and other markers as predictors of preeclampsia did not find a significant elevation in α-fetoprotein

levels between patients who developed preeclampsia and those who remained normal.⁵⁵ Although that study was retrospective and involved the collection of samples in the second trimester before the onset of preeclampsia, the result obtained is not in keeping with the supposed placental secretory dysfunction postulated in patients with preeclampsia and that is expected to be worse with increasing severity of disease. Shenhav et al⁵⁴ however reported a different finding in a similar work done evaluating the levels of maternal serum markers including α-fetoprotein patients with early and late onset severe preeclampsia. In that study, the levels of α-fetoprotein in patients who developed early onset severe preeclampsia was significantly higher than in patients with late onset severe preeclampsia (p=0.01). Walters et al⁵⁰ also reported a significant elevation in α-fetoprotein in patients who developed preeclampsia compared to those in the normal population and proposed that an abnormality of the placenta predisposes to the development of this disorder. While most authors have evaluated the role of α-fetoprotein as a predictor of occurrence of preeclampsia with varied conclusions, my findings suggest that α-fetoprotein is a marker only of severe preeclampsia and does not differentiate between mild and severe disease.

In my study, the mean level of maternal serum β-HCG for normal pregnant women in the preliminary study was 5,989.65 ± 670.39 mIU/ml; that of patients with mild preeclampsia was 9,470 ± 126.7mIU/ml while the mean for patients with severe preeclampsia was 10,912 ± 741.37 mIU/ml. There was a marked increase in the level of serum β-HCG between normal patients and those with mild preeclampsia and a further increase between women with mild and severe disease.

This differential increase in mean levels of maternal serum β-HCG is similarly reported by Kanika et al in a study to determine the value of serum β-HCG in pathogenesis of

preeclampsia⁷³. Kanika et al found that maternal serum β-HCG was markedly raised in preeclampsia in comparison to normal population. In their study, the mean level of maternal serum β-HCG in normal patients was 8,391.06 ± 1,909.64, while that of patients with mild and severe disease was 16,950 ± 1,709.22 mIU/ml and 19,793.40 ± 950 mIU/ml respectively.

Gokdeniz et al⁶¹, Basirat et al⁷⁴, and Hsu et al⁷⁵also reported similar findings of significantly elevated levels of β-HCG in severely preeclamptic women compared with those in matched controls. Contrary results have been reported in by Teoh and Sivasamboo.⁷⁶

In my study, the difference in mean levels of maternal serum β-HCG between patients with mild preeclampsia and those with severe preeclampsia was not statistically significant (p = 0.557). This finding is similar to that observed by Hsu et al who reported that although β-HCG levels were significantly higher in severely preeclamptic women (p<0.05), it was not in those with mild preeclampsia, compared with those in their matched controls.⁷⁵

In contrast, Kanika et al ⁷³ and Basirat et al⁷⁴ reported a statistically significant difference in the mean of maternal serum β-HCG between patients with mild preeclampsia and those with severe preeclampsia (p <0.0001 in both studies).

Again, as with α-fetoprotein in my study, β-HCG appears to be a marker of severe preeclampsia but not so for mild disease. It appears that the degree of focal placental damage must be such as to allow for significantly elevated levels of these placental markers into the maternal circulation for the markers to be useful in identifying severe preeclampsia. Lesser placental damage which ordinarily is expected to result in mild disease appears not to allow for a significant elaboration of these markers in the maternal circulation.

This study also showed that there was no statistically significant relationship between α-fetoprotein and both clinical and biochemical parameters of disease severity of preeclampsia.

β-HCG had a statistically significant relationship with hyperreflexia / clonus (p = 0.005) and dipstick proteinuria (p = 0.009). It thus appears from my study that the expectation that α-fetoprotein and β-HCG would be earlier and more objective markers of disease severity compared to clinical features which may be subjectively assessed and haematological / biochemical parameters which reflect end-organ damage is unfounded.

Furthermore, in this study, there was a poor correlation (-0.046) between α-fetoprotein and disease severity. The correlation of β-hCG with disease severity was however perfect (1.0).

Thus, β-hCG may be a more reliable marker of severe disease than α-fetoprotein. Also, there may be no added benefit of combined measure of both assays.

CONCLUSION

This study showed that α-fetoprotein and β-HCG are significantly elevated only in patients with severe preeclampsia compared to the normal pregnant population. Neither of these markers differentiated between mild and severe preeclampsia nor showed significant relationship with conventional clinical and biochemical features of disease severity. There was also no added benefit of combined measure of both assays.

RECOMMENDATION

There is still a need to identify early markers of disease severity of preeclampsia.

These markers need to affordable and readily available. These two factors were major constraints in the performance of this study. Also, markers of disease severity which can be easily evaluated without the need for sophisticated machines and highly trained personnel, particularly in developing countries will greatly help in curbing the rising incidence of maternal mortality attributable to the enigma of preeclampsia.

To achieve the above, there must be a sustained partnership and support involving the public and private sectors as well as collaboration with international agencies with particular interest in research in developing countries.

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