Abstract
The relationship between predictors and the variable of interest was estimated using a structural equation model which is used to predict latent variables. The main advantage of the SEM is the ability to estimate the direct and indirect pathways of the effect of the primary independent variable on the outcome, given sufficient sample sizes. Despite not directly modeling the mediated pathways, GLMMs excluding mediating variables performed well with respect to power, bias and coverage probability in modeling the total effect of the primary independent variables on the outcome. In longitudinal studies, data are collected from subjects at several time points. The main purpose of longitudinal analysis is to detecting the trends or trajectories of the variables of interest.
A longitudinal study was conducted on 792 adults living with HIV/AIDS who commenced HAART. Structural equation modeling was used to construct a model to detecting predictors of CD4 cell count change. The procedure was illustrated by applying it to longitudinal health-related quality-of-life data on HIV/AIDS patients, collected from September 2008 to August 2012 monthly for the first six months and quarterly for remaining study period.
The result of current investigation indicates that CD4 cell count change was highly influenced by certain socio-demographic and clinical variables. Out of all the participants, 141 (82%) have been considered 100% adherent to antiretroviral therapy. Structural equation modeling has confirmed the direct effect that personality (decision-making and tolerance of frustration) has on motives to behave, or act accordingly, which was in turn directly related to medication adherence behaviors. In addition, these behaviors have had a direct and significant effect on viral load, as well as an indirect effect on CD4 cell count. The final model demonstrates the congruence between theory and data (
The results of this study support our theoretical model as a conceptual framework for the prediction of medication adherence behaviors in persons living with HIV/AIDS. Implications for designing, implementing, and evaluating intervention programs based on the model are to be discussed.
Author Contributions
Copyright© 2020
Seyoum Tegegne Awoke.
License
This work is licensed under a Creative Commons Attribution 4.0 International License.
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Competing interests The authors declare that they have n competing interests, which may have inappropriate influenced them in writing this article.
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Results
The baseline characteristics of study variables are indicated in As shown in Model fitting for CD4 cell count data using structural equation modelling One means of assessing the determinants of the change of CD4 cell count is Structural Equation Modelling (SEM). Considering the commonly significant covariates on the variable of interest on the previous chapters, let us apply structural equation modelling to see whether or not the significant variables found above are also significant in this case. In our case, all dependent and independent variables are manifest/observable variables. Let rectangles in Considering the current change of CD4 cell count as endogenous variable, the predictor variables (HAART adherence, weight, age, baseline CD4 cell count, visiting time and Cell phone ownership) found as significant variables from the previous chapters can be considered as exogenous variables. Since CD4 cell count results from the two previous results (prior one unit from the current and prior two units from the current) in transition model were significant for the current change, they had been included as predictor variables. Consider the first two lag variables (lag-2 and lag-1) as exogenous variable as shown in In The goodness-of-fit statistic is indicated in From ( The correlation structure between E1<--->E4, E2<--->E3, E3<--->E5, E2<--->E8, E6<--->E8, E4<--->E8, E7<--->E8 and E3<--->E8 had significant effect on the relationship between endogenous and exogenous variables. In order to assess estimated value of linkage for each covariate on CD4 cell count change, standardized regression weights and the structural equation model are needed.
Variable
Average
No (%)
Weight (kg)
62 (58-70)
-
Base line CD4 cells/ mm3
134 (113-180)
-
Age (years)
36 (28-48)
-
First month / initial CD4 cell count change/mm3
15.9 (12-26)
-
Sex
Male
391 (49.4)
Female
401 (50.6)
Educational status
no education
160 (20.2)
Primary
205 (25.9)
Secondary
273 (34.5)
Tertiary
154 (19.4)
Residence area
Urban
468 (59.1)
Rural
324 (40.9)
Marital status
Living with partner
355 (44.8)
Living without Partner
437 (55.2)
Level of income
Low income (< 500 ETB per month)
355 (44.8)
Middle income (5001-999 ETB per month)
346 (43.7)
High income ( ≥ 1000ETB per month)
91 (11.5)
WHO HIV stage
Stage I
101 (12.8)
Stage II
258 (32.6)
Stage III
199 (25.1)
Stage IV
234 (29.5)
Disclosure
Yes
575 (72.6)
No
217 (27.4)
Cell ownership
yes
400 (50.5)
No
392 (49.5)
First monthHAART adherence
Good
540 (68.2)
Fair
160 (20.2)
Poor
92 (11.6)
RMSEA model
GFI model
RMSEA
95 % C.I
P-value
RMR
GFI
AGFI
PGFI
Saturated model
0.0320
-0.0002
0.0653
0.7820
0.0805
0.9973
0.9855
Null model
0.2970
0.3769
0.4047
0.0001
4.2453
0.4821
0.2896
0.4353
Estimate
Current CD4 cell count change <------------ CD4 cell count change (lag-2)
0.62463
Current CD4 cell count change <------------ CD4 cell count change (lag-1)
0.21497
Current CD4 cell count change <------------------------------------ adherence
0.56231
Current CD4 cell count change <-----------------------------------------weight
0.22354
Current CD4 cell count change <---------------------------------------------- age
0.83452
Current CD4 cell count change <-----------------------baseline CD4 cell count
0.35463
Current CD4 cell count change <-------------------------------------Visiting times
0.21487
Measurement
coefficient
S.E
Z
P-value
95% C.I
Adherence <------- CD4 count change
1(const.)
Constant
96.31
1.38
74.5
<0.001
92.79
98.77
Weight <------ CD4 count change
3.27
0.12
9.7
<0.001
1.95
5.52
Constant
97.08
1.47
72.6
<0.001
94.42
102.44
Age <------ CD4 count change
4.03
0.13
8.91
<0.001
1.81
7.45
Constant
97.10
1.35
71.6
<0.001
94.44
99.76
Baseline CD4count <------CD4 count change
1.05
0.61
11.42
<0.001
0.08
3.98
Constant
45.77
5.88
75.43
<0.001
26.34
64.44
Visiting time <------CD4 count change
1.02
0.51
10.42
<0.001
0.01
2.89
Constant
60.77
5.88
97.43
<0.001
36.34
74.43
Owner of phone <------CD4 count change
1.24
0.61
11.42
<0.001
0.07
3.98
Constant
36.76
4.85
94.43
<0.001
22.34
92.43
Lag-2 <------CD4 count change
1.14
0.54
34.32
0.012
0.02
3.35
Constant
32.38
4.68
65.32
0.003
28.76
42.53
Lag-1 <------ CD4 count change
1.07
0.84
43.42
0.012
0.01
4.45
Constant
35.48
5.58
68.52
0.003
26.76
45.43
Variance of E *weight
53.47
1.92
37.15
76.17
Variance of E *age
34.25
9.81
23..36
58.33
Variance of E* visiting times
96.15
67.62
54.84
98.61
Variance of CD4 cell count
18.20
24.32
12.43
27.46
Estimate
S.E
C.R
P-value
Adherence <--------CD4 cell count change at lag2
0.6546
0.0568
10.0462
***
Adherence<-------- CD4 cell count change at lag1
0.22497
0.0551
4.0839
***
0.28497
0.0451
4.0839
***
weight <------------- CD4 cell count change at lag2
0.58916
0.0558
10.5581
***
weight <------------- CD4 cell count change at lag1
0.38916
0.0458
8.5581
***
weight <-------------- current CD4 cell count change
0.38916
0.0458
8.5581
0.2312
Age <------------------ CD4 cell count change at lag2
0.24762
0.0453
6.4352
***
Age <------------------ CD4 cell count change at lag1
0.83452
0.0874
6.3542
***
0.65483
0.4563
4.5433
***
Initial CD4<----------- CD4 cell count change at lag2
0.65463
0.0568
10.0462
***
Initial CD4<------------ CD4 cell count change at lag1
0.22487
0.0551
4.0839
***
0.58916
0.0558
10.5581
***
Owner of Cell phone<---- CD4 cell count change at lag2
0.65326
0.0568
1.0462
***
Owner of Cell phone <-- CD4 cell count change at lag1
0.23497
0.0551
4.0839
***
0.67916
0.0558
12.5581
***
CD4 count(lag-2) <------ CD4 cell count change (lag-1)
0.56326
0.05682
1.04618
***
0.32497
0.15409
4.06390
***
Covariance for saturated model
E1<------->E4
1.45324
0.34524
4.65421
***
E6<------->E7
0.65224
0.64824
4.65421
0.08532
E2<------->E3
0.64327
.65482
3.12537
***
E6<------->E7
0.75412
.06831
2.3451
0.32130
E3<------->E8
0.82453
.67543
3.45632
***
E3<------->E5
1.43271
.86541
2.54321
***
E5<------->E6
0.94231
.32107
0.97421
0.32172
E2<------->E8
1.63261
.85321
2.54511
***
E1<------->E2
0.68261
.95321
0.84511
0.14522
E4<------->E8
0.98212
.54132
3.42152
***
E7<------->E8
1.34252
1.22412
2.53214
***
E4<------->E5
0.86521
.86241
1.86912
0.08321
E6<------->E8
-0.86312
.94321
1.86321
***
Discussion
In current investigation, the structural equation models for analysis of longitudinal data on univariate models of observable variables (CD4 cell count change) that are conditional to the other variables (time-varying or time invariant) were reviewed. Hence, in the paper keeping the statistical theory to be a practical guide for analysing longitudinal data, SEM applied for analysis of longitudinal data(CD4 cell count change and its predictors). However, considering the readers concept and prior knowledge of SEM, the investigators largely avoid dwelling on the basis of SEM. Although common software packages such as SAS and R have the capability to run SEMs, software designed specifically for SEMs The current study examines one specific setting of mediated longitudinal data. Other situations with different data structures where mediation is present could also be explored, e.g. situations where the mediator and the primary independent variable as well as the outcome are repeatedly measured, categorical outcomes, and settings with more complex pathways between variables. In addition, we specifically explored the question of whether the LMM performs sufficiently in a setting favorable to the SEM. Future studies examining broader settings where the data arise from non-SEMs would provide further insight into the use of the LMM and SEM in mediated longitudinal settings. First, we found the factor loadings and intercepts of HD (health distress) and EF (energy and fatigue) not to be invariant across measurement occasions and, second, we found direct effects of CD4-cell count on EF and RF (role-functioning) The Bonferroni adjustment of the level of significance guards against inflation of the family-wise error rate, but the chi-square difference test can still be affected by model complexity and sample size It should be noted that most response shift researchers in substantive areas of psychology contend that response shifts are the result of some catalyst event, such as an intervention in educational research (Howard et al. 1979), or a health state change in medical research (Sprangers and Schwartz 1999). In the HRQL study of HIV/AIDS patients, there is not a well defined event that all respondents have in common, other than having been diagnosed with HIV or AIDS some time ago. However, the time since diagnosis and the time on HAART vary greatly across patients and cannot be considered true catalysts. The one thing all patients have in common is that they participate in the HRQL study, and that they complete HRQL tests every half year. The test taking itself can have an effect on their response behaviour, which may change with time. The patients may become more accustomed to both their disease and taking the test, which perhaps induces a response shift. It should also be noted that most work on response shift in substantive psychological research was not aimed at investigating measurement invariance, but rather at explaining paradoxical intervention effects. Seeing that research into response shift was hampered by researchers having different conceptions of response shift, Oort (2005b) proposed to formally define response shift as a special case of measurement bias, although some researchers may still have another perspective on response shift (Oort et al. 2009). As is illustrated by the empirical example, Step 2 and Step 3 of the detection procedure are laborious and time consuming. Especially if the numbers of observed variables and exogenous variables are large, these two steps involve the fitting of numerous models, in order to evaluate the chi-difference tests. An advantage of using modification indices is that, within each iteration, the researcher only has to fit a single model. Therefore, although perhaps less sound (Kaplan 1990), we explored the use of the modification index as an alternative to the global tests with multiple degrees of freedom. When we evaluated the modification indices with the Bonferroni adjusted levels of significance, none of the findings were significant because of the large number of tests under consideration (e.g. 120 in Step 2). When testing at less conservative levels of significance, for example by considering tests of intercept constraints first and factor loading constraints second, or by simply raising the family-wise level of significance, there was a number of modification indices that reached significance. However, as multiple modification indices were about equally large, the choice of which constraint to remove first seemed arbitrary, yet highly consequential for the removal of constraints in subsequent iterations, leading to very different conclusions. In addition, we also had to be careful not to run into constraint interactions. Still, the most important problem with relying on modification indices and less conservative testing was that many of the modifications were difficult to interpret and that the number of iterations grew very large. Saris et al. (2009) suggest only modifying models if the modification indices are associated either with moderate (instead of high) statistical power or with substantial expected parameter changes. When statistical power is high, one can only rely on substantive arguments for modification (ibidem), which we did, as in the present analyses the power to find medium sized differences was consistently above 99%. In such situations, the decision making becomes increasingly subjective, as researchers will have to base their decisions between modifications and when to stop modifications on the interpretability of the different modifications. It is therefore highly likely that different researchers, with different substantive knowledge and different interpretation skills, will end up with different conclusions when analysing the same data. As can be seen from the procedure using modification indices, subjectivity in measurement bias detection influences whether and where bias is found. Notall researchers may want to test every possible combination of tenable equality constraints. When this is the case, a priori hypotheses driven by theory should be stated before analysis and only these tests should be conducted. Under these circumstances, chance findings may further be reduced and more generalisable results found. The problems associated with devising an objective procedure for measurement bias detection is common to specification searches in general. Bollen (2000): Modelling strategies are subject to debate for virtually all statistical procedures. Witness the sharp disagreements over stepwise regression, the interpretation of clusters in cluster analysis, or the identification of outliers and influential points. The largely objective basis of statistical algorithms does not remove the need for human judgment in their implementation. Similarly, when investigating measurement invariance, it is impossible to completely remove the element of human judgement. This is certainly true for the substantive interpretation of apparent measurement bias. However, we think that the procedure presented in this paper, with its safeguards against chance findings, at least helps to more objectively decide which measurements are biased and which are not. Ethical clearance certificate had been obtained from two universities namely Bahir Dar University, Ethiopia with Ref ≠ RCS/1412/2006 and University of South Africa (UNISA), South Africa, Ref ≠ : 2015-ssr-ERC_006 . We can attach the ethical clearances certificate up on request. This manuscript has not been published elsewhere and is not under consideration by another journal. The secondary data used for current investigation is available with the corresponding author.