Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 20  |  Issue : 2  |  Page : 117-122

Ultrasound features of placental changes and their obstetric correlates among HIV patients and controls at Aminu Kano Teaching Hospital, Kano


1 Department of Obstetrics and Gynaecology, Bayero University Kano/Aminu Kano Teaching Hospital, Kano State, Nigeria
2 Department of Radiology, Bayero University Kano/Aminu Kano Teaching Hospital, Kano State, Nigeria
3 Department of Obstetrics and Gynaecology, Aminu Kano Teaching Hospital, Kano, Nigeria

Date of Web Publication17-Jul-2019

Correspondence Address:
Dr. Ayyuba Rabiu
FWACS, FMCOG, Department of Obstetrics and Gynaecology, Bayero University Kano/Aminu Kano Teaching Hospital, P.M.B. 3011, Kano State
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jomt.jomt_15_18

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  Abstract 


Background: One of the serious health problems in the world today is the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome pandemic, with Nigeria having the second largest number of new cases. During pregnancy, HIV-infected women face more adverse effects than uninfected women. This study aimed at evaluating ultrasound features of placentas of HIV-positive women and controls to demonstrate a difference in vasculoplacental complications between the two groups. Methods: A comparative study was conducted among HIV-positive women and their matched controls. Informed consent was obtained and a pretested interviewer-administered questionnaire was used. The women had ultrasound assessment of the placenta and an obstetric ultrasound scan. Results: There were no differences in placental surface area (t = −1.122, df = 6, P = 0.305, 95% confidence interval: −17.46 to 15.56) and placental thickness (t = 1.846, df = 58, P = 0.07, 95% confidence interval: −0.405 to 9.99). Calcifications were found but not related to HIV status. The most common complication among the HIV-infected women was miscarriage. No complications were recorded among the controls. Conclusion: There was no difference in the vasculopathological changes detectable by ultrasound scan in the placentas of HIV-infected and uninfected pregnant women.

Keywords: HIV, placenta, ultrasound vasculopathological changes


How to cite this article:
Rabiu A, Ismail A, Lawal Y, Mu'uta JI. Ultrasound features of placental changes and their obstetric correlates among HIV patients and controls at Aminu Kano Teaching Hospital, Kano. J Med Trop 2018;20:117-22

How to cite this URL:
Rabiu A, Ismail A, Lawal Y, Mu'uta JI. Ultrasound features of placental changes and their obstetric correlates among HIV patients and controls at Aminu Kano Teaching Hospital, Kano. J Med Trop [serial online] 2018 [cited 2020 Jul 11];20:117-22. Available from: http://www.jmedtropics.org/text.asp?2018/20/2/117/262750




  Introduction Top


The human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) pandemic is one of the most serious health problems with lasting consequences that is ravaging the world today. Sub-Saharan Africa bears the greatest burden of HIV/AIDS epidemic hosting 67.6% of the total number of people living with HIV, 69.2% of the 2.6% of total new cases, and 72.0% of the 1.8 million deaths in 2009.[1]

Globally, Nigeria is the country with the second highest number of new cases of HIV infection with an estimated 3.7% of the population living with HIV.[2],[3] In 2008, the national seroprevalence based on antenatal survey was 4.6%.[1]

HIV-infected women are more at risk of pregnancy-related complications like pregnancy-induced hypertension, anemia, breech presentation, stillbirths, and fetal death than HIV-uninfected women.[4] In addition, intrauterine fetal death is more common among HIV-positive women who did not receive mother-to-child transmission prophylaxis or had breech presentation.[4]

Studies have shown mixed results in the incidence of vasculoplacental complications between HIV-positive and negative patients, based on histological findings. Canlorbe et al.[5] showed no difference in the incidence of vasculoplacental complications between HIV-positive pregnant women and their matched controls. However, Vermaak et al.[6] reported both microscopic and macroscopic differences relating to the degree of immune status; placentas of HIV-positive patients were characterized by decreased weight and increased number of marginal infarcts.

The placenta is a dynamic vital organ for the fetus that performs several functions within a short lifespan. Its integrity is indispensable for fetal well-being, growth, and development.[7] Due to the dynamic nature of the placenta, its size changes in response to fetal needs. In pregnancies complicated by conditions such as diabetes mellitus or Rhesus isoimmunization, the thickness, length, and volume of the placenta increases.[8] A variety of pathologic changes like placental infarction, intraplacental hematoma, deposition of immunoglobulin and complement, and thickening of the trophoblastic basement membrane in patients with systemic lupus erythematosus was also noted.[9] Placental surfaces in women with diabetes mellitus were found to have infarction, hematoma, calcification, and fibrin deposits.[10]

Limited data exist on radiological features of placental changes in HIV-infected women. Rabelo et al.[11] reported a case on placental histopathology and clinical presentation of severe congenital Zika syndrome in a HIV-exposed but uninfected infant. In their report, clinical, imaging, and laboratory examinations of the pregnant woman and the newborn were performed. Unfortunately, there was no report on the radiological features of placental changes in HIV-positive woman coinfected with Zika virus.

This study postulated that ultrasound scan of the placenta of HIV-positive pregnant women and their matched controls would reveal remarkable differences in pathologic changes. Therefore, we sought to evaluate the ultrasound features of placentas in HIV-positive patients and their matched controls at Aminu Kano Teaching Hospital, Nigeria.


  Methodology Top


It was a comparative study between HIV-positive pregnant women and HIV-negative matched controls, who attended antenatal care clinic in Aminu Kano teaching Hospital. Ethical approval was obtained from the hospital ethics committee. A questionnaire was designed and pretested before administration. Information on obstetric correlates, HIV status, the duration of antiretroviral therapy, and complications among others was asked and documented. An informed consent was obtained from each participant before questionnaire administration. Recruited patients were sent to the radiology unit of the hospital for ultrasound assessment of the placenta and other relevant obstetric scan. These entailed sonographic documentation of the gestational age and screening for gross morphologic abnormality. Maximum placental thickness was measured to the nearest millimeter. Maturity of the placenta was graded using the suggestions of Grannum et al.[12] In addition, effort was made to screen for possible foci of infarction (as evidenced by decreased parenchymal echogenicity).

Obstetric ultrasound findings of multiple gestations and congenital morphologic abnormalities were excluded from the study.

The data were analyzed using Statistical Package for Social Sciences (SPSS) Version 18 Electronic Software (SPSS Inc., Chicago, IL, USA). P values less than 0.05 were considered significant. Findings were presented numerically and in tabular form.


  Results Top


During the study period (from July 1, 2016 to July 31, 2017), 31 HIV-positive pregnant women and their controls were recruited. The mean age ± standard deviation (SD) was 30 ± 5 and 27 ± 5 years for HIV and control groups, respectively (P = 0.032).

The mean parity for the HIV and control groups was 3.3 ± 2.15 and 2.2 ± 2.48, respectively. The median parity was 3.0 (quartile range (QR): 25th = 2; 50th = 3; 75th = 5) for HIV-positive and 2.0 (QR: 25th = 0; 50th = 2; 75th = 3) for the control group. There was no difference in the mean parity between the two groups (t = 1.804, df = 60, P = 0.07, 95% confidence interval, CI: −0.116 to +2.245).

The mean gestational age for HIV-positive and control groups was 30.0 ± 6.48 and 29.5 ± 4.70 weeks, respectively. There was no difference between the mean gestational age of the two groups (t = 0.404, df = 60, P = 0.68, 95% CI: −2.295 to +3.457).

The mean number of living children for the HIV group was 2.3 ± 1.6 and for the control group was 1.9 ± 2.0.

[Table 1] depicts the sociodemographic characteristics of the respondents. Both the HIV-positive and control groups were married.
Table 1: Sociodemographic characteristics of the respondents

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Seventeen (54.8%) of the HIV-positive group were in the second order of marriage whereas 14 (45.2%) were in the first order of marriage. All the participants in the control group were in the first order of marriage.

The average number of years following HIV diagnosis was 5.7 ± 2.56 and the average number of years on treatment was 5.6 ± 2.65. They were all regular on medications. The median number of years following HIV diagnosis and treatment was 6 for both diagnosis and treatment (QR: 25th= 4; 50th= 6; 75th=8).

The mean placental surface area ± SD was 26.1 ± 18.60 and 43.5 ± 19.15 cm2 for the HIV-positive and control groups, respectively. There was no difference between the mean placental surface area (t = –1.122, df = 60, P = 0.30, 95% CI: −17.46 to +15.56).

The mean placental thickness ± SD was 8.4 ± 13.95 and 3.6 ± 0.94 cm2 for the HIV-positive and control groups, respectively. There was no difference between the mean placental thickness in the two groups (t = 1.846, df = 58, P = 0.07, 95% CI: −0.405 to +9.99).

Grade I placenta was observed more commonly among the HIV-positive group when compared to the controls (51.8% vs. 20.0%) whereas grade II was less prevalent among the HIV-positive group (24.1% vs. 73.3%) as shown in [Table 2].
Table 2: Placental grade and distribution of placental infarct among HIV and control groups

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No placental hematoma was seen in both the control and the study groups.

[Table 3] shows the association between placental calcification and HIV status.
Table 3: Placental calcification

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Presence of placental calcification was not associated with HIV status (χ2 = 0.182, P = 0.67).

[Figure 1] shows the history of complications among the HIV-positive group prior to the index pregnancies. Miscarriage (70%) was reported by the majority followed by stillbirth (15%). There was no history of complications among the control groups.
Figure 1: History of complications among HIV group. ENND, early neonatal death; IUFD, intrauterine fetal death.

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  Discussion Top


This study evaluated the ultrasound features of placental changes in HIV-positive and negative pregnant women with assumption that HIV infections would invariably affect the placental morphology as HIV infection is associated with pregnancy-related complications.[4] However, the study showed no remarkable differences between the placenta of HIV-positive pregnant women and that of the controls.

The average number of living children was more in the HIV group than the control group. This can be explained by the fact that the average parity of the HIV group was more than the control group 3.3 ± 2.15 and 2.2 ± 2.48, but this was not statistically significant (t = 1.804, df = 60, P = 0.076, 95% CI: −0.116 to +2.245). The mean age ± SD was 30.8 ± 5.50 and 27.6 ± 5.34 years for HIV-positive and control groups, respectively. A study conducted by Kalk et al.[13] also showed that HIV-infected women were older (median [interquartile range (IQR)] 27.4 years [24–31] vs. 25.8 [23–30]), more likely to be multiparous (81.7% vs. 71.8%). Our findings are also similar to this study.

In this study, the average number of years following diagnosis was 5.7 ± 2.56 and the average number of years on treatment was 5.6 ± 2.65. This means most of the women commenced on antiretroviral therapy, almost immediately after diagnosis, so as to improve their quality of life and general well-being. Maternal placental vasculopathological syndromes are an interrelated group of disorders that include preeclampsia, eclampsia, placental infarction, and abruption. Whether the risk is increased in HIV-positive women is unknown. These risks are associated with preterm birth, intrauterine growth restriction, and low birth weight, which are common findings in HIV-positive women.[14] A recent meta-analysis found no difference in risk of preeclampsia between HIV-positive and negative women.[15] Another study by Canlorbe et al.[5] also found no difference in the incidence of pregnancy-related hypertension, preeclampsia, eclampsia, and vascular growth restriction between HIV-infected and noninfected women. These findings are in agreement with the findings of this study, in which no significant difference in the placental surface area was found between the two groups of the HIV-infected and uninfected groups, respectively. Likewise, no difference was found in the mean placental thickness in the HIV-infected and noninfected groups, respectively. The major complication encountered in the HIV group was miscarriage (70.0%) and stillbirth (15.0%). No complication was observed in the control group. A rare association between HIV infection and stillbirth has been reported by Shapiro et al.[16] in Botswana among women receiving highly active antiretroviral therapy.There were two (6.9%) women among the HIV-positive group found to have placental infarcts and one (6.7%) among the controls. No hematoma was found in both the groups. The incidence of calcifications was more in the HIV group than the control group (12 and 7), respectively, although there was no association between these findings and HIV status. This does not agree with the study by Vermaak et al.[6] wherein microscopic differences found were related to the immune status of the women that included decreased weight and increased marginal infarcts. Our study that was based on the radiological features and not histological findings could be responsible for the difference.


  Limitation Top


This was a comparative study; we did not follow these women up to delivery to determine fetal outcome in relation to the changes found in the placentas for both the groups. Histological examination of the placenta should be done for women found to have pathologies after delivery and the findings correlated with fetal outcome and immune status.

The small sample size could have influenced the end results of no statistically significant difference in the pathological changes seen between the two groups.


  Conclusion Top


The mean placental surface area was higher in the control group than the HIV-infected group, although this was not statistically significant. Likewise, the placental thickness was greater in the HIV group than the control group, but this was also not significant. Calcifications observed in both the groups were unrelated to HIV status. There was no difference in the vasculopathological changes in the placentas of HIV-infected women and uninfected women; early commencement of highly active antiretroviral therapy following diagnosis of HIV infection could be responsible for the findings. A follow-up study should be done and the women should be followed up till delivery to determine the fetal outcome, in those found to have pathologies in the placentas.

Recommendation

The placental pathologies found should be correlated with viral load/CD4 counts of the women.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Federal Ministry of Health. National Guidelines for Prevention of Mother-To-Child Transmission of HIV (PMTCT); HIV and AIDS Division: Federal Ministry of Health, 4th ed. Abuja, Nigeria: Federal Secretariat; 2010. pp. 1-9.  Back to cited text no. 1
    
2.
UNAID. Global Report: Annexes. 2012. Available at: www.unaids.org/en/resources/campaigns/20121120_globalreport2012/annexes. [Accessed June 21, 2015].  Back to cited text no. 2
    
3.
Federal Republic of Nigeria. Global AIDS responses Country Progress Report, Nigeria. Available at: www.unaids.org/en/dataanlysis/knowyourresponse/countryprogressreports/2012countries/#a_52910. [Accessed June 21, 2015].  Back to cited text no. 3
    
4.
Lionel J, Aleyamma TK, Varghese L, Buck J, Gopalakrishnan K, Chaguturu S et al. HIV and obstetric complications and fetal death outcomes in Vellore, India. Trop Doct 2008;38:144-6.  Back to cited text no. 4
    
5.
Canlorbe G, Matheron S, Mandelbrot L, Oudet B, Luton D, Azria E. Vasculo-placental complications in pregnant women with HIV infection: a case control study. Am J Obstet Gynecol 2015;213:241.e1–9.  Back to cited text no. 5
    
6.
Vermaak A, Theron G, Schubert PT, Kidd M, Rabie U, Adjiba BM et al. Morphologic changes in the placentas of HIV-positive women and their association with degree of immune suppression. Int J Obstet Gynecol 2012;119:239-43.  Back to cited text no. 6
    
7.
Yui-Chiu V, Chiu L. Sonographic features of placental complications in pregnancy. Am J Rad 1982;138:879-85.  Back to cited text no. 7
    
8.
Fox H. Pathology of the placenta. In: Bennington L, ed. Major Problems in Pathology, Volume 7. Philadelphia: Saunders 1978. pp. 97-105.  Back to cited text no. 8
    
9.
Hanly JG, Gladman DD, Rose TH, Laskin CA, Urowitz MB. Lupus pregnancy. A prospective study of placental changes. Arthritis Rheumatol 1988;31:358-66.  Back to cited text no. 9
    
10.
Salge AKM, Rocha KMN, Xavier RM, Ramalho WS, Rocha EL, Guimaraes JV et al. Macroscopic placental changes associated with fetal and maternal events in diabetes mellitus. Clinics (Sao Paulo) 2012;67:1203-8.  Back to cited text no. 10
    
11.
Rabelo K, Fernandes RCSC, de Souza LJ, de Souza TL, Santos FB, Nunes PCGN et al. Placental histopathology and clinical presentation of severe congenital Zika syndrome in a human immunodeficiency virus-exposed uninfected infant. Front Immunol 2017;8:1704.  Back to cited text no. 11
    
12.
Grannum PAT, Berkowitz RL, Hobbins JC. The ultrasonic changes in the maturing placenta and their relations to fetal pulmonic maturity. Am J Obstet Gynecol 1979;33:915-7.  Back to cited text no. 12
    
13.
Kalk E, Schubert P, Bettinger JA, Cotton MF, Esser M, Slogrove A et al. Placental pathology in HIV infection at term: a comparison with HIV-uninfected women. Trop Med Int Health 2017;22:604-13.  Back to cited text no. 13
    
14.
Ng R, Macdonald EM, Yudin HM, Bayoumi AM, Loutfy MR, Raboud J et al. Maternal placental syndrome among women living with HIV in Ontario: a population based study. CMAJO 2015;3:e360-5.  Back to cited text no. 14
    
15.
Calvert C, Ronsmans C. HIV and risk of direct obstetric complications; a systematic review and meta analysis. PLoS One 2013;8:e74848.  Back to cited text no. 15
    
16.
Shapiro RL, Souda S, Parekh N, Binda K, Kayembe M, Lockman S et al. High prevalence of hypertension and placental insufficiency, but no in utero HIV transmission, among women on HAART with stillbirths in Botswana. PLoS One 2012;7:e31580.  Back to cited text no. 16
    


    Figures

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    Tables

  [Table 1], [Table 2], [Table 3]



 

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