Recurrent miscarriage associated with rare anti-PP1Pk antibody: a case series and literature review

doi:10.21203/rs.3.rs-2728370/v1

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Recurrent miscarriage associated with rare anti-PP1Pk antibody: a case series and literature review

https://doi.org/10.21203/rs.3.rs-2728370/v1

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Background: The anti-PP1Pk antibody is a rare antibody associated with recurrent spontaneous abortion (RSA) in the first trimester. As it is a rare entity, few reports have been published, especially in China. Currently, there is no specific treatment for RSA associated with anti-PP1Pk antibody because it is a naturally occurring antibody. This study aims to report three cases of RSA associated with the anti-PP1Pk antibody to share our experiences with its management.

Methods: The three patients' medical information was obtained from the medical records. Intravenous immunoglobulin and/or plasmapheresis was offered to the patients. We also made an extension research of the related literature about RSA associated with anti-PP1Pk antibody.

Results: Although patients received intervention, the maternal anti-PP1Pk antibody titer remained stable and did not decrease. There were no live births. We summarized publications about pregnancy in women with anti-PP1Pk antibodies.

Conclusions: Early initiation of plasmapheresis in high-risk patients with anti-PP1Pk antibodies should be strongly considered.

pregnancy

anti-PP1Pk antibody

recurrent spontaneous abortion

intravenous immunoglobulin

plasmapheresis

Recurrent spontaneous abortion (RSA) is the natural loss of two or more consecutive pregnancies before 20–28 weeks gestation with the same sexual partner [1–3]. RSA occurs in about 1–2% of all childbearing-age couples [4]. The etiology of RSA is very complex, including genetic factors, anatomical factors, endocrine factors, infectious factors, immune factors, thrombus-prone factors, male factors, systemic diseases of pregnant women, environmental factors, and others [4].

Recent evidence shows that more than 60% of RSA is caused by immune disorders [5]. Maternal-fetal blood group incompatibility is an alloimmune abnormality, the first cause of fetal and neonatal anemia [6]. The PP1Pk blood group system, discovered in 1927, is an extremely rare blood group. The blood system is based on the presence of any of the three glycosphingolipid antigens (P, P1, and Pk) on the surface of erythrocytes. There are five phenotypes in the PP1Pk blood group system named P₁, P₂, P₁^k, P₂^k, and p, according to the presence of a combination of any three antigens [6].

An individual with a phenotype has none of all three P, P1, and Pk antigens. The P phenotype is autosomal recessive, inherited, and extremely rare, with an estimated worldwide prevalence of about 5.8 per 100,000 [7].

The P phenotype is closely associated with spontaneous abortion in the first trimester. Unlike neonatal anemia caused by other maternal-fetal blood group systems, in which antibodies are induced by contact with fetal erythrocytes, individuals with the p phenotype spontaneously produce anti-PP1Pk antibodies, mostly IgG antibodies, without contact with fetal erythrocytes [8]. Embryonic trophoblasts produce antigens as early as the 3rd week of pregnancy, while anti-PP1Pk antibodies in pregnant women with the P phenotype recognize these antigens and affect the trophoblast/placental function. The placenta has a high level of P antigen than fetal erythrocytes [9]; thus, the maternal anti-PP1Pk antibody may bind to these antigens affecting the placental function, finally leading to spontaneous abortion or stillbirth [10, 11]. The risk of miscarriage is related to anti-PP1Pk antibody titer and antibody type, especially IgG antibody [12].

Currently, there is no specific treatment for RSA-associated anti-PP1Pk antibody because it is naturally occurring. To date, only twenty-one cases have been reported worldwide, with none from China. Here we report three cases of RSA caused by the anti-PP1Pk antibody to share our experience of its management and provide a reference for Chinese clinicians.

Patients

This case series includes three patients with RSA-associated anti-PP1Pk antibodies admitted to the Reproductive Immunology Department of Shanghai First Maternity and Infant Hospital. The three patients' medical information was collected from the medical records. The study was approved by the Ethics Committee of Shanghai First Maternity and Infant Hospital (NO: KS22297).

Serological test and antibody titration

The anti-PP1Pk antibody was detected in Shanghai Blood Center. The antibody titer was assessed using series dilution methods.

Intervention

During each plasmapheresis, 1800ml of plasma was collected and replaced with 500ml of albumin and 750ml of normal saline.

Three patients were included.

Case presentation

Case 1

A 35-year-old woman who had lost all nine previous pregnancies was admitted to the ** Hospital in May 2016. The woman and her husband were married for the first time and had nine miscarried natural pregnancies between 2008 and 2014. No fetal heart activity was found in each pregnancy. She was the only child of her parents and reported no history of chronic disease, her parents’ marriage was not consanguineous and they reported no family history of MSA. Systematic etiological studies revealed that both she and her husband had normal chromosomes, and she had a normal uterus. She was negative for antinuclear antibodies and antiphospholipid antibodies. She had normal sex hormone levels, insulin, blood glucose, protein S, protein C, ATIII antigen activity, and homocysteine. She was positive for thyroid peroxidase antibody while negative for thyroglobulin antibody, with normal TSH. Our hospital’s blood bank found that the irregular antibody screening test was positive, and the blood sample was sent to the Shanghai Blood Center for further examination. She was anti-PP1Pk antibody IgG positive with a titer of 1:256.

In her 10th pregnancy, she was given oral dydrogesterone and folic acid in the first trimester, and the nuchal translucency (NT) was normal at 12 weeks gestation. The anti-PP1Pk antibody titer was still 1:256, and intravenous immunoglobulin (IVIG) was given at 20 g/day for five days from 12 to 12^+ 5 weeks of pregnancy. The anti-PP1Pk antibody titer remained at 1:256, and plasmapheresis was performed at 14 weeks of pregnancy. However, fetal growth ceased at 14^+ 5 weeks of pregnancy. The treatment procedure is shown in Table 1.

Table 1

Treatment procedure of the Case 1
Week of gestation	treatment	The titer of anti-PP1Pk antibody
8–11^+ 6	dydrogesterone and folic acid	NA
12–12^+ 5	IVIG 20 g/day for 5 days	1:256
14	Plasmapheresis: 1800ml of plasma was collected, and 500ml of albumin and 750ml of normal saline	1:256

Case 2

A 39-year-old woman with one biochemical pregnancy and three spontaneous miscarriages in the first trimester was referred to our department in December 2021. She did not use any drugs in the first three pregnancies. In the fourth pregnancy, she used low molecular weight heparin, aspirin, prednisone, and metformin. However, there was still no fetal heart activity at eight weeks, and the pregnancy was terminated. The woman and her husband were married for the first time. The patient had a normal regular menstrual pattern, a heterozygous gene mutation for citrin deficiency, and a heterozygous gene mutation for mucopolysaccharidosis. Her parents had a consanguineous marriage, and she had one brother and sister. Her sister gave birth to two healthy children, and her brother had one healthy child. Systematic etiological studies revealed that both she and her husband had normal chromosomes, and she had a normal uterus. She was negative for antinuclear and antiphospholipid antibodies and had normal sex hormone levels, blood glucose, protein S, protein C, ATIII antigen activity, and homocysteine. She was negative for thyroid peroxidase antibody and thyroglobulin antibody. Fasting insulin: 8.82 µIU/mL, insulin 0.5 h: 79.27 µIU/mL, insulin 1h: 95.54µIU/mL, insulin 2h: 123.99 µIU/mL, insulin 3h: 122.81 µIU/mL. The irregular antibody screening test was positive. Shanghai Blood Center confirmed she was anti-PP1Pk antibody positive with an IgG titer of 1:128.

The fifth pregnancy was accidental during the COVID-19 pandemic in April 2022, and she could not go to the hospital for treatment. She had a miscarriage again in the first trimester and denied another pregnancy.

Case 3

A 24-year-old woman who had one biochemical pregnancy and one spontaneous miscarriage in the first trimester was admitted to our department in December 2021. Her first pregnancy was a biochemical pregnancy, and the embryo stopped developing in the first trimester of the second pregnancy. The fetus had edema of the neck and back, and the embryo’s gene chip was normal. Both the patient and her husband were married for the first time. The patient had a normal regular menstrual pattern, one miscarriage, and no live birth. She denied a history of chronic diseases and a family history of RSA. Systematic etiological studies revealed that both she and her husband had normal chromosomes, and she had a normal uterus. She was negative for antinuclear and antiphospholipid antibodies. She had normal sex hormone levels, insulin, blood glucose, protein S, protein C, ATIII antigen activity, and homocysteine and was euthyroid. The irregular antibody screening test was positive. Shanghai Blood Center confirmed she was anti-PP1Pk antibody positive with an IgG titer of 1:32.

In the third pregnancy, plasmapheresis was performed thrice at 11 + weeks, 12^+ 1 weeks, and 13^+ 4 weeks gestation. The NT was normal. The anti-PP1Pk IgG antibody titer was 1:32 at 11^+ 4 weeks gestation. The anti-PP1Pk IgM and IgG antibody titers were 1:8 and 1:16 at 12^+ 1 weeks gestation, and 1:32 and 1:32 at 13^+ 3 weeks gestation, respectively. The fetal heart activity disappeared at 14^+ 3 weeks gestation.

In this study, we reported three cases of RSA associated with anti-PP1Pk antibody. Although we performed IVIG and plasma exchange for patients 1 and 3, the outcome was adverse.

The anti-PP1Pk antibody is found in the serum of individuals with the p phenotype, one reason for RSA in pregnancy. A previous study reported that the P antigen was higher in the placenta than in fetal erythrocytes [9]. Currently, there is no specific treatment for recurrent miscarriage associated with anti-PP1Pk antibody positivity at home and abroad. An extensive literature search was conducted to find references about pregnant women with the P phenotype. The literature search’s results are shown in Table 1. A total of 19 papers reported on 21 patients; four papers [13–16] were not published in English and were not included in Table 2. IVIG and plasmapheresis were the two most available strategies to manage it.

Table 2

Summary of publication about pregnant women with p phenotype
Article	Patient’s age	Country	Parents with consanguineous marriage	Previous miscarriages	Maternal serum anti-PP1Pk antibody titers	Management	Fetal outcome
Weiss 1975(Weiss et al., 1975)	39	Israel	NA	5	1:64	NA	Pregnancy loss
Levene 1977 (Levene et al., 1977)	32	Israel	NA	2	NA	NA	An infant with hemolytic disease was delivered
Biale 1982 (Biale and Dvilansky, 1982)	32	Israel	NA	NA	NA	NA	A male infant weighing 2500 was delivered at 36 weeks of gestation
Cantin, 1983(Cantin and Lyonnais, 1983)	NA	Canada	No	3	1:256	NA	NA
Shechter 1987 (Shechter et al., 1987)	36	Israel	NA	8	1:128	plasmapheresis	A male infant weighing 2500 was delivered at 36 weeks of gestation
Yoshida 1994(Yoshida et al., 1994)	35	Japan	NA	6	1:128	56 times of plasmapheresis during 7–34 gestational weeks	A male infant weighing 2554g was delivered at 34 weeks of gestation
Haentjens-verbeke1996(Haentjens-Verbeke et al., 1996)	20	France	NA	1	NA	3 times/week of plasmapheresis during 5–21 gestational weeks	First: A boy weighing 950g was delivered at 31 weeks of gestation Second: A boy weighing 820g was delivered at 29 + 2 weeks of gestation
Fernández-Jiménez 2001(Fernández-Jiménez et al., 2001)	28	Spain	NA	7	NA	63 times of plasmapheresis and IVIG per week during 8–36 gestational weeks	An infant weighing 3000g was delivered at 36 weeks of gestation
Taniguchi, 2003(Taniguchi et al., 2003)	31	Japan	NA	1	1:512	51 times of double filtration plasmapheresis during 5–35 gestational weeks	A healthy female infant weighing 1978g was delivered at the 36 + 1 week of gestation.
Colon 2004(Conlan, 2004)	25	Australia	NA	3	1:64	59 times of plasmapheresis during 6–36 gestational weeks	An infant was delivered at 37 weeks of gestation
Hanafusa 2006(Hanafusa et al., 2006)	36	Japan	NA	2	1:256	57 times of double filtration plasmapheresis during 7–36 gestational weeks	A female infant weighing 2496g was delivered at 37 + 3 weeks of gestation
Benidt 2010(Benidt et al., 2010)	21	USA	NA	0	1:16	Supportive	A female infant was delivered at 34 + 3 weeks of gestation
Mohd Azri 2014(Mohd Azri et al., 2014)	27	Malaysia	Yes	2	NA	oral dydrogesterone	An infant weighing 2860g was delivered at 37 weeks of gestation
Nascimento 2020 (Nascimento et al., 2020)	30	Portugal	NA	2	1:4 (1:128 in her second miscarriage)	Prednisolone and prophylactic LMWH	A female infant weighing 2445g was delivered at 37 weeks of gestation
Di Ciaccio 2021(Di Ciaccio et al., 2021) Case 1	22	Australia	NA	0	1:8	Aspirin	An infant weighing 3140g was delivered at 38 weeks of gestation
Di Ciaccio 2021(Di Ciaccio et al., 2021) Case 2	31	Australia	NA	2	First: 1:2 Second: 1:2	Aspirin	First: An infant weighing 2668g was delivered at 37 + 6 weeks of gestation Second: An infant weighing 2740g was delivered at 35 weeks of gestation
Di Ciaccio 2021(Di Ciaccio et al., 2021) Case 3	28	Australia	NA	0	1:4	None	An infant weighing 2248g was delivered at 36 + 6 weeks of gestation
Li Case 1	35	China	No	9	1:256	IVIG for five days and plasmapheresis	Failure at 14 + 5 weeks of gestation
Li Case 2	39	China	Yes	3	1:128	None	Failure
Li Case 3	24	China	No	1	1:32	plasmapheresis	Failure

IVIG can prevent hemolysis caused by maternal-fetal blood type incompatibility by reducing the maternal antibody level [30]. The possible mechanism may be as follows: avoidance of the rebound in antibody synthesis following immunoglobulin depletion; reduction of placental transfer of unnecessary antibodies by competing with placental Fc receptors; high-dose IVIG may saturate the FcRn receptor, which is a protective receptor against IgG catabolism; thus IVIG treatment may increase IgG catabolism [23]. However, IVIG treatment for anti-PP1Pk antibody positivity in pregnancy is not evidence-based [31]. Currently, successful pregnancies of RSA associated with anti-PP1PK antibody positivity are treated with plasmapheresis or plasmapheresis combined with IVIG, but not IVIG alone. Plasmapheresis can reduce the anti-PP1Pk antibody titer to prevent miscarriage. Trophoblast cells can express antigens in the first trimester, so plasmapheresis should be started at 5–7 weeks gestation to reduce the antibody titer to between 1:16 and 1:32 [22]. Plasmapheresis is usually performed using a centrifugal plasma separator for simple plasmapheresis, while some studies have found that double-filtration plasmapheresis is safer for pregnant women [26]. In Case 3, the anti-PP1Pk antibody titer was stable at 1:32 before and after pregnancy but dropped to 1:16 on the day after plasmapheresis at 12^+ 1 weeks gestation. Since the fetus had fetal neck and back edema in the second pregnancy, plasmapheresis should be performed in the first trimester.

However, medical limitations may make some patients ineligible for IVIG and plasmapheresis. Mohd Azri et al. [28] first reported that a 27-year-old Malaysian with 2 RSA associated with anti-PP1Pk antibody positivity was treated with oral dydrogesterone at 10 weeks gestation and delivered a healthy baby in her third pregnancy. However, the anti-PP1Pk titer was only 1:2 during her third pregnancy. Nascimento et al. [29] reported that a Portuguese woman with 2 RSA associated with anti-PP1PK antibody positivity received prednisolone and prophylactic LMWH and delivered a healthy baby at 37 weeks gestation. The antibody titer during pregnancy was maintained between 1:4 and 1:16, while the titer was 1:128 during her second pregnancy loss. Di Ciaccio et al. [6] reported four pregnancies in three patients with anti-PP1PK antibody positivity and all four cases delivered healthy babies with only supportive aspirin treatment. The antibody titers for the pregnancies were only 1:2 to 1:8. For patients with low anti-PP1Pk antibody titers, plasmapheresis may not be necessary.

In Case 1 in our case series, the patient had nine previous pregnancies without fetal heart activity. In this pregnancy, oral dydrogesterone was used once the pregnancy was confirmed. Because the anti-PP1Pk antibody titer was maintained at 1:256, IVIG was started at 12 weeks, and plasmapheresis was applied at 13 weeks. However, the fetus stopped developing at 14 weeks gestation. We suspected that plasmapheresis might have been offered too late. For high-risk patients with high antibody titers and many miscarriages, plasmapheresis should be started as soon as possible to reduce antibody titers once pregnancy is diagnosed. However, the therapy may fail in pregnant women whose antibody titers continue to increase or rebound [26].

Only homozygotes present the rare P phenotype, so family members of those with positive anti-P1Pk antibodies should be screened [32]. Moreover, individuals with the p phenotype are easily identified among the same generation, and a consanguineous marriage between parents will lead to a higher incidence of the p phenotype in their children. In the case of the above Malaysian, her parents’ marriagewas consanguineous, and her siblings were all rare p phenotypes [28]. In her case, although her parents’ marriage was consanguineous, both her brother and sister had completely normal childbearing. Because the serum of anti-PP1Pk antibody-positive individuals has agglutination reactions with the normal red blood cells of all-known blood types, it is difficult to obtain suitable blood products for individuals with this rare blood type [33]. Regular autologous blood donation and red blood cell freezing can be considered in this population for future use.

In conclusion, here we reported three cases of pregnancy with anti-PP1Pk antibody positivity. Although plasmapheresis was offered in two cases, the outcomes were adverse. For individuals with the p phenotype, their siblings should be screened, and their blood should regularly be preserved. Moreover, plasmapheresis should be started as soon as possible once pregnancy is confirmed.

RSA: recurrent spontaneous abortion

NT: nuchal translucency

IVIG: intravenous immunoglobulin

Ethics approval and consent to participate

This study was approved by the Institutional Ethics Committee (Shanghai First Maternity and Infant Hospital) (approval number/protocol number KS22297).

Consent for publication

This study is a retrospective study, and the data obtained are owned by the medical record itself, so no informed consent was signed.

Availability of data and materials

The data underlying this article will be shared on reasonable request to the corresponding author.

Competing interests

The authors have no conflicts of interest to declare.

Funding

This work was supported by Natural Science Foundation of Shanghai (No:23ZR1450100). The funders of the study had no role in the study design, data collection, data analysis, data interpretation, or writing of the manuscript.

Acknowledgments

We thank Medjaden Inc. for scientific editing of this manuscript.

Authors' contributions

Data curation, GHL, MYD, XJD and SPW; Methodology, QLD and SHB; Writing – original draft, GHLand MYD; Writing – review & editing, GHL, MYD, QLD and SHB. All authors read and approved the final manuscript.

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No competing interests reported.

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Recurrent miscarriage associated with rare anti-PP1Pk antibody: a case series and literature review

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