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Obstetrics & Gynecology 2002;100:1196-1202
© 2002 by The American College of Obstetricians and Gynecologists
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ORIGINAL RESEARCH

The Recurrence Risk of Adverse Outcome in the Second Pregnancy in Women With Rheumatic Disease

Johan F. Skomsvoll, MD, Valborg Baste, MSc, Lorentz M. Irgens, MD, PhD and Monika Østensen, MD, PhD

From the Department of Rheumatology, Center for Mothers with Rheumatic Disease, University Hospital of Trondheim, Trondheim; and Medical Birth Registry of Norway, Locus of Registry Based Epidemiology, University of Bergen, Bergen, Norway.

Address reprint requests to: Johan F. Skomsvoll, MD, University Hospital of Trondheim, Center for Mothers With Rheumatic Disease, Department of Rheumatology, 7006 Trondheim, Norway; E-mail: johan.skomsvoll{at}medisin.ntnu.no.


   ABSTRACT
TOP
ABSTRACT
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
OBJECTIVE: To study recurrence risks of adverse pregnancy outcome in the second pregnancy in women with rheumatic disease.

METHODS: In a national population-based cohort study, women with rheumatic disease recorded from 1967 to 1995 in the Medical Birth Registry of Norway were compared with mothers without such diagnoses with regard to recurrence risks of adverse pregnancy outcomes in the second pregnancy. The odds ratios (ORs) of all outcomes were adjusted for maternal age, those of cesarean delivery for time period, and those of preeclampsia for interpregnancy interval.

RESULTS: Women with rheumatic disease and adverse pregnancy outcome in the first pregnancy had a statistically significant higher recurrence risk of the same event in the second pregnancy than women without rheumatic disease (preeclampsia: OR 2.22; 95% confidence interval [CI] 1.18, 4.19) (cesarean delivery: OR 1.52; 95% CI 1.05, 2.21) (preterm birth: OR 1.86; 95% CI 1.12, 3.11). In women with rheumatic disease diagnosed between the first and second births, a significantly increased recurrence risk of low birth weight occurred. Women with rheumatic disease also had a higher occurrence of markers for placental dysfunction (preeclampsia, preterm birth, or small for gestational age) in the second birth after any of these outcomes in the first birth (OR 1.35; 95% CI 1.02, 1.78) (35.1% versus 29.2%).

CONCLUSION: The recurrence risk of an adverse outcome in the second pregnancy is increased in any woman, but was even higher in women with a rheumatic disease. These patients should be counseled accordingly, be closely monitored during pregnancy, and have access to appropriate subspecialists.

Inflammatory and autoimmune disorders occur preferentially in women of fertile years. A large number of studies have reported an increased rate of fetal loss, preterm birth, and low birth weight in connective tissue diseases like systemic lupus erythematosus and systemic sclerosis.1–3 Even when pregnancies are planned, effectively treated, and closely monitored, an increased risk of adverse pregnancy outcome persists. The mechanisms are not clear, but placental lesions such as decidual vasculopathy, decidual or fetal thrombi, and extensive infarction truly contribute.4–8

Also, a subclinical disease process or the presence of autoantibodies may compromise placental function. Recently, we reported an increased risk of adverse pregnancy outcome not only in connective tissue diseases but also in inflammatory rheumatic diseases like rheumatoid arthritis.9,10 An extended MEDLINE search showed that recurrence of adverse outcomes like preeclampsia, preterm birth, and low birth weight has rarely been addressed in mothers with systemic lupus and other connective tissue diseases11,12 and is lacking for the inflammatory rheumatic diseases. Considerable evidence indicates that adverse pregnancy outcomes in general tend to recur from one pregnancy to the next. The purpose of this study was to analyze the recurrence risk of an adverse outcome in the second pregnancy of women with rheumatic disease. Because an increasing number of women wish to plan their pregnancies and this is felt more urgently when a chronic disease is present, the clarification of this issue has become increasingly important.


   MATERIALS AND METHODS
TOP
ABSTRACT
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Established in 1967, the Medical Birth Registry of Norway is based on compulsory notification of all births after 16 weeks’ gestation and comprises data relevant to the clarification of the epidemiology of health problems among pregnant women and infants.13 On a notification form unchanged in the period 1967–1995, data on demographic variables, pregnancy, delivery, and the newborn have been reported by the attending midwife and doctor and coded at the birth registry using the Classification of Diseases, 8th Revision.

We analyzed data for all single births in Norway from 1967 to 1995. Using the mother’s national identification number, all the births were linked into a sibship, which was the unit of analysis. Women with only one birth, sibships with multiple births, and sibships in which the first birth occurred before 1967 were excluded. Patients were defined as all women for whom onset of a rheumatic disease was noted before the first pregnancy (birth order one) (RD1; n = 1065) or after the first but before the second birth (birth order two) (RD2; n = 919). All women without a diagnosis of rheumatic disease formed the control group (n = 487,432).

Women with rheumatic disease (RD1 or RD2) fall into three subcategories according to Classification of Diseases, 8th Revision:

connective tissue diseases (Classification of Diseases, 8th Revision codes 734 and 716: systemic lupus, systemic sclerosis, Sjögren syndrome, polymyositis or dermatomyositis)

specified inflammatory arthritides (Classification of Diseases, 8th Revision code 712: rheumatoid arthritis, juvenile rheumatoid arthritis, ankylosing spondylitis)

nonspecified inflammatory arthritides (Classification of Diseases, 8th Revision code 715)

The present study is based on data on maternal health before and during pregnancy, birth order, maternal age, preeclampsia, preterm birth, induction, cesarean delivery, low birth weight (less than 2500 g), and small for gestational age. In a previous study of women with rheumatic disease, we found a higher perinatal and postperinatal mortality than in references.9 The numbers of perinatal and postperinatal loss were too small to assess recurrence risk.

Preterm birth was defined as gestation of less than 37 weeks. Induction of labor included any method notified as induction (eg, amniotomy, oxytocin, prostaglandin). Cesarean delivery comprised both emergency and elective. Smallness for gestational age was defined as birth weight less than the tenth percentile for the actual gestational age. Low birth weight was defined as less than 2500 g.

To assess the recurrence risk of adverse outcome among women with rheumatic disease, the women were categorized into six groups according to whether the diagnosis was made before the first birth (RD1) or before the second birth (RD2) or if there was no diagnosis (controls), and whether the first pregnancy outcome was normal or adverse. The occurrence of adverse outcome in the second pregnancy in these six groups was compared by logistic regression analysis. Odds ratios (ORs) were adjusted for maternal age (younger than 19 years, 20–24, 25–29, 30–34, 35–39, and 40 or older) at second birth. Because of secular trends in cesarean delivery and induction of birth, the ORs were also adjusted for time period (1967–1976, 1977–1986, 1987–1995). Because an increased interpregnancy interval, as observed in women with rheumatic disease,14 is associated with a higher risk of preeclampsia,15 ORs were also adjusted for interpregnancy interval. We compared the recurrence rates in mothers with rheumatic disease with rates among mothers without rheumatic disease and with no adverse outcome in the first pregnancy (Tables 1Go–6Go). Furthermore, we attempted to assess the excessive risk attributable to rheumatic disease by comparing with women without rheumatic disease and with an adverse outcome in the first pregnancy (Table 7Go). The analyses were performed by SPSS for Windows 10.05 (SPSS Inc., Chicago, IL). The present study was approved by a regional ethical committee.


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  		Table 1. The Risk of Preeclampsia in Second Pregnancy by Preeclampsia Status in First Pregnancy in Women With Rheumatic Disease and in Controls, Medical Birth Registry of Norway, 1967–1995
 

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  		Table 6. The Risk of any Adverse Outcome* in Second Pregnancy by Any Adverse Outcome in First Pregnancy in Women With Rheumatic Disease and Controls, Medical Birth Registry of Norway, 1967–1995
 

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  		Table 7. The Recurrence Risks of Adverse Outcomes in Second Pregnancy Among Mothers With Rheumatic Disease Diagnosed Before First Birth and Second Birth, Respectively, Compared With Recurrence Risks Among Mothers Without any Rheumatic Disease, Medical Birth Registry of Norway, 1967–1995
 

   RESULTS
TOP
ABSTRACT
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
In this study we included mainly women with specified inflammatory arthritides, which represented 85.3% of all women with a rheumatic disease and with a diagnosis before first birth and 82.5% with a diagnosis before second birth (Table 8Go). Women with connective tissue disease represented only 5.4% (before first birth) and 7.8% (before second birth) of all women with rheumatic disease included in this study.


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  		Table 8. Proportions of Women With Rheumatic Disease Classified in a Diagnostic Group and by Time of Diagnosis, Medical Birth Registry of Norway, 1967–1995
 
In women whose first pregnancy was complicated by preeclampsia, the recurrence risk in women diagnosed before first birth (RD1) was significantly increased relative to women without rheumatic disease (25.9% versus 13.9%) (Table 1Go) (OR 2.22; 95% confidence interval [CI] 1.18, 4.19) (Table 7Go).

In women whose first pregnancy was complicated by low birth weight, the recurrence risk in women diagnosed before the second birth (RD2) was significantly increased relative to controls (29.5% versus 15.9%) (Table 2Go) (OR 2.22; 95% CI 1.16, 4.26) (Table 7Go). Although no significant increased recurrence risk of low birth weight was found in RD1 relative to controls who had low birth weight in their first pregnancy, the OR was 1.71 and close to significant (95% CI 0.99, 2.96) (Table 7Go) (23.9% versus 15.9%) (Table 2Go).


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  		Table 2. The Risk of Low Birth Weight (<2500 g) in Second Pregnancy by Low Birth Weight Status in First Pregnancy in Women with Rheumatic Disease and in Controls, Medical Birth Registry of Norway, 1967–1995
 
The recurrence risk in RD1 was significantly higher in women whose first pregnancy was complicated by preterm birth than in controls (26.0% versus 15.7%) (Table 3Go) (OR 1.86; 95% CI 1.12, 3.11) (Table 7Go).


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  		Table 3. The Risk of Preterm Birth in Second Pregnancy by Preterm Birth Status in First Pregnancy in Women With Rheumatic Disease and in Controls, Medical Birth Registry of Norway, 1967–1995
 
In women who had a cesarean delivery in the first pregnancy, the recurrence risks in RD1 and RD2 were similar to and higher than the recurrence risk in controls who had cesarean delivery in the first pregnancy (RD1: 61.2% versus 48.1%; OR 1.52; 95% CI 1.05, 2.21) (RD2: 59.2% versus 48.1%; OR 1.47; 95% CI 0.99, 2.19) (Tables 5Go and 7Go).


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  		Table 5. The Risk of Cesarean Delivery in Second Pregnancy by Cesarean Delivery Status in First Pregnancy in Women With Rheumatic Disease and in Controls, Medical Birth Registry of Norway, 1967–1995
 
The occurrence of preeclampsia, preterm birth, or small for gestational age (placental dysfunction syndrome) in the second birth after any of these conditions in the first birth was significantly higher in RD1 than in controls (35.1% versus 29.2%) (Table 6Go) (OR 1.35; 95% CI 1.02, 1.78) (Table 7Go).


   DISCUSSION
TOP
ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The two main findings in this nationwide population-based study that included all mothers in Norway during a period of almost 30 years were that previous adverse outcomes were predictors of subsequent adverse pregnancy outcomes and that rheumatic disease increased the risk of recurrence up to two-fold and independently of the time of diagnosis (before first or second birth).

The validity of diagnosis may be a concern. However, 0.5% of all mothers had a rheumatic disease (specified inflammatory arthritides [0.43%] and connective tissue disease [0.035%]), which fits with the prevalence rates of rheumatic diseases among fertile women in other Scandinavian studies.16 Furthermore, the validity of a diagnosis of rheumatic disease in the Medical Birth Registry of Norway was assessed in comparison with a "gold standard" comprising clinically verified diagnoses.16 In that study, 88.2% of all mothers diagnosed as patients with rheumatic disease were represented with a corresponding diagnosis in the registry, and in 97.3% of the cases the diagnoses were correct with respect to type.

Mothers may underreport rheumatic disease, particularly women without adverse pregnancy outcome, causing inflated ORs. However, such a recall bias would probably not apply to any extent because the data on maternal disease are registered before the birth. Furthermore, the high ascertainment of rheumatic disease in the registry is not compatible with such a recall bias.16

We had no information on smoking or drug therapy during pregnancy. Our results could be biased if women with rheumatic disease were more or less likely to smoke than the control group. There is no evidence to suppose different smoking habits during pregnancy.3,17 Active rheumatic disease is an indication for drug therapy and indeed is associated with lower birth weight.18 However, to perform a controlled study to delineate effects of treatment from disease would raise important ethical issues.

Possible socioeconomic differences between case subjects and controls are of minor concern in the Norwegian population, which comprises approximately 95% whites and is socioeconomically rather homogeneous.14 There are no indications that the rheumatic diseases are more prevalent in lower socioeconomic groups.19 The Norwegian health and social security system covers all citizens and provides free antenatal and obstetric care to all inhabitants.

Our study confirmed the recurrence risk of preeclampsia and preterm birth in an obstetric population.20,21 This risk was nearly doubled in women with rheumatic disease. In another population-based study, previous low birth weight was associated with an increased risk of preeclampsia.22 One study found that the risk of a small for gestational age (SGA) child was dramatically higher in women with recurrent preeclampsia.23 Possibly a shared etiological mechanism could account for fetal growth restriction in the first pregnancy and preeclampsia in the next. Similar placental pathology has been documented in pregnancies with idiopathic fetal growth restriction, preeclampsia, and idiopathic preterm labor,24,25 and a placental dysfunction syndrome has been proposed.26 Outcomes related to placental dysfunction were more frequent in women with rheumatic disease in the second birth after any of these outcomes in the first birth. Our data suggest that autoimmune mechanisms may be involved.4,27,28

Conditions associated with preterm birth are preeclampsia, premature rupture of membranes, intrauterine infections, and previous preterm birth.29–31 Additional factors contribute in rheumatic disease like vasculopathy, active disease, and immunosuppressive treatment including high doses of corticosteroids.4–6,32,33 Several of these factors persist throughout the reproductive life span of a patient and can negatively affect fetal growth, resulting in an SGA child or low birth weight.1–3,9,34 The fact that rheumatic disease did not increase the risk of a second SGA infant but had an impact on low birth weight may partly relate to the higher frequency of induction and cesarean delivery in our study. Cesarean delivery is associated with the risk of repeated surgical delivery in subsequent pregnancies,35 relating to pregnancy complications or sometimes preferences of the patients and their obstetricians.

Adverse pregnancy outcome9 and recurrent pregnancy complications are increased in women with rheumatic disease, particularly those with connective tissue disease. As a consequence, we have established an interdisciplinary pregnancy clinic for women with rheumatic disease where patients are monitored and treated according to the risk calculated from individual disease characteristics and previous pregnancy experience. Counseling before a planned pregnancy by specialists of internal medicine and obstetrics is always offered, as well as monitoring of placental function and fetal surveillance by a specialist of fetal medicine in case of any known risks.


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  		Table 4. The Risk of Small for Gestational Age in Second Pregnancy by Small for Gestational Age Status in First Pregnancy in Women With Rheumatic Disease and in Controls, Medical Birth Registry of Norway, 1967–1995
 

   Footnotes
 
This study has been supported in part by the Norwegian Women’s Public Health Association, Norwegian Foundation for Health and Rehabilitation, and Norwegian Society for Rheumatology.

The authors thank Dr. John M. D. Thompson, Department of Paediatrics, University of Auckland, for valuable comments on the manuscript.

PII S0029-7844(02)02340-2

Received November 5, 2001. Received in revised form June 5, 2002. Accepted June 27, 2002.


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ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
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2. Julkunen H, Jouhikainen T, Kaaja R, Leirisal-Repo M, Stephansson E, Palusuo T. Fetal outcome in lupus pregnancy: A retrospective case-control study of 242 pregnancies in 112 patients. Lupus 1993;2:125–31.[Abstract/Free Full Text]

3. Steen VD, Medsger TA. Fertility and pregnancy outcome in women with systemic sclerosis. Arthritis Rheum 1999; 42:763–8.[Medline]

4. Stone S, Khamashta MA, Poston L. Placentation, antiphospholipid syndrome and pregnancy outcome. Lupus 2001;10:67–74.[Abstract/Free Full Text]

5. Salafia CM. Parke AL. Placental pathology in systemic lupus erythematosus and phospholipid antibody syndrome. Rheum Dis Clin North Am 1997;23:85–97.[Medline]

6. Magid MS, Kaplan C, Sammaritano LR, Peterson M, Druzin ML, Lockshin MD. Placental pathology in systemic lupus erythematosus: A prospective study. Am J Obstet Gynecol 1998;179:226–34.[Medline]

7. Ogishima D, Matsumoto T, Nakumura Y, Yoshida K, Kuwabara Y. Placental pathology in systemic lupus erythematosus with antiphospholipid antibodies. Pathol Int 2000;50:224–9.[Medline]

8. Abromovsky CR, Vegas ME, Swinehart G, Gyves MT. Decidual vasculopathy in lupus erythematosus. N Engl J Med 1980;303:668–72.[Medline]

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10. Skomsvoll JF, Østensen M, Irgens LM, Baste V. Pregnancy complications and delivery practice in women with connective tissue disease and inflammatory rheumatic disease in Norway. Acta Obstet Gynecol Scand 2000;79: 490–5.[Medline]

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12. Le Thi Huong D, Wechsler B, Vauthier-Brouzes D, See-bacher J, Lefebvre G, Bletry O, et al. Outcome of planned pregnancies in systemic lupus erythematosus: A prospective study on 62 pregnancies. Br J Rheumatol 1997;36: 772–7.[Abstract/Free Full Text]

13. Irgens LM. The Medical Birth Registry of Norway, epidemiological research and surveillance through 30 years.Acta Obstet Gynecol Scand 2000;79:435–9.[Medline]

14. Skomsvoll JF, Østensen M, Baste V. Number of births, interpregnancy interval, and subsequent pregnancy rate after a diagnosis of inflammatory rheumatic disease in Norwegian women. J Rheumatol 2001;28:2310–4.[Medline]

15. Skjærven R, Wilcox AJ, Lie RT. The interval between pregnancies and the risk of preeclampsia. N Engl J Med 2002;346:33–8.[Abstract/Free Full Text]

16. Skomsvoll JF, Østensen M, Baste V, Irgens LM. Validity of a diagnosis of rheumatic disease in the Medical Birth Registry of Norway. Acta Obstet Gynecol Scand 2002;81: 831–4.[Medline]

17. Pope JE, Bellamy N, Stevens A. The lack of associations between rheumatoid arthritis and both nulliparity and infertility. Semin Arthritis Rheum 1999;28:342–50.[Medline]

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19. Brekke M, Hjortdahl P, Thelle DS, Celius EG, Heldal E, Joner G. Differences in morbidity between the Eastern central city district and the suburban Western district of Oslo. Tidsskr Nor Laegeforen 1998;118:14–7.[Medline]

20. Odegard RA, Vatten LJ, Nilsen ST, Salvesen KA, Austgulen R. Risk factors and clinical manifestation of preeclampsia. BJOG 2000;107:1410–6.[Medline]

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22. Rasmussen S, Irgens LM, Albrechtsen S, Dalaker K. Predicting preeclampsia in the second pregnancy from low birth weight in the first pregnancy. Obstet Gynecol 2000; 96:696–700.[Abstract/Free Full Text]

23. Odegard RA, Vatten LJ, Nilsen ST, Salvesen KA, Austgulen R. Preeclampsia and fetal growth. Obstet Gynecol 2000;96:950–5.[Abstract/Free Full Text]

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