Aust NZ f Obstet Gynaecol 1998; 38: 4: 428

Hepatitis G Virus Infection Detected in a Woman with Intrahepatic Cholestasis of Pregnancy

Mark Morton” FRACP, Ming Qiao’5 MB, BS, PhD and Grace Chang” BSc(Hon) Women ’s and Children ’s Hospital4 and Infectious Diseases Laborutories, Institute of Medical and Veterinaly Science,’ Adelaide, South Australia

This is thought to be the first case report of intra- hepatic cholestasis of pregnancy in which hepatitis G virus has been detected.

Case report The patient was a 32-year-old woman who

presented in her first pregnancy with generalized pruritus at 32 weeks’ gestation. She had a past history of Graves disease which had been treated with radioactive iodine 3 years before. She subsequently became hypothyroid and was taking thyroxine 150 pg mane. She was taking no other medication. There was no past history of hepatitis, blood transfusion or intravenous drug use.

The patient had onset of generalized pruritus at 26 weeks’ gestation and was referred to the medical clinic at 32 weeks’ gestation. Examination did not reveal any signs of chronic liver disease and there was no jaundice. Biochemistry at 32 weeks’ gestation showed an ALT of 11 7U/L (N: 11-52), GGT of 40UL (N: 4-33), and serum bile acids of 40 pmol/L (N: 0-7). An ultrasound examination of the liver and biliary system was normal. Serological tests did not indicate recent infection with hepatitis A, B, and C, Epstein- Barr virus, or cytomegalovirus. Antimitochondrial and antismooth muscle antibodies were also negative.

GBV-C (hepatitis G) RNA by reverse transcrip- tion polymerase chain reaction (RT-PCR) was detected in the woman’s serum by using Abbott LCx GBV-C assay.

Glucose intolerance of pregnancy had been diagnosed at 30 weeks’ gestation by a 75 g oral glucose tolerance test, with a fasting blood glucose of 5.8 mmol/L and a 2-hour value of 10.4 mmol/L. Despite treatment with diet, blood glucose values were frequently above 7.0 mmol/L and she was commenced on insulin from 32 weeks’ gestation.

The patient was commenced on ursodeoxycholic acid 450 mg tds in an attempt to improve the cholestasis and relieve the pruritus. She was also

I . Senior Consultant Physician. 2. Virology Registrar. 3. Senior Medical Scientist.

Address for correspondence: Dr Mark Morton, FRACP, Women’s and Children’s Hospital, King William Road, North Adelaide, South Australia 5006

started on hydroxyzine 25 mg tds. There was initial improvement in the pruritus and after 4 days of treat- ment the ALT and GGT levels had returned to normal.

The cholestasis was controlled for 3 weeks but at 35 weeks’ gestation the pruritus worsened and liver function tests started to deteriorate. ALT rose to 135 U/L (N: 11-52), and serum bile acids rose from 16 pmol/L at 34 weeks’ gestation to I22 umol/L (N: 0-7) at 35 weeks’ gestation. In view of the worsening cholestasis induction of labour was performed at 36 weeks’ gestation. During the induction and subse- quent labour there was evidence of fetal distress so an emergency lower segment Caesarean section was performed. A live female infant, birth-weight 2,720 g was delivered with Apgar scores of 7 and 9. The infant’s cord blood was negative for hepatitis G RNA.

After delivery the ursodeoxycholic acid and hydroxyzine were ceased. The pruritus improved markedly in the first 24 hours after delivery and liver enzymes improved.

A liver biopsy was performed 14 days postpartum. This showed a very mild nonspecific hepatitis in keeping with a drug or viral aetiology. Numerous hepatocytes contained pseudoinclusions of glycogen which were attributed to the recent gestational diabetes. There was no evidence of chronic liver disease. GBV-C (hepatitis G) RNA by RT-PCR was also performed on the liver biopsy and was negative indicating that the hepatitis G virus was not present in the liver or else very few hepatocytes were infected.

Liver enzymes remained slightly elevated 2 weeks postpartum with a GGT of 8 8 U L (N: 4-33) and an ALT of 122 U/L (N: 1 1-52). The patient has remained well. The source of the patient’s hepatitis G virus infection remains unknown.

The infant was also followed up for evidence of hepatitis G virus infection. Although GBV-C RNA was not detected in the cord blood of the infant, a blood sample at 10 weeks of age was positive for GBV-C (hepatitis G) RNA by RT-PCR, suggesting mother to baby transmission of hepatitis G virus. However, the infant remains well.

MAKK MORTON ET AL 429

DISCUSSION There is much controversy regarding the hepatitis G

virus and whether it causes liver disease (1). There is very little information available regarding hepatitis G virus infection occurring in pregnancy. As in this case, mother to baby transmission of hepatitis G virus has been described (2). Moaven et a1 also found that the baby was negative for HGV RNA on cord blood at birth, but positive at 4 and 6 weeks of age.

Cholestasis of pregnancy is a condition of unknown aetiology but oestrogens and progesterone appear to be involved in its pathogenesis. There also appears to be an interplay between genetic and environmental factors (3) , and patients presenting with cholestasis in pregnancy should be investigated to exclude other causes of liver dysfunction. Hepatitis G virus infection occurs in 1% to 2% of blood donors (1) and cholestasis of pregnancy occurs in 0.2% to 12% of deliveries, depending on the population studied (4). Although we cannot exclude the possibility that the 2 conditions occurred by chance in the same individual, it is conceivable that the presence of hepatitis G virus in this patient predisposed her to developing symptoms of cholestasis when the hormonal changes of pregnancy occurred.

Furthermore, one report has suggested that hepatitis G virus may cause a cholestatic type of liver disease ( 5 ) . The possible role of hepatitis G virus infection in patients presenting with cholestasis of pregnancy warrants further study.

Acknowledgements Work carried out at the Women's and Children's

Hospital, Adelaide, South Australia. GBV-C (hepatitis G) RNA testing was carried out at the Infectious Diseases Laboratories, Institute of Medical and Veterinary Science, Adelaide, South Australia.

References 1. Miyakawa Y, Mayurni M. Hepatitis G virus - A true hepatitis

virus or an accidental tourist. N Engl J Med 1997; 336: 795-796. 2. Moaven LD, Tennakoon PS, Bowden DS, Locarnini SA. Mother-

to-baby transmission of hepatitis G virus. Med J Aust 1996; 165: 84-85.

3. Reyes H. Review: intrahepatic cholestasis. A puzzling disorder of pregnancy. J Gastro Hepat 1997; 12: 211-216.

4. Williamson C, Nelson-Piercy C. Liver disease in pregnancy. Br J Hosp Med 1997; 58: 213-216.

5 . Colombatto P, Randone A, Civitico G et al. Hepatitis G RNA in the serum of patients with elevated gamma glutamyl transpeptidase and alkaline phosphatase: a specific liver disease. J Viral Hep 1996; 3: 301-306.

Aust NZ J Obstet Gynaecol 1998; 38: 4: 429

Conservative Management of Placenta Praevia with a High Risk of Placenta Accreta

Simon J. Dunstone" DCH, FRCOG, FRACOG and Charles B. Leibowitz' MBBCh, FF RAD (D) SA, Mackay Base Hospital, Mackay, Queensland

EDITORIAL COMMENT We accepted this case f o r publication because, together with the 2 following papers concerning interstitial pregnancies, they form an interesting trilogy of case reports where the women were given methotrexate during pregnancy. We do not argue with the management of this patient because of the high risk of a morbidly adherent placenta and the formidable surgery that can be required when such a placenta is dislodged at Caesarean section. Although the authors did not make this comment, it seems to the editor that a normally implanted placenta would be likely to separate at Caesarean section even if it was not handled. The editor can recall a horrendous experience with a patient who had a placenta praevia percreta where the plan of leaving the placenta after classical Caesarean section had to be abandoned because of massive haemorrhage that occurred spontaneously after the

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1. Staff Specialist. 2. Clinical Senior Lecturer, The University of Queensland 3. Visiting Radiologist.

Address for correspondence: Dr Simon Dunstone, Mackay Base Hospital, PO Box 5580, Mackay Mail Centre, Queensland 4741.