It may be helpful to have this page or the booklet to hand to show them. Bile passes from the liver cells via small ducts to the common bile duct and on into the duodenum part of your gut. It plays a central role in helping the body digest fat. It acts as a detergent, breaking the fat into very small droplets so that it can be absorbed from food in your gut.
It also makes it possible for your body to take up the fat-soluble vitamins A, D, E and K from the food passing through the gut. We do not yet know what causes the restriction of the flow of bile from the liver in ICP. Evidence suggests that it is caused by a combination of hormonal, genetic and environmental factors. All hormones are metabolised broken down in the liver. One theory is that the liver cannot cope with the high levels of hormones during pregnancy oestrogen and progesterone.
This is supported by observations that:. ICP also has a genetic cause. This means it has been linked to genetic changes making some women more susceptible to the disease. This can also explain cases where ICP occurs within families and why it is more common in some ethnic groups.
Although ICP affects one in 0. In other places, such as South America and Scandinavia, the number of women affected is higher still. However these genetic changes do not explain all the causes of the disorder and other factors such as diet and hormones may play a part.
Further research is being carried out to investigate these areas. Itching is often the only symptom of ICP. The itching typically begins on the arms, legs, hands and soles of the feet.
It may also occur on other parts of the body such as the face, back and breasts. It is usually worse at night, leading to sleeplessness and exhaustion. Some women scratch themselves so frantically that they make themselves bleed. A few lose their appetite and feel generally unwell. A number of women thought to be around one in ten will develop jaundice in pregnancy. However, most women with ICP do not have jaundice. Chronic hepatitis B or C infections may be transmitted to neonates; however, hepatitis B virus transmission is effectively prevented with perinatal hepatitis B vaccination and prophylaxis with hepatitis B immune globulin.
Cholelithiasis occurs in 6 percent of pregnancies; complications can safely be treated with surgery. Women with chronic liver disease or cirrhosis exhibit a higher risk of fetal loss during pregnancy. Preeclampsia is associated with HELLP hemolysis, elevated liver enzymes and low platelet count syndrome, acute fatty liver of pregnancy, and hepatic infarction and rupture. These rare diseases result in increased maternal and fetal mortality.
Treatment involves prompt delivery, whereupon the liver disease quickly reverses. Therapy with penicillamine, trientine, prednisone or azathioprine can be safely continued during pregnancy.
Isolated hepatic disease rarely occurs during pregnancy. A number of associations between hepatic dysfunction and pregnancy exist. This review discusses these relationships in the context of obstetric management. The liver serves multiple functions: the biotransformation of insoluble compounds e. No single liver function test is available to quantify liver disease.
Cholestasis and biliary obstruction are evaluated by measuring alkaline phosphatase, bilirubin, 5'-nucleotidase or gamma glutamyl transpeptidase levels 1 Figure 1. In normal pregnancies, alkaline phosphatase levels may be elevated three- to fourfold, secondary to placental alkaline phosphatase levels.
Elevations of ALT occurring during pregnancy can be evaluated using a diagnostic algorithm Figure 2.
Elevated ALT is frequently the result of viral hepatitis, which can be easily diagnosed using serologic tests. Other possible etiologies of mild or moderate elevations of ALT are drug-induced hepatotoxicity, hyperemesis gravidarum, cholelithiasis, HELLP hemolysis, elevated liver enzymes and low platelet count syndrome or acute fatty liver of pregnancy.
Algorithm for the evaluation of alanine aminotransferase elevation during pregnancy. Viral hepatitis is the most common cause of jaundice in pregnancy. Hepatitis E is a waterborne virus spread through fecal-oral transmission. Infection occurs most commonly in developing countries after flooding. Pregnant women with hepatitis E infection exhibit markedly increased fatality rates 10 to 20 percent.
Disseminated HSV infection is associated with prodromal systemic illness, vesicular skin rash and leukopenia. Acyclovir Zovirax effectively treats early disseminated HSV infection. Infants of HBsAg-positive mothers should receive hepatitis B immune globulin immunoprophylaxis at birth and hepatitis B vaccine at one week, one month and six months after birth. In cases of acute hepatitis B virus infection complicating pregnancy, the prevalence of neonatal infection depends on the time during gestation that maternal infection occurs.
The infection occurs in 6 percent of neonates of women infected in the second trimester, in 67 percent of those infected in the third trimester and in virtually all of those infected in the immediate postpartum period. Chronic hepatitis C virus infection affects 1.
Therefore, an increasing number of patients with hepatitis C virus infection are requesting information about vertical transmission of the virus during pregnancy. Patients with risk factors for hepatitis C virus infection, such as intravenous drug use or other parenteral exposures, should undergo screening for hepatitis C virus infection before pregnancy with second- or third-generation hepatitis C virus antibody assays to confirm exposure to the virus.
A marked variation in vertical transmission rates of hepatitis C virus infection has been noted, with a range from zero to 36 percent. In patients who are HIV negative with ongoing intravenous drug abuse or blood transfusions during pregnancy, a 23 percent hepatitis C virus vertical transmission rate has been reported.
Vertical transmission of the virus has been reported to occur in two of three infants of mothers with acute hepatitis C virus infection, suggesting a higher risk of vertical transmission than occurs in patients with chronic infection, secondary to the high levels of hepatitis C virus RNA that occur in acute infection. Cholelithiasis is noted in as many as 6 percent of pregnant women. Symptoms of cholelithiasis are similiar in pregnant and nonpregnant patients.
The alkaline phosphatase level progressively increases during normal pregnancy and is unhelpful in distinguishing hepatobiliary disease. A liver ultrasound examination is most helpful in determining the presence of cholelithiasis or sludge in symptomatic patients. Surgical treatment i. A retrospective review 17 of 19, pregnancies revealed that 11 percent of surgical emergencies were attributable to biliary tract disease.
Choledocholithiasis accounts for approximately 7 percent of patients with jaundice in pregnancy. One group of investigators 17 reported safely performing endoscopic retrograde cholangiopancreatography and endoscopic retrograde sphincterotomy without complications in five pregnant women in the second and third trimesters with choledocholithiasis using minimal fluoroscopy and lead aprons to shield the abdomen.
All of the women delivered healthy babies at term. Intrahepatic cholestasis of pregnancy occurs in 0. It typically arises in the third trimester of pregnancy, although it has been reported as early as 13 weeks' gestation. Liver histopathology reveals centrilobular bile stasis. A clear racial and genetic predisposition for this disorder has been described. Intrahepatic cholestasis complicates 0. Multiple medications have been tried as treatments for cholestasis of pregnancy.
Ursodeoxycholic acid Actigall , given at dosages of 15 mg per kg per day, has been the most successful therapy for cholestasis of pregnancy, as it ameliorates both the pruritus and liver function abnormalities and is well-tolerated by both mother and fetus.
Studies in rats, mice and rabbits have revealed no teratogenicity or other negative effects on the developing fetus. Studies in humans examining the use of ursodeoxycholic acid in pregnancy have been uncontrolled and limited by small patient numbers. However, in pregnant patients with cholestatic liver disease, the pruritus can be severely disabling, and ursodeoxycholic acid therapy provides safe and effective relief.
Cholestyramine Questran binds bile acids and may improve pruritus; however, it may exacerbate steatorrhea and does not alter liver function or fetal prognosis. Patients exhibiting cholestasis of pregnancy should receive close fetal surveillance at delivery. Elevated serum bilirubin and alkaline phosphatase levels return to normal four to six weeks after delivery.
Hepatic dysfunction with preeclampsia has long been recognized. This syndrome may complicate the course in 3 to 10 percent of patients with preeclampsia and is noted in 0. Liver biopsy reveals periportal hemorrhage and fibrin deposition. The maternal mortality rate is 2 percent, and the perinatal mortality rate is 33 percent. Following delivery, laboratory abnormalities peak in the first one to two days postpartum and return to normal within three to 11 days.
Proper interpretation of liver function tests LFTs at an early stage can lead to timely management and may reduce complications in both mother and fetus. Normal LFTs do not always mean that the liver is normal. A number of pitfalls can be encountered in the interpretation of basic blood LFTs. The commonly used LFTs primarily assess liver injury rather than hepatic function.
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