What Hepatic Changes Are Considered Normal During Pregnancy?
Liver Affliction in Pregnancy
Am Fam Md. 1999 Feb 15;59(iv):829-836.
Commodity Sections
- Abstract
- Pregnancy and Hepatitis
- Cholelithiasis in Pregnancy
- Pregnancy-Specific Liver Disease
- References
Acute viral hepatitis is the well-nigh mutual cause of jaundice in pregnancy. The grade of acute hepatitis is unaffected past pregnancy, except in patients with hepatitis East and disseminated herpes simplex infections, in which maternal and fetal mortality rates are significantly increased. Chronic hepatitis B or C infections may be transmitted to neonates; still, hepatitis B virus transmission is effectively prevented with perinatal hepatitis B vaccination and prophylaxis with hepatitis B immune globulin. Cholelithiasis occurs in 6 per centum of pregnancies; complications can safely be treated with surgery. Women with chronic liver illness or cirrhosis showroom a higher risk of fetal loss during pregnancy. Preeclampsia is associated with HELLP (hemolysis, elevated liver enzymes and low platelet count) syndrome, astute fatty liver of pregnancy, and hepatic infarction and rupture. These rare diseases upshot in increased maternal and fetal bloodshed. Treatment involves prompt commitment, whereupon the liver disease quickly reverses. Therapy with penicillamine, trientine, prednisone or azathioprine tin can be safely continued during pregnancy.
Isolated hepatic disease rarely occurs during pregnancy. A number of associations betwixt hepatic dysfunction and pregnancy be. This review discusses these relationships in the context of obstetric management.
The liver serves multiple functions: the biotransformation of insoluble compounds (e.g., drugs, toxins, bilirubin), the metabolism and excretion of cholesterol and bilirubin, the production of plasma proteins (due east.thousand., albumin, coagulation factors, alpha- and beta-globulins, transferrin, haptoglobin), and the metabolism of amino acids, carbohydrates and lipids.
No single liver office examination is available to quantify liver disease. The designation "liver part tests" describes a panel of laboratory tests profiling discrete aspects of liver function.1 Liver cell injury or necrosis is measured by determining aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, while liver synthetic part (depressed in cirrhosis or severe acute liver disease) is quantified past determining albumin level and prothrombin time. Cholestasis and biliary obstruction are evaluated by measuring alkaline phosphatase, bilirubin, five'-nucleotidase or gamma glutamyl transpeptidase levels1 (Figure 1). In normal pregnancies, alkaline phosphatase levels may exist elevated 3- to fourfold, secondary to placental element of group i phosphatase levels.2–5
Cholestasis During Pregnancy
Figure 1.
Evaluation of cholestasis during pregnancy. (RUQ = right upper quadrant)
Elevations of ALT occurring during pregnancy can be evaluated using a diagnostic algorithm (Effigy 2). Elevated ALT is frequently the result of viral hepatitis, which can exist easily diagnosed using serologic tests. Other possible etiologies of balmy or moderate elevations of ALT are drug-induced hepatotoxicity, hyperemesis gravidarum, cholelithiasis, HELLP (hemolysis, elevated liver enzymes and low platelet count) syndrome or astute fatty liver of pregnancy.
Alanine Aminotransferase Elevation During Pregnancy
Figure 2.
Algorithm for the evaluation of alanine aminotransferase acme during pregnancy. (HBsAg = hepatitis B surface antigen; ALT = alanine aminotransferase; RUQ = right upper quadrant; DIC = disseminated intravascular coagulopathy; HELLP = hemolysis, elevated liver enzymes, low platelets)
Pregnancy and Hepatitis
- Abstract
- Pregnancy and Hepatitis
- Cholelithiasis in Pregnancy
- Pregnancy-Specific Liver Affliction
- References
Acute VIRAL HEPATITIS
Viral hepatitis is the nigh common cause of jaundice in pregnancy.4 The course of most viral hepatitis infections (due east.thou., hepatitis A, B, C and D) is unaltered by pregnancy.6,7 However, a more severe course of viral hepatitis in pregnancy has been noted in patients with hepatitis E and disseminated herpes simplex virus (HSV) infections.2,6,8–11
Hepatitis E is a waterborne virus spread through fecal-oral transmission. Infection occurs near commonly in developing countries later flooding. Pregnant women with hepatitis East infection showroom markedly increased fatality rates (10 to 20 pct).6,eight,9
Disseminated HSV infection is associated with prodromal systemic disease, vesicular pare rash and leukopenia.10,11 Maternal and fetal mortality rates achieve 50 per centum without treatment. Acyclovir (Zovirax) effectively treats early disseminated HSV infection.11
HEPATITIS B VIRUS
In the United States, 15,000 pregnant women who are hepatitis B surface antigen (HBsAg)-positive deliver annually.6 Universal screening of pregnant women for HBsAg is now performed to reduce perinatal transmission of hepatitis B virus.three The risk of hepatitis B virus transmission to the fetus is proportional to maternal hepatitis B virus Deoxyribonucleic acid, as reflected in hepatitis B antigen (HBeAg) and antibody (HBeAb) status.3 The risk of hepatitis B virus vertical transmission is x per centum in mothers with negative HBeAg and positive HBeAb and 90 percent in those with positive HBeAg.3,6 The risk of chronic hepatitis B virus infection in a neonate who does not receive immunoprophylaxis and vaccination for hepatitis B virus is 40 percent.3
Infants of HBsAg-positive mothers should receive hepatitis B allowed globulin immunoprophylaxis at birth and hepatitis B vaccine at one calendar week, ane calendar month and six months after nascence.3,6 This regimen reduces the incidence of hepatitis B virus vertical transmission to zero to iii percent.six
In cases of astute hepatitis B virus infection complicating pregnancy, the prevalence of neonatal infection depends on the time during gestation that maternal infection occurs.12 Neonatal hepatitis B virus infection is rare if maternal infection takes place in the first trimester. The infection occurs in 6 percent of neonates of women infected in the second trimester, in 67 pct of those infected in the third trimester and in virtually all of those infected in the immediate postpartum period.12 Neonates of mothers experiencing acute hepatitis B virus infection should receive immunoprophylaxis and vaccination, as outlined above.
HEPATITIS C VIRUS
Chronic hepatitis C virus infection affects 1.four percent of the U.Southward. population.13 The incidence of hepatitis C virus infection is rise most rapidly amid persons twenty to 45 years of age. Therefore, an increasing number of patients with hepatitis C virus infection are requesting information virtually vertical transmission of the virus during pregnancy.13
Patients with take a chance factors for hepatitis C virus infection, such equally intravenous drug utilize or other parenteral exposures, should undergo screening for hepatitis C virus infection earlier pregnancy with second- or third-generation hepatitis C virus antibody assays to confirm exposure to the virus.12 Women with documented hepatitis C virus infection who are contemplating pregnancy should be encouraged to undergo human immunodeficiency virus (HIV) testing and repeated quantitative hepatitis C virus RNA measurements to determine their likely risk of hepatitis C virus vertical manual.
A marked variation in vertical manual rates of hepatitis C virus infection has been noted, with a range from zero to 36 per centum.xiv Vertical transmission is strongly supported by the finding of identical hepatitis C virus subtypes in mothers and infants infected with hepatitis C virus.xiv In hepatitis C virus–positive, HIV–negative mothers without a history of active intravenous drug use or transfusion exposure, the risk of hepatitis C virus vertical manual is zero to 18 pct.14 Perinatal transmission of hepatitis C virus is greatest in patients with hepatitis C virus RNA titers greater than i million copies per mL; mothers who did not accept hepatitis C virus RNA did not transmit hepatitis C virus infection to their neonates.xiv
In patients who are HIV negative with ongoing intravenous drug corruption (or blood transfusions) during pregnancy, a 23 percent hepatitis C virus vertical transmission charge per unit has been reported.14 The highest reported rate of vertical transmission in this grouping occurs in infants born to hepatitis C virus–positive, HIV–positive mothers, with transmission rates of 6 to 36 percent.fourteen
No therapy has been shown to influence neonatal transmission of hepatitis C virus.
Vertical transmission of the virus has been reported to occur in ii of iii 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.14 Interferon therapy should not exist administered during pregnancy because of its possible adverse effects on the fetus.fifteen
Cholelithiasis in Pregnancy
- Abstruse
- Pregnancy and Hepatitis
- Cholelithiasis in Pregnancy
- Pregnancy-Specific Liver Disease
- References
Cholelithiasis is noted in every bit many as 6 percent of pregnant women.4,16 Pregnancy-induced changes in bile composition predispose these patients to cholelithiasis.15,17 The bile salt pool decreases in the second trimester, and biliary cholesterol levels may increase, resulting in lithogenic bile.15 In addition, gallbladder emptying slows in the second trimester, increasing the risk of cholelithiasis.
Symptoms of cholelithiasis are similiar in pregnant and nonpregnant patients.xv Patients with cholecystitis typically present with laboratory abnormalities, including leukocytosis and mild to moderate elevations of transaminase and bilirubin levels. 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.fifteen
Surgical handling (i.eastward., laparoscopic cholecystectomy) of biliary colic can exist safely accomplished in the beginning or 2d trimester.four Every bit the uterus enlarges, surgery becomes more than hard and should be avoided during the third trimester.15
A retrospective review17 of 19,000 pregnancies revealed that 11 pct of surgical emergencies were attributable to biliary tract disease. Choledocholithiasis accounts for approximately 7 percent of patients with jaundice in pregnancy.17 Of patients presenting with pancreatitis during pregnancy, xc percent have choledocholithiasis.17 Gallstone pancreatitis is associated with a 15 percent maternal mortality rate and a sixty percentage fetal mortality charge per unit. One group of investigators17 reported safely performing endoscopic retrograde cholangiopancreatography and endoscopic retrograde sphincterotomy without complications in five meaning women (in the second and third trimesters) with choledocholithiasis using minimal fluoroscopy and pb aprons to shield the belly. All of the women delivered good for you babies at term.17
Pregnancy-Specific Liver Disease
- Abstract
- Pregnancy and Hepatitis
- Cholelithiasis in Pregnancy
- Pregnancy-Specific Liver Disease
- References
INTRAHEPATIC CHOLESTASIS OF PREGNANCY
Intrahepatic cholestasis of pregnancy occurs in 0.01 percent of pregnancies in the United States. It typically arises in the third trimester of pregnancy, although information technology has been reported as early as 13 weeks' gestation.eighteen–20 The pathophysiology of intrahepatic cholestasis of pregnancy remains poorly understood.xix Pruritus alone occurs in 80 percent of patients; pruritus and jaundice develop in 20 percentage of patients.twenty Laboratory abnormalities include a bilirubin level less than 5 mg per dL (85.5 μmol per L), minimal or no top in transaminase, cholesterol and triglyceride levels, and exceptional, mild to moderate steatorrhea. Liver histopathology reveals centrilobular bile stasis.20 Intrahepatic cholestasis of pregnancy is associated with a 12 to 44 percent incidence of prematurity, a sixteen to 25 pct incidence of fetal distress and an increased perinatal mortality charge per unit (1.3 to 3.5 percent).3,18
A clear racial and genetic predisposition for this disorder has been described. Intrahepatic cholestasis complicates 0.01 to 0.02 percent of pregnancies in North America, one to 1.v per centum of pregnancies in Sweden and 5 to 21 per centum of pregnancies in Chile.20 The disease is rare in black patients.20 A strong family history of cholestasis of pregnancy is typically described by the patient.20 Kindred studies reveal alterations in bromosulfophthalein clearance post-obit estrogen treatment in both male and female relatives of women afflicted by intrahepatic cholestasis of pregnancy.19
Multiple medications have been tried as treatments for cholestasis of pregnancy.19 Parenteral vitamin K (phytonadione; Aqua-Mephyton) supplementation is advocated in patients with prolonged cholestasis (secondary to malabsorption of this fat-soluble vitamin). Ursodeoxycholic acid (Actigall), given at dosages of fifteen mg per kg per day, has been the almost 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.21 Ursodeoxycholic acrid has been proved condom in trials of cholestatic liver disease in infants, children and adults. Studies in rats, mice and rabbits have revealed no teratogenicity or other negative furnishings on the developing fetus. Studies in humans examining the use of ursodeoxycholic acrid in pregnancy have been uncontrolled and limited past small patient numbers. However, in pregnant patients with cholestatic liver disease, the pruritus can be severely disabling, and ursodeoxycholic acrid therapy provides safe and constructive relief.
Cholestyramine (Questran) binds bile acids and may improve pruritus; however, it may exacerbate steatorrhea and does not alter liver function or fetal prognosis.19 Phenobarbital has non been shown to improve pruritus or alter liver tests and may cause neonatal respiratory low.19
Patients exhibiting cholestasis of pregnancy should receive close fetal surveillance at delivery.3,twenty Symptoms of cholestasis normally resolve within ii days of commitment. Elevated serum bilirubin and alkaline phosphatase levels render to normal four to six weeks later delivery.3 Cholestasis of pregnancy recurs in 60 to 70 per centum of subsequent pregnancies.three
PREECLAMPSIA
Hepatic dysfunction with preeclampsia has long been recognized.22 More recently, this dysfunction has been associated with other findings in the HELLP syndrome. This syndrome may complicate the form in 3 to 10 percent of patients with preeclampsia and is noted in 0.1 percent of all pregnancies.23,24 The pathophysiology of HELLP syndrome reflects that of preeclampsia, with microvascular damage, platelet activation and vasospasm. Liver biopsy reveals periportal hemorrhage and fibrin deposition.25 Recent data propose that a defect in nitric oxide metabolism may contribute to preeclampsia and HELLP syndrome.26,27
Notable hepatic abnormalities in the HELLP syndrome include hemolysis (with elevated bilirubin levels and lactate dehydrogenase levels greater than 600 IU per L), moderately elevated transaminase levels (AST and ALT levels of 200 to 700 IU per L) and a platelet count less than 100,000 per mL (100 × 109 per L).2,3 Patients typically present with right upper quadrant pain and malaise.2,3 Threescore percent of patients exhibit significant weight proceeds or edema; fifty per centum have nausea or emesis.3 No correlation has been noted betwixt extent of hypertension, liver function examination abnormalities or liver biopsy findings.25
The maternal and fetal complications of HELLP syndrome are meaning. The maternal bloodshed charge per unit is ii percentage, and the perinatal mortality rate is 33 percent.24 Among the hepatic consequences are a 2 percent incidence of ruptured liver hematoma (with frequent concomitant bloodshed) and a 4 to 38 percent incidence of disseminated intravascular coagulation.3
The most effective treatment for HELLP syndrome is prompt delivery.two,3 Postpartum corticosteroids have proved efficacious in improving maternal platelet counts, ALT levels and blood pressure.28 Therapies that accept not proved efficacious include plasmapheresis,29 antithrombotic agents and immunosuppression.3
Post-obit delivery, laboratory abnormalities peak in the first one to 2 days postpartum and render to normal within 3 to 11 days. The adventure of recurrence of HELLP syndrome in subsequent pregnancies has been reported equally 3.4 percent.24
Acute Fatty LIVER OF PREGNANCY
Acute fat liver of pregnancy most oftentimes complicates the tertiary trimester and is normally associated with preeclampsia (l to 100 per centum).2,3 Although rare (with an incidence of 1 in thirteen,000), astute fat liver of pregnancy is a life-threatening condition, with an 18 percent maternal and a 23 pct fetal mortality rate.30
Symptoms associated with acute fatty liver of pregnancy include anorexia, nausea, emesis, intestinal pain, jaundice, headache and cardinal nervous system disturbances.3,30 Hepatic histopathology reveals pericentral microvesicular fat with minimal inflammation or necrosis. Liver biopsy is not indicated for diagnosis.31 The laboratory abnormalities in acute fatty liver of pregnancy include moderate elevations of transaminase levels (AST and ALT less than 1,000 IU per L), prolongation of prothrombin time and partial thromboplastin time, decreased fibrinogen, renal failure, profound hypoglycemia and bilirubin levels of i to 10 mg per dL (17.1 to 171.0 μmol per 50).
Some children of mothers with acute fatty liver of pregnancy have been noted to limited homozygous deficiency of long-chain 3-hydroxyacyl-CoA dehydrogenase, resulting in severe metabolic and neurologic consequences to the infants.32,33 Their mothers were found to exhibit a heterozygous deficiency of long-chain 3-hydroxyacyl-CoA dehydrogenase, contributing to astute fatty liver of pregnancy. Such defects in fatty acid oxidation are initially suggested by elevations in urinary organic acid levels and in plasma carnitine and acylcarnitine levels, detected after an overnight fast.32 Recurrent astute fatty liver of pregnancy has been reported in mothers expressing heterozygous long-chain three-hydroxyacyl-CoA dehydrogenase deficiency.31,32,34
The handling of astute fatty liver of pregnancy is expeditious commitment and intensive care. Patients usually improve promptly post-obit delivery and, in the absence of long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency, the prognosis in pregnancies following astute fatty liver of pregnancy is good.
HEPATIC RUPTURE AND INFARCTION
Hepatic rupture and infarction, extremely rare complications of preeclamptic liver illness, usually occur in the third trimester.four The incidence of hepatic rupture varies from one in 40,000 to one in 250,000 pregnancies35; hepatic infarction is even more rare. Older multigravida mothers with preeclampsia (75 to 85 percent) are at higher take a chance. Less commonly, hepatic rupture complicates growth of hepatic adenomata or other masses during pregnancy.3 Hepatic rupture most commonly involves the correct lobe.iv It is believed to be a continuum of preeclampsia, in which areas of coalescing hemorrhage result in thinning of the capsule and intraperitoneal hemorrhage.4 Instance reports have documented numerous pseudoaneurysms in the area of hemorrhage, raising the possibility of a vasculopathy contributing to this rare disorder.35
Patients with hepatic rupture typically present in stupor, with preceding right upper quadrant pain, hypertension, elevated transaminase levels (greater than 1,000 IU per L) and coagulopathy.four Therapy for hepatic rupture has included transfusion of blood products and intravenous fluids, surgical evacuation and arterial embolization.4 These therapies have met with only moderate success; a 59 to 70 percentage maternal bloodshed rate and a 75 per centum perinatal mortality charge per unit have been noted in hepatic rupture.4 Late complications arising after treatment of hepatic rupture include hepatic abscess formation and pleural effusions.
Hepatic infarction is best detected by using computed tomographic scans or magnetic resonance imaging.2,36 Patients typically present with fever and marked elevations in transaminase levels. In surviving patients, liver office and histopathology are normal inside six months of delivery.2,36 Intrahepatic hemorrhage has been reported to recur in a minority of subsequent pregnancies.35
CHRONIC LIVER Illness
An increased risk of fetal loss has been noted in pregnant patients with chronic liver illness.37 Therapy with penicillamine (Cuprimine), trientine (Syprine), prednisone or azathioprine (Imuran) tin can be safely continued during pregnancy in patients with Wilson's disease or autoimmune hepatitis.37 In patients with primary biliary cirrhosis, ursodeoxycholic acid therapy can be safely continued.37 In patients with chronic hepatitis B or C infection, interferon therapy should exist discontinued during pregnancy, as its furnishings on the fetus are unknown.37
A marked reduction in fertility has been noted in cirrhotic patients.37 Cholestasis may worsen during pregnancy in patients with primary biliary cirrhosis. Infants of patients with marked hyperbilirubinemia during pregnancy may crave exchange transfusion at birth.37
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What Hepatic Changes Are Considered Normal During Pregnancy?,
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