How Long Can a Baby Live With Elevated Liver Enzymes Without Treatment?
Liver Disease in Pregnancy
Am Fam Physician. 1999 Feb 15;59(4):829-836.
Article Sections
- Abstract
- Pregnancy and Hepatitis
- Cholelithiasis in Pregnancy
- Pregnancy-Specific Liver Disease
- References
Astute viral hepatitis is the most common cause of jaundice in pregnancy. The form of acute hepatitis is unaffected past pregnancy, except in patients with hepatitis E and disseminated canker simplex infections, in which maternal and fetal mortality rates are significantly increased. 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 half-dozen percent of pregnancies; complications can safely exist treated with surgery. Women with chronic liver illness 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. Handling involves prompt delivery, whereupon the liver illness quickly reverses. Therapy with penicillamine, trientine, prednisone or azathioprine can be safely continued during pregnancy.
Isolated hepatic affliction 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.grand., drugs, toxins, bilirubin), the metabolism and excretion of cholesterol and bilirubin, the production of plasma proteins (east.grand., albumin, coagulation factors, alpha- and beta-globulins, transferrin, haptoglobin), and the metabolism of amino acids, carbohydrates and lipids.
No single liver function exam is bachelor to quantify liver disease. The designation "liver role tests" describes a console of laboratory tests profiling discrete aspects of liver function.one Liver jail cell injury or necrosis is measured by determining aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, while liver synthetic office (depressed in cirrhosis or astringent acute liver disease) is quantified by determining albumin level and prothrombin time. Cholestasis and biliary obstruction are evaluated past measuring element of group i phosphatase, bilirubin, 5'-nucleotidase or gamma glutamyl transpeptidase levels1 (Figure 1). In normal pregnancies, alkaline phosphatase levels may be elevated three- to fourfold, secondary to placental alkaline phosphatase levels.ii–5
Cholestasis During Pregnancy
FIGURE 1.
Evaluation of cholestasis during pregnancy. (RUQ = right upper quadrant)
Elevations of ALT occurring during pregnancy tin exist evaluated using a diagnostic algorithm (Effigy 2). Elevated ALT is frequently the result of viral hepatitis, which tin be 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 elevation 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
- Abstruse
- Pregnancy and Hepatitis
- Cholelithiasis in Pregnancy
- Pregnancy-Specific Liver Disease
- References
Astute VIRAL HEPATITIS
Viral hepatitis is the well-nigh common cause of jaundice in pregnancy.four The class of well-nigh viral hepatitis infections (e.chiliad., hepatitis A, B, C and D) is unaltered by pregnancy.6,7 However, a more than astringent class of viral hepatitis in pregnancy has been noted in patients with hepatitis E and disseminated herpes simplex virus (HSV) infections.ii,6,8–11
Hepatitis E is a waterborne virus spread through fecal-oral transmission. Infection occurs about usually in developing countries after flooding. Pregnant women with hepatitis E infection exhibit markedly increased fatality rates (10 to twenty percent).six,8,9
Disseminated HSV infection is associated with prodromal systemic illness, vesicular skin rash and leukopenia.x,11 Maternal and fetal mortality rates reach 50 percent without treatment. Acyclovir (Zovirax) effectively treats early disseminated HSV infection.11
HEPATITIS B VIRUS
In the United States, 15,000 meaning women who are hepatitis B surface antigen (HBsAg)-positive evangelize annually.6 Universal screening of meaning women for HBsAg is at present performed to reduce perinatal transmission of hepatitis B virus.3 The take chances of hepatitis B virus transmission to the fetus is proportional to maternal hepatitis B virus DNA, every bit reflected in hepatitis B antigen (HBeAg) and antibody (HBeAb) condition.3 The take chances of hepatitis B virus vertical transmission is 10 percent in mothers with negative HBeAg and positive HBeAb and 90 percent in those with positive HBeAg.3,vi The risk of chronic hepatitis B virus infection in a neonate who does not receive immunoprophylaxis and vaccination for hepatitis B virus is twoscore per centum.3
Infants of HBsAg-positive mothers should receive hepatitis B immune globulin immunoprophylaxis at birth and hepatitis B vaccine at one week, one month and vi months after birth.3,6 This regimen reduces the incidence of hepatitis B virus vertical transmission to zilch to 3 percent.vi
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.12 Neonatal hepatitis B virus infection is rare if maternal infection takes identify in the first trimester. The infection occurs in six percent of neonates of women infected in the second trimester, in 67 per centum of those infected in the tertiary 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.iv pct of the U.S. population.thirteen The incidence of hepatitis C virus infection is rise nigh chop-chop amid persons 20 to 45 years of age. Therefore, an increasing number of patients with hepatitis C virus infection are requesting information about vertical transmission of the virus during pregnancy.xiii
Patients with run a risk factors for hepatitis C virus infection, such as intravenous drug apply 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 ostend 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 probable risk of hepatitis C virus vertical transmission.
A marked variation in vertical transmission rates of hepatitis C virus infection has been noted, with a range from goose egg to 36 pct.xiv Vertical transmission is strongly supported by the finding of identical hepatitis C virus subtypes in mothers and infants infected with hepatitis C virus.fourteen In hepatitis C virus–positive, HIV–negative mothers without a history of active intravenous drug use or transfusion exposure, the adventure of hepatitis C virus vertical transmission is zero to eighteen percent.fourteen Perinatal transmission of hepatitis C virus is greatest in patients with hepatitis C virus RNA titers greater than 1 1000000 copies per mL; mothers who did not have hepatitis C virus RNA did not transmit hepatitis C virus infection to their neonates.14
In patients who are HIV negative with ongoing intravenous drug abuse (or blood transfusions) during pregnancy, a 23 percentage hepatitis C virus vertical transmission rate has been reported.14 The highest reported charge per unit of vertical manual in this group occurs in infants born to hepatitis C virus–positive, HIV–positive mothers, with manual rates of 6 to 36 percent.14
No therapy has been shown to influence neonatal transmission of hepatitis C virus.
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 college take chances of vertical manual than occurs in patients with chronic infection, secondary to the high levels of hepatitis C virus RNA that occur in astute infection.fourteen Interferon therapy should not be administered during pregnancy because of its possible adverse furnishings on the fetus.15
Cholelithiasis in Pregnancy
- Abstract
- Pregnancy and Hepatitis
- Cholelithiasis in Pregnancy
- Pregnancy-Specific Liver Disease
- References
Cholelithiasis is noted in as many as half dozen percent of meaning women.four,16 Pregnancy-induced changes in bile composition predispose these patients to cholelithiasis.15,17 The bile common salt pool decreases in the second trimester, and biliary cholesterol levels may increment, resulting in lithogenic bile.15 In addition, gallbladder emptying slows in the second trimester, increasing the adventure 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 test is most helpful in determining the presence of cholelithiasis or sludge in symptomatic patients.15
Surgical handling (i.e., laparoscopic cholecystectomy) of biliary colic can exist safely accomplished in the first or 2d trimester.iv Every bit the uterus enlarges, surgery becomes more hard and should exist avoided during the third trimester.xv
A retrospective review17 of 19,000 pregnancies revealed that xi percentage of surgical emergencies were attributable to biliary tract illness. Choledocholithiasis accounts for approximately 7 percent of patients with jaundice in pregnancy.17 Of patients presenting with pancreatitis during pregnancy, 90 percent have choledocholithiasis.17 Gallstone pancreatitis is associated with a xv percent maternal mortality charge per unit and a 60 percent fetal mortality rate. Ane grouping of investigators17 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.17
Pregnancy-Specific Liver Disease
- Abstract
- Pregnancy and Hepatitis
- Cholelithiasis in Pregnancy
- Pregnancy-Specific Liver Illness
- References
INTRAHEPATIC CHOLESTASIS OF PREGNANCY
Intrahepatic cholestasis of pregnancy occurs in 0.01 pct of pregnancies in the The states. It typically arises in the third trimester of pregnancy, although information technology has been reported as early equally thirteen weeks' gestation.18–20 The pathophysiology of intrahepatic cholestasis of pregnancy remains poorly understood.19 Pruritus alone occurs in 80 pct of patients; pruritus and jaundice develop in twenty percentage of patients.20 Laboratory abnormalities include a bilirubin level less than v mg per dL (85.5 μmol per L), minimal or no elevation in transaminase, cholesterol and triglyceride levels, and infrequent, mild to moderate steatorrhea. Liver histopathology reveals centrilobular bile stasis.xx Intrahepatic cholestasis of pregnancy is associated with a 12 to 44 percent incidence of prematurity, a 16 to 25 percentage incidence of fetal distress and an increased perinatal bloodshed rate (one.three to 3.v pct).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, 1 to 1.v percent of pregnancies in Sweden and 5 to 21 percent of pregnancies in Chile.20 The disease is rare in black patients.20 A strong family unit history of cholestasis of pregnancy is typically described by the patient.twenty Kindred studies reveal alterations in bromosulfophthalein clearance following estrogen handling in both male and female relatives of women affected by intrahepatic cholestasis of pregnancy.nineteen
Multiple medications accept been tried as treatments for cholestasis of pregnancy.xix Parenteral vitamin G (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 15 mg per kg per day, has been the most successful therapy for cholestasis of pregnancy, equally it ameliorates both the pruritus and liver function abnormalities and is well-tolerated by both mother and fetus.21 Ursodeoxycholic acrid has been proved safe in trials of cholestatic liver disease in infants, children and adults. 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 acrid in pregnancy have been uncontrolled and limited by small patient numbers. However, in pregnant patients with cholestatic liver illness, the pruritus tin be severely disabling, and ursodeoxycholic acid therapy provides safe and constructive relief.
Cholestyramine (Questran) binds bile acids and may ameliorate pruritus; however, it may exacerbate steatorrhea and does not alter liver role or fetal prognosis.xix Phenobarbital has non been shown to improve pruritus or alter liver tests and may cause neonatal respiratory depression.19
Patients exhibiting cholestasis of pregnancy should receive close fetal surveillance at delivery.3,xx Symptoms of cholestasis usually resolve within ii days of delivery. Elevated serum bilirubin and alkali metal phosphatase levels return to normal 4 to half dozen weeks after delivery.3 Cholestasis of pregnancy recurs in threescore to seventy pct of subsequent pregnancies.3
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.i percent of all pregnancies.23,24 The pathophysiology of HELLP syndrome reflects that of preeclampsia, with microvascular impairment, platelet activation and vasospasm. Liver biopsy reveals periportal hemorrhage and fibrin degradation.25 Recent data suggest 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 Fifty), 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 correct upper quadrant pain and malaise.2,iii Sixty pct of patients showroom significant weight gain or edema; 50 per centum have nausea or emesis.three No correlation has been noted between extent of hypertension, liver role test abnormalities or liver biopsy findings.25
The maternal and fetal complications of HELLP syndrome are significant. The maternal bloodshed rate is ii percent, and the perinatal bloodshed rate is 33 percent.24 Among the hepatic consequences are a 2 per centum incidence of ruptured liver hematoma (with frequent concomitant mortality) and a 4 to 38 pct incidence of disseminated intravascular coagulation.three
The most effective treatment for HELLP syndrome is prompt delivery.2,3 Postpartum corticosteroids have proved efficacious in improving maternal platelet counts, ALT levels and claret pressure level.28 Therapies that take not proved efficacious include plasmapheresis,29 antithrombotic agents and immunosuppression.three
Following delivery, laboratory abnormalities peak in the first one to 2 days postpartum and render to normal within 3 to xi days. The risk of recurrence of HELLP syndrome in subsequent pregnancies has been reported as iii.iv percent.24
Acute Fatty LIVER OF PREGNANCY
Acute fatty liver of pregnancy nearly frequently complicates the third trimester and is unremarkably associated with preeclampsia (50 to 100 percent).2,iii Although rare (with an incidence of one in 13,000), acute fatty liver of pregnancy is a life-threatening status, with an 18 percent maternal and a 23 percent fetal bloodshed charge per unit.xxx
Symptoms associated with acute fat liver of pregnancy include anorexia, nausea, emesis, abdominal hurting, jaundice, headache and central nervous arrangement disturbances.three,30 Hepatic histopathology reveals pericentral microvesicular fatty with minimal inflammation or necrosis. Liver biopsy is not indicated for diagnosis.31 The laboratory abnormalities in astute fat liver of pregnancy include moderate elevations of transaminase levels (AST and ALT less than 1,000 IU per Fifty), prolongation of prothrombin time and partial thromboplastin time, decreased fibrinogen, renal failure, profound hypoglycemia and bilirubin levels of one to ten mg per dL (17.1 to 171.0 μmol per L).
Some children of mothers with astute fatty liver of pregnancy have been noted to express homozygous deficiency of long-chain iii-hydroxyacyl-CoA dehydrogenase, resulting in severe metabolic and neurologic consequences to the infants.32,33 Their mothers were institute to exhibit a heterozygous deficiency of long-chain iii-hydroxyacyl-CoA dehydrogenase, contributing to acute fat liver of pregnancy. Such defects in fatty acid oxidation are initially suggested past elevations in urinary organic acrid levels and in plasma carnitine and acylcarnitine levels, detected subsequently an overnight fast.32 Recurrent astute fatty liver of pregnancy has been reported in mothers expressing heterozygous long-concatenation 3-hydroxyacyl-CoA dehydrogenase deficiency.31,32,34
The treatment of acute fatty liver of pregnancy is expeditious delivery and intensive care. Patients usually better promptly post-obit delivery and, in the absence of long-concatenation iii-hydroxyacyl-CoA dehydrogenase deficiency, the prognosis in pregnancies following acute fat liver of pregnancy is good.
HEPATIC RUPTURE AND INFARCTION
Hepatic rupture and infarction, extremely rare complications of preeclamptic liver illness, usually occur in the 3rd trimester.4 The incidence of hepatic rupture varies from one in 40,000 to one in 250,000 pregnancies35; hepatic infarction is fifty-fifty more than rare. Older multigravida mothers with preeclampsia (75 to 85 percent) are at higher take chances. Less ordinarily, hepatic rupture complicates growth of hepatic adenomata or other masses during pregnancy.3 Hepatic rupture most normally involves the right lobe.iv It is believed to be a continuum of preeclampsia, in which areas of coalescing hemorrhage effect in thinning of the sheathing and intraperitoneal hemorrhage.four Case reports have documented numerous pseudoaneurysms in the surface area of hemorrhage, raising the possibility of a vasculopathy contributing to this rare disorder.35
Patients with hepatic rupture typically present in shock, with preceding right upper quadrant pain, hypertension, elevated transaminase levels (greater than i,000 IU per L) and coagulopathy.iv 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 per centum maternal mortality rate and a 75 pct perinatal bloodshed charge per unit accept 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 role and histopathology are normal inside half dozen months of delivery.2,36 Intrahepatic hemorrhage has been reported to recur in a minority of subsequent pregnancies.35
CHRONIC LIVER Disease
An increased run a risk of fetal loss has been noted in pregnant patients with chronic liver disease.37 Therapy with penicillamine (Cuprimine), trientine (Syprine), prednisone or azathioprine (Imuran) can be safely continued during pregnancy in patients with Wilson's disease or autoimmune hepatitis.37 In patients with master biliary cirrhosis, ursodeoxycholic acrid therapy can be safely continued.37 In patients with chronic hepatitis B or C infection, interferon therapy should exist discontinued during pregnancy, every bit its effects 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 require substitution transfusion at birth.37
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REFERENCES
prove all references
one. Chopra S, Griffin PH. Laboratory tests and diagnostic procedures in evaluation of liver affliction. Am J Med. 1985;79:221–30. ...
2. Riely CA. Hepatic disease in pregnancy. Am J Med. 1994;96(1A):18S–22S.
iii. Samuels P, Cohen AW. Pregnancies complicated by liver disease and liver dysfunction. Obstet Gynecol Clin Northward Am. 1992;nineteen:745–63.
4. Smoleniec JS, James DK. Gastrointestinal crises during pregnancy. Dig Dis. 1993;11:313–24.
5. Sjogren MH. Hepatic emergencies in pregnancy. Med Clin North Am. 1993;77:1115–27.
six. Mishra L, Seeff LB. Viral hepatitis, A through Eastward, complicating pregnancy. Gastroenterol Clin Northward Am. 1992;21:873–87.
vii. Snydman DR. Hepatitis in pregnancy. N Engl J Med. 1985;313:1398–401.
8. Tsega E, Hansson BG, Krawczynski Chiliad, Nordenfelt Eastward. Astute sporadic viral hepatitis in Ethiopia: causes, risk factors, and furnishings on pregnancy. Clin Infect Dis. 1992;fourteen:961–v.
9. Bile K, Isse A, Mohamud O, Allebeck P, Nilsson L, Norder H, et al. Contrasting roles of rivers and wells every bit sources of drinking water on set on and fatality rates in a hepatitis Due east epidemic in Somalia. Am J Trop Med Hyg. 1994;51:466–74.
10. Stagno Southward, Whitley RJ. Herpesvirus infections of pregnancy. Part II: Herpes simplex virus and varicellazoster virus infections. N Engl J Med. 1985;313:1327–30.
11. Glorioso DV, Molloy PJ, Van Thiel DH, Kania RJ. Successful empiric treatment of HSV hepatitis in pregnancy. Example study and review of the literature. Dig Dis Sci. 1996;41:1273–5.
12. Tong MJ, Thursby M, Rakela J, McPeak C, Edwards VM, Mosley JW. Studies on the maternal-baby transmission of the viruses which cause acute hepatitis. Gastroenterology. 1981;80(five Pt 1):999–1004.
xiii. Sharara AI, Hunt CM, Hamilton JD. Hepatitis C. Ann Intern Med. 1996;125:658–68.
fourteen. Hunt CM, Carson KL, Sharara AI. Hepatitis C in pregnancy. Obstet Gynecol. 1997;89(five Pt 2):883–ninety.
15. Fallon WF Jr, Newman JS, Fallon GL, Malangoni MA. The surgical management of intra-abdominal inflammatory conditions during pregnancy. Surg Clin North Am. 1995;75:xv–31.
sixteen. Mabie WC. Obstetric management of gastroenterologic complications of pregnancy. Gastroenterol Clin North Am. 1992;21:923–35.
17. Baillie J, Cairns SR, Putman WS, Cotton wool PB. Endoscopic management of choledocholithiasis during pregnancy. Surg Gynecol Obstet. 1990;171:one–4.
18. Rioseco AJ, Ivankovic MB, Manzur A, Hamed F, Kato SR, Parer JT, et al. Intrahepatic cholestasis of pregnancy: a retrospective case-control report of perinatal consequence. Am J Obstet Gynecol. 1994;170:890–v.
nineteen. Reyes H, Simon FR. Intrahepatic cholestasis of pregnancy: an estrogen-related disease. Semin Liver Dis. 1993;13:289–301.
20. Reyes H. The spectrum of liver and gastrointestinal disease seen in cholestasis of pregnancy. Gastroenterol Clin North Am. 1992;21:905–21.
21. Palma J, Reyes H, Ribalta J, Iglesias J, Gonzalez MC, Hernandez I, et al. Effects of ursodeoxycholic acid in patients with intrahepatic cholestasis of pregnancy. Hepatology. 1992;xv:1043–7.
22. Barron WM. The syndrome of preeclampsia. Gastroenterol Clin North Am. 1992;21:851–72.
23. Roberts WE, Perry KG Jr, Woods JB, Files JC, Blake PG, Martin JN Jr. The intrapartum platelet count in patients with HELLP (hemolysis, elevated liver enzymes, and depression platelets) syndrome: is it predictive of afterward hemorrhagic complications? Am J Obstet Gynecol. 1994;171:799–804.
24. Sibai BM, Ramadan MK, Chari RS, Friedman SA. Pregnancies complicated by HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets): subsequent pregnancy outcome and long-term prognosis. Am J Obstet Gynecol. 1995;172(1 Pt i):125–9.
25. Barton JR, Riely CA, Adamec TA, Shanklin DR, Khoury AD, Sibai BM. Hepatic histopathologic condition does not correlate with laboratory abnormalities in HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count). Am J Obstet Gynecol. 1992;167:1538–43.
26. Cameron Information technology, van Papendorp CL, Palmer RM, Smith SK, Moncada S. Relationship between nitric oxide synthesis and increase in systolic blood pressure in women with hypertension in pregnancy. Hypertens Pregnancy. 1993;12:85–92.
27. de Belder A, Lees C, Martin J, Moncada S, Campbell S. Treatment of HELLP syndrome with nitric oxide donor [Alphabetic character]. Lancet. 1995;345:124–5.
28. Magann EF, Perry KG Jr, Meydrech EF, Harris RL, Chauhan SP, Martin JN Jr. Postpartum corticosteroids: accelerated recovery from the syndrome of hemolysis, elevated liver enzymes, and depression platelets (HELLP). Am J Obstet Gynecol. 1994;171:1154–8.
29. Martin JN Jr, Files JC, Blake PG, Perry KG Jr, Morrison JC, Norman PH. Postpartum plasma commutation for singular preeclampsia-eclampsia as HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome. Am J Obstet Gynecol. 1995;172(iv Pt 1):1107–25.
30. Kaplan MM. Acute fatty liver of pregnancy. N Engl J Med. 1985;313:367–seventy.
31. Riely CA, Latham PS, Romero R, Duffy TP. Acute fatty liver of pregnancy. A reassessment based on observations in nine patients. Ann Intern Med. 1987;106:703–6.
32. Treem WR, Rinaldo P, Hale DE, Stanley CA, Millington DS, Hyams JS, et al. Acute fatty liver of pregnancy and long-chain iii-hydroxyacyl-coenzyme A dehydrogenase deficiency. Hepatology. 1994;19:339–45.
33. Sims HF, Brackett JC, Powell CK, Treem WR, Hale DE, Bennett MJ, et al. The molecular basis of pediatric long chain 3-hydroxyacyl-CoA dehydrogenase deficiency associated with maternal acute fatty liver of pregnancy. Proc Natl Acad Sci U Southward A. 1995;92:841–five.
34. Barton JR, Sibai BM, Mabie WC, Shanklin DR. Recurrent astute fat liver of pregnancy. Am J Obstet Gynecol. 1990;163:534–viii.
35. Greenstein D, Henderson JM, Boyer TD. Liver hemorrhage: recurrent episodes during pregnancy complicated by preeclampsia. Gastroenterology. 1994;106:1668–71.
36. Hosono M, Togashi Chiliad, Kawakami S, Itoh Grand, Fukuoka Yard, Kobayashi F, et al. MR demonstration of reversible periportal aberrant intensity in eclampsia. J Comput Assist Tomogr. 1994;18:143–5.
37. Lee WM. Pregnancy in patients with chronic liver affliction. Gastroenterol Clin North Am. 1992;21:889–903.
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