Acute Fatty Liver of Pregnancy

Table of Contents

1. What Acute Fatty Liver of Pregnancy Is
2. How Common It Is
3. The Link to the Baby's Fat-Burning Enzymes
4. Symptoms Reported at Presentation
5. Blood Test and Scan Findings
6. The Swansea Criteria and How Well They Perform
7. How It Differs From HELLP Syndrome and Preeclampsia
8. What Hospitals Do
9. Outcomes for Mother and Baby
10. Recurrence in Later Pregnancies
11. Testing the Baby for Fat-Burning Defects
12. Signs Hospitals Treat as Urgent
13. Key Research Papers
14. Connections
15. Featured Videos

What Acute Fatty Liver of Pregnancy Is

In a healthy liver, fat is either stored in a few large drops or burned for energy inside the cell's power units, the mitochondria. In acute fatty liver of pregnancy, the liver cells instead fill with a fine "foam" of very small fat droplets. Doctors call this pattern microvesicular steatosis. When it is seen under the microscope, it shows that the cells' fat-burning machinery has broken down rather than that too much fat has arrived.

A liver in this state cannot do its everyday jobs. It stops releasing enough sugar into the blood, so blood sugar falls. It makes fewer clotting proteins, so the blood clots poorly. It clears less ammonia and bilirubin, so jaundice appears and, in severe cases, the brain is affected. The kidneys are often drawn in as well. A team at a large Texas hospital that reviewed 51 cases over 37 years summed it up this way: the clinical features and laboratory findings all come from one central process, liver failure (Nelson et al., 2013).

A 2017 review in the American Journal of Gastroenterology calls acute fatty liver of pregnancy an obstetric emergency of maternal liver failure. It links the illness to defects in fatty-acid metabolism during pregnancy, especially when the baby carries a genetic defect in fatty-acid oxidation (Liu et al., 2017).

How Common It Is

The best population count comes from the United Kingdom. The UK Obstetric Surveillance System asked all 229 consultant-led maternity units in the country to report every case between February 2005 and August 2006. Among an estimated 1,132,964 women giving birth, 57 had acute fatty liver of pregnancy, an incidence of 5.0 per 100,000 maternities, or roughly 1 in 20,000 births (Knight et al., 2008).

The same study found two features that were more common than expected among the women affected:

• Twins: 18% of the women were carrying twins. The authors concluded that women with twin pregnancies appear to be at higher risk.
• Low body weight: 20% had a body mass index under 20. The authors noted that more research is needed on this link.

Counts from single hospitals vary widely. A prospective study in one obstetric unit in Southwest Wales found 5 cases among 4,377 deliveries over 15 months, a rate the authors described as much greater than previously reported (Ch'ng et al., 2002). In Olmsted County, Minnesota, a population-based search covering 35,101 pregnancies between 1996 and 2010 found only 1 case (Allen et al., 2016). The UK authors pointed out that their national figure was lower than those from earlier hospital-based studies, which tend to collect the most severe cases.

The Link to the Baby's Fat-Burning Enzymes

The most striking discovery about acute fatty liver of pregnancy is that the cause can lie partly in the baby. Long-chain fatty acids are broken down in the mitochondria by a group of enzymes. One of them, long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD), sits inside a larger enzyme complex called the mitochondrial trifunctional protein. A child who inherits two faulty copies of the gene, one from each parent, cannot burn long-chain fats properly.

In 1999, a study in the New England Journal of Medicine examined 24 children with this kind of enzyme deficiency. Nineteen had a deficiency of long-chain 3-hydroxyacyl-CoA dehydrogenase alone and became ill with low blood sugar without ketones (hypoketotic hypoglycemia) and a fatty liver. All 19 carried a particular change in the gene, in which the amino acid glutamic acid at position 474 is replaced by glutamine (called E474Q, or Glu474Gln). Eight had two copies of it, and eleven had it on one copy alongside a different mutation. While they were carrying these babies, 79% of the mothers who carried one copy of the change had acute fatty liver of pregnancy or HELLP syndrome. Five other children had a complete loss of all three enzymes in the complex, and none of their mothers had liver disease in pregnancy (Ibdah et al., 1999).

The same research group then screened, in the other direction, starting from the mothers. Between 1997 and 2001, 108 consecutive samples from women who had acute fatty liver of pregnancy or HELLP syndrome, or from their children or partners, were sent for molecular testing. Mutations that cause long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency in the child were found in 5 of the 27 families with acute fatty liver of pregnancy (19%). In every one, the mother's gene copy carried the E474Q change. Among the 81 women with HELLP syndrome, only one carried a single copy of E474Q, and her newborn had no mutation. The authors described the link between acute fatty liver of pregnancy and E474Q in the fetus as significant (Yang et al., 2002).

A 2026 systematic review gathered 27 studies with 77 cases of acute fatty liver of pregnancy in which the mother or baby had genetic or biochemical testing. A fat-burning disorder was confirmed in the baby in 27 of the 77 pregnancies (35.1%). Of those 27 babies, 22 (81.5%) had long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency, three had medium-chain acyl-CoA dehydrogenase deficiency, one had short-chain acyl-CoA dehydrogenase deficiency and one had carnitine palmitoyltransferase-I deficiency (Varotsis et al., 2026).

The screening study describes this as a fetal-maternal link: the mother carries one faulty copy, the baby carries two, and the mother falls ill while carrying that baby (Yang et al., 2002). Even so, in the systematic review nearly two in three tested pregnancies had no fat-burning disorder confirmed in the baby (Varotsis et al., 2026), so in many cases the cause is not explained.

Symptoms Reported at Presentation

The early symptoms are ordinary ones, which is part of why the condition is hard to spot. Studies from three countries report similar patterns:

• Panama, 35 cases (1996–2010): nausea or vomiting in 88.5%, jaundice in 71.4% and abdominal pain in 51.4%. The mean gestational age at delivery was 36 weeks (Vigil-de Gracia and Montufar-Rueda, 2011).
• Texas, 51 cases (1975–2012): persistent nausea and vomiting in 57%, high blood pressure in 57% and abdominal pain in 53%. More than 90% had at least one of these findings (Nelson et al., 2013).
• Beijing, 55 cases (2008–2018): jaundice in 89.1%, nausea or vomiting in 58.2%, loss of appetite in 49.1%, tiredness in 45.5% and excessive thirst in 30.9%. The mean gestational week at diagnosis was 35.25. Three women (5.5%) were diagnosed only after the birth (Chang et al., 2020).

In the 2026 systematic review of cases with genetic testing, 87.8% of the women presented with digestive symptoms such as nausea, vomiting or abdominal pain (Varotsis et al., 2026).

Blood Test and Scan Findings

Blood tests show a liver that has stopped making and clearing what it normally does. In the Panama series, low blood sugar was found in 94.2% of women, kidney failure in 94.2%, clotting problems in 77.1%, fluid in the abdomen (ascites) in 48.5% and brain involvement from liver failure (encephalopathy) in 40% (Vigil-de Gracia and Montufar-Rueda, 2011).

In the Texas series, a combination of liver and kidney dysfunction was nearly universal, though its severity varied. The liver's production of clotting proteins was impaired in more than three-quarters of the women. That made bleeding at delivery heavier, and 50% of the 51 women received blood or blood-component transfusions (Nelson et al., 2013).

A Japanese review drew attention to two findings that change how early the disease can be recognized. About 50% of women with acute fatty liver of pregnancy did not have a low platelet count when they first arrived. And the condition was closely tied to a drop in antithrombin, a clotting-control protein the liver makes. The authors proposed adding antithrombin activity below 65% to the diagnostic criteria, so that the disease could be suspected before life-threatening complications appear (Minakami et al., 2014).

Liver biopsy shows the microvesicular fat directly, but it is rarely done in practice; the Chinese Swansea study relied on the non-biopsy criteria for that reason (Wang et al., 2017). An ultrasound may show fluid in the abdomen or a "bright" liver, which is one of the Swansea features listed below.

The Swansea Criteria and How Well They Perform

The Swansea criteria come from the prospective study of liver problems in pregnancy run in Swansea, Southwest Wales (Ch'ng et al., 2002). They turn the scattered findings above into a checklist. A 2026 review describes the rule used in guidelines and in most published studies: six or more of fourteen features, with no other explanation for them (Solomon Condriuc et al., 2026). The fourteen features are:

1. Vomiting
2. Abdominal pain
3. Excessive thirst or urination
4. Encephalopathy (confusion or drowsiness from liver failure)
5. Raised bilirubin
6. Low blood sugar
7. Raised uric acid
8. Raised white blood cell count
9. Fluid in the abdomen or a bright liver on ultrasound
10. Raised liver enzymes (transaminases)
11. Raised ammonia
12. Kidney impairment
13. Abnormal clotting tests
14. Microvesicular fat on liver biopsy

The criteria have been tested in several ways:

• Agreement with expert diagnosis: in the UK national study, 55 of the 57 cases (90%) were confirmed by the diagnostic criteria together with clinical assessment and 2 by clinical assessment alone, a 97% agreement with a kappa statistic of 0.78. The authors described this as substantial agreement (Knight et al., 2008).
• Without a biopsy: in a Chinese series of 52 women, 90.4% met five or more criteria without a biopsy. Women who met seven or more criteria had a significantly higher risk of stillbirth and more often needed continuous blood purification treatment (Wang et al., 2017).
• Pregnancy's own effects on blood tests: normal pregnancy changes several of the blood values the criteria use. Five of 11 case series that reported laboratory values used cut-offs different from the Swansea ones. The authors favoured pregnancy-specific reference ranges (Morton and Laurie, 2018).
• Accuracy against a true reference standard: the 2026 review found that the criteria's accuracy against an independent standard comes from one small biopsy series with a high share of cases. Their ability to tell acute fatty liver of pregnancy apart from HELLP syndrome and other causes of acute liver failure appears limited. Because several criteria measure organ failure that is already present, the threshold may not yet be met early in the illness, and no study has tested the criteria prospectively at first presentation (Solomon Condriuc et al., 2026).

In short, the Swansea criteria describe the established disease well, but they are less proven as an early warning tool.

How It Differs From HELLP Syndrome and Preeclampsia

Hemolysis, elevated liver enzymes and low platelets (HELLP) syndrome and preeclampsia are also third-trimester conditions that affect the liver, and both are far more common. The HELLP Syndrome page covers that condition in depth. The Minnesota population study gives a sense of the balance: among 247 women with a liver disease unique to pregnancy, 134 had preeclampsia with liver dysfunction, 72 had HELLP syndrome and 1 had acute fatty liver of pregnancy (Allen et al., 2016).

The conditions overlap a great deal. A review that compared them found they share clinical, laboratory, tissue and genetic features, and that telling them apart is often difficult. The differences it reported were:

• Blood pressure: HELLP syndrome was likely to occur in women with high blood pressure, while acute fatty liver of pregnancy often occurred without it (Minakami et al., 2014). In the Texas series, however, 57% of women with acute fatty liver of pregnancy did have high blood pressure (Nelson et al., 2013), so blood pressure alone does not separate them.
• Antithrombin: a pregnancy-related fall in antithrombin was linked specifically to acute fatty liver of pregnancy (Minakami et al., 2014).
• Platelets: low platelets define HELLP syndrome, but about half of women with acute fatty liver of pregnancy had normal platelet counts when they first presented (Minakami et al., 2014).
• Liver failure markers: low blood sugar, poor clotting and kidney failure, the signs of a failing liver, dominate acute fatty liver of pregnancy (Vigil-de Gracia and Montufar-Rueda, 2011; Nelson et al., 2013).
• The baby's genes: in the screening study, the baby's fat-burning defect was found in families with acute fatty liver of pregnancy but not in the HELLP syndrome group (Yang et al., 2002).

The 2017 review notes that distinguishing acute fatty liver of pregnancy from HELLP syndrome and preeclampsia can be challenging and that further work is needed to diagnose it more quickly (Liu et al., 2017).

What Hospitals Do

No medicine reverses acute fatty liver of pregnancy. Care rests on two things: ending the pregnancy promptly, and supporting the mother's organs until her liver recovers. The 2017 review states that delay in diagnosis and treatment has life-threatening consequences (Liu et al., 2017).

Prompt delivery

In the Beijing series, the median time from diagnosis to delivery was 1.55 days, and 75% of the pregnancies (39 of 52) were ended on the day of diagnosis. Cesarean delivery was used in 78.8% (Chang et al., 2020). A 2016 meta-analysis of observational studies compared cesarean with vaginal delivery: the maternal death rate was 44% lower (relative risk 0.56) and the perinatal death rate was also lower (relative risk 0.52) with cesarean delivery. It found no association with the type of newborn death or with complications in multiple maternal organs (Wang et al., 2016). Because these were observational studies, the sicker women and the way each hospital chose may explain part of the difference.

Supportive care

Many women need intensive care. In the UK national study, 60% were admitted to intensive care and 15% to a specialist liver unit, and one woman received a liver transplant (Knight et al., 2008). Supportive care reported in the studies includes:

• Correction of low blood sugar, which was present in 94.2% of the Panama series (Vigil-de Gracia and Montufar-Rueda, 2011).
• Blood products to correct clotting and replace blood lost at delivery. In Beijing, 53.6% of women having a cesarean were given plasma before surgery (Chang et al., 2020).
• Kidney support, including blood purification, in the more severe cases (Wang et al., 2017).
• Plasma exchange, in which the patient's plasma is removed and replaced. In a retrospective study of 290 women at two Chinese hospitals, women treated with plasma exchange had a significantly lower 60-day death rate in a propensity-matched comparison (Li et al., 2023). This is a retrospective result, and no randomized trial is cited here.
• Liver transplant, in rare cases where the liver does not recover (Knight et al., 2008).

In the Beijing series, among women whose bleeding after birth went past 500 ml, those treated with a balloon pressed inside the womb had less uncontrollable bleeding and fewer hysterectomies, though the differences were not statistically significant in so small a group (Chang et al., 2020).

Recovery

The Texas team measured how long recovery takes. After delivery, clinical improvement was typically seen within 3–4 days, and most laboratory values returned to normal within 7–10 days, though some abnormalities lasted much longer (Nelson et al., 2013).

Outcomes for Mother and Baby

Reported outcomes vary greatly between settings, partly because hospital studies collect the sickest cases.

• United Kingdom, national (57 women): one woman died, a case fatality rate of 1.8%. There were 7 deaths among 67 babies, a perinatal mortality rate of 104 per 1,000 births. The authors judged outcomes better than previously reported, possibly because milder cases were now being counted (Knight et al., 2008).
• Texas (51 women): 2 maternal deaths and a stillbirth rate of 120 per 1,000 pregnancies (Nelson et al., 2013).
• Panama (35 women): 4 maternal deaths (11.4%) and 5 perinatal deaths (12.5%) (Vigil-de Gracia and Montufar-Rueda, 2011).
• Beijing (55 women): 3 mothers (5.5%) died of multiple organ failure and 6 babies (9.8%) died. Compared with 220 matched mothers without the disease, severe negative outcomes were far more common (27.3% vs. 0.9%), as was newborn asphyxia (24.6% vs. 0.9%) (Chang et al., 2020).
• Two Chinese referral hospitals (290 women, 2012–2022): 50 women (17.2%) died. Those who died more often had encephalopathy, bleeding after birth, fetal distress and fetal death (Li et al., 2023).

For babies, the fat-burning defect matters a great deal. In the 2026 systematic review, stillbirth or infant death was reported in 14 of 22 cases (63.6%) with long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency. No fetal or newborn deaths were recorded with the other fat-burning disorders or when genetic testing was negative (Varotsis et al., 2026).

Recurrence in Later Pregnancies

The chance of acute fatty liver of pregnancy happening again is not well known, and the two main sources point in different directions.

• Case series: a 2025 review of 10 small case series found only one recurrence in 35 later pregnancies (Morton et al., 2025).
• Patient survey: a questionnaire spread through an international online patient group reached 69 women with a past case. Of the 24 who had another baby, 5 were diagnosed again, about 1 in 5. In 4 of those 5 the second episode was milder, while in one it was worse. In the second affected pregnancy the women were delivered earlier, by planned cesarean before labour, at a median of 245 days instead of 265. A male baby was not linked to a higher risk of recurrence (Glavind et al., 2020).

A survey of this kind may over-represent women who had a recurrence, while small case series may miss recurrences that happened elsewhere. The 2025 review concluded that studies following women through later pregnancies are needed to define the risk (Morton et al., 2025). When a fat-burning defect is found in the baby, the screening study notes that it is inherited recessively, from both parents, which is why its authors describe genetic counselling and prenatal diagnosis for later pregnancies (Yang et al., 2002).

Testing the Baby for Fat-Burning Defects

Because a baby with long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency can become dangerously ill with low blood sugar and fatty liver after birth (Ibdah et al., 1999), the researchers who found the link argued for testing. They concluded that screening newborns for the E474Q mutation in pregnancies complicated by acute fatty liver of pregnancy could allow early diagnosis and treatment in the newborn, and genetic counselling and prenatal diagnosis in later pregnancies (Yang et al., 2002). The 2026 systematic review concluded that evaluation for fetal and maternal long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency belongs in the diagnostic workup of acute fatty liver of pregnancy (Varotsis et al., 2026).

Not every expert agrees testing every case is proven worthwhile. The 2017 review states that the value of screening all patients for these genetic defects remains to be determined (Liu et al., 2017).

Case reports show what is at stake. A Spanish team described a 7-month-old girl with long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency and low blood sugar without ketones. In a previous pregnancy, her mother had acute fatty liver of pregnancy that ended in fetal death at 34 weeks. The girl carried the 1528G>C change (the DNA form of E474Q) on both gene copies, and each parent carried one. The authors called for screening newborns of mothers with liver complications in pregnancy such as acute fatty liver of pregnancy or severe or recurrent HELLP syndrome (Gutiérrez Junquera et al., 2009).

Signs Hospitals Treat as Urgent

In the studies on this page, these findings in the last months of pregnancy, or in the days after the birth, marked the start of the illness. Maternity and emergency teams treat them as urgent and check blood sugar, liver tests, kidney tests and clotting:

• New nausea and vomiting late in pregnancy, especially with tiredness or loss of appetite
• Pain in the upper abdomen
• Yellowing of the skin or the whites of the eyes
• Unusual thirst or passing a lot of urine
• Confusion, drowsiness or shakiness from low blood sugar
• Bleeding that is hard to stop, or easy bruising

The reviews describe the cost of delay: the 2017 review states that late diagnosis and treatment have life-threatening consequences (Liu et al., 2017), and the Japanese review found that diagnosis was often delayed until life-threatening complications appeared (Minakami et al., 2014). Because the early symptoms resemble ordinary pregnancy complaints or a stomach upset, the blood tests are what reveal the failing liver.

Key Research Papers

1. Knight M, Nelson-Piercy C, Kurinczuk JJ, Spark P, Brocklehurst P. A prospective national study of acute fatty liver of pregnancy in the UK. Gut. 2008;57(7):951-6. PubMed PMID: 18332072
2. Ibdah JA, Bennett MJ, Rinaldo P, Zhao Y, Gibson B, Sims HF, Strauss AW. A fetal fatty-acid oxidation disorder as a cause of liver disease in pregnant women. N Engl J Med. 1999;340(22):1723-31. PubMed PMID: 10352164
3. Yang Z, Yamada J, Zhao Y, Strauss AW, Ibdah JA. Prospective screening for pediatric mitochondrial trifunctional protein defects in pregnancies complicated by liver disease. JAMA. 2002;288(17):2163-6. PubMed PMID: 12413376
4. Varotsis D, Araji S, Horgan R, Powel JE, McLaren R Jr, Kirmse B, Makhamreh MM, Al-Kouatly HB. Acute Fatty Liver of Pregnancy and Fetal Fatty Acid Oxidation Disorders: A Systematic Review. O G Open. 2026;3(1):e148. PubMed PMID: 41727930
5. Vigil-de Gracia P, Montufar-Rueda C. Acute fatty liver of pregnancy: diagnosis, treatment, and outcome based on 35 consecutive cases. J Matern Fetal Neonatal Med. 2011;24(9):1143-6. PubMed PMID: 21668324
6. Nelson DB, Yost NP, Cunningham FG. Acute fatty liver of pregnancy: clinical outcomes and expected duration of recovery. Am J Obstet Gynecol. 2013;209(5):456.e1-7. PubMed PMID: 23860212
7. Chang L, Wang M, Liu H, Meng Q, Yu H, Wu YM, Zhu Y. Pregnancy outcomes of patients with acute fatty liver of pregnancy: a case control study. BMC Pregnancy Childbirth. 2020;20(1):282. PubMed PMID: 32393199
8. Ch'ng CL, Morgan M, Hainsworth I, Kingham JG. Prospective study of liver dysfunction in pregnancy in Southwest Wales. Gut. 2002;51(6):876-80. PubMed PMID: 12427793
9. Solomon Condriuc IP, Popovici R, Cosovanu EO, Mogos RA, Haba R, Sescu VA, Stan RS, Mogos SJ, Buzduga CM, Carauleanu A. Metabolic and Synthetic Dysfunction in Acute Fatty Liver of Pregnancy: Reappraising the Swansea Criteria-A Narrative Review. Metabolites. 2026;16(10):799. PubMed PMID: 42941274
10. Wang S, Li SL, Cao YX, Li YP, Meng JL, Wang XT. Noninvasive Swansea criteria are valuable alternatives for diagnosing acute fatty liver of pregnancy in a Chinese population. J Matern Fetal Neonatal Med. 2017;30(24):2951-2955. PubMed PMID: 27923319
11. Morton A, Laurie J. Physiological changes of pregnancy and the Swansea criteria in diagnosing acute fatty liver of pregnancy. Obstet Med. 2018;11(3):126-131. PubMed PMID: 30214478
12. Minakami H, Morikawa M, Yamada T, Yamada T, Akaishi R, Nishida R. Differentiation of acute fatty liver of pregnancy from syndrome of hemolysis, elevated liver enzymes and low platelet counts. J Obstet Gynaecol Res. 2014;40(3):641-9. PubMed PMID: 24428400
13. Allen AM, Kim WR, Larson JJ, Rosedahl JK, Yawn BP, McKeon K, Hay JE. The Epidemiology of Liver Diseases Unique to Pregnancy in a US Community: A Population-Based Study. Clin Gastroenterol Hepatol. 2016;14(2):287-94.e1-2. PubMed PMID: 26305066
14. Liu J, Ghaziani TT, Wolf JL. Acute Fatty Liver Disease of Pregnancy: Updates in Pathogenesis, Diagnosis, and Management. Am J Gastroenterol. 2017;112(6):838-846. PubMed PMID: 28291236
15. Wang HY, Jiang Q, Shi H, Xu YQ, Shi AC, Sun YL, Li J, Ning Q, Shen GX. Effect of caesarean section on maternal and foetal outcomes in acute fatty liver of pregnancy: a systematic review and meta-analysis. Sci Rep. 2016;6:28826. PubMed PMID: 27387594
16. Li L, Huang D, Xu J, Li M, Zhao J, Shi Q, Guo Q. The assessment in patients with acute fatty liver of pregnancy (AFLP) treated with plasma exchange: a cohort study of 298 patients. BMC Pregnancy Childbirth. 2023;23(1):171. PubMed PMID: 36915067
17. Glavind J, Boie S, Glavind E, Fuglsang J. Risk of recurrent acute fatty liver of pregnancy: survey from a social media group. Am J Obstet Gynecol MFM. 2020;2(2):100085. PubMed PMID: 33345956
18. Morton A, Phillips L, Nisbet J, He JW. The risk of recurrence of acute fatty liver of pregnancy - a review of the current literature. Obstet Med. 2025;18(4):210-213. PubMed PMID: 39906898
19. Gutiérrez Junquera C, Balmaseda E, Gil E, Martínez A, Sorli M, Cuartero I, Merinero B, Ugarte M. Acute fatty liver of pregnancy and neonatal long-chain 3-hydroxyacyl-coenzyme A dehydrogenase (LCHAD) deficiency. Eur J Pediatr. 2009;168(1):103-6. PubMed PMID: 18408953

PubMed Topic Searches

1. PubMed: acute fatty liver of pregnancy
2. PubMed: acute fatty liver of pregnancy and the Swansea criteria
3. PubMed: acute fatty liver of pregnancy and LCHAD deficiency
4. PubMed: recurrence of acute fatty liver of pregnancy

Connections

• Nephrology & Hepatology — the parent category
• HELLP Syndrome — the more common third-trimester liver emergency it is most often confused with
• Preeclampsia — high blood pressure of pregnancy, which can also affect the liver
• Hyperemesis Gravidarum — severe pregnancy vomiting, another liver disease unique to pregnancy
• Liver Disease — an overview of liver conditions
• Hepatic Encephalopathy — brain effects of liver failure
• Fatty Liver Disease (MASLD) — the common, slowly developing form of fatty liver
• Jaundice — yellowing of the skin and eyes

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