Pregnancy and liver disease pdf

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pregnancy and liver disease pdf

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Liver Disease: Reproductive Considerations

The journal's aim is to publish articles focused on basic, clinic care and translational research that seeks to prevent rather than treat the complications of endstage liver disease. The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two receding years. CiteScore measures average citations received per document published. Read more. SRJ is a prestige metric based on the idea that not all citations are the same.

SJR uses a similar algorithm as the Google page rank; it provides a quantitative and qualitative measure of the journal's impact. SNIP measures contextual citation impact by wighting citations based on the total number of citations in a subject field.

Liver disease during pregnancy is more common than expected and may require specialized intervention. It is important to determine if changes in liver physiology may develop into liver disease, to assure early diagnosis. For adequate surveillance of mother-fetus health outcome, liver disease during pregnancy might require intervention from a hepatologist. In this review we describe and discuss the main characteristics of those liver diseases associated with pregnancy and only some frequent pre-existing and co-incidental in pregnancy are considered..

In addition to the literature review, we compiled the data of liver disease occurring during pregnancies attended at the National Institute of Perinatology in Mexico City in a three-year period.. In our tertiary referral women hospital, liver disease was present in Associated liver disease was found in Only 0. When managing pregnancy in referral hospitals in Latin America, it is important to discard liver alterations early for adequate follow up of the disease and to prevent adverse consequences for the mother and child..

Liver disease is a serious complication of pregnancy and poses a challenge for the gynecologist and hepatologist.

Liver disorders may present themselves inconspicuously during gestation. Due to the physiological changes in the liver that occur during pregnancy, it is difficult to diagnose and manage a liver disease. A systematic approach is needed for its treatment and must include a detailed clinical history, examination, laboratory analyses and radiographic evaluation.

The clinical history should include previous pregnancy diseases and associated liver complications, intravenous drug use, transfusions, if pregnancies were taken to term, and oral contraceptive use. Also, the patient should be evaluated for clinical data that may suggest liver dysfunction such as nausea, vomiting, jaundice, generalized pruritus, abdominal pain, polyuria and polydipsia in the absence of other morbidities as chronic metabolic disease such as diabetes [6—10].

Liver disease during pregnancy is classified into two main categories: those related to pregnancy; and those non-related or coincidental to pregnancy that are present de novo, or are pre-existing chronic liver disease exacerbated by pregnancy Table 1 [2,6,9]. In addition, pre-eclampsia PE and hyperemesis gravidarum HG are frequently associated to liver abnormalities [4,5,7]. Non-related pregnancy hepatic diseases include acute and chronic viral hepatitis, cirrhosis with or without portal hypertension, biliary diseases such as gallstones and primary sclerosing cholangitis, vascular alterations such as Budd—Chiari syndrome BCS , Wilson's disease, autoimmune liver diseases, metabolic disorders, drug induced hepatotoxicity and post liver transplantation state Table 1 [2,5,6,11].

Classification of liver diseases in pregnancy [2,11]. HELLP: hemolysis, elevated liver enzymes and low platelets count. Pregnancy associated liver disorders exhibit specific trimester occurrence, while non-pregnancy-related liver diseases can occur at any time. The timing of the occurrence of clinical manifestations and abnormal liver function tests LFTs are critical for determining diagnosis and treatment strategies.

Therapeutic decisions must be made considering the implications for both the mother and the child, and rapid diagnosis is required in severe liver diseases because the decision of immediate delivery will determine maternal and fetal outcome.

The main factors that determine maternal prognosis depend on the type of liver disease, the degree of impaired synthetic, metabolic, and excretory liver function, and timing of delivery [6,8,10]. In this review we will focus on the description of main liver pathologies associated to pregnancy, and an overview of some co-incidental or pre-existing liver diseases will be summarized.

We compared these data to reports of liver disorder frequencies during pregnancy. Pregnancy-specific disorders are the leading cause of abnormal LFTs during pregnancy, particularly in the third trimester. Pre-eclampsia-related disorder is the most common among these [12]. Physiological changes in pregnancy can mimic liver disease; therefore, these must be considered when diagnosing suspected pregnancy related liver disease.

However, increased levels in transaminases, bilirubin, fasting total bile acids, or the prothrombin time PT above the normal range during pregnancy, are abnormal and require prompt evaluation [5,6,15—17].

The main characteristics of pregnancy related liver diseases are shown in Table 2. Major characteristics of pregnancy related liver diseases and differential diagnoses [8,9,11,15—17]. HG occurs in approximately 0. Symptoms usually start before the 9th week of gestation wg and disappear by the 20th wg [5,6,8,10].

HG should be established as exclusion diagnostic criteria in most cases. However, the evaluation of HG by exclusion and evaluation for other causes is warranted in atypical cases, especially if the vomiting begins or persists during the 2nd trimester. HG is not considered a true liver disease, but it is associated to abnormal LFTs in approximately half of patients [5,6,9,11,18]. Clinical signs lead to dehydration and increased renal values, electrolyte abnormalities, metabolic alkalosis, and erythrocytosis.

Other biochemical abnormalities, such as increased serum amylase and lipase values may also be observed [5,15,16]. In addition, an abdominal ultrasound must demonstrate normal liver parenchyma without biliary obstruction.

However, an obstetrical ultrasound is mandatory because HG may be associated with multiple and molar pregnancies. Increased body mass index, pre-existing diabetes, asthma, psychiatric illness, hyperthyroid disorders in a previous pregnancy or a previous pregnancy with HG, have also been shown to be risk factors for this disease [6,7,9,18]. The major etiologies proposed for the development of HG are: I High levels of human chorionic gonadotropin HCG exert a stimulating effect on the secretory process in the upper gastrointestinal tract; the production of thyroid-binding globulin also increases under estrogen stimulation, leading to a decrease in free thyroxine T4.

The transient decrease in the free T4 level stimulates the thyroid where the patient may develop gestational transient thyrotoxicosis, leading to vomiting. Thus, higher levels of estrogens during pregnancy can raise the risk of HG. The cause of liver dysfunction is unclear but is usually resolved when vomiting decreases [7,9].

No single therapy has been found to be significantly beneficial for HG patients. The medical approach is based on correcting electrolyte levels and preventing dehydration [23]. Sometimes patients required hospitalization requiring a complex management including vitamins, parenteral nutrition and general support medical control. If treated early, HG is usually not associated with any major adverse maternal or fetal outcome.

Few studies have shown an increased incidence of low birth-weight and prematurity in the babies of these patients. No specific treatment is required for liver dysfunction and liver failure is only rarely reported [7,9,18,19]. ICP, also known as obstetric cholestasis, is characterized by cholestasis and pruritus, with onset in the late second and third trimester of pregnancy.

It is associated with abnormal liver function in the absence of other liver diseases and is resolved completely after delivery.

Seasonal variations indicate a higher incidence in the winter months in some countries [20,21]. Risk factors include advanced maternal age, a history of cholestasis secondary to oral contraceptives, personal or family history of ICP, multiple pregnancy and fertility treatment.

Some studies suggest a higher prevalence in patients with hepatitis C, cholelithiasis and non-alcohol fatty liver disease NAFLD [8,22,23]. A typical symptom of ICP is intense pruritus, commonly localized on palms and soles, which progresses during pregnancy. Increased serum bilirubin levels have been observed in a small number of cases, while jaundice occurs in [8,24]. The serum autotaxin, a lysophospholipase D, essential for angiogenesis and neuronal development during embryogenesis, was found to be a highly sensitive and specific diagnostic marker that distinguishes ICP from other pruritic disorders of pregnancy and pregnancy-related liver diseases [16,25].

Ultrasonography should be performed to exclude cholelithiasis [8,22,26]. The etiology of ICP is multifactorial, and involves genetic, hormonal, and environmental factors [21,22,24]. Estrogens and progesterone metabolites have been involved in the pathogenesis of ICP. Cholestasis, in women using oral contraceptives with high estrogen content, is similar to ICP.

A high level of estrogen, in genetically predisposed individuals, may induce ICP by impaired sulfation and the transport of bile acids. Genetic predisposition in ICP has been suggested by family clustering, presence of ethnic and geographic variations, and by variants in genes coding for hepatobiliary transport proteins. Genetic predisposition may alter the bile ducts and hepatocytes cell membrane composition, as well as produce a dysfunction of biliary canalicular transporters.

ABCB4 variants with subsequent loss of MDR3 protein are associated to low levels of phospholipids in bile and a high biliary cholesterol saturation index [27]. Placental gene expression profiles in ICP women have also revealed that the core regulatory genes where involved in the immune response, the vascular endothelial growth factor VEGF signaling pathway, and G-protein coupled receptor signaling, suggesting an essential role of the immune response and angiogenesis in the pathophysiology of ICP [29,30].

Bile acid homeostasis and transport in hepatocytes were found to be tightly regulated by the nuclear hormone receptor, farnesoid X receptor, encoded by NR1H4. The variants in NR1H4 may possibly be implicated via downregulation of BSEP expression [24—28,31] ; and during recent years increasingly ICP is recognized to be associated with an abnormal metabolic profile, including glucose intolerance and dyslipidemia, although it is considered to be secondary to maternal aberrant BA homeostasis reviewed in [32].

However, frequencies and types of genetic variants in Latin American and Mexican population have not been described and need further investigation. UDCA increases the expression of bile salt export pumps and increases placental bile transporters. UDCA improves clinical symptoms, predominantly pruritus, and may even reduce the risk of premature birth.

It is more effective than cholestyramine or dexamethasone in controlling pruritus. Fat malabsorption can result in fat-soluble vitamin deficiencies. Some women do not respond to UDCA. In these cases combining treatment with rifampicin can improve the symptoms and biochemical results [22,33—35].

ICP usually resolves within six weeks after delivery. Maternal outcomes are excellent, however, there is a risk of fetal distress, preterm labor, stillbirth, or even intrauterine death by fetal asphyxia. Delivery at 37 wg should be considered because intrauterine death is more common in the last month of pregnancy, and fewer deaths before 37 wg.

Decisions should be tailored to each pregnancy [8,16,22,33]. ICP may also be associated with an abnormal metabolic profile in afflicted women, and an especially higher prevalence of dyslipidemia, impaired glucose tolerance, and maternal comorbidities e. ICP has a high recurrence rate.

ICP affected women also have an increased risk of hepatobiliary disease later in life, most commonly gallstones, hepatobiliary malignancies and immune mediated and cardiovascular diseases. AFLP is a rare but highly threatening hepatic disease occurring during the last trimester of pregnancy, that generally begins between 30 and 38 wg [5] although it can appear at early post-partum [13,36].

This pathology is characterized by microvesicular steatosis in the hepatocytes of zone 3 centrolobular , rapid loss of liver function, jaundice, and coagulopathy requiring maternal supportive care [1]. Delivery is necessary to assure maternal survival [17,37]. Early diagnosis is also crucial in order to save maternal and fetal lives. Liver biopsy is useful to confirm AFLP diagnosis, but has been suggested as nonessential. Clinical evaluation with at least six Swansea criteria Table 3 is considered sufficient to accurately diagnose the disease [1,38—40].

These criteria include unspecific symptoms starting during the third trimester such as nausea, vomiting, jaundice, malaise, and anorexia, characteristic with higher levels of transaminases and bilirubins in a short period of time.

Liver Disease: Reproductive Considerations

Of particular importance are those diseases that exclusively affect pregnant women and have adverse effects on maternal, fetal, or neonatal outcomes. Acute viral hepatitis is an important cause of liver disease in pregnant women, and hepatitis E virus infection is associated with substantial mortality. An increasing number of women have chronic liver diseases caused by viral hepatitis, alcoholic liver disease and nonalcoholic fatty liver disease, autoimmune liver diseases, and genetic liver diseases. The presence of chronic liver diseases or cirrhosis in pregnant or nonpregnant women requires alterations in gynecologic care, including contraception, pregnancy planning, cervical cancer screening, human papillomavirus vaccination, and postmenopausal hormone therapy. Women who have had liver and other solid organ transplants require gynecologic care tailored to their immunosuppressed status. Collaboration between obstetrician—gynecologists and hepatologists is essential to provide optimal care to women with acute or chronic liver diseases.

Background: Different spectrum of liver disease can affect outcome of pregnancy. The incidence of liver disorders in pregnancy varies in different parts of the world. The present study was designed to see the incidence, spectrum, and outcome of liver disease in pregnancy. Methods: All pregnant women with deranged liver profile, attending antenatal clinic and labour room in the department of Obstetrics and Gynecology of BRD Medical College over the period of one year August to July were included in the study. Enrolled cases were followed up till discharge in respect to maternal and fetal outcome. Results: Liver disease was found in 2. Pregnancy specific liver disease was the most common type

The journal's aim is to publish articles focused on basic, clinic care and translational research that seeks to prevent rather than treat the complications of endstage liver disease. The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two receding years. CiteScore measures average citations received per document published. Read more. SRJ is a prestige metric based on the idea that not all citations are the same. SJR uses a similar algorithm as the Google page rank; it provides a quantitative and qualitative measure of the journal's impact.

Liver Disease in Pregnancy and Transplant

The purpose of this review is to discuss current and new knowledge regarding liver disease in pregnancy and pregnancy post-liver transplantation. Severe liver disease associated with pregnancy is rare. Liver biopsy is rarely needed for diagnosis but is safe in selected cases. Ursodeoxycholic acid should be initiated at diagnosis.

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