Liver Problems In Pregnancy
Liver disease is serious and requires treatment and regular monitoring by a liver specialist.
A liver specialist is known as a hepatologist and you need to be referred by your family doctor or general practitioner. Over nearly 40 years of practicing medicine, I have seen many patients develop severe liver disease, which sadly could have been prevented by early detection and early referral to a hepatologist. There needs to be more awareness of liver disease so that patients can be treated early so that we can prevent cirrhosis, liver failure and liver cancer. Make sure you have your liver function checked annually with a blood test.
I have presented my ideas on how to help those with liver diseases using nutritional medicine, which I have been using for many years with good success rates. However, my recommendations do not replace the care of your own doctor and you should remain under the care of your own doctor whilst using nutritional therapies.
If you have any questions you may contact my naturopath, Christine, on 623 334 3232 or email us at [email protected]
Liver problems in pregnancy
Certain liver diseases only occur during pregnancy and can vary from mild to severe.
It is important to try to keep your liver healthy at all times so that if you do fall pregnant your liver can cope with an increased work load during pregnancy. If you enter pregnancy with a fatty liver or a sluggish or inflamed gallbladder you will be at increased risk of liver disorders during pregnancy. Keeping your nutritional status high and your weight in the healthy range will help to a significant degree to prevent liver problems during pregnancy.
The most common types of liver disease unique to pregnancy include:
- hyperemesis gravidarum
- acute fatty liver of pregnancy
- intrahepatic cholestasis of pregnancy
Hyperemesis gravidarum occurs in around 1 per 100 pregnancies, in other words 1% of pregnancies.
It usually starts in the first trimester (first third of pregnancy), around 4 to 10 weeks after conception, but can occur as late as 20 weeks gestation. Other causes of vomiting during pregnancy, that are not due to hyperemesis gravidarum, can be uncomplicated nausea, stomach ulcers, infections of the gut (gastroenteritis), gallstones, viral hepatitis and kidney infections.
Who is likely to get hyperemesis gravidarum?
You are at a higher risk if you –
- have a previous history of hyperemesis gravidarum
- have an overactive thyroid gland
- have a molar pregnancy
- have diabetes
- have a multiple pregnancy (twins or triplets etc)
- are overweight with a fatty liver
What causes hyperemesis gravidarum?
The causes are not fully understood. Hormone levels play a role because nausea and vomiting peak when the pregnancy hormones human chorionic gonadotropin (HCG) and estradiol are at their highest levels.
Symptoms include severe continual nausea and vomiting, which often requires hospitalization and intravenous fluids. Patients are often very dehydrated and may show signs of malnutrition. Maternal weight gain is usually poor and weight loss is frequent.
Ketones are often present in urine testing. Severe sufferers often have abnormally elevated liver enzymes, which indicate liver inflammation. Blood tests may show elevations in the liver enzymes (aminotransferase and alkaline phosphatase) and bilirubin. Abnormal levels of pancreatic enzymes may be present in the blood - amylase and lipase levels may rise up to 5 times of normal values, which indicate inflammation of the pancreas.
Thankfully, a liver biopsy is usually not necessary, but if a more serious liver disease must be ruled out, a liver biopsy may be performed. In patients with hyperemesis gravidarum, a liver biopsy usually shows normal looking liver cells or the existence of sluggish bile flow in the tiny liver bile ducts.
Treatment of hyperemesis gravidarum
- Avoid things that make you feel nauseated, such as odors from perfume, smoke, chemical household products and cooking strong smelling foods.
- Eating low fat small meals and taking digestive enzymes in the middle of meals may help to reduce symptoms.
- Raw juices may help enormously and good things to juice are apples, pears, celery, cabbage, mint, parsley, carrot and ginger. Drink 3 ounces (100mls) at a time. Vitamin C powder in a dose of 500mg can be added to the juice.
- Ultimate Gut Health Powder in a dose of 1 level scoop (8g) can be added to certain milks – try rice milk, almond milk or coconut milk. Do not heat the milks. Take the gut powder once daily.
- Selenium in a dose of 100 mcg to 200 mcg daily may help the liver function and reduce inflammation.
- N Acetyl Cysteine (NAC) capsules in a dose of 600 mg three times daily will help to reduce inflammation in the liver and bile ducts.
- Homeopathic drops of Ipecac or Nux Vomica may help and are harmless; try taking 5 drops in water every hour.
- Crystallized ginger or ginger capsules (250 mg by mouth 4 times per day) have been used with some success.
- Acupuncture and wristbands that apply pressure to the front of the wrist can be tried. In a Cochrane review, the wristband demonstrated no benefit over placebo, but all of the studies had a large placebo effect, and no side effects were associated with the treatment. Another strategy that has proven successful is multivitamin and mineral use at the time of conception, so any patient with a history of hyperemesis gravidarum should be prescribed multivitamins and minerals before conception.
- Injections of B vitamins can sometimes be very effective, especially if the patient is unable to keep oral tablets in their stomach. These injections must be prescribed by a doctor and the most important B vitamins are vitamin B 12 and B 6. These can be given weekly into the buttocks. Vitamin B 6 in a dose of 25 mg taken orally 3-4 times per day can be used safely.
The drug doxylamine, which is an H1 receptor blocker, can be given as 12.5 mg by mouth 3-4 times per day along with the vitamin B.
If dehydration is present, intravenous fluids must be started, and anti-vomiting drugs may be prescribed in hospital such as promethazine or steroids such as methylprednisolone orally or intravenously.
It is better to be admitted to hospital earlier rather than later to avoid serious dehydration and weight loss. Intravenous fluids along with electrolytes and vitamins, especially vitamin B 1 (thiamine), should be given for patients who cannot tolerate liquids for a prolonged period of time. In severe cases, tube feeds and intravenous (parenteral) nutrition may be necessary.
Thiamine should be given in a dose of 100 mg intravenously before the administration of any glucose-electrolyte containing fluids, and then continued until an adequate diet is able to be tolerated. It is wise to supplement with thiamine and indeed the injections of B 12 and B 6 as well in any patient with more than 4 weeks of vomiting.
As well as physical complications, some patients can experience significant mental issues including anxiety and depression.
If effective treatment is given early most studies have shown the mother and baby progress normally. In very severe cases the birth weight of the baby is significantly lower than those with mild disease. Thankfully, there is no evidence of increased risk of congenital malformations. Cases of intrauterine death have been reported, but these are extremely rare and have only been seen in cases of severe disease.
Acute fatty liver of pregnancy (AFLP)
Acute fatty liver of pregnancy (AFLP) occurs in 1 per 10,000 to 15,000 pregnancies. AFLP often starts in the second half of pregnancy (from 27 to 40 weeks gestation), usually close to the end of the pregnancy. It may be missed and may not be diagnosed until after the birth.
There is an increased risk of AFLP in older mothers, multiple gestations (twins or triplets etc), pre-eclampsia, and a prior history of AFLP.
Complicated genetic and metabolic factors may be underlying and there is an increased risk of AFLP in women who have a genetic defect (mutation) that affects their mitochondrial fatty acid oxidation pathway and women who carry a fetus with a long-chain 3-hydroxyacyl-coenzyme-A-dehydrogenase (LCHAD) deficiency.
In many cases, AFLP is associated with mutations in LCHAD, which is 1 of 4 enzymes that break down long-chain fatty acids in the liver. This deficiency leads to a buildup of these fatty acids in the liver. There is an 18-fold increase in maternal liver disease in mothers carrying infants with fatty acid oxidation (FAO) deficiencies.
Symptoms of acute fatty liver of pregnancy (AFLP)
AFLP manifests as nausea, vomiting, loss of appetite, abdominal pain, fluid inside the abdomen (ascites) and worsening jaundice. Kidney failure may occur and severe mental confusion (hepatic encephalopathy) occurs in 60% of patients. Around half of patients also have signs of preeclampsia – namely high blood pressure, protein in the urine and severe fluid retention.
Blood tests for liver function tests will show elevation of liver enzymes and bilirubin. Severe problems such as low blood sugar (hypoglycemia), high blood ammonia levels, low platelets and bleeding disorders are often present.
Treatment of acute fatty liver of pregnancy (AFLP)
AFLP is a serious life threatening disease and the patient should be immediately admitted to hospital. The condition of the fetus must be continually monitored. The treatment is delivery of the fetus, which stops the overload of fatty acids on the mother’s liver. This is urgent, as recovery before delivery of the baby has not been reported.
Because of the requirement for immediate delivery of the baby, around 75% of babies are born preterm, with an average delivery at 34 weeks of pregnancy. Infants of mothers with AFLP must be tested for defects in their fatty acid oxidation because early treatment can decrease infant mortality and morbidity.
Most patients start to improve within 48 to 72 hours after delivery. Severe cases require intensive care level monitoring and possible transfer to centers capable of liver transplants.
Liver function usually normalizes within a week of delivery but may take several months. Complete recovery usually occurs. In the past, many women with AFLP died and mortality rates were as high as 70%. Today mortality rates are estimated from 7-18% and the causes of death include liver and/or kidney failure, postpartum hemorrhage, wide spread blood clots, pancreatitis, and respiratory failure.
Recurrence of AFLP in future pregnancies is rare, but has occurred, usually in carriers of LCHAD mutations. These women must be monitored by specialists in maternal-fetal medicine.
Intrahepatic cholestasis of pregnancy (ICP)
Intrahepatic means inside the liver. Cholestasis means stasis (lack of flow) of bile inside the tiny bile ducts, which are situated within all liver tissue. Intrahepatic cholestasis of pregnancy (ICP) occurs in around 2 per 1,000 pregnancies. It usually starts in the last third of pregnancy (third trimester), around 30 weeks gestation.
It is more common in older mothers and in women who had sluggish bile flow (cholestasis) while taking oral contraceptives. The causes of ICP include genetic and hormonal factors.
What causes ICP?
ICP is caused by abnormal transport of bile fluid, which causes saturation of the liver’s biliary system. ICP can occur in families during pregnancy and is thought to be an inherited defect in the MDR3 gene, which encodes for a canalicular phospholipid translocator involved in bile duct secretion of phospholipids. Mutations in the MDR3 gene are not the only cause and probably account for up to 15% of cases of ICP.
Female sex hormones play a large causal role, as almost all cases are seen in the third trimester, when estrogen levels are rising. Estrogen hormones are known to cause stasis of bile (cholestasis).
The sex hormone progesterone has also shown a role in causing ICP. One study demonstrated that 64% of patients who developed ICP were taking progesterone tablets to reduce the risk of premature birth. A large percentage of women with ICP had relief of symptoms after cessation of progesterone therapy and another 10% after a reduction in their dose of progesterone.
Symptoms of ICP
Patients with ICP develop generalized itching (pruritus) that is often most severe on the palms and soles, and then moves to the face and trunk. The pruritus worsens over time and is gone within 48 hours of birth. Pruritus may be so severe that it causes poor sleep, skin trauma, sores, anxiety and depression. Around 20% of patients become jaundiced which means that the buildup of bile in the skin causes yellow eyes and skin. Because the bile is not flowing from the liver into the intestines, problems with digestion and absorption of fats in the diet results in diarrhea or fatty stools in some patients.
Blood tests usually show elevated bilirubin levels and elevated liver enzymes. The most accurate laboratory test is serum bile acids, which may be the first or only blood abnormality and this test is used to make a definitive diagnosis of ICP. Women with ICP usually show elevated bile acids which may sometimes be as high as 100 fold of normal. These tests usually show normal values within 2-8 weeks after birth.
Treatment of intrahepatic cholestasis of pregnancy (ICP)
ICP can have severe outcomes such as premature labor and stillbirth, so patients should be treated at centers capable of treating premature infants. Early delivery of the fetus may be required.
Treatment consists of the drug Ursodeoxycholic acid (UDCA), which reduces itching and liver enzymes and then allows birth to occur closer to full term. Another drug called cholestyramine can be used to reduce pruritus, but it is less effective than UDCA and can cause more side effects.
You can talk to your doctor about the use of nutritional supplements to support bile transport and liver detoxification and these include the amino acids taurine and glycine. Theoretically, supplements of NAC 600mg three times daily, selenium 100 to 200mcg daily, vitamin C 2000mg daily and vitamin E 1000 UI daily may reduce inflammation in the bile ducts and liver cells, but have not been studied in a controlled way.
The incidence of spontaneous premature labor in women with ICP ranges from 30-40%. The risk of stillbirth increases after 37 weeks gestation, which supports active treatment of induced delivery at 37 weeks.
Fetal death rates in women with ICP have been recorded to be as high as 11%. Delivery of the fetus is recommended when fetal lung maturity is demonstrated.
Generally all symptoms of ICP go after delivery of the baby, and there is only a very small chance of persistence after birth, mostly in rare inherited forms of ICP. There is a high chance of recurrence of ICP in future pregnancies, which is estimated to be 45-70%, so this is an important factor to consider.
One study found that ICP may cause an increased susceptibility to developing more serious liver diseases in the future. These include infection of the gallbladder (cholecystitis), gallstones, fatty liver and cirrhosis. Thus, if you have suffered with ICP it is important to start taking extra care of your liver by following a healthy diet and avoiding excess alcohol. The use of a good liver formula containing Milk Thistle, B vitamins, taurine and selenium can help to support healthy liver tissue and function.
Avoid becoming overweight and if you have a fatty liver it is important to reverse it through a healthy diet and a regular exercise program. For more information see my book titled Fatty Liver – You can reverse it.
The above statements have not been evaluated by the FDA and are not intended to diagnose, treat or cure any disease.