Can terminate Ampiclox one month of pregnancy

Liver disease complicates about 5% of all pregnancies. Since liver diseases that are not adequately diagnosed and treated can have serious consequences for mother and child, a structured and reliable diagnosis is important during pregnancy.

Physiological changes in liver values:
The adequate interpretation of hepatologically (affecting the liver) relevant biochemical laboratory parameters as a prerequisite for the correct causal and prognostic classification of liver diseases during pregnancy has specific characteristics due to changes in pregnancy physiology. The liver values ​​in the narrower sense (GOT / GPT) as well as the gamma-glutamyltransferase (γ-GT) and the serum bilirubin generally remain in the normal range during pregnancy. This means that any increase in these parameters, which is observed in about 5% of all pregnancies, should lead to a differential diagnostic evaluation. In contrast, alkaline phosphatase (AP) often increases significantly towards the end of pregnancy due to increased secretion of the placenta (so-called placental isoenzyme). The most important physiological changes in pregnancy that are relevant for the assessment of liver function are shown in Table 1.

Liver diseases during pregnancy:

An increase in liver values ​​must be expected in up to 5% of all pregnancies. The following categorization of liver diseases during pregnancy has proven itself:


1. Pregnancy-specific liver diseases (caused by pregnancy):
  • Intrahepatic pregnancy cholestasis
  • Acute pregnancy fat liver
  • HELLP syndrome
  • Liver involvement in preeclampsia / eclampsia
  • Liver involvement in hyperemesis gravidarum

2. Selection of coincident hepatobiliary diseases (occurring randomly during pregnancy):
  • Cholelithiasis
  • Acute viral hepatitis
  • Drug-toxic hepatopathies
  • Bacterial diseases
  • Budd-Chiari Syndrome

3. Selection of pre-existing hepatobiliary diseases (pre-existing):
  • Chronic viral hepatitis
  • Primary biliary cirrhosis
  • Autoimmune hepatitis
  • Liver cirrhosis / portal hypertension

Due to the specific mechanisms of disease development and the knowledge required to avoid possible complications, pregnancy-specific liver diseases are of great importance. These are triggered by the pregnancy itself and usually occur in typical pregnancy stages (Fig. 1).

Fig. 1 Causes of jaundice depending on the gestational age, percentages in brackets. ICP: Intrahepatic Pregnancy Cholestasis; HG: Hyperemesis gravidarum; AFLP: Acute pregnancy fat liver

Diagnosis:
A hepatological diagnosis is indicated for every pregnant patient with elevated liver values ​​or itching or the occurrence of upper abdominal pain, especially in late pregnancy.

If the routinely recommended hepatitis B virus (HBV) screening of a pregnant woman shows evidence of hepatitis B surface (HBs) antigen, further specific diagnostics are also necessary.

In addition to the appropriate laboratory diagnostics, the anamnesis, especially with regard to previous pregnancies, the family anamnesis and drug-toxic causes of the liver disease, is of particular importance.

The extensive laboratory-chemical differential diagnosis aims v. a. for the exclusion or detection of previously undetected pre-existing or coincident hepatopathies.

In addition, an upper abdominal sonography should be performed to evaluate any changes in the liver parenchyma and possible gallstones. The liver biopsy, which is often still performed, should be handled very restrictively and is reserved for special, less invasive clinical situations that cannot be clarified.

Intrahepatic Pregnancy Cholestasis (ICP):
Intrahepatic pregnancy cholestasis, triggered by a reversible disruption of biliary secretion, is the prototypical pregnancy-specific liver disease. The main symptom is itching, which is why the disease is also described under the subject of skin.
In Germany, around one ICP case per 100 pregnancies is observed today.
The disease typically occurs in late pregnancy, as this is where the highest levels of female sex hormones can be detected.
Recent studies indicate that ICP is more common in patients with other gastroenterological conditions such as chronic hepatitis C virus (HCV) infection, non-alcoholic steatohepatitis, cholelithiasis, and pancreatitis. There are mutual relationships between chronic HCV infection and ICP: while HCV-positive patients develop ICP more often (16-fold increased risk), HCV infection is 3.5 times more likely to be detected in pregnant women with ICP. All patients with pregnancy cholestasis should therefore receive a virus serological diagnosis. If there is a familial accumulation of intrahepatic cholestases, genetic factors can also be considered, which can now be investigated.

Clinic: Clinically groundbreaking for the diagnosis of ICP are:

  • Itching (main clinical finding)
  • GPT increase usually <300 U / l
  • Bile acids> 10 µmol / l
  • γ-GT mostly normal
  • Exclusion of other liver or biliary tract diseases
  • Complete remission after childbirth

Further clinical symptoms can include jaundice (<10% of cases) and steatorrhea (fatty stools) with potentially accompanying vitamin K deficiency and altered coagulation. In this case, close INR controls are necessary to reduce the risk of fetal bleeding.

Diagnosis: An upper abdominal sonography is part of the obligatory initial diagnosis, in particular to detect or exclude changes in the liver parenchyma and gallstones. A liver biopsy is not indicated.

Acute pregnancy fat liver: (steatohepatitis)
The very rare clinical picture of acute pregnancy fat liver with an incidence of 1: 13,000 represents the most serious hepatological complication of pregnancy with pronounced microvesicular liver disease and the risk of fulminant liver failure.

Pathophysiology: Steatohepatitis is caused by a dysfunction of the so-called mitochondria based on a genetic predisposition with exogenous triggering from drugs or infections. In order to understand the disease, it is important that it develops when the child is a homozygous carrier of a mutation. The result is a defect in the metabolism of long-chain fatty acids, called LCHAD.

Clinic: