LIVER DISEASES AND ITS CURE

 Therapy for liver disease has improved significantly in recent decades and includes everything from diet to medication and highly advanced surgery. The diagnosis has been improved considerably in terms of serum samples and radiological technology. Despite this, part of the diagnosis is still based on liver biopsy when recommended by liver consultants.

LIVER DISEASES AND ITS CURE


Patients with liver disease develop symptoms late in the course of the disease, and we often discover them because liver samples have been included as part of another investigation. The commonly used samples (aminotransferases) only indicate the presence of an injury but not the diseases that are causing the injury. In our country, there are relatively few diseases that cause serious liver damage. In the chapter, there is a proposal for an investigation to be able to identify these quickly. Most often, patients are worried about finding a good doctor or physician for the treatment because only a specialist doctor can accurately diagnose the real issue; Doctors with the title as liver consultants or liver and gastrointestinal consultants are referred for liver and its related diseases.

Investigation of elevated liver samples

To detect liver disease, the activity of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), alkaline phosphatases (ALP), and glutamyl transferase (GT) in serum are examined. Other samples that indicate damage, such as lactate dehydrogenase (LD), do not provide additional information.

Experience has shown that patients with elevated liver samples can be divided into those who have only aminotransferase elevations and those who also have an increase in ALP. In connection with infections or drug side effects, temporary increases in aminotransferases are common, and these should, if ALP is normal, only be investigated if the patient is generally affected or if the values ​​rise continuously. A general rule is that if the patient is unaffected and the aminotransferases are <5 times the normal value, you can wait and only follow the patient for six months before further investigation, see Fact Box 2. If there are other indications of a specific disease, this should, of course, be investigated.

GT is most often elevated in liver disease. If the GT is not high, ALP increase is not due to liver disease, but the cause should be sought in other organs, for example, in the skeleton. Patients with elevated ALP (above normal value) should be investigated more quickly, as these are sometimes diseases that must be investigated immediately.

Occasional findings of an isolated increase in aminotransferases in children aged 0–2 years are not uncommon. The values ​​are usually normalized within a year or so, and if the child is otherwise healthy and has no cholestasis, these children can probably be followed conservatively. A pediatrician's contact is indicated in the initial stage.

However, in children, there are two types of early-onset liver disease with suspended bile flow to the intestine (neonatal cholestasis), bile duct atresia, and Byler's disease, respectively. Surgical action may be indicated before 8 weeks of age.

 

Anamnesis

Alcohol is the most common cause of severe liver damage in the western world. See also the chapter Alcohol - risk use, harmful use and dependence, the section Measurement methods and laboratory tests. Anamnesis is the most sensitive method of finding these patients, and a patient with elevated liver values ​​should therefore be asked about their alcohol consumption. More than 60 g alcohol/day for men and 20 g / day for women are considered to cause liver damage. A glass (equivalent to 4 cl of spirits, 15 cl of wine or 30 cl of strong beer) contains about 15 g of alcohol.

One of the most common causes of aminotransferase elevation is fatty liver due to obesity, so one should also address a diet history and ask about weight gain. Abdominal pain and weight loss indicate malignant disease. The epidemiology of hepatitis B and hepatitis C are described below. The most common inherited liver disease is hemochromatosis.

Status

Spider naevi and palmarerytem indicate that the patient has cirrhosis. Abdominal palpation can reveal liver enlargement and if the liver is uneven and lumpy, such as cirrhosis or tumor. With abdominal palpation, ascites can be detected.

The weight should be noted because being overweight is a cause of fatty liver. Increased skin pigmentation and swollen metacarpophalangeal joints are seen in hemochromatosis.

Laboratory samples

Elevated aminotransferases are caused by these enzymes leaking into the bloodstream due to cell damage. There is a correlation between the size of the ongoing damage and how high the values ​​are. In the case of a chronic injury, the values ​​are usually relatively low, while they are sky-high, for example, in an acute intoxication with paracetamol.

In bile stasis, elevated levels of ALP are seen due to induction of the enzyme, which leads to increased intracellular production and increased activity in serum. Thus, the increased serum activity is not due to cell damage. GT is formed at the same site in the cell as ALP and will rise in serum if ALP rises. Rising GT, on the other hand, often occurs without ALP rising. Many diseases only give an increase in aminotransferases and sometimes GT, while some diseases always give an increase in ALP / GT.

Some samples provide information on etiology. For the diagnosis of hepatitis, see Table 1. In chronic right-sided heart failure, a moderate increase in aminotransferases and alkaline phosphatases / GT is sometimes seen. In acute forward failure, the patient often receives sharply increased aminotransferases (> 50 times) for a few days. However, these normalize quickly.

S-ferritin and iron saturation provide information on hemochromatosis, alpha-1-antitrypsin on alpha-1-antitrypsin deficiency and the presence of antibodies to smooth muscle and mitochondria are seen in autoimmune hepatitis and primary biliary cirrhosis, respectively.

Liver function is reflected by albumin and PK / INR. These values ​​are relatively insensitive and change only when the function is significantly affected. Bilirubin rises in both bile stasis and liver failure and is therefore difficult to evaluate as a functional test.

Radiology

Fatty liver can be diagnosed with ultrasound, but not inflammation and fibrosis/cirrhosis. Patients with focal changes have usually elevated ALP, and these should be performed with ultrasound or CT. If the ultrasound is normal in patients with elevated ALP, the bile ducts are examined with MRC (magnetic camera cholangiography) to rule out bile duct obstruction, such as stones and tumors (see Figure 1). ERC (endoscopic retrograde cholangiography) and PTC (percutaneous transhepatic cholangiography) are now used only to perform therapeutic procedures.

Elastography

Elastography (often Fibro-scan, which is ultrasound-based) is used to measure the degree of fibrosis in the liver, especially in chronic hepatitis B and C. With the help of a so-called shear wave, the elasticity of the liver is measured, which can be used as a marker for fibrosis. Elastography is mainly tested in chronic hepatitis C, where it is very useful and can often replace liver biopsy. A big advantage is that the examination is done in a few minutes and can be performed in connection with a reception visit. In addition, it is painless and harmless. Elastography cannot be used in acute liver damage as you can get high values ​​for reasons other than fibrosis1.

Liver biopsy

Liver biopsy is performed to diagnose and stage diseases of the liver, i.e. to map the degree of fibrosis and inflammation. All patients who are uncertain about diagnosis and prognosis should take a liver biopsy, as no method can yet replace histology to clarify the degree of fibrosis and inflammation.

Investigation of jaundice

The flow chart in Figure 1 can be used in the investigation of jaundice. Patients with jaundice should always be investigated immediately. If the mildly jaundiced patient has normal liver values, it is likely that it is Gilbert's syndrome. Gilbert's syndrome involves intermittent unconjugated hyperbilirubinemia and is due to a reduced conjugation capacity of the liver cells. The disease is common, harmless, and gives no symptoms. Bilirubin values ​​are usually <50 micromol / l. Differential diagnostic should consider hemolytic anemia.

Parenchymal jaundice is usually caused by alcohol, viral hepatitis, drugs, or other toxic substances, while jaundice is caused by cholecystitis or biliary tract, or pancreatic cancer. The patient is referred urgently for an ultrasound examination of the liver and bile ducts. If the examination shows dilated bile ducts, further investigation of bile ducts is carried out with MRC and ERC. If the bile ducts are normal, it indicates parenchymal liver disease. If these patients show signs of liver failure with rising PK / INR levels and declining albumin, contact a liver transplant center. Liver transplantation is a very complex procedure performed when there are is almost no external medicine or procurement remain effective, and this procedure need to be done by highly practiced surgeons and technologically well-equipped operation theatres are required,  gastroenterologist in Irvine (a city in Canada) is very known and trained in these kinds of interventions.

Viral hepatitis

There are currently five known viral hepatitis - hepatitis A – E, of which hepatitis A, B, and C are most common. Viral hepatitis is classified as a generally dangerous disease, and every newly diagnosed case must be reported in accordance with the Swedish Communicable Diseases Act. Hepatitis A and E are transmitted focally-orally, while hepatitis B, C, and D are transmitted through body fluids. Hepatitis C is very common in people with intravenous addiction. The notifying doctor must give advice on infection control and start infection tracing.

In addition to the above-mentioned actual hepatitis virus, other viruses, such as Epstein-Barr virus and cytomegalovirus, can also cause liver effects and, in rare cases, clinical hepatitis.

Acute viral hepatitis can be clinical or subclinical. In clinical acute hepatitis, there are first general symptoms, such as fatigue, fever, joint pain, and muscle aches. Thereafter, jaundice may occur, reducing general symptoms. The urine becomes dark, and the stool light. Acute hepatitis B and C can, regardless of the clinical picture, turn into a chronic form. Chronic hepatitis progresses insidiously and is usually asymptomatic, but patients sometimes experience general fatigue. Only in advanced liver damage with impaired liver function do symptoms such as severe fatigue, ascites, and increased tendency to bleed appear. Chronic hepatitis can lead to liver cirrhosis and primary liver cancer. For the different forms of hepatitis, incidence, routes of infection, incubation period, disease picture, and risks of developing chronicity.

In the laboratory, elevated aminotransferases are seen in viral hepatitis, where ALT is normally higher than AST. In acute hepatitis, the aminotransferases, as well as bilirubin (conjugated), can be greatly increased, while ALP and GT are slight to moderately elevated. The PK / INR value may be increased in the event of severe liver damage. The majority of patients with acute hepatitis are followed up in outpatient care - initially approximately once a week with control of blood and liver status and PK / INR. If there is a risk of fulminant hepatitis, the patient is admitted for observation. An approximate laboratory benchmark for hospitalization may be PK / INR> 1.7, but the patient's general condition should be considered. In chronic hepatitis, the aminotransferases are usually only slightly elevated and sometimes completely normal. It is not possible to distinguish different hepatitis on the clinical picture or on biochemical parameters. The etiology is determined via serological tests and PCR.

Patients with acute hepatitis can eat a normal diet. Alcohol and drugs should be avoided. Immune prophylaxis should be given to those in the environment who may have been infected. Prophylaxis of hepatitis C does not exist. Specific antiviral therapy is not given in acute hepatitis except possibly in acute fulminant hepatitis with liver failure. In chronic hepatitis B and C, however, specific antiviral therapy should always be considered.

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