Differential diagnosis of viral hepatitis, its essence, markers, the need for

The term viral hepatitis can describe either clinical disease or histological findings associated with the disease. Acute infection with the hepatitis virus can range from subclinical illness, symptomatic illness to fulminant liver failure.

Adults with acute hepatitis A or B usually have symptomatic signs, while those with acute hepatitis C may not have symptoms.

The clinical picture of most viral hepatitis is very similar, differing only in value in terms of the severity of the disease and its results. Viral hepatitis A and E are characterized by a cyclic benign course with complete recovery.

In a complex chronic course of hepatitis B, C and D, in some cases, lethal outcomes are observed. The primary action for timely treatment is the differential diagnosis of viral hepatitis.

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Symptoms and insidiousness of the disease

Typical symptoms of acute chronic hepatitis are: fatigue, anorexia, nausea and vomiting. Very high aminotransferase values ​​(> 1000 U/L) and hyperbilirubinemia are often observed.

Severe cases of acute hepatitis can rapidly progress to acute liver failure, characterized by poor hepatic synthetic function. This is often defined as a prothrombin time (PT) of 16 seconds or an international normalized ratio (MHR) of 1,5 in the absence of preexisting liver disease.

Fulminant hepatic failure (FPF) is defined as acute failure that is complicated by encephalopathy. Unlike encephalopathy associated with liver cirrhosis, FPI is explained by increased permeability of the blood-brain barrier and impaired osmoregulation in the brain, which leads to edema of brain cells.

The resultant cerebral edema is a potentially fatal complication of fulminant hepatic failure.

FPI can occur in 1% of cases of acute hepatitis due to hepatitis A or B. Hepatitis E is common in Asia, and hepatitis C is questionable. Although the problem of fulminant liver failure can be resolved, more than half of all cases are fatal if liver transplantation is not performed on time.

Provided that acute viral hepatitis does not progress to FPI, many cases resolve within days, weeks, or months. Alternatively, acute viral hepatitis can develop into chronic hepatitis. Hepatitis A and hepatitis E never progress to chronic hepatitis, both clinically and histologically.

The histological evolution of chronic hepatitis has been demonstrated in approximately 90-95% of cases of acute hepatitis B in newborns, 5% of cases of acute hepatitis B in adults, and up to 85% of cases of acute hepatitis C. In some patients with chronic hepatitis, the disease remains asymptomatic throughout their lives. others may complain of fatigue (mild to severe) and indigestion.

Approximately 20% of patients with chronic hepatitis B or hepatitis C eventually develop cirrhosis, as evidenced by histological changes, severe fibrosis, and nodular regeneration. While some patients with cirrhosis are asymptomatic, others develop life-threatening complications. Clinical diseases of chronic hepatitis and cirrhosis can take months, years or decades.

Indications for

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Differential diagnosis of viral hepatitis is necessary for the treatment of leptospirosis, yersiniosis, mononucleosis, malaria, obstructive and hemolytic jaundice, toxic hepatosis.

Some acute viral diseases trigger an immune system response that causes several types of white blood cells to increase. Differential diagnosis can provide clues to the specific cause of this immune process.

For example, it can help determine if an infection is caused by bacteria or viruses.

In malaria, there is a clear alternation of attacks of fever with chills, replaced by fever and sweat, and periods of apyrexia. The enlargement of the inflamed spleen in size is very painful. Hemolytic anemia is observed, an indirect proportion of bilirubin in the blood serum prevails.

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With a course of obstructive jaundice, stones in the gallbladder and passages, an increase in the head of the pancreas and other symptomatic signs are detected using ultrasound.

With such a diagnosis, most patients have a moderate increase in the activity of ALT, AST, leukocytosis, and accelerated ESR. Hemolytic jaundice is characterized by anemia, accelerated ESR, an increase in the indirect proportion of bilirubin in the blood. Stercobilin is always present in the stool.

Differential diagnosis of GV with hepatosis is complicated and requires thoughtful and painstaking work from the doctor. In this case, a correctly collected anamnesis is essential. Indications for treatment are based on viral studies (including viral nucleic acid determination), determination of disease activity and stage (including biochemical, pathological and/or non-invasive methods) and excluding contraindications.

To avoid unnecessary side effects and for a cost-effective approach, emphasis is placed on the importance of rapid and detailed virologic assessments, the applicability of transient elastography as an acceptable alternative to liver biopsy, and the relevance of an appropriate consistent follow-up schedule for viral response during therapy.

Suprahepatic jaundice

In suprahepatic jaundice, excessive breakdown of red blood cells occurs, which suppresses the liver’s ability to conjugate bilirubin. This causes unconjugated hyperbilirubinemia. Any bilirubin that can be combined will be cleared from the body normally, but unconjugated bilirubin remaining in the bloodstream causes jaundice.

Hepatic jaundice

Liver diseases of all kinds threaten the organ’s ability to keep pace with bilirubin processing. Hunger, circulating infections, certain medications, hepatitis, and cirrhosis can cause hepatic jaundice, as well as some hereditary liver chemistry defects, including Gilbert syndrome and Crigler-Najjar syndrome.

In hepatocellular (or intrahepatic) jaundice, there is dysfunction of the liver itself. The liver loses its ability to conjugate bilirubin, but in cases where it can also become cirrhotic, it compresses the intrahepatic portions of the biliary tree to cause some degree of obstruction. This results in both unconjugated and conjugated bilirubin in the blood, called a “mixed” picture.

Subhepatic jaundice

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Subhepatic forms of jaundice include jaundice caused by the inability of soluble bilirubin to reach the intestine after it has left the liver. These disorders are called obstructive jaundice.

The most common cause is the presence of gallstones in the ducts. Other causes are associated with birth defects and infections that damage the bile ducts: drugs, infections, cancer, and physical injury.

Some medications, and rarely pregnancy, simply cause bile to stop in the ducts.

Subhepatic jaundice refers to the obstruction of the bile drainage system. Bilirubin, which is not excreted from the body, combines with the liver, resulting in conjugated hyperbilirubinemia.

Differential diagnostic markers

Definitive diagnosis of hepatitis B or hepatitis C requires various immunological and molecular diagnostic tests and takes a significant amount of time before starting treatment.

Recently there have been table reports suggesting a screening marker using CBC with cell population data (CPD) for infectious diseases such as sepsis and tuberculosis. If such screening markers for hepatitis are developed, it will help reduce time to treatment and medical costs.

192 patients with acute viral hepatitis (AVH) from three different hospitals in the Madras metropolitan area, between November 1985 and January 1986, were tested for serological markers of hepatitis A virus (anti-HAVIgM) and hepatitis B virus (HBsAg, HBeAg , anti-HBcIgM and anti-HBs) using an enzyme linked immunosorbent assay (ELISA).

Hepatitis B was diagnosed as the main type of AVH in the hospital (48,9%). Using the anti-HBcIgM marker of the hepatitis B virus and anti-HAVIgM, it was possible to find out that 13,5% of cases currently suffering from hepatitis A were either HBV carriers (8,3%), or cases recovering from a previous attack on hepatitis B (5,3%).

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Various combinations of positivity of HBV markers have been observed and their diagnostic value has been suggested.

Diagnosis of congenital hepatitis in children

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Certain chemicals in bile can cause itching when too much of them gets into the skin. In newborns, insoluble bilirubin can enter the brain and cause irreparable harm.

Prolonged jaundice can disrupt the balance of chemicals in the bile and cause stones to form. Apart from these potential complications and discoloration of the skin and eyes, jaundice itself is harmless.

Other symptoms are determined by the disease causing the jaundice.

Newborns are the only large patient population in whom jaundice itself requires attention. Since insoluble bilirubin can enter the brain, the amount in the blood should not exceed a certain level. If there is a suspicion of increased hemolysis in the newborn, the bilirubin level should be measured again within the first few days of life. If the bilirubin level is too high soon after birth, treatment should be started immediately.

Transfusing most of a child’s blood was the only way to reduce the amount of bilirubin several decades ago. Then it was discovered that the bright blue light turns bilirubin harmless.

The light chemically changes the bilirubin in the blood as it passes through the baby’s skin. In 2003, researchers tested a new drug called Stanat, which promised to block the production of bilirubin, but was never finally approved or widely used.

Differentiating hepatitis from other diseases

In medicine, differentiation is looking for differences in different but similar diseases.

Common causes of liver cirrhosis include prolonged treatment of viral hepatitis C and excessive alcohol abuse. Obesity is common and can be a risk factor on its own or in combination with excessive alcohol consumption and hepatitis C.

According to the US National Institutes of Health, the differential diagnosis of hepatitis has revealed that people who have consumed more than two alcoholic beverages a day (including beer and wine) are more likely to develop hepatitis C for several years, especially in women. For men, consuming three a day for the same period may put them at risk of cirrhosis.

However, the amount for each person varies, and this does not mean that everyone who has ever drunk more than the average is bound to develop cirrhosis. Alcohol-induced cirrhosis is often the result of the systematic use of alcohol in volumes that are several times higher than this value and for 10-12 years.

Hepatitis C can be acquired through sexual intercourse or contact with infected blood. Infection can be acquired through syringes, including tattooing, body piercings, intravenous drug use, and needle sharing.

Inflammation caused by autoimmune disease: Autoimmune hepatitis may have a genetic cause. About 70 percent of people with autoimmune hepatitis are women.

VIDEO

Lecture: “Diagnostics, treatment and prevention of chronic hepatitis.”

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Svetlana Borszavich

General practitioner, cardiologist, with active work in therapy, gastroenterology, cardiology, rheumatology, immunology with allergology.
Fluent in general clinical methods for the diagnosis and treatment of heart disease, as well as electrocardiography, echocardiography, monitoring of cholera on an ECG and daily monitoring of blood pressure.
The treatment complex developed by the author significantly helps with cerebrovascular injuries and metabolic disorders in the brain and vascular diseases: hypertension and complications caused by diabetes.
The author is a member of the European Society of Therapists, a regular participant in scientific conferences and congresses in the field of cardiology and general medicine. She has repeatedly participated in a research program at a private university in Japan in the field of reconstructive medicine.

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