Tratamiento de enfermedades hepáticas en CDMX

Specialty

Treatment for liver diseases in CDMX, Mexico Col del Valle

Doctor:

Octavio Rojas Diaz

Specialty

Gastrosurgeon / Liver Diseases

Address

Av. Coyoacán 715

Cp 03100 Col Del Valle CDMX

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liver diseases

viral hepatitis

Viral hepatitis are contagious diseases caused by viruses that specifically affect the liver and alter its function. There are five known types of viral hepatitis: A, B, C, D, and E.

Despite prevention and vaccination efforts, viral hepatitis continues to be a frequent cause of medical consultation. Diagnosis is based on history and physical examination, along with interpretation of elevated liver pigment and enzyme levels.

The definitive diagnosis is confirmed by the detection of specific markers of these viruses in the blood of patients, either antigens or their genome, as well as the antibodies produced against them.

The interpretation of the results of the serological tests is facilitated by correlating them with the clinical symptoms, knowing the routes of transmission of the infection, the natural history of the disease and the process of viral replication.

Hepatitis A

Hepatitis A is a highly contagious disease that affects the liver and is the most common form of hepatitis in Mexico. Anyone, regardless of age or gender, can get it. It is generally transmitted from person to person through the fecal-oral route, by putting objects contaminated with the feces of a person infected with the virus in the mouth. The lack of adequate sanitary conditions and inadequate personal hygiene increase the risk of transmission.

Most cases of infection are due to contact with an infected housemate or sexual partner. The virus can also be transmitted through food or drink handled by an infected person. Although outbreaks of the waterborne disease are rare, they can occur if the water is contaminated with sewage or is not properly treated. The virus is not transmitted by casual contact at work, factory, or school.

Symptoms of the disease may include fever, malaise, fatigue, loss of appetite, nausea, abdominal pain, dark urine, and jaundice (yellowing of the skin and eyes). Most people recover without complications within a few weeks, and symptoms are more common in adults than children. The contagious period begins about a week or two before the onset of symptoms and is minimal for the week following the onset of jaundice. Once recovered, people are immunized for life and are no longer carriers of the virus.

There is no specific treatment for hepatitis A, and bed rest is generally recommended. The best long-term protection is the hepatitis A vaccine. To prevent person-to-person transmission, it is essential to wash your hands thoroughly after using the bathroom and changing diapers, and before preparing or eating food. In case of close contact with an infected person, immunoglobulin vaccinations are recommended to minimize the risk of contracting the disease.

Hepatitis A virus (HAV):

Hepatitis A virus (HAV) belongs to the Picornaviridae family and can be found in blood and feces during the incubation phase and early illness, making it difficult to detect once symptoms appear.

In this phase, the presence of the virus in the blood coincides with its excretion in the feces.

To diagnose Hepatitis A, a test is performed to detect the presence of IgM antibodies, which rise rapidly at the onset of symptoms and peak shortly thereafter. This is the most reliable method for early diagnosis of the disease.

Over time, IgM levels decrease to almost undetectable. On the other hand, IgG antibodies also increase during the acute phase and decrease slowly during convalescence, but they remain in the serum for decades and only become negative at very advanced ages.

Total anti-HAV antibodies refer to the pool of IgA, IgG and IgM in the serum against HAV. These levels indicate whether there has been or continues to be an HAV infection and resistance to subsequent infection with the virus. If an individual is total anti-HAV positive, they are immune, whereas those with total anti-HAV negative are susceptible to infection.

During acute hepatitis, a negative total anti-HAV result excludes HAV as an etiologic agent. In acute HAV hepatitis, a positive result is obtained in most cases, but this is not sufficient for an etiological diagnosis. In endemic areas, where the majority of the population has positive titres, it is necessary to determine the anti-HAV IgM to confirm that it is acute HAV hepatitis and not another type of viral hepatitis in a subject immune to HAV.

On the other hand, in areas of low prevalence, it is also necessary to determine the anti-HAV IgM to confirm the etiology of the infection. If a positive result for anti-HAV IgM is obtained, it should be confirmed by detecting total anti-HAV.

anti-HAV IgM:

Its half-life is five days and it is detected in serum at the end of the incubation period, persisting during the illness and the first weeks of convalescence. The presence of IgM indicates current or recent infection with the virus, making it the preferred marker for diagnosing acute hepatitis A. In the event of a negative result for acute hepatitis, a second determination may be recommended after a few days. It usually appears at the same time as the clinical symptoms of hepatitis.

A acute and disappears in a period that varies between six weeks and six months. The reaction of immunocompromised individuals is unknown.

anti-HAV IgG:

It appears before the first symptoms and persists indefinitely. In the absence of IgM, it indicates a previous infection and immunity.

HAV detection:

It has little use in clinical practice and is used in epidemiological studies and in outbreaks to detect the virus in shellfish or other materials that may be contaminated. HAV antigen and/or RNA can be determined.

In summary, hepatitis A is a very common infectious disease caused by an enterovirus from the Picornaviridae family, known as hepatitis A virus (HAV), which causes acute inflammation of the liver in most cases. It is transmitted by the oro-fecal route, such as through contaminated food. It causes an acute form of hepatitis (inflammation of the liver) and does not have a chronic phase.

The patient's immune system creates antibodies against hepatitis A, which provide immunity against future infection. There is a vaccine available that prevents hepatitis A infection for life.

Characteristics of hepatitis A

Hepatitis A Virus (HAV) is a hepatotropic virus that can cause mild or severe symptoms, including jaundice (yellowing of the skin or eyes).

Although it rarely causes fulminant hepatitis, most people make a complete recovery. Unlike hepatitis B or C, hepatitis A does not become chronic or cause a carrier state.

Transmission occurs mainly through food contaminated with saliva or feces. Children and adolescents in developing countries are more likely to contract HAV, but in developed countries it can also affect adults and cause serious complications.

Fortunately, there is an effective vaccine against hepatitis A that is administered in the vaccination schedule in Mexico.

Common symptoms of hepatitis A include tiredness, nausea, fever, loss of appetite, abdominal pain, and diarrhea. Some people may also experience dark urine, light-colored stools, or jaundice.

Although some people may not have symptoms, it is important to see a doctor if you think you may have hepatitis A. Diagnosis is made through blood tests, and treatment focuses on relieving symptoms and allowing the body to recover.

Hepatitis A Treatment

hepatitis B treatment varies depending on the severity of the disease and the stage it is in. In some cases, no treatment is needed, but in others, antiviral or immunomodulatory drugs may be prescribed to control the virus and reduce liver damage.

It is important that people diagnosed with hepatitis B avoid alcohol and drugs, and that they eat a healthy and balanced diet. Bed rest may also be necessary in severe cases.

Symptoms

Hepatitis B can present with flu-like symptoms, although some people may not experience any symptoms at all.

Possible symptoms include:

Fatigue and muscle aches
Nausea and loss of appetite
Fever
General discomfort
Abdominal pain
Diarrhea
Darkening of the urine (choluria)
Light colored stool (acolia)
Yellowing of the eyes and skin (jaundice)

It is important to see a doctor if you experience these symptoms or if you think you have been exposed to the hepatitis B virus.

Diagnosis of Hepatitis B

The detection of Hepatitis B is done through a blood test in the laboratory to determine serology. However, the antigenic system of Hepatitis B Virus is more complex than that of other Hepatitis-causing viruses. The following are the serological highlights of Hepatitis B:

HBsAg

Hepatitis B Virus Surface Antigen (HBsAg) indicates a current infection. Its presence is not enough to determine if HBV is the cause of Acute Hepatitis, nor does its absence exclude its responsibility for the disease.

Reasons for a negative test may be a blood sample drawn weeks after the onset of Hepatitis, very low antigenemia, or fulminant hepatitis.

Chronic Hepatitis B is suspected when HBsAg persists six months after illness onset. In patients with Chronic Hepatitis B, HBsAg persists even though viral replication and transaminases have normalized.

anti-HBs

Anti-HBs antibodies are detected in blood a few weeks after the disappearance of HBsAg. They indicate immunity against HBV, which may be secondary to previous Hepatitis or vaccination against the disease.

In some situations, the detection of Anti-HBs may be transient, such as in neonates of HBsAg-positive mothers or in patients who have received specific gamma globulin against HBV.

Anti-HBc IgM

If this antibody is present, it indicates that the infection is current or recent. It is positive before the first symptoms appear and is found in all cases of acute infection, even in the absence of HBsAg (during the window period and fulminant hepatitis). Therefore, it is the preferred marker to identify acute hepatitis B virus infection.

Anti-HBc IgG

It appears simultaneously with IgM, but remains in the body for life. It indicates natural immunity to the virus when associated with the anti-HBs antibody. However, the latter antibody may not be detectable if levels are low years after acute hepatitis. In the case of chronic hepatitis, this antibody is detected together with HBsAg.

HBeAg

If this antigen is present, it indicates that there is active viral replication, which means that the infection is acute or chronic. In the case of acute hepatitis, it can be detected from the end of the incubation period until two months after the onset of the acute phase. If the disease develops into chronic hepatitis, this antigen remains detectable.

Its negativization in chronic hepatitis (seroconversion to anti-HBe), either spontaneously or after treatment, indicates a significant decrease in viral replication that precedes inactivation of the disease. It is encoded in the Pre-Core region of the HBV genome, so a mutation in this region of the genome prevents the secretion of antigen outside the hepatocyte. This genomic variant represents up to 50% of chronic hepatitis B in our environment, is called precore mutant or "e less" and is characterized by presenting viral replication (DNA+) with negative HBeAg.

anti-HBe

In the case of acute hepatitis, this antibody appears early, before HBsAg becomes negative, indicating a good prognosis. In the case of chronic hepatitis, its appearance (seroconversion) implies a decrease in replication and less infectivity.

HBV-DNA

This marker is the most reliable for detecting viral replication. It is very useful for detecting the "e minus" mutant.

Contagion Hepatitis B is spread by contact with the blood, semen, or other body fluids of an infected person. Contagion can occur by:

Having sex with an infected person without using a condom.
Sharing needles to inject drugs.
Getting a tattoo or body piercing with dirty instruments that were used on other people.
Sticking yourself with a needle contaminated with infected blood (healthcare workers can contract hepatitis B this way).
Living with someone who has hepatitis B.
Sharing a toothbrush or razor with an infected person.
Travel to countries where hepatitis B is common.
Transmission from mother to fetus.

Prevention and treatment

Vaccination is the best way to prevent hepatitis B, and is currently included in the childhood vaccination schedule.

Regarding treatment, there are various options that can be recommended by a specialist doctor depending on the severity and evolution of the disease. Some of them are:

Interferon: It is administered by injection and the treatment usually lasts about four months.
Lamivudine: Taken as a pill once a day, a one-year course is generally recommended.
Adefovir dipivoxil: It is also taken as a pill once a day, and treatment can last for a year.
In some cases, hepatitis B can lead to cirrhosis of the liver, which may require a liver transplant. This procedure consists of removing the damaged liver and replacing it with a healthy one from a donor.

It is important to remember that you should always consult a doctor in case of any suspicion of hepatitis B infection, and follow all the recommendations and treatments prescribed by a specialist in the field.

Hepatitis C

Hepatitis C is an inflammation of the liver caused by infection with the hepatitis C virus.

Symptoms

In most cases, people infected with the hepatitis C virus have no symptoms. Often, the infection is detected through routine medical exams or medical procedures, in which laboratory tests are done to assess liver function.

If the infection has been present for many years, the liver may become permanently scarred, a condition known as cirrhosis. In many cases, there may be no symptoms of the disease until cirrhosis has developed.

The following symptoms may appear in case of hepatitis C infection:

Jaundice (yellow coloration)
Abdominal pain (in the upper right part of the abdomen)
Fatigue and muscle aches
Nausea and loss of appetite
vomiting
low fever
Pale-colored stools (acholia)
Dark urine (choluria)
generalized pruritus
Ascites (fluid in the abdominal cavity)
Bleeding varices (dilated veins in the esophagus)

HCV is a virus from the Flaviviridae family. Its structure is largely unknown due to the lack of suitable in vitro systems or animal models. It is characterized by a high mutation rate because the virus-dependent RNA polymerase does not possess the 3'-5' exonuclease error-correcting capacity, which translates into an increase in the heterogeneity of the virus in each replication cycle.

Heterogeneity is evident at two levels: 1) genotypes or variants between different individuals, and 2) existence of quasispecies in the same individual. The global prevalence of infection (anti-HCV+) is approximately 3%, ranging from 0.4% to 1.1% in Western Europe and the US, to 9.6% to 28% in North Africa. .

Its incidence has decreased due to the decrease in transmission through blood products and the application of universal precautions in medical procedures. HCV is responsible for 20% of cases of acute hepatitis, but due to its silent presentation, it is rarely diagnosed. Only 25% of cases develop jaundice.

There is a window period of 4-8 weeks in which there is no increase in transaminases or anti-HCV seroconversion, but viraemia is positive.

In the diagnosis of hepatitis C, we use both immunological and virological tests.

In the case of serological tests, there are three different generations. The first-line tests, such as the ELISA, and the complementary ones, such as the RIBA, seek to detect antibodies against HCV.

With the latest first-line tests, the seronegativity window time has decreased, increasing its sensitivity to almost 100%. However, complementary tests have a higher specificity although lower sensitivity.

It is important to note that the sensitivity and specificity of these tests depend on the prevalence of infection in the population studied. For example, ELISA-positive but RIBA-negative and low-risk patients are usually not viraemic and therefore do not have HCV infection. In some cases, the absence of viremia in patients with positive ELISA and RIBA results may be due to a false negative HCV-RNA test, intermittently negative viremia, or a false positive serological result.

On the other hand, virological tests are useful for the detection of active infection and contagiousness. Qualitative detection of HCV-RNA by PCR provides evidence of acute infection and is used to verify the diagnosis of vertical infection, confirm chronic hepatitis C, and monitor response to treatment.

Viremia quantification is also useful for monitoring response to treatment. In addition, genotyping aids in patient evaluation, prognosis, and treatment planning.

Hepatitis C can be spread in a variety of ways, including through a blood transfusion before July 1992, contact with blood at work, sharing needles when injecting drugs, having multiple sexual partners, etc. others.

There is currently no cure for hepatitis C, but some patients may benefit from treatment with alpha interferon or a combination of alpha interferon and ribavirin.

Alcohol-related hepatitis

Alcohol-related hepatitis is diagnosed by clinical and laboratory criteria in patients with heavy alcohol consumption and characteristic clinical and laboratory symptoms. Signs and symptoms include fever, anorexia, jaundice, and hepatomegaly, with liver inflammation caused by alcohol-induced damage to liver cells.

This form of hepatitis is a complex problem that can lead to chronic liver disease and cirrhosis. However, if the patient stops drinking, the inflammation may be reversible, but if cirrhosis is already present, the disease may rapidly progress to liver failure.

The most common symptoms of hepatitis from alcohol use include:

Abdominal tenderness
Blood vessels in the skin in the form of a spider
Accumulation of fluid in the abdominal cavity (ascites)
loss of appetite
Jaundice (yellow skin and eyes)
low fever
Fatigue
Nausea

To diagnose alcohol-related hepatitis, liver function tests, blood counts, coagulation tests, serum electrolytes, and tests for other body chemicals may be performed. Also, liver ultrasound and liver biopsy can be used to obtain more detailed information.

Treatment of alcohol-related hepatitis involves abstaining from alcohol and, in some cases, an alcoholism treatment program.

There are no specific medications to cure alcohol-related hepatitis, so treatment focuses on reducing symptoms and stopping the progression of the disease. Depending on the severity of the disease, the patient may be treated on an outpatient basis or may need to be hospitalized.

Toxic Hepatitis

Toxic hepatitis is an inflammatory and necrotic process that affects liver cells, and can be caused by a wide variety of toxins, drugs, and chemicals. Liver damage induced by these elements is increasing, and can manifest itself in various ways, from a simple elevation of aminotransferase levels to more serious diseases such as acute hepatitis and fulminant hepatic necrosis.

The etiopathogenesis of toxic hepatitis is complex and cannot be predicted. There are many drugs and chemicals that can cause hepatitis, and these reactions are idiosyncratic, meaning they depend on the individual and are not dose related.

The liver has a great functional reserve capacity, so its function is not altered when there are only localized or focal lesions. However, when the damage is diffuse, physiological disturbances occur that can lead to liver failure syndrome.

Liver injuries are classified based on the mechanism of damage, which can be direct or idiosyncratic. Drugs and chemicals that cause direct damage trigger reproducible reactions and are dose dependent.

On the other hand, hepatotoxins cause damage that is difficult to reproduce, affecting only a minority of exposed people, and may or may not depend on the dose. They usually require several weeks of exposure before clinical symptoms appear, and their response is an immunological hypersensitivity reaction that includes hyperthermia, lymphadenopathy, arthritis or arthralgia, rash, and eosinophilia.

In any case, an individual immunological predisposition is recognized in which the major histocompatibility complex of HLA leukocytes participates.

When liver cells are injured, defense mechanisms are activated that include the enzymatic action of glutathione -S-transferases, peroxidases, hydrolases, and glucuronyl transferases. The genetic deficiency of these substances can be a determining factor in the special susceptibility to damage by drugs (see Table No. 1).