Hepatitis D: symptoms

Acute hepatitis B with delta-agent (coinfection) with and without hepatic coma

Symptoms of hepatitis D, which develops as a result of co-infection, are extremely similar to those in acute hepatitis B. The incubation period is from 6 to 10 weeks. Characteristic cyclic flow.

[1], [2], [3], [4], [5], [6], [7], [8]

Pre-Cheetah period

It begins more sharply than with viral hepatitis B, with deterioration of health, malaise, weakness, fatigue, headache. Simultaneously, dyspeptic phenomena are noted: a decrease in appetite right up to anorexia, nausea, vomiting. More often than with viral hepatitis B, migratory pain occurs in large joints. Almost half of the patients have pain in the right hypochondrium, which is not typical for viral hepatitis B. Another difference from viral hepatitis B is fever, and in 30% of patients the body temperature rises above 38 C. The duration of the pre-jaundice period is shorter than with viral hepatitis B, and averages about 5 days.

Jaundice period

With the appearance of jaundice, the symptoms of hepatitis D and intoxication are increasing. Against the background of jaundice, arthralgia (in 30%) and subfebrile condition are preserved. Strengthen weakness, fatigue: more often reveal a skin itch; pains remain in the right upper quadrant, not related to food intake. Often, there are urtic rashes on the skin. The longest symptoms of icteric period: weakness, decreased appetite, pain in the right upper quadrant. In all patients, the liver is enlarged by 1-3 cm, its edge is elastic, smooth, sensitive on palpation. More often than with viral hepatitis B, the spleen increases. In the blood serum, the bilirubin content is increased due to bound fraction, the activity of transferases is much higher than in acute hepatitis B. The index of thymol test significantly increases, which is unusual for viral hepatitis B: the sulemic test remains normal. Hyperbilirubinemia lasts an average of 1.5 months, hyperfermentemia - up to 2-3 months.

The disease often has a two-wave course with clinico-enzymatic exacerbation, which can be explained by the presence in the body of two viruses with different biological properties. It is assumed that the first wave is a manifestation of HBV infection, and the second is due to delta infection, since by this time the body already has enough HBs-antengene molecules necessary for HDV reproduction. However, some researchers explain the presence of a second peak of ALT by activating HBV replication after the period of inhibition of its replication by the delta virus. In 60% of patients on the 18-32th day from the onset of jaundice, on the background of the beginning improvement, weakness, dizziness, pains in the liver area increase: the liver is again enlarged, the index of thymol test and the activity of transferases increase. Often, ACT activity is higher than ALT activity, the de Ritis coefficient is more than 1. A decrease in the sulemic test and prothrombin index is possible. In some patients, only an enzymatic exacerbation is observed without any clinical manifestations. The disease often occurs in a moderate and severe form; in 5-25% of cases fulminant (fulminant) form develops, which ends lethal. In adults, 60-80% of fulminant forms of HBsAg-positive hepatitis are caused by HDV infection. With a successful course of hepatitis of mixed etiology, the duration of the disease is 1.5-3 months. The disease ends in recovery (approximately 75% of cases) or death - with fulminant form of the disease. The development of chronic hepatitis is rarely observed (1-5%), the disappearance of HBsAg also indicates a recovery from delta infection.

Acute delta (super) -infection of the hepatitis B virus

This variant of the disease can occur both manifestly and clinically latent, but in 60-70% of patients still register either an episode of jaundice, or a classic picture of icteric variant of acute hepatitis. The incubation period lasts 3-4 weeks. The pre-zheltushny period characterizes an acute, sometimes turbulent beginning. The duration does not exceed 3-4 days. In contrast to acute viral hepatitis B, more than half of the patients have a body temperature above 38 C, arthralgia and pain in the right upper quadrant occur, and some patients have a urticaria rash on the skin. After 2-3 days, the urine becomes dark, the feces discolor, the liver and spleen increase, the sclera and skin appear yellow.

In the icteric period, the patients feel worse, the symptoms of hepatitis D and intoxication increase, the body temperature remains elevated for another 3-4 days, pains in the joints continue, and pain in the right upper quadrant is recorded more often than before jaundice, and they are permanent.

When examining patients, a considerable increase and density of both the liver and spleen attracts attention. More than 40% of patients develop edematous-ascitic syndrome. In the blood serum - hyperbilirubinemia (persists usually more than 2 months). Hyperfermentemia (often with a distortion of the de Ritis coefficient). The activity of ALT and ACT remains high longer than with viral hepatitis B and hepatitis of mixed etiology, and practically none of the patients have a level of enzyme activity.

Unlike other viral hepatitis in acute hepatitis delta in carriers of HBAg, the protein-synthetic function of the liver is significantly impaired, which is manifested by a decrease in the index of the sulemic test in the first 10 days of icteric period and an increase in thymol test. The number of albumins decreases, the content of the y-globulin fraction increases. The development of edematous-ascitic syndrome in this variant of HDV infection is associated both with a decrease in the synthesis of albumins and with a qualitative change in albumin levels. In the overwhelming majority of patients, the disease proceeds wavyly with repeated clinical and enzymatic exacerbations accompanied by jaundice, symptoms of intoxication, development of edematous-ascitic syndrome, short-term (1-2-day) waves of fever with scrounging, the appearance of an ephemeral rash on the skin. The severity of clinical symptoms in individual patients decreases with each new wave, while in others the disease assumes a progredient character: subacute liver disease, hepatic encephalopathy develop, and a fatal outcome occurs.

Recovering occurs very rarely, the outcomes are almost always unfavorable: either a fatal outcome (with fulminant form or with severe form with the development of subacute liver disease), or the formation of chronic viral hepatitis D (approximately 80%) with high process activity and rapid transition to cirrhosis .

Another possible variant of superinfection is infection with the delta virus of patients with chronic hepatitis B. Clinically, this is manifested by exacerbation of a so-favorable hepatitis, the appearance of intoxication, jaundice, hyperfermentemia, and also progression to cirrhosis of the liver.

[9], [10],