Hepatitis C in children in the first year of life

It is quite obvious that in the first year of life, a child is most likely to acquire hepatitis C from the mother.

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Causes Hepatitis C in children in the first year of life

The likelihood of an infant becoming infected with the hepatitis C virus from a mother with any form of HCV infection is high, but when the virus is most likely transmitted - in utero, during labor or birth, or through close contact - is not yet clear. In addition, the clinical variants of hepatitis C in this age group are practically unknown.

In some cases, hepatitis C was observed to develop in infants born to mothers with chronic hepatitis C. In this case, the children were born with anti-HCV and no symptoms of hepatitis; later, at 6-12 months of life, they developed hepatitis C in an icteric form with subsequent chronicization of the process.

T. Kuroki et al. (1993) revealed a high frequency (33%) of transmission of HCV infection to infants from mothers with CHC; the researchers believe that infection of children most likely occurs during childbirth or in the first months of life, when there is close contact between mother and child.

The frequency of perinatal infection with the hepatitis C virus is 7.2%, and when the mother has CHC and HIV infection, it increases to 14.8%.

M. Giovannnini et al. (1990), observing 25 pairs - anti-HCV-positive mother - newborn, found anti-HCV in the blood serum of all infants, which disappeared in the next 2-4 months of life. In 11 children aged 6-12 months, anti-HCV reappeared, which was assessed as seroconversion as a result of HCV infection. When studying the anamnesis, it was found that 6 of 11 children aged 3-12 weeks of life had increased ALT activity, which was not given due attention.

The presented data are ambiguous, but still indicate that vertical transmission of the hepatitis C virus from the mother is possible; in this case, there is a high probability of developing primary chronic hepatitis.

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Symptoms Hepatitis C in children in the first year of life

Forty-one children aged 2 months to 1 year, admitted to the clinic with a diagnosis of viral hepatitis, were under clinical observation. Hepatitis A was verified in 2 children (4.9%), hepatitis B in 15 (36.6%), hepatitis C in 17 (41.5%), cytomegalovirus hepatitis in 3 (7.3%), and viral hepatitis of unknown etiology in 4 (9.7%). Thus, hepatitis B and C occupied the leading place in the structure of viral liver lesions in children in the first year of life.

Among 17 children in their first year of life who were sick with hepatitis C, there were 11 girls and 6 boys. Mothers of 3 children suffered from drug addiction, while in 2 women, during simultaneous examination with their children, anti-HCV was found in the blood without clinical and laboratory signs of liver damage, another 9 children were born to mothers sick with CHC, 1 child - to a mother who developed serologically confirmed hepatitis C 2 weeks after delivery. Only 4 children were from healthy mothers. All infants, with the exception of one, were born full-term, with a body weight from 2800 to 4000 g.

Based on the available epidemiological data, it could be assumed that the source of HCV infection in 11 children were mothers with acute or chronic hepatitis C (9 people) and drug addicts (2 people) with latent HCV infection. None of these children received blood products. Of the remaining 6 children, 3 were most likely infected through blood products, since 2-3 months before they became ill with hepatitis C, they were in neonatal wards, where one child was transfused with blood and two were transfused with plasma. Specific markers of hepatitis C were not detected in the mothers of these children. Another two children (who were abandoned by their mothers) were constantly treated in hospitals from birth, received multiple parenteral manipulations, through which, apparently, they became infected with the hepatitis C virus. One child from a healthy mother had an indication for a single blood draw for clinical analysis at the polyclinic.

Acute hepatitis development is observed in 2 girls aged 3 and 4.5 months. The mother of one of them fell ill with typical hepatitis C 2 weeks after birth. The girl fell ill 2.5 months after the onset of the disease in her mother - acutely, with a rise in body temperature to 38.3 ° C and the appearance of lethargy. The next day, darkening of urine was noted, and on the 3rd day - jaundice, due to which the child was hospitalized in the clinic with a diagnosis of hepatitis C. The condition in the hospital was assessed as moderate. The girl was lethargic, regurgitated. The skin and sclera were moderately icteric. The abdomen was swollen, painless. The liver was of a dense consistency, protruded from the hypochondrium by 3 cm on palpation, the spleen - by 1.5 cm. In the biochemical blood test, the total bilirubin level was 70 μmol / l, conjugated - 50 μmol / l, ALT activity - 1520 U, AST - 616 U, ALP - 970 U, beta-lipoproteins - 63 U, prothrombin index - 68%, thymol test indicators - 11.8 U. When testing blood for serological markers of viral hepatitis, anti-HBc, anti-HBs, anti-HCV were detected; HCV RNA was not detected.

Ultrasound scanning revealed moderate liver parenchyma compaction with echo signals up to 1/3 of the maximum, a normal gallbladder, and a sharp increase in the pancreas. The spleen is slightly enlarged.

Based on clinical and serological data, hepatitis C, mild form, pancreatitis was diagnosed.

The presence of antibodies to the hepatitis B virus is explained by their transplacental transmission from the mother, who had them in her medical history.

The course of the disease was smooth, by the end of the 2nd week from the onset of the disease, jaundice disappeared, the liver decreased, and a biochemical blood test revealed only moderately increased transaminase activity: ALT - 414 U and AST - 241 U. The girl was discharged home in satisfactory condition.

Considering that the mother fell ill with acute hepatitis C 2 weeks after giving birth, and the child - 2.5 months after the mother's illness, one can think about postnatal infection through close contact in the maternity hospital, but at the same time, infection during childbirth (intranatal) cannot be ruled out, since it is known that the hepatitis C virus appears in the blood 2-4 weeks before the first clinical signs of the disease.

Another girl, 4.5 months old, had a drug-addicted mother who contracted hepatitis B one week before giving birth. The girl had been receiving parenteral treatment since birth due to a cerebrovascular accident, and after being discharged she was admitted to a children's home (her mother abandoned her), where she developed unsatisfactorily, gained weight poorly, and was therefore treated in hospital again.

The present disease began with the appearance of jaundice, for which the girl was hospitalized in our clinic in a moderate condition. She was restless, ate poorly. The skin and sclera were slightly icteric. The liver protruded from the hypochondrium by 1.5 cm, the spleen was determined at the edge of the costal arch. Biochemical blood test: total bilirubin - 58 μmol / l, conjugated - 30 μmol / l, ALT activity - 473 U, ACT - 310 U, beta-lipoproteins - 63 U, prothrombin index - 64%, thymol test indicators - 10 U. Serological markers: HBsAg, anti-HCV were detected.

Over the next 3 days, the condition steadily worsened: agitation gave way to lethargy, the girl periodically did not respond to others, icterus of the skin and sclera increased to moderate. Increasing pastosity of the tissues was noted. Breathing became frequent, shallow. Heart sounds were distinct, increased to 200 beats per minute. The abdomen was moderately distended. The liver decreased in size and was palpated by 0.5 cm from the hypochondrium. The girl fell into a coma, and soon, with signs of respiratory and cardiac arrest, death occurred. On the same day, a biochemical analysis recorded a sharp increase in the bilirubin level - up to 236 μmol / l, half of which was unconjugated fraction; ALT and AST activity decreased to 160 and 190 U, respectively. Morphological examination diagnosed acute massive liver necrosis. Clinical diagnosis: combined hepatitis B and C, malignant form, hepatic coma with a fatal outcome.

Considering multiple episodes of hospital treatment starting from the neonatal period, parenteral infection with the hepatitis C virus can be assumed. The girl could have been infected with the hepatitis B virus from her mother, who had acute hepatitis B 1 week before giving birth.

The third child was admitted to the clinic at the age of 5 months due to the fact that 2 weeks before, the mother had an increase in body temperature to 39°C, dark urine and jaundice.

Blood biochemistry: total bilirubin - 113 μmol/l, conjugated - 65 μmol/l, ALT - 530 U, ACT - 380 U. Serological markers of hepatitis: HBsAg "-", anti-HBc IgM "-", anti-HCV "+", anti-HAV IgM "+", HCV RNA "-". This gave grounds to diagnose hepatitis A in her against the background of chronic hepatitis C.

From the child's medical history it is known that he was born full-term from the first time birth, with a body weight of 4000 g, length 54 cm. At the age of 1 month he was operated on for pyloric stenosis (while he did not receive blood products)

On admission to the clinic, the child's condition was assessed as satisfactory. The skin and sclera are of normal color. There is a 4 cm long postoperative scar on the skin in the epigastric region. The abdomen is soft and painless. The liver is compacted and protrudes from the hypochondrium by 2.5 cm,

Blood biochemistry: total bilirubin - 4 μmol/l, ALT - 177 U, AST - 123 U, thymol test results - 10 U. Serological markers of hepatitis; HBsAg "-", anti-HCV "+", anti-HAVIgM "-". HCV RNA "+".

These data provided grounds for diagnosing the child with hepatitis C, which most likely occurred during childbirth, and not during surgery for pyloric stenosis, since the surgery was not accompanied by a transfusion of blood products.

Primary chronic hepatitis C was diagnosed in another 14 children aged 3.5 months to 1 year. None of them had a clear onset of the disease. They were admitted to the clinic due to long-term hepatosplenomegaly. Neurological symptoms (hyperexcitability, increased muscle tone, hypertension syndrome) were observed in 3 of them from birth, and anti-CMV IgM was detected in the blood serum, which made it possible to diagnose congenital cytomegalovirus infection. Subsequently, neurological manifestations decreased, but psychomotor developmental delay persisted, hepatosplenic syndrome progressed, and increased AJTT and AST activity was detected. Progression of hepatosplenic syndrome, increased transaminase activity during repeated biochemical studies made it possible to suspect viral hepatitis. Upon admission to the clinic, the children were lethargic, had a decreased appetite; Three of them (with congenital cytomegalovirus infection) had a clearly expressed delay in psychomotor development. Two infants had isolated telangiectasias on the extremities, in one case - a pronounced venous network on the abdomen. All had a dense palpable liver, protruding from the hypochondrium by 2.5-4 cm. In 8 children, the spleen protruded 1-2 cm below the costal margin.

Blood biochemistry: ALT and AST activity from 75 to 200 U, alkaline phosphatase increased by 1.5-3 times above the norm. Bilirubin level in all patients was normal, there were practically no changes in the protein spectrum of blood serum. Ultrasound scanning revealed heterogeneity of liver tissue with echosignatures from 1/3 to 1/2 of the maximum in 7 patients. Anti-HCV was detected in the blood serum of all children; HCV RNA was also detected in 7 children.

Thus, the majority (11 of 17 children) were infected with the hepatitis C virus from their mothers. Acute and chronic hepatitis was detected in 6 mothers, and anti-HCV was detected in 2 more mothers during parallel examination with their children.

It is most likely that the transmission of HCV infection from mother to infant in most cases occurs during childbirth, which is confirmed by the appearance of clinical symptoms of hepatitis C 2-3 months after birth. 5 children became infected with hepatitis C after birth (3 as a result of plasma and blood transfusions and 2 as a result of multiple parenteral manipulations).

As observations show, in 15 out of 17 children in the first year of life, hepatitis C developed as a primary chronic disease, with a torpid course and fluctuations in the increased activity of transaminases. Only in 2 infants did hepatitis C manifest itself in the icteric form, and in one - in the fulminant variant as a result of mixed infection with hepatitis B.

Thus, hepanitis C in children of the first year of life can occur due to ante-, intra- and postnatal infection. According to research data, infection during childbirth can be considered predominant, while vertical transmission of НСV, if it occurs, is most likely extremely rare.

Our own observations and a few reports from other researchers show that hepatitis C in children of the first year of life occurs as a primary chronic process. In this regard, they require careful long-term monitoring and interferon therapy.