Sarsekeyeva N.Y., Kosherova B.N.
Liver cirrhosis in patients with HIV infection
(clinical case)
Karaganda,
Kazakhstan
Virus hepatitis
and HIV infection have become a majorpublic health problem in our country and
in most countries of the world. 1.5-2 million people annually die from viral
hepatitis related to diseases, including cirrhosis and hepatocellular
carcinoma. Compared with patients infected with only viral hepatitis
co-infected patients have a higher degree of necrotic and inflammatory changes
histologically, slow response to treatment, increased frequency of cirrhosis,
hepatic decompensation and liver failure and increased level of mortality
[1-3].
HIV infection
disrupts the immune system and thus accelerates the development of viral hepatitis,
provokes usually more rapid development of complications, namely the formation
of liver cirrhosis and hepatocellular carcinoma development [4,5].
At the end of
2014 2216 cumulative cases of HIV-infection were registered in Karaganda
region. The viral hepatitis B+C was diagnosed in 54 patients (with the
increase) among the surveyed people living with HIV in the Karaganda region,
2014.
As an
illustration, we present a clinical example.
Patient D., born
in1972, was followed up from 2009 in the SI "Karaganda Regional Center for
the Prevention and Control of AIDS". Diagnosis: HIV infection, clinical
stage 2. Chronic mixed-hepatitis B+C with transformation into cirrhosis,
hemangioma of the liver. From the epidemiological history: from 2007 he has been
a user of injecting drugs (tetralgin intravenous).
In March 2012,
the patient noted deterioration when intoxication and dyspeptic syndromes
started to appear, against this background, there was noted the appearing of
jaundice. The patient came to the Karaganda Regional Center for the Prevention
and Control of AIDS, at that moment the number of CD4 lymphocytes was 308
cells/mcl, viral load – 38,700 c/ml. Considering the clinical and laboratory
deterioration, the patient was sent to hospital treatment in the regional
infectious diseases hospital in the city of Karaganda.
Upon admission to
the RIH he had bad health condition, severity of the condition was due to a
pronounced intoxication syndrome, initial signs of hepatic encephalopathy,
severe cholestasis. Consciousness was clear. He had high fever and was making
lots of mistakes in febrile figures. There was malnutrition, peripheral edema
in the extremities, the phenomenon of ascites. Skin and mucous bright icteric
had saffron tinge like trophic changes in the skin in the form of dryness,
hyperkeratosis. There have been bright extra hepatic vascular signs.
Manifestations of hemorrhagic syndrome were not observed. Belly was increased
in volume due to flatulence, ascites. There were venous collaterals on the sides
of the chest, abdomen, blunting in sloping areas of the abdomen. The liver was
big +7+8+10 cm, densely-woody, had sharpened edge, the surface is rough,
painful on palpation. Spleen was +5 cm thick, sensitive to palpation. Urine was
dark.
In RIH clinical
diagnosis: Chronic mixed B+C hepatitis, a high degree of activity with
cholesteric component, severe degrees of severity with the transformation in
cirrhosis was appeared. Portal hypertension. Edematous-ascitic syndrome.
Related diagnosed with HIV infection. Addiction. Deficiency anemia 1 degree.
Hemangioma of the liver. Holetsistoholangit.
When laboratory and instrumental examination
are revealed the following data: a general analysis of blood – hemoglobin 102
g/l, ESR 15 mm/h, erythrocytes 3.9õ1012/l,
leukocytes 4.2õ109/l, platelets 1.31õ1011/l, 1%
eosinophils, segmented 54%, 36% lymphocytes, 9% monocytes, the color index of
0.78. In the biochemical analysis of blood: total bilirubin 374.0 mcmol/l,
direct bilirubin 235.6 mcmol/l, thymol test 27.4 units, ALT 1262.9 nms/l, AST
589.5 nms/l, sugar 6.32 mmol/l, alkaline phosphatase of 295 nmol/s-l, amylase
28.2 mg/s-l. In proteinogram: total protein 88.3 g/l, albumin 23 g/l, α1 –
5%, α2 – 6%, β – 10%, γ – 56%.
Under the marker
diagnostics: HBsAg – was discovered, anti-HBcorIgM – was discovered,
anti-HBcorIgG – was discovered, anti-HCVtotal – was detected.
On abdominal
ultrasound revealed the following changes: hepatosplenomegaly, diffuse changes
in the liver parenchyma, portal hypertension. Manifestations cholecystitis,
cholangitis. Hemangioma of the liver segment 5. Salts in
the kidneys.
Against the
background of the therapy the patient was noted clinical and biochemical
improvement in the form of fading jaundice, normalization of appetite. Liver was
decreased slightly +5+6+7 cm, has become more elastic, painless on palpation,
splenomegaly persisted, evening due to persistent low-grade fever cholangitis.
At discharge in the biochemical analysis of blood: total bilirubin 64.0
mcmol/l, ALT 159.8 nms/l, AST 98.3 nms/l, thymol test 19.2 units.
Thus, chronic
viral hepatitis are increasingly becoming the cause of hospitalization for
cirrhosis, severe and death among HIV-infected patients.
References:
1. Soriano V,
Permanyer P. HIV and viral hepatitis coinfection. Eds. 2007; 118.
2. Sogni P,
Salmon-Ceron D, Dodevin P. Management of cirrhosis complications in HIV
patients coinfected with hepatitis  or Ñ vims. La Presse Medicaid. 2005; 20 (34): 1579-1783.
3. Appay V, Sauce D. Immune activation and inflammation in
HIV-1 infection: causes and consequences. The Journal of Pathology. 2008; 214
(2): 231-241.
4. Fåvrier M, Dorgham K, Rebollo A. CD4+ T cell depletion
in human immunodeficiency virus (HIV) infection: role of apoptosis. 2011; Viruses 3 (5):
586-612.
5. Wandeler G et
al. Hepatitis C virus infections in the swiss HIV cohort study: a rapidly
evolving epidemic. Clin Infect Dis. 2012; 55: 1408-1416.