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 3.91012/l, leukocytes 4.2109/l, platelets 1.311011/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 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. Fvrier 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.