الفهرس 
Hepatitis C VirusOnly 14 pages are availabe for public view
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Abstract
Summary
Hepatitis C virus is positive-strand RNA virus and can
replicate inside the liver, transmitted by apparent and inapparent
parenteral procedures representing a frequent cause of liver
disease worldwide. HCV exists as a multiple genotypes and is
hyperendemic in Egypt. HCV infection causes acute symptoms
in 15% of cases and not associated with jaundice. chronic
infection develops in 85% of cases. Both acute and chronic
HCV infection may affect the hepatic and extrahepatic tissues.
There are a number of diagnostic tests for hepatitis C
including: HCV antibody enzyme immunoassay or ELISA,
recombinant immunoblot assay and quantitative HCV RNA
polymerase chain reaction (PCR). HCV RNA can be detected
by PCR typically one to two weeks after infection. 40-80% of
HCV can clear with INF therapy and antiviral medications, no
vaccine protects against HCV infection.
Numerous extrahepatic disorders have been recognized in
association with HCV infection among which dermatological
disease occupy a central part.
NAE was first described in 1996 by El-Darouti and
Abou El Ela, it was presented as a cutaneous marker for
HCV infection. NAE was initially classified as one of the
necrolytic erythemas, a group which includes acrodermatitis
enteropathica (associated most commonly with zinc
deficiency), necrolytic migratory erythema (associated most
commonly with glucoagonoma syndrome), pellagra
(associated most commonly with niacin deficiency) and
others. A lot of clinical and histologic similarities exist
between these disease entities.
Clinically, NAE is categorized into 3 phases; initial
stage with a scaly erythematous papule or plaque with a deep
red to violaceous center and a surrounding erythematous
macule, fully developed stage with erythematous to
violaceous lichenified plaques having sharply defined
margins surmounted by adherent scales with finely
mammillated surface in less scaly areas and occasional crusts
over sites of necrosis, and late stage with progressively
thinner lesions and increased hyperpigmentation. The
distribution of the lesions is exclusively acral and the dorsal
of the feet are the predominant site in all patients.
Electron microscopic examination of lesional skin biopsy
from necrolytic acral erythema shows no viral particles but only
clumped tonofilaments.
Most reported NAE cases are HCV positive as proven by
ELISA and PCR. Liver enzymes are elevated in all cases.
However, there are few cases reported with negative hepatitis
C-virus infection.
Several pathogenic mechanisms for NAE were postulated.
NAE appears to be an immune mediated response in chronic
HCV patients, associated with, lower C3 and C4 (complements
C3 and C4), and higher frequency of positive ASMA (antismooth
muscle antibody). Another postulated theory is low serum
zinc levels. Lipopolysaccaride (LPS), a major signal transduction
protein that accumulates in hepatic patients because of failure to
detoxify, elevates in the plasma of HCV patients compared to
controls. LPS significantly increases the cytokines beta interferon
(IFN-ß) and interleukin-6 (IL-6) secretion from B cells. So, LPSstimulated
hypozincemia is mediated, at least partly, by a
cytokine-directed internal redistribution of zinc.
The aim of this work is to assess the presence of HCV
RNA in skin biopsy of Necrolytic acral erythema lesion since
no other studies were done for this aim except for ElSummary
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Ghandour et al. (2005) which was done on 5 patients only. To
achieve this goal, 42 patients divided into two groups were
recruited. The first group included 21 patients suffering from
NAE and hepatitis C virus infection, and the other group
included 21 HCV patients without any cutaneous
manifestations.
All patients and controls were subjected to full history
taking, general and dermatological examination, and assessment
of serum: Alanine amino transferase (ALT), Aspartate amino
transferase (AST), total (Bilirubin) and alkaline phosphatase
(ALK phos), skin biopsy taking and evaluation of the presence
of HCV RNA in these biopsies by RT- PCR.
No statistically significant difference was found between
NAE and control group regarding age, sex, smoking, presence
of HBV, ascites, bilharziasis, DM and regarding elevated liver
enzymes.
All patients in the NAE and control groups showed
negative results regarding the detection of HCV RNA in the
skin biopsies by PCR.
In conclusion, although HCV may play a role in
pathogenesis and development of cutaneous NAE, this is
probably not through direct proliferation in NAE lesion.
Further larger scale studies are needed for detection of
HCV RNA by PCR in skin, with biopsies frozen as soon as
possible to avoid destruction of the virus. Other investigations
for the mechanism of association between HCV and NAE are
warranted.