3.5 Differences in cytopenia by cirrhosis etiology
The rate of leukopenia was notably
higher and the rate of
erythropenia was lower in
HBV-related cirrhotic patients than alcohol-related cirrhotic patients
(leukopenia: 18.33% vs 7.26%, P = 0.034; erythropenia: 48.14% vs
64.18%, P = 0.018). No significant
difference was observed in the rate of thrombocytopenia between the two
groups (Table 5). After adjusting for confounders, the risk of
erythropenia (OR = 0.13, 95% CI:
0.02–0.85, P = 0.033) was higher
in alcohol-related cirrhotic patients, while the risk of leukopenia (OR
= 13.39, 95% CI: 1.80–99.76, P = 0.011) was higher in HBV-related
cirrhotic patients (Table 6).
4 DISCUSSION
In the present study, HBV-related cirrhotic patients
had higher adjusted risks of HCC
and hypersplenism than alcohol-related cirrhotic patients. In contrast,
the adjusted risks of HE and ACLF were notably greater in
alcohol-related cirrhotic patients. The differences in complications
between cirrhotic patients with different etiologies indicate that
cirrhosis is not a single disease.
A retrospective cohort study indicated that the rate of HCC in
HBV-related cirrhotic patients was higher than that in alcohol-related
cirrhotic patients (32.6% vs 6.0%).18 Consistently,
we observed that the rate of HCC was notably higher in HBV-related
cirrhotic patients than alcohol-related cirrhotic patients (39.55% vs
1.45%). Another study revealed that viral hepatitis promoted the
development of HCC more than alcoholic hepatitis, which meant that
patients with HCC due to viral hepatitis had worse
outcomes.19 Therefore,
rigorous HCC surveillance is
needed in HBV-related cirrhotic patients.
We also found that HBV-related cirrhotic patients had a higher rate of
hypersplenism than alcohol-related cirrhotic patients (45.84% vs
28.99%). As one of the most common cirrhotic complications,
hypersplenism often causes rapid and premature destruction of blood
cells, especially platelets and leukocytes, which can lead to infection
and bleeding.20 A study reported that leukopenia in
cirrhotic patients led to a much higher risk of infection and poor
prognosis.21 We discovered that the rate of leukopenia
was substantially higher in HBV-related cirrhotic patients than
alcohol-related cirrhotic patients (18.33% vs 7.26%). Thus, more
attention should be paid to preventing infection among patients with
HBV-related cirrhosis. In contrast, erythropenia was more common in
alcohol-related cirrhotic patients (64.18% vs 48.14%). This may be
because alcohol suppresses erythropoiesis in the
bone.22,23
We found that the rate of HE was
significantly higher in alcohol-related cirrhotic patients than
HBV-related cirrhotic patients (15.94% vs 4.49%). Similarly, a
retrospective cohort study of 598 cirrhotic patients by Vaz et al24 reported that alcohol-related cirrhotic patients
had a higher rate of HE than hepatitis C virus-related cirrhotic
patients (11.0% vs 5.0%). This may be because chronic alcohol abuse
may cause more severe neocortical injury and cognition impairment than
chronic hepatitis virus
infection.25 Furthermore, the severity of HE has been
shown to be associated with the serum ammonia level 26and we found that alcohol-related cirrhotic patients with HE had a
higher serum ammonia level than HBV-related cirrhotic patients
with HE (134.00 ± 62.99 vs 82.16 ±
17.82 μmol/L), indicating more severe HE in alcohol-related cirrhotic
patients. Therefore, early detection and treatment of HE in
alcohol-related cirrhotic patients should be considered.
Additionally, we found that the rate of ACLF was higher in
alcohol-related cirrhotic patients than HBV-related cirrhotic patients
(7.25% vs 2.28%). Our result was similar to that of research by Axley
et al 27, which demonstrated that the rate of ACLF was
clearly higher in alcohol-related cirrhotic patients than hepatitis
virus-related cirrhotic patients (7.2% vs 4.1%). Moreover, another
study reported that alcohol-related cirrhotic patients exhibited more
severe ACLF than patients with viral liver disease.28Thus, it is necessary to be aware of the high risk of ACLF when treating
patients with alcohol-related cirrhosis.
There were, admittedly, several limitations in our study, particularly
the small sample size. Additionally, we only included hospitalized
patients (who may have had greater
disease severity), which may have caused selection bias. Furthermore,
several potential confounders, such as diet (especially a high-protein
diet), that may influence the occurrence of HE in cirrhotic patients,
were not taken into consideration. Future studies with large sample
sizes are warranted to confirm our findings.
5 CONCLUSION
HBV-related cirrhotic patients had increased risks of HCC
and hypersplenism, whereas
alcohol-related cirrhotic patients more readily developed HE and
ACLF. Therefore, there should be a
greater focus on regular screening
for HCC and hypersplenism in HBV-related cirrhotic patients and for HE
and ACLF in alcohol-related cirrhotic patients.