Prevalence of Anaemia in Decompensated Chronic Liver Disease
Prevalence of Anaemia in Decompensated Chronic Liver Disease
Prevalence of Anaemia in Decompensated Chronic Liver Disease
ISSN 1817-3055
© IDOSI Publications, 2014
DOI: 10.5829/idosi.wjms.2014.10.1.82114
Abstract: Aim of the study: To assess the prevalence of anaemia in decompensated chronic liver disease
patients.Objectives:1)To detect the abnormalities of rbcs in a cirrhotic patient.2)To find the type of anaemia in
a patient with decompensated chronic liver disease. Materials and methods:1)To asses the precvalance of
anaemia in decompensated chronic liver disease. The study was conducted in sreebalaji medical college and
hospital from 2011 to 2013.2). About 100 patients were selected in random from patients coming to department
of general medicine opd and ward patients.CONCLUSION The study revealed 86 percent had anaemia helping
in early diagnosis of anaemia in decompensated chronic liver disease patients and could play a role in in
treatment of patients earlier and prevent morbidity and mortality
Corresponding Author: E. Halleys Kumar, Sree Balaji Medical College And Hospital, No 7, Clc Works Road,
Chromepet, Chennai- 600044, Tamilnadu, India.
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MATERIALS AND METHODS exposure risk or involve intravenous contrast with the
potential for nephrotoxicity as does computed
Study Population: tomography (CT).
Nodularity, irregularity, increased echogenicity and
To asses the prevalence of anaemia in atrophy are ultrasonographic hallmarks of cirrhosis.
decompensated chronic liver disease, the prevalence In advanced disease, the gross liver appears small
study was conducted in sree balaji medical college and multinodular, ascites may be detected and Doppler
and hospital from 2011 to 2013. flow can be significantly decreased in the portal
About hundred patients were selected in random for circulation.
this study, from patients coming to department of
general medicine opd and ward patients. RBC Count: RBC count was done in neubauers chamber
using hayems fluid or auto analyser. normal value: 4.5 to
Inclusion Criteria: 5.5 millon per cu mm.
All liver disease patients whose symptoms and signs Hemoglobin Estimation: Done by sahlis method, based
persists more than six months. on the conversion of hemoglobin to acid hematin or acid
Alcoholic, post infective,metabolic causes of liver analyser. normal values : male 14 to 18 gm/dl female 12 to
diseases are taken in consideration. 16 gm/dl
Blood investigations such as complete blood count, Table 1 shows hemoglobin abnormalities in
liver function test,,UGI scopy and ultrasound decompensated chronic liver disease patients .
abdomen were done for all the patients. ONCE the
patients were confirmed as a case of decompensated (70 males and 30 females).
chronic liver disease then the patients were said to
undergo other tests such as Rbc, Hb,,reticulocyte In this study we found that 10 males(14.3 percent ),
count and peripheral smear to find the type of 6(20 percent) of the patients had severe anemia
anaemia. 30 males (42.9 percent), 12 females( 40.0 percent) had
oral and written consent of the patients got for the moderate anaemia and 20 males ( 28.6percent ), 8
clinical examination and for the lab investigations. females (26.7 percent) had mild anaemia.
A detailed history was taken such as abdominal pain, About 10 males and 4 females had normal
abdominal distension, decreased urine output, hemoglobin levels.iv) female patients had a greater
yellowish discolouration of urine and eyes, loss of proportion of severe anaemia in other studies
appetite, loss of weight, early satiety and fever. contrary to our study in which male patients has
severe anaemia compared to females.
Ultrasonography: Abdominal ultrasonography with Female patients had a greater proportion of severe
Doppler is a noninvasive, widely available modality that anaemia in other studies contrary to our study in
provides valuable information regarding the gross which male patients has severe anaemia compared to
appearance of the liver and blood flow in the portal females.
and hepatic veins in patients suspected to have
cirrhosis. TABLE 2 showing type of anemia more prevalent in
Ultrasonography should be the first radiographic decompensated chronic liver disease patients.
study performed in the evaluation of cirrhosis because it
is the least expensive and does not pose a radiation ( 70 males and 30 females)
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Table 1: Hemoglobin ( Anaemia In Chronic Liver Disease Patients) Which is followed by microcytic hypochromic and
Gender macrocytic.
----------------------------------
Microcytic hypochromic anaemia is more prevalent in
Male Female Total
------------- ------------- ----------------
men than women.
Hemoglobin (gm/dl) N % N % N % Macrocyticanaemia is more common among
SEVERE (<6gm/dl) 10 14.3 6 20.0 16 16.0 alcoholics.
MODERATE ( 6 TO 8.9/dl) 30 42.9 12 40.0 42 42.0 About 18 males(30 percent) and 6 females (23
MILD ( 9 TO 12.9gm/dl) 20 28.6 8 26.7 28 28.0 percent) had microcytic hypochromic anaemia
NORMAL 10 14.3 4 13.3 14 14.0 About 11 males(18.3 percent) and 4 females(15.4
Total 70 100.0 30 100.0 100 100.0 percent) had macrocytic anaemia. All 11males gave
history of alcoholism.
1 male(1.7 percent) and 1 female(3.8 percent) had
dimorphic anaemia.
About 10 males and 4 females had normal
hemoglobin level( 14 patients)
DISCUSSION
Anaemia in Cirrhosis:
Anaemia in Cirrhosis Is Mostly Due To:
Hemodilution
Decreased erythropoietin level as per study
sicilianohepatol 1995 who showed decreased
Table 2: Type OfAnaemia In Chronic Liver Disease Patients erythropoietin level in cirrhotic patients with anaemia.
Patients with Anaemia Cirrhosis without anaemia is not associated with low
----------------------------------------- erythropoietin levels ( pirsi,jhepatol 1994)
Male Female Total Where as Yang et al [3] investigated the significance
--------------- --------------- ----------------
of erythropoietin in 67 patients with varying severity
Type of Rbcs N % N % N %
NORMOCYTIC 30 50.0 15 57.7 45 16.0
of cirrhosis and reported that plasma erythropoietin
MICROCYTIC 18 30.0 6 23.1 24 42.0 levels were significantly higher in cirrhotic patients
MACROCYTIC 11 18.3 4 15.4 15 28.0 than in controls. They also found levels to be higher
DIMORPHIC 1 1.7 1 3.8 2 14.0 in patients with anemia.
Total 60 100.0 26 100.0 86 100.0 Inflammatory cytokines suppresing the bone marrow
( chronic inflammation)
Folic acid and vitamin B12 deficiencies and iron
deficeincy develop frequently in patients with
cirrhosis producing severe anaemia.
Spur cell anaemia - seen in advanced chronic liver
disease especially in alcoholics and has a poor
prognosis. It is related to abnormal cholesterol
loading of the red cell membrane and reduced
deformability of the red cells. In the presence of
hyperlipidemia, it is referred to as Zieve’s
syndrome.[4]
Wilson’s disease may be associated with a hemolytic
anaemia in 1-12%.2 Hepatic necrosis leads to release
In my study, normocytic normochromic anaemia is of copper, which in turn has an oxidative action on
more prevalent than other type of anaemias,about 30 RBC cell membrane phospholipids leading to their
males( 50 percent) and 15 females( 57.7 percent) had breakdown. These patients typically present as
normocytic normochromic anaemia. fulminant hepatic failure with hemolysis [5].
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World J. Med. Sci., 10 (1): 56-60, 2014
Ribavirin-induced hemolytic anaemia Ribavirin is Esophageal and gastric varices and/or portal
used for treatment of hepatitis C along with interferon hypertensive gastropathy may be associated with
or pegylated interferon. It can cause significant slow chronic loss of blood into the gut and
dose-dependent hemolytic anaemia in about 10% of development of chronic iron deficiency anemia.The
patients on interferon and ribavirin therapy [6]. most important approach to management is
There are clear recommendations on dose reduction prevention of variceal hemorrhage [11,13,14].
depending on the fall in haemoglobin. Alternatively, serum iron is bound to beta globulin transferrin and
erythropoietin growth factor up to a dose of 40,000 total iron bindingcapacity largely depends on
units s.c. weekly can be given. Newer growth factors transferrin concenteration.
with longer half-lives such as darbopoietin and TIBC is often low.
pegylated erythropoietin are convenient for the lesser
number of doses required. CERA (continuous Abnormalites of rbcs:
erythropoietin receptor activator), a pegylated
erythropoietin is one such agent with once monthly Target cells are particularly prominent in cholestasis
dosing [7]. where a rise in bile acids may contribute LCAT
activity [15].
Characteristics of Anaemia: Anemia of diverse etiology It is seen in 2 percentage of the patients in our study.
occurs in about 75% of patients with chronic liver Acanthocytosis or spur cells can refer generally to
disease[8] the presence of this type of crenated red blood cells,
may be found in severe cirrhosis or pancreatitis[16],
According to sheilasherlock and oxford text book of they are a bad prgnosticindicator.these abnormal rbcs
are not found in our study.
hepatology. most common anaemia seen in cirrhotic
patients is normochromic and normocytic
CONCLUSION
anaemia[9,10]
According to study done by malhotra,1951 incidence
86 percentage of patients had anaemia in some forms.
was 90 percentage.in studies done by
Normocytic normochromic anaemia is most common
bhatia(1961)and mishra et al (1982), incidence were 59
type of anaemia present in our study in patients
and 79 percentage respectively.
having cirrhosis.
In study done by kimber et al reported 43 percent of
Microcytic anaemia is more common in men than
macrocytosis supported by bingham et al.
women in my study.
Macrocytic Anemia in an alcoholic arise as a
Macrocytic anaemia patients gave history of
consequence of the direct toxic effects of alcohol on alcoholism.
erythrocyte precursors in the bone marrow. 2% of target cells are found in my study.
Folic acid and vitamin B12 deficiencies develop In my study 86 percent had anaemia, which indicates
frequently in patients with cirrhosis. These that earlier diagnosis of hematological abnormalities
deficiencies may be related to inadequate food intake in decompensated chronic liver disease patients
or intestinal malabsorption. They are suspected when would help us to treat patients earlier and prevent
examination of a blood film reveals hypersegmented morbidity and mortality.
cells and oval macrocytes, in addition to round
macrocytes characteristic of chronic liver disease. REFERENCES
When anemia is caused by these deficiencies, the
mean corpuscular volume is increased and bone 1. Middle-East Journal of Scientific Research 7(6):1001-
marrow shows megaloblastic erythropoiesis. 1007,2011 ISSN 1990-9233 © idosi publications, 2011.
Consumption of alcohol appears to be associated 2. Middle-East Journal of Scientific Research 14 (4): 461-
with an approximately 40% reduction in the risk of 470, 2013 ISSN 1990-9233,© IDOSI Publications, 2013
development of iron deficiency anemia. DOI: 10.5829/idosi.mejsr.2013.14.4.7321.
Acute gastrointestinal hemorrhage is a common and 3. Yang, Y.Y., H.C. Lin, W.C. Lee Wc, Huang, Y.T. Hou,
potentially serious complication of portal M.C. Lee, F.Y. Chang and F.Y. Lee Sd, 2003. Plasma
hypertension[11-14].Acute hemorrhage may induce erythropoietin level in patients with cirrhosis and its
severe hypovolemia and subsequently secondary relationship to the severity of cirrhosis and renal
iron deficiency anemia. function. J. Gastroenterol. Hepatol., 18: 1156-61.
59
World J. Med. Sci., 10 (1): 56-60, 2014
4. Zieve L. Jaundice, 1958. Hyperlipidemia and 9. Schmidt, Sca J. Hematol, 1983. 30: 465
hemolytic anaemia: a heretofore unrecognized 10. Rubiee, Cry Med, 1977. 40: 338.
syndrome associated with alcoholic liver cirrhosis. 11. Garcia-Pagan, J.C., A. De Gottardiand J.Bosch,2008.
Ann. Intern Med., 48: 471-96. Review article: the modern management of portal
5. Roberts, E.A. and M.L.Schilsky, 2003. American hypertension--primary and secondary prophylaxis of
Association for Study of Liver Diseases (AASLD). variceal bleeding in cirrhotic patients. Aliment
Practice guidelines on Wilson disease. Hepatology, Pharmacol Ther., 28: 178-186 [PubMed].
37: 1475-92. 12. Abraldes, J.G. and J. Bosch, 2007. The treatment of
6. Manns, M.P., J.G. McHutchison, S.C. Gordon, acute variceal bleeding. J. Clin Gastroenterol.,
V.K. Rustgi, M. Shiffman and R. Reindollar, Good 41(Suppl 3): S312-S317 [PubMed].
Man Zd, Koury K, Ling M, Albrecht Jk. 2001. 13. Kravetz, D., 2007. Prevention of recurrent
Peginterferon alfa-2b plus ribavirin compared with esophageal variceal hemorrhage: review and current
interferon alfa-2b plus ribavirin for initial treatment of recommendations. J. Clin Gastroenterol., 41(Suppl 3):
chronic hepatitis C: a randomised trial. Lancet. S318-S322 [PubMed].
358: 958-65. 14. Albillos, A., 2007. Preventing first variceal
7. Macdougall, I.C., CERA (Continuous Erythropoietin hemorrhage in cirrhosis. J. Clin Gastroenterol.,
Receptor Activator), 2005. A new erythropoiesis- 41(Suppl 3): S305-S311 [PubMed].
stimulating agent for the treatment of anemia. Curr. 15. Carr, J.M., 1989. Disseminted intravascular
Hematol. Rep., 4: 436-40. coagulation in cirrhosis. Hepatology, 10: 103-10.
8. McHutchison, J.G., M.P. Mannsand and D.L. Longo, 16. ^a b Hillman, R.S.K.A. Ault, M. Leporrier and
2006. Definition and management of anemia in H.M. Rinder, 2011. Hematology in Clinical Practice.
patients infected with hepatitis C virus. Liver Int.,
26: 389-398.
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