Common causes of anemia include acute and chronic blood loss due to upper gastrointestinal
(GI) bleeding, malnutrition, hemolysis, hypersplenism secondary to portal hypertension, and
impaired coagulation. Alcohol causes anemia by its direct bone marrow toxicity, vitamin B12
and folate deficiency due to poor oral intake, and intestinal malabsorption. Treatment
related anemia is seen in patients with chronic hepatitis C virus infection receiving
ribavirin and interferon. Hepatitis associated aplastic anemia, characterized by pancytopenia
and hypocellular bone marrow, is an entity seen concurrently with or within 6 months of
infection with hepatotropic viruses such as hepatitis B, hepatitis C and Epstein-Barr virus.
Acute and chronic blood loss from varices, portal hypertensive gastropathy and gastric antral
vascular ectasia can give rise to iron-deficiency anemia, in which the picture is one of
microcytic hypochromic anemia. Another common hematological abnormality seen in liver
cirrhosis is macrocytosis. The causes of macrocytosis in liver cirrhosis are also multi
factorial. Vitamin B12 and folate deficiency is also frequently seen in liver cirrhosis,
particularly of alcoholic origin, due to malnutrition and increased intestinal permeability,
and gut dysbiosis.
Patients with cirrhosis patients have a high incidence of sepsis which can trigger
decompensation and may result in prolonged hospital stay and increased mortality. Many
studies have estimated that about 30%-50% admissions of patients with cirrhosis have sepsis.
Of those who don't have sepsis at presentation, about 15% patients admitted to hospital
develop sepsis during the hospital stay. After infection develops, the patient may develop
acute kidney injury (AKI), shock, encephalopathy or disseminated intravascular coagulation
(DIC) further decreasing the chances of survival. Sepsis and the associated cytokines have a
myelosuppressive effect and prevent the erythron from making blood cells. This results in an
increase in ferritin as an inflammatory biomarker and alters iron metabolism by affecting the
production of hepcidin in the liver. The worsening of anemia in patients with sepsis is well
documented, and this is further impacted using drugs like antibiotics which trigger
inflammation mediated suppression of the erythron and other hematopoietic precursors like
megakaryocytes and leucoblasts.
In the study, after taking informed consent, participants will be evaluated for etiology of
chronic liver disease with proper history, clinical examination and investigations which will
include viral markers (HbsAg, Anti-HCV, Total anti-Hbc, AIH markers (Anti-nuclear antibody/
anti-smooth muscle antibody/anti- liver kidney microsomal antibody), serum ceruloplasmin,
non-alcoholic fatty liver disease (NAFLD) work up and radiological investigations for
cirrhosis. The severity of cirrhosis will be determined by Child-Pugh's and MELD/MELD-Na
score.
To evaluate for anemia, following results would be noted: Complete hemogram with RBC indices,
reticulocyte count and peripheral blood smear, RFT, LFT, INR, iron studies - serum iron,
ferritin, total iron binding capacity and %transferrin saturation, serum vitamin B12, folate
levels. Workup for hemolysis would include lactate dehydrogenase, serum haptoglobin, direct
coombs test and plasma hemoglobin. Upper GI endoscopy findings will also be noted to evaluate
the contribution of gastrointestinal blood loss in causing anemia.