From the Research
The pathophysiology of a low white blood cell count (leukopenia) in acute hepatitis primarily involves bone marrow suppression and increased peripheral destruction of white blood cells. During acute viral hepatitis, the infecting virus can directly suppress bone marrow function, reducing the production of all blood cell lines including leukocytes, as seen in a study of 324 adults with acute viral hepatitis, where 7.4% of patients developed leukopenia 1. Additionally, the liver inflammation triggers the release of inflammatory cytokines that can further inhibit normal bone marrow function. The spleen often enlarges (splenomegaly) during acute hepatitis, leading to increased sequestration and destruction of white blood cells. Autoimmune mechanisms may also develop, with the production of antibodies against white blood cells, accelerating their clearance from circulation. In severe cases, the liver's compromised function affects the metabolism of toxins that can be harmful to bone marrow. Nutritional deficiencies that commonly occur during acute hepatitis, particularly folate deficiency, can further impair white blood cell production. This leukopenia typically resolves as the hepatitis improves, but may require supportive care and close monitoring to prevent infectious complications during the acute phase of illness. Some studies have investigated the efficacy of antiviral agents in treating hepatitis B, such as tenofovir and entecavir, but these do not directly address the pathophysiology of leukopenia in acute hepatitis 2, 3, 4, 5. However, understanding the treatment options for hepatitis B can inform the management of patients with leukopenia in this context. Key factors to consider in the management of leukopenia in acute hepatitis include:
- Monitoring of white blood cell counts
- Supportive care to prevent infectious complications
- Treatment of underlying hepatitis
- Management of nutritional deficiencies and splenomegaly.