Journal of Liver

Thrombocytopenia during Liver Cirrhosis Condition and its Clinical Complications

Hideo Maehara^* Department of Hepatology and Surgery, Heinrich Heine University Medical Center, Dusseldorf, Germany
^*Correspondence: Hideo Maehara, Department of Hepatology and Surgery, Heinrich Heine University Medical Center, Dusseldorf, Germany, Email:

Received: 03-Jul-2023, Manuscript No. JLR-23-22830; Editor assigned: 06-Jul-2023, Pre QC No. JLR-23-22830 (PQ); Reviewed: 19-Jul-2023, QC No. JLR-23-22830; Revised: 26-Jul-2023, Manuscript No. JLR-23-22830 (R); Published: 02-Aug-2023, DOI: 10.35248/2167-0889.23.12.190.

Description

Platelets are small blood cells that play a vital role in hemostasis, the process of stopping bleeding after an injury. Platelets form clumps at the site of injury and release substances that activate the coagulation cascade, resulting in the formation of a fibrin clot that seals the wound. Normal platelet count ranges from 150,000 to 400,000 per microliter of blood. Thrombocytopenia is a condition in which the platelet count falls below 150,000 per microliter, increasing the risk of bleeding. Thrombocytopenia is a common complication of Chronic Liver Disease (CLD), affecting up to 76% of patients with cirrhosis. Cirrhosis is a condition in which the liver is scarred and damaged by various causes, such as viral infections, alcohol abuse, autoimmune disorders, or metabolic diseases. Cirrhosis impairs the liver’s ability to perform its essential functions, such as detoxifying the blood, producing bile, synthesizing proteins, and regulating glucose and lipid metabolism. Cirrhosis also causes portal hypertension, which is an increase in the pressure within the portal vein that carries blood from the digestive organs to the liver. Portal hypertension leads to the formation of varies, which are enlarged and fragile blood vessels that can rupture and bleed.

Patients with liver disease may have increased platelet consumption due to various factors, such as Disseminated Intravascular Coagulation (DIC), infection, sepsis, or hypersplenism. Some patients with liver disease may develop Immune Thrombocytopenia (ITP), a condition in which autoantibodies target and destroy platelets. ITP may coexist with liver disease, especially in patients with autoimmune hepatitis or chronic hepatitis C. ITP may also be induced by some drugs used to treat liver disease or its complications, such as interferon, immunosuppressants, and antibiotics. The liver is the main source of Thrombopoietin (TPO), a hormone that stimulates the production of platelets by megakaryocytes in the bone marrow. Cirrhosis reduces the synthesis and secretion of TPO by the liver, resulting in decreased platelet production. Moreover, some factors that cause liver disease, such as alcohol and certain viruses, may also suppress the bone marrow function and inhibit megakaryopoiesis. In conclusion, thrombocytopenia is a frequent and complex complication of liver disease that involves multiple mechanisms and has variable clinical implications.

The management of thrombocytopenia in liver disease requires individualized assessment and treatment based on the patient’s characteristics and needs. Hemophagocytic Lymphohistiocytosis (HLH) is a rare and life-threatening condition in which certain white blood cells (histiocytes and lymphocytes) become overactive and attack other blood cells. HLH can be triggered by infections, malignancies, or autoimmune diseases. Liver disease can cause HLH by activating the immune system or impairing its regulation. Coagulopathy is a condition in which the blood does not clot normally, resulting in increased bleeding or bruising. Liver disease can cause coagulopathy by impairing the synthesis of clotting factors and inhibitors, reducing the clearance of activated clotting factors, or altering the balance of vitamin Kdependent factors. There are several mechanisms that contribute to thrombocytopenia in patients with liver disease. The clinical significance of thrombocytopenia in liver disease is controversial. Some studies have suggested that thrombocytopenia may be associated with increased bleeding risk, especially from varies. Leukopenia is a condition in which the white blood cell count is lower than normal. White blood cells are part of the immune system and help fight infections and inflammation. Liver disease can cause leukopenia by reducing the production of white blood cells in the bone marrow, increasing the sequestration of white blood cells by the spleen, or causing immune-mediated destruction of white blood cells.

Conclusion

However, other studies have found no correlation between platelet count and bleeding outcomes. This may be explained by the fact that bleeding in liver disease is multifactorial and depends on other factors besides platelet count, such as coagulation abnormalities, vascular integrity, infection, inflammation, and medication use. The management of thrombocytopenia in liver disease depends on several factors, such as the severity of thrombocytopenia, the underlying cause of liver disease, the presence of other bleeding risk factors, and the type and urgency of the procedure or intervention that requires hemostasis.