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Improvement in Thrombocytopenia after Carvedilol use in Hepatitis C cirrhotic patients.

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Carvedilol is a β-blocker (non-selective). It causes vasoconstriction in the splanchnic vessels and causes reduction of portal inflow. Hence this change causes less destruction of platelets in the patients having splenomegaly with portal hypertension and cirrhosis. Objectives: The objective of the study is to find out the effect of carvedilol on thrombocytopenia in cirrhotic patients of hepatitis C. Study Design: Descriptive study. Settings: Department of Gastroenterology, Fatima Memorial Hospital, Lahore. Period: Six months from 17th October 2015 to 16th April 2016. Material & Method: Data was collected using designed proformas. All patients with hepatitis C having cirrhosis of liver, splenomegaly and a platelet count of less than 100,000/mm3 were included after taking informed consent. Dose of carvedilol was managed so that 25% reduction in heart rate was achieved. Platelet count was repeated after two weeks. Blood pressure, pulse and platelet count before and after 25% reduction in heart rate with carvedilol was compared. Changes in platelet count, blood pressure, pulse and dose of carvedilol were also calculated. <0.05 p value was taken as significant. Results: A total of 66% patients responded to carvedilol therapy and showedmean rise in platelet count of 16 ± 10.3. (P-Value <0.05). Changes in platelet count with change in blood pressure, pulse and with dose of carvedilol were found to be significant. (P<0.05). Conclusion: Carvedilol causes improvement in thrombocytopenia in cirrhotic patients.
Title: Improvement in Thrombocytopenia after Carvedilol use in Hepatitis C cirrhotic patients.
Description:
Carvedilol is a β-blocker (non-selective).
It causes vasoconstriction in the splanchnic vessels and causes reduction of portal inflow.
Hence this change causes less destruction of platelets in the patients having splenomegaly with portal hypertension and cirrhosis.
Objectives: The objective of the study is to find out the effect of carvedilol on thrombocytopenia in cirrhotic patients of hepatitis C.
Study Design: Descriptive study.
Settings: Department of Gastroenterology, Fatima Memorial Hospital, Lahore.
Period: Six months from 17th October 2015 to 16th April 2016.
Material & Method: Data was collected using designed proformas.
All patients with hepatitis C having cirrhosis of liver, splenomegaly and a platelet count of less than 100,000/mm3 were included after taking informed consent.
Dose of carvedilol was managed so that 25% reduction in heart rate was achieved.
Platelet count was repeated after two weeks.
Blood pressure, pulse and platelet count before and after 25% reduction in heart rate with carvedilol was compared.
Changes in platelet count, blood pressure, pulse and dose of carvedilol were also calculated.
<0.
05 p value was taken as significant.
Results: A total of 66% patients responded to carvedilol therapy and showedmean rise in platelet count of 16 ± 10.
3.
(P-Value <0.
05).
Changes in platelet count with change in blood pressure, pulse and with dose of carvedilol were found to be significant.
(P<0.
05).
Conclusion: Carvedilol causes improvement in thrombocytopenia in cirrhotic patients.

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