RACIONAL: A medida do gradiente de pressão venosa hepática é o método mais utilizado para a avaliação da pressão portal. Mais recentemente, a contagem de plaquetas no sangue tem sido apontada como um ...marcador não-invasivo da presença de hipertensão portal. OBJETIVO: Correlacionar a contagem de plaquetas com os valores do gradiente de pressão venosa hepática em uma população de pacientes cirróticos. PACIENTES E MÉTODOS: Foram estudados 83 pacientes com hepatopatia crônica que realizaram estudo hemodinâmico hepático, em período de 6 anos. Os pacientes foram divididos em grupos conforme a classificação de Child-Pugh e todos realizaram endoscopia digestiva alta para constatar a presença de varizes de esôfago, assim como tiveram a contagem sérica de plaquetas determinada. RESULTADOS: O número de plaquetas variou entre 45.000/mm³ e 389.000/mm³, com média 104.099 e desvio-padrão 58.776. O gradiente de pressão venosa apresentou média igual a 15,2 mm Hg e desvio-padrão igual a 6,4 mm Hg, variando de 1 a 29 mm Hg. Realizou-se regressão linear simples para verificar a correlação entre o gradiente de pressão venosa e o número de plaquetas, o que permitiu constatar fraca correlação entre ambos. Embora se tenha observado menor número de plaquetas, à medida que o calibre das varizes aumentava e nos pacientes com maior grau de disfunção hepatocelular - medida pela classificação de Child-Pugh - não se encontrou significância estatística. CONCLUSÃO: A despeito de não haver demonstrado correlação estatística entre o número de plaquetas com o gradiente de pressão venosa hepática e o grau de disfunção hepatocelular, pelas tendências observadas, acredita-se que ambos os fatores podem estar implicados na patogenia da plaquetopenia em pacientes cirróticos.
RACIONAL: A medida do gradiente de pressão venosa hepática é o método mais utilizado para a avaliação da pressão portal. Mais recentemente, a contagem de plaquetas no sangue tem sido apontada como um ...marcador não-invasivo da presença de hipertensão portal. OBJETIVO: Correlacionar a contagem de plaquetas com os valores do gradiente de pressão venosa hepática em uma população de pacientes cirróticos. PACIENTES E MÉTODOS: Foram estudados 83 pacientes com hepatopatia crônica que realizaram estudo hemodinâmico hepático, em período de 6 anos. Os pacientes foram divididos em grupos conforme a classificação de Child-Pugh e todos realizaram endoscopia digestiva alta para constatar a presença de varizes de esôfago, assim como tiveram a contagem sérica de plaquetas determinada. RESULTADOS: O número de plaquetas variou entre 45.000/mm³ e 389.000/mm³, com média 104.099 e desvio-padrão 58.776. O gradiente de pressão venosa apresentou média igual a 15,2 mm Hg e desvio-padrão igual a 6,4 mm Hg, variando de 1 a 29 mm Hg. Realizou-se regressão linear simples para verificar a correlação entre o gradiente de pressão venosa e o número de plaquetas, o que permitiu constatar fraca correlação entre ambos. Embora se tenha observado menor número de plaquetas, à medida que o calibre das varizes aumentava e nos pacientes com maior grau de disfunção hepatocelular - medida pela classificação de Child-Pugh - não se encontrou significância estatística. CONCLUSÃO: A despeito de não haver demonstrado correlação estatística entre o número de plaquetas com o gradiente de pressão venosa hepática e o grau de disfunção hepatocelular, pelas tendências observadas, acredita-se que ambos os fatores podem estar implicados na patogenia da plaquetopenia em pacientes cirróticos.BACKGROUND: Determination of hepatic venous pressure gradient is the main method used to assess portal pressure. Recently, platelet blood levels has been indicated as a non-invasive marker of the presence of portal hypertension. AIM: To correlate platelet blood levels with the hepatic venous pressure gradient among patients with cirrhosis. PATIENTS AND METHODS: A total of 83 cirrhotic patients who had undergone hepatic venous pressure gradient over the last 6 years were included. Patients were divided in groups according to Child-Pugh classification. All had upper digestive endoscopy to assess the presence of esophageal varices and platelet serum levels were recorded. RESULTS: Platelet serum levels range varied between 45,000/mm³ and 389,000/mm³ (mean: 104,099; standard deviation: 58,776). Mean hepatic venous pressure gradient was 15.2 mm Hg with a standard deviation of 6.4 mm Hg (range: 1 to 29 mm Hg). Simple linear regression analysis was applied to verify an association of hepatic venous pressure gradient and platelet serum levels, revealing a weak correlation between both variables. We observed a progressive reduction of serum platelet levels as esophageal varices diameter increased and hepatocellular function (established by Child-Pugh classification) decreased. However, these findings did not reach statistical significance. CONCLUSION: Despite the lack of a statistical significant correlation among serum platelet levels and hepatic venous pressure gradient or hepatocellular function, there was a clear tendency indicating that those variables could be involved in the pathogenesis of low platelet levels.
RACIONAL: A medida do gradiente de pressão venosa hepática é o método mais utilizado para a avaliação da pressão portal. Mais recentemente, a contagem de plaquetas no sangue tem sido apontada como um ...marcador não-invasivo da presença de hipertensão portal. OBJETIVO: Correlacionar a contagem de plaquetas com os valores do gradiente de pressão venosa hepática em uma população de pacientes cirróticos. PACIENTES E MÉTODOS: Foram estudados 83 pacientes com hepatopatia crônica que realizaram estudo hemodinâmico hepático, em período de 6 anos. Os pacientes foram divididos em grupos conforme a classificação de Child-Pugh e todos realizaram endoscopia digestiva alta para constatar a presença de varizes de esôfago, assim como tiveram a contagem sérica de plaquetas determinada. RESULTADOS: O número de plaquetas variou entre 45.000/mm³ e 389.000/mm³, com média 104.099 e desvio-padrão 58.776. O gradiente de pressão venosa apresentou média igual a 15,2 mm Hg e desvio-padrão igual a 6,4 mm Hg, variando de 1 a 29 mm Hg. Realizou-se regressão linear simples para verificar a correlação entre o gradiente de pressão venosa e o número de plaquetas, o que permitiu constatar fraca correlação entre ambos. Embora se tenha observado menor número de plaquetas, à medida que o calibre das varizes aumentava e nos pacientes com maior grau de disfunção hepatocelular - medida pela classificação de Child-Pugh - não se encontrou significância estatística. CONCLUSÃO: A despeito de não haver demonstrado correlação estatística entre o número de plaquetas com o gradiente de pressão venosa hepática e o grau de disfunção hepatocelular, pelas tendências observadas, acredita-se que ambos os fatores podem estar implicados na patogenia da plaquetopenia em pacientes cirróticos.
BACKGROUND: Determination of hepatic venous pressure gradient is the main method used to assess portal pressure. Recently, platelet blood levels has been indicated as a non-invasive marker of the presence of portal hypertension. AIM: To correlate platelet blood levels with the hepatic venous pressure gradient among patients with cirrhosis. PATIENTS AND METHODS: A total of 83 cirrhotic patients who had undergone hepatic venous pressure gradient over the last 6 years were included. Patients were divided in groups according to Child-Pugh classification. All had upper digestive endoscopy to assess the presence of esophageal varices and platelet serum levels were recorded. RESULTS: Platelet serum levels range varied between 45,000/mm³ and 389,000/mm³ (mean: 104,099; standard deviation: 58,776). Mean hepatic venous pressure gradient was 15.2 mm Hg with a standard deviation of 6.4 mm Hg (range: 1 to 29 mm Hg). Simple linear regression analysis was applied to verify an association of hepatic venous pressure gradient and platelet serum levels, revealing a weak correlation between both variables. We observed a progressive reduction of serum platelet levels as esophageal varices diameter increased and hepatocellular function (established by Child-Pugh classification) decreased. However, these findings did not reach statistical significance. CONCLUSION: Despite the lack of a statistical significant correlation among serum platelet levels and hepatic venous pressure gradient or hepatocellular function, there was a clear tendency indicating that those variables could be involved in the pathogenesis of low platelet levels.
Determination of hepatic venous pressure gradient is the main method used to assess portal pressure. Recently, platelet blood levels has been indicated as a non-invasive marker of the presence of ...portal hypertension.
To correlate platelet blood levels with the hepatic venous pressure gradient among patients with cirrhosis.
A total of 83 cirrhotic patients who had undergone hepatic venous pressure gradient over the last 6 years were included. Patients were divided in groups according to Child-Pugh classification. All had upper digestive endoscopy to assess the presence of esophageal varices and platelet serum levels were recorded.
Platelet serum levels range varied between 45,000/mm(3) and 389,000/mm(3) (mean: 104,099; standard deviation: 58,776). Mean hepatic venous pressure gradient was 15.2 mm Hg with a standard deviation of 6.4 mm Hg (range: 1 to 29 mm Hg). Simple linear regression analysis was applied to verify an association of hepatic venous pressure gradient and platelet serum levels, revealing a weak correlation between both variables. We observed a progressive reduction of serum platelet levels as esophageal varices diameter increased and hepatocellular function (established by Child-Pugh classification) decreased. However, these findings did not reach statistical significance.
Despite the lack of a statistical significant correlation among serum platelet levels and hepatic venous pressure gradient or hepatocellular function, there was a clear tendency indicating that those variables could be involved in the pathogenesis of low platelet levels.
Hepatic dysfunction frequently develops in patients infected with the human immunodeficiency virus (HIV). This retrospective study was undertaken to determine the laparoscopic and histologic findings ...in a group of HIV-seropositive patients with or without the acquired immune deficiency syndrome (AIDS). Fifty-four patients, 44 with AIDS and 10 HIV-positive, underwent laparoscopic examination and visually guided biopsies for the assessment of clinical or biochemical evidence of liver injury. Significant abnormalities were detected in 31/44 (70%) AIDS patients and 3/10 (30%) HIV-positive patients. Overall, specific laparoscopic findings were described in 25/54 (46%). The most common findings were peritoneal involvement, massive intra-abdominal adhesions, focal lesions of the liver or spleen, and diffuse nodularity of the liver; these were usually related to opportunistic infections or neoplasms such as non-Hodgkin's lymphomas and Kaposi's sarcoma. No procedure-related deaths occurred. Laparoscopy is a safe and accurate method to detect underlying disease in a selected population of HIV-seropositive patients.
Chronic hepatitis B virus infection is closely associated with the development of hepatocellular carcinoma, which is a major cause of cancer death worldwide. Recent studies have implicated hepatitis ...C virus infection as a major pathogenic agent of HBsAg-negative hepatocellular carcinoma. The significance of hepatitis C virus and hepatitis B virus infections in the occurrence of HBsAg-negative hepatocellular carcinoma has not been well established in the United States. We studied 91 HBsAg-negative American patients with hepatocellular carcinoma for evidence of hepatitis C virus or hepatitis B virus infection. These patients had no other predisposing factors to hepatocellular carcinoma. A sensitive polymerase chain reaction was employed to detect hepatitis C virus RNA and hepatitis B virus DNA in serum and liver. Three sets of hepatitis C virus and hepatitis B virus primers were used to optimize the detection of viral genomes. Hepatitis C virus antibodies were measured with second-generation immunoassays. Twenty-six (29%) of these patients carried low levels of hepatitis B virus DNA in either serum, liver/tumor tissue or both. On the basis of the results from serological and polymerase chain reaction analyses of serum and liver, we found that 53 of 91 patients (58%) exhibited evidence of hepatitis C virus infection. When data were combined, 14 patients (15%) had evidence of hepatitis B virus/hepatitis C virus coinfection, whereas 12 (13%) were infected with hepatitis B virus alone and 39 (43%) had hepatitis C virus only. Twenty-six (29%) had no markers of hepatitis B virus or hepatitis C virus infection. All patients with identifiable viral markers had coexisting chronic liver disease. Our study suggests that hepatitis C virus and occult hepatitis B virus infections account for most (71%) hepatocellular carcinoma cases of unknown pathogenesis in the United States. However, in some patients with hepatocellular carcinoma no defined pathogenesis is associated with development of disease.
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