January 7, 2011
Researchers at the University of California in San Francisco (UCSF) have launched a study to discover the best comprehensive care methods for people living with HIV as they get older. In a news article by the university about the project, the study’s leaders explain they will be integrating the expertise of specialists in geriatric medicine with that of infectious disease experts to address the fact that HIV-positive people are experiencing age-related problems at a younger age than HIV-negative people.
“I know I’m getting older,” Lou Grosso, a 57-year-old UCSF HIV clinic patient, said in the article. “So is that why I have the aches and pains and memory issues? Or is it because I have been taking all those antiretroviral drug cocktails that have been keeping me alive all these years? I never thought I would live this long to ask these questions.”
These are some of the issues that the new study aims to answer, as well as how to choose the best care models for people with age-related problems. At present, doctors really don’t know how best to manage aging HIV-positive patients.
Are the same comprehensive care guidelines used for HIV-negative people appropriate? Currently, there are no easy answers to that question.
“Conditions that you might normally see in patients in their 60s or 70s are showing up in HIV patients who are only in their 40s and 50s,” said Brad Hare, MD, Grosso’s doctor and medical director of the UCSF Positive Health Program at San Francisco General Hospital.
Hare explains that he and a colleague, Malcolm John, MD, who heads UCSF’s comprehensive HIV care clinic, will use the study funds to identify which screening tests should be conducted to monitor for diseases of aging, along with when they should be used. The study will also explore the value of bringing in nutritionists and pharmacists as essential members of the care team.
John stresses that they will also be looking beyond the physical manifestations of HIV disease. Specialists in psychology and social support will also be involved.
UCSF’s Positive Care Center, one of the country’s model integrated care programs, will serve as the template upon which to study the best care strategies for people as they age.
“It’s our legacy and responsibility at UC to be leaders in research and caring for people with HIV,” Hare concluded.
Source
January 9, 2011
Cirrhosis Is Present in Most Patients With Hepatitis B and Hepatocellular Carcinoma
Clinical Gastroenterology and Hepatology
Volume 9, Issue 1 , Pages 64-70, January 2011
Ju Dong Yang, W. Ray Kim, Ritika Coelho, Teresa A. Mettler, Joanne T. Benson, Schuyler O. Sanderson, Terry M. Therneau, Bohyun Kim, Lewis R. Roberts
Abstract
Background & Aims
There are few data available about the prevalence or effects of cirrhosis in patients with hepatocellular carcinoma (HCC) from viral hepatitis. We compared patients with HCC and hepatitis B virus (HBV) or hepatitis C virus (HCV) infections to determine the proportions of cirrhosis in each group, virologic and tumor characteristics, and overall survival.
Methods
This analysis included patients with HBV (n = 64) or HCV (n = 118) infection who were diagnosed with HCC at the Mayo Clinic in Rochester, Minnesota from 1994–2008; groups were matched for age and sex. The diagnosis of cirrhosis was based on histology and, if histologic information was insufficient or unavailable, clinical indicators that included ascites or varices, thrombocytopenia or splenomegaly, and radiographic configuration of cirrhosis. Virologic characteristics, tumor stage, and patient survival were also assessed.
Results
The prevalence of histologic cirrhosis was 88% among patients with HBV infection and 93% among those with HCV infection (P = .46). When the most inclusive criteria for cirrhosis were applied, cirrhosis was present in 94% of patients with HBV and 97% with HCV (P = .24). Among HCV patients, 5.2% were negative for HCV RNA after antiviral treatment; 63.4% of HBV patients had HBV DNA <2000 IU/mL with or without treatment. Patients with HBV tended to have less surveillance and more advanced stages of HCC, without differences in survival from those with HCV infection (P = .75).
Conclusions
Most patients with HCC and chronic viral hepatitis had evidence of cirrhosis, including those with HBV infection and those without active viral replication.
Keywords: Liver Cancer, Liver Disease, Virology, Survival
Source
Volume 9, Issue 1 , Pages 64-70, January 2011
Ju Dong Yang, W. Ray Kim, Ritika Coelho, Teresa A. Mettler, Joanne T. Benson, Schuyler O. Sanderson, Terry M. Therneau, Bohyun Kim, Lewis R. Roberts
Abstract
Background & Aims
There are few data available about the prevalence or effects of cirrhosis in patients with hepatocellular carcinoma (HCC) from viral hepatitis. We compared patients with HCC and hepatitis B virus (HBV) or hepatitis C virus (HCV) infections to determine the proportions of cirrhosis in each group, virologic and tumor characteristics, and overall survival.
Methods
This analysis included patients with HBV (n = 64) or HCV (n = 118) infection who were diagnosed with HCC at the Mayo Clinic in Rochester, Minnesota from 1994–2008; groups were matched for age and sex. The diagnosis of cirrhosis was based on histology and, if histologic information was insufficient or unavailable, clinical indicators that included ascites or varices, thrombocytopenia or splenomegaly, and radiographic configuration of cirrhosis. Virologic characteristics, tumor stage, and patient survival were also assessed.
Results
The prevalence of histologic cirrhosis was 88% among patients with HBV infection and 93% among those with HCV infection (P = .46). When the most inclusive criteria for cirrhosis were applied, cirrhosis was present in 94% of patients with HBV and 97% with HCV (P = .24). Among HCV patients, 5.2% were negative for HCV RNA after antiviral treatment; 63.4% of HBV patients had HBV DNA <2000 IU/mL with or without treatment. Patients with HBV tended to have less surveillance and more advanced stages of HCC, without differences in survival from those with HCV infection (P = .75).
Conclusions
Most patients with HCC and chronic viral hepatitis had evidence of cirrhosis, including those with HBV infection and those without active viral replication.
Keywords: Liver Cancer, Liver Disease, Virology, Survival
Source
Thrombocytopenia in chronic hepatitis C
J Gastrointestin Liver Dis. 2010 Dec;19(4):381-5.
Olariu M, Olariu C, Olteanu D.
National Institute of Infectious Diseases "Prof.Dr.Matei Balş" Bucharest,Romania; Email: ol_mihai@yahoo.com.
Abstract
BACKGROUND AND AIMS: Thrombocytopenia in patients with chronic hepatitis C may be the result of several factors: bone marrow inhibition, the decrease of liver thrombopoietin production and an autoimmune mechanism. Clinical variables such as age, gender, severity of liver disease and degree of viremia could influence the severity of platelet reduction. The goal of this study is to determine the prevalent mechanism of thrombocytopenia in patients with chronic hepatitis C and the clinical predictors of its severity.
METHODS: Eighty-one patients with chronic hepatitis C and thrombocytopenia were included. The viral inhibition on the bone marrow (central mechanism) was studied by performing bone marrow biopsy from the iliac crest. The presence of antiplatelet antibodies by ELISA assessed the peripheral mechanism. The clinical predictors included in the analysis were: age, gender, ALT level, liver fibrosis stage and HCV RNA.
RESULTS: Coexistence of a central and peripheral mechanism was found in the vast majority (93.3%) of patients with severe thrombocytopenia (< 100,000/microL) and in most patients (61.53%) with moderate thrombocytopenia (100,000- 125,000/microL). In patients with less severe thrombocytopenia (126,000-149,000/microL), autoimmune destruction was the sole mechanism (85%). Thrombocytopenia was significantly associated with ALT values, viral load and stage of fibrosis.
CONCLUSIONS: Our data demonstrates that chronic hepatitis C is associated with a variable degree of thrombocytopenia. As the disease advances, the platelet count decreases and, in most cases, both mechanisms are involved. The stage of fibrosis is one of the major determinants of thrombocytopenia.
PMID: 21188328 [PubMed - in process]
Source
Olariu M, Olariu C, Olteanu D.
National Institute of Infectious Diseases "Prof.Dr.Matei Balş" Bucharest,Romania; Email: ol_mihai@yahoo.com.
Abstract
BACKGROUND AND AIMS: Thrombocytopenia in patients with chronic hepatitis C may be the result of several factors: bone marrow inhibition, the decrease of liver thrombopoietin production and an autoimmune mechanism. Clinical variables such as age, gender, severity of liver disease and degree of viremia could influence the severity of platelet reduction. The goal of this study is to determine the prevalent mechanism of thrombocytopenia in patients with chronic hepatitis C and the clinical predictors of its severity.
METHODS: Eighty-one patients with chronic hepatitis C and thrombocytopenia were included. The viral inhibition on the bone marrow (central mechanism) was studied by performing bone marrow biopsy from the iliac crest. The presence of antiplatelet antibodies by ELISA assessed the peripheral mechanism. The clinical predictors included in the analysis were: age, gender, ALT level, liver fibrosis stage and HCV RNA.
RESULTS: Coexistence of a central and peripheral mechanism was found in the vast majority (93.3%) of patients with severe thrombocytopenia (< 100,000/microL) and in most patients (61.53%) with moderate thrombocytopenia (100,000- 125,000/microL). In patients with less severe thrombocytopenia (126,000-149,000/microL), autoimmune destruction was the sole mechanism (85%). Thrombocytopenia was significantly associated with ALT values, viral load and stage of fibrosis.
CONCLUSIONS: Our data demonstrates that chronic hepatitis C is associated with a variable degree of thrombocytopenia. As the disease advances, the platelet count decreases and, in most cases, both mechanisms are involved. The stage of fibrosis is one of the major determinants of thrombocytopenia.
PMID: 21188328 [PubMed - in process]
Source
Vitamins B status and antioxidative defense in patients with chronic hepatitis B or hepatitis C virus infection
European Journal of Nutrition
DOI: 10.1007/s00394-010-0156-1
Published Online 24 December 2010
Original Contribution
Chun-che Lin, Wen-hu Liu, Zhi-hong Wang and Mei-chin Yin
Abstract
Background & Aims
The impact of hepatitis B virus (HBV) or hepatitis C virus (HCV) infection upon B vitamins status and antioxidative defense in infected patients was examined.
Methods
Dietary record and blood levels of B vitamins and oxidative stress–associated biomarkers were determined for 195 healthy controls, 132 HBV, and 114 HCV patients.
Results
HBV-infected patients had significantly higher levels of total cholesterol, free fatty acids (FFA), and lower ghrelin level (p < 0.05); and HCV-infected patients had significantly higher Ishak inflammation score and lactate dehydrogenase activity (p < 0.05). HBV patients had significantly lower red blood cell (RBC) vitamins B2 and B6 levels, and HCV infection significantly decreased vitamins B2, B6 and folate levels in RBC and/or plasma (p < 0.05). Correlation coefficients of RBC vitamin B2 versus serum FFA in HBV patients, RBC vitamins B2 and B6 versus HCV RNA and Ishak inflammation score, and plasma vitamin B6 vs Ishak inflammation score in HCV patients were <−0.5. HBV-infected patients had significantly higher oxidized glutathione level and lower glutathione peroxidase activity (p < 0.05), but HCV patients had significantly lower superoxide dismutase and catalase activities (p < 0.05).
Conclusion
HBV or HCV infection enhanced oxidative stress and lowered B vitamins in circulation. In order to avoid other healthy risk, nutrition status should be monitored and limitation or supplementation of certain nutrients might be helpful for HBV- or HCV-infected patients.
Keywords Hepatitis B virus – Hepatitis C virus – B vitamins – Oxidative stress – Lipid metabolism
Source
DOI: 10.1007/s00394-010-0156-1
Published Online 24 December 2010
Original Contribution
Chun-che Lin, Wen-hu Liu, Zhi-hong Wang and Mei-chin Yin
Abstract
Background & Aims
The impact of hepatitis B virus (HBV) or hepatitis C virus (HCV) infection upon B vitamins status and antioxidative defense in infected patients was examined.
Methods
Dietary record and blood levels of B vitamins and oxidative stress–associated biomarkers were determined for 195 healthy controls, 132 HBV, and 114 HCV patients.
Results
HBV-infected patients had significantly higher levels of total cholesterol, free fatty acids (FFA), and lower ghrelin level (p < 0.05); and HCV-infected patients had significantly higher Ishak inflammation score and lactate dehydrogenase activity (p < 0.05). HBV patients had significantly lower red blood cell (RBC) vitamins B2 and B6 levels, and HCV infection significantly decreased vitamins B2, B6 and folate levels in RBC and/or plasma (p < 0.05). Correlation coefficients of RBC vitamin B2 versus serum FFA in HBV patients, RBC vitamins B2 and B6 versus HCV RNA and Ishak inflammation score, and plasma vitamin B6 vs Ishak inflammation score in HCV patients were <−0.5. HBV-infected patients had significantly higher oxidized glutathione level and lower glutathione peroxidase activity (p < 0.05), but HCV patients had significantly lower superoxide dismutase and catalase activities (p < 0.05).
Conclusion
HBV or HCV infection enhanced oxidative stress and lowered B vitamins in circulation. In order to avoid other healthy risk, nutrition status should be monitored and limitation or supplementation of certain nutrients might be helpful for HBV- or HCV-infected patients.
Keywords Hepatitis B virus – Hepatitis C virus – B vitamins – Oxidative stress – Lipid metabolism
Source
The relationship between liver disease stage and liver fibrosis: a tangled web
Authors: Germani, Giacomo 1; Burroughs, Andrew K 1; Dhillon, Amar P 2
Source: Histopathology, Volume 57, Number 6, December 2010 , pp. 773-784(12)
Publisher: Wiley-Blackwell
Abstract:
The structural consequences of chronic liver disease are described as a series of liver disease `stages' with scarring and architectural change that eventually destroys and replaces the normal lobular structure of the liver. Fibrosis (`excess collagen') and stage have been confused in histological staging systems. Fibrosis is part of increasing liver disease stage, but fibrosis and stage are different. Staging liver disease is important in routine histopathological assessment. Measurement of liver fibrosis is another process. The collagenous proportion of a liver biopsy [collagen proportionate area (CPA)] correlates with hepatic venous pressure gradient (HVPG), which is of recognized prognostic value. CPA at 1 year post-transplantation in hepatitis C virus-infected patients predicts subsequent clinical decompensation. CPA in cirrhotic patients predicts decompensation more accurately than staging or HVPG. The `cirrhosis' stage category has poor prognostic power, and CPA effectively substages cirrhosis. CPA improves the description of liver disease stage. Proper validation of antifibrotic treatments and `non-invasive markers of liver fibrosis' requires measurement of liver fibrosis (and not liver biopsy stage scores). It is unacceptable for the words `fibrosis' and `score' to remain next to each other. There are benefits to properly understanding liver fibrosis and liver disease stage and properly assessing each of them.
Keywords: liver; fibrosis; stage; collagen proportionate area; image analysis
Source
Source: Histopathology, Volume 57, Number 6, December 2010 , pp. 773-784(12)
Publisher: Wiley-Blackwell
Abstract:
The structural consequences of chronic liver disease are described as a series of liver disease `stages' with scarring and architectural change that eventually destroys and replaces the normal lobular structure of the liver. Fibrosis (`excess collagen') and stage have been confused in histological staging systems. Fibrosis is part of increasing liver disease stage, but fibrosis and stage are different. Staging liver disease is important in routine histopathological assessment. Measurement of liver fibrosis is another process. The collagenous proportion of a liver biopsy [collagen proportionate area (CPA)] correlates with hepatic venous pressure gradient (HVPG), which is of recognized prognostic value. CPA at 1 year post-transplantation in hepatitis C virus-infected patients predicts subsequent clinical decompensation. CPA in cirrhotic patients predicts decompensation more accurately than staging or HVPG. The `cirrhosis' stage category has poor prognostic power, and CPA effectively substages cirrhosis. CPA improves the description of liver disease stage. Proper validation of antifibrotic treatments and `non-invasive markers of liver fibrosis' requires measurement of liver fibrosis (and not liver biopsy stage scores). It is unacceptable for the words `fibrosis' and `score' to remain next to each other. There are benefits to properly understanding liver fibrosis and liver disease stage and properly assessing each of them.
Keywords: liver; fibrosis; stage; collagen proportionate area; image analysis
Source
Metabolic syndrome found in 52 percent of patients after liver transplantation
Published: Thursday, January 6, 2011 - 10:11
Researchers from Israel have determined that more than half of liver transplant recipients develop post-transplantation metabolic syndrome (PTMS), placing them at greater risk for cardiovascular disease. Prior to transplantation only 5% of the patients were diagnosed with metabolic syndrome, but rates of obesity, hypertriglyceridemia, hypertension, and diabetes were significantly higher post transplantation. Full details of this retrospective-prevalence study are available in the January 2011 issue of Liver Transplantation, a journal published by Wiley-Blackwell on behalf of the American Association for the Study of Liver Diseases. Metabolic syndrome, which is comprised of obesity, hypertension, hyperglycemia, and dyslipidemia, is commonly seen in patients following liver transplantation and is double the rate reported for the general population. Prior studies have found that immunosuppressive medications including calcineurin inhibitors and corticosteroids; modifiable lifestyle choices such as food intake, which can contribute to weight gain and insulin resistance; and the underlying liver disease itself (chronic hepatitis C virus infection and nonalcoholic fatty liver disease), all play a significant role in the development of metabolic syndrome.
In order to determine the prevalence and risk factors associated with PTMS, Professor Ziv Ben Ari and colleagues from the Liver Transplant Unit at Rabin Medical Center—the largest such unit in Israel—reviewed the files of 252 patients who received a liver transplant between 1985 and 2007. Researchers analyzed pre- and post-transplant clinical and laboratory data, including height, weight, waist circumference, presence of diabetes, hypertension, or hyperlipidemia, and prescribed medications (immunosuppressive, anti-hypertensive, hypoglycemic, and lipid-lowering drugs).
Researchers diagnosed PTMS when at least three of the following criteria were met: increased waist circumference, elevated fasting serum triglycerides, elevated blood pressure, abnormally high fasting serum glucose, high BMI and low high-density lipoprotein-cholesterol. Major vascular events were defined as transient ischemic attack, cerebrovascular accident, acute coronary syndrome, and myocardial infarction. Coronary events were identified by coronary angiography or coronary revascularization.
"We found significantly higher rates of obesity, hypertriglyceridemia, hypertension, diabetes and low HDL cholesterol, in patients following liver transplantation," said Professor Ben Ari. Researchers determined that PTMS patients were older and heavier than those in the non-PTMS group, and had a higher rate of pre-transplant chronic hepatitis C virus infection.
Further analysis showed significant independent predictors of PTMS were age, pre-transplant nonalcoholic fatty liver disease, BMI, diabetes, and triglycerides. Patients with PTMS also experienced more major vascular and cardiac events following their transplants than those without PTMS (15% versus 5%). "PTMS is associated with cardiovascular morbidity but not mortality, and it may be predicted by pre-transplantation conditions," concluded Professor Ben Ari.
In an editorial also published this month in Liver Transplantation, Michael Charlton, MD, FRCP, from the Mayo Clinic Transplant Center commented, "Professor Ben Ari and colleagues provide new evidence of the increasingly high prevalence and important associated outcomes of PTMS. Well designed, prospective studies are needed to validate these new observations and to establish optimal strategies for the diagnosis, prevention and management of post-transplant metabolic syndrome."
Source: Wiley-Blackwell
Soure
Researchers from Israel have determined that more than half of liver transplant recipients develop post-transplantation metabolic syndrome (PTMS), placing them at greater risk for cardiovascular disease. Prior to transplantation only 5% of the patients were diagnosed with metabolic syndrome, but rates of obesity, hypertriglyceridemia, hypertension, and diabetes were significantly higher post transplantation. Full details of this retrospective-prevalence study are available in the January 2011 issue of Liver Transplantation, a journal published by Wiley-Blackwell on behalf of the American Association for the Study of Liver Diseases. Metabolic syndrome, which is comprised of obesity, hypertension, hyperglycemia, and dyslipidemia, is commonly seen in patients following liver transplantation and is double the rate reported for the general population. Prior studies have found that immunosuppressive medications including calcineurin inhibitors and corticosteroids; modifiable lifestyle choices such as food intake, which can contribute to weight gain and insulin resistance; and the underlying liver disease itself (chronic hepatitis C virus infection and nonalcoholic fatty liver disease), all play a significant role in the development of metabolic syndrome.
In order to determine the prevalence and risk factors associated with PTMS, Professor Ziv Ben Ari and colleagues from the Liver Transplant Unit at Rabin Medical Center—the largest such unit in Israel—reviewed the files of 252 patients who received a liver transplant between 1985 and 2007. Researchers analyzed pre- and post-transplant clinical and laboratory data, including height, weight, waist circumference, presence of diabetes, hypertension, or hyperlipidemia, and prescribed medications (immunosuppressive, anti-hypertensive, hypoglycemic, and lipid-lowering drugs).
Researchers diagnosed PTMS when at least three of the following criteria were met: increased waist circumference, elevated fasting serum triglycerides, elevated blood pressure, abnormally high fasting serum glucose, high BMI and low high-density lipoprotein-cholesterol. Major vascular events were defined as transient ischemic attack, cerebrovascular accident, acute coronary syndrome, and myocardial infarction. Coronary events were identified by coronary angiography or coronary revascularization.
"We found significantly higher rates of obesity, hypertriglyceridemia, hypertension, diabetes and low HDL cholesterol, in patients following liver transplantation," said Professor Ben Ari. Researchers determined that PTMS patients were older and heavier than those in the non-PTMS group, and had a higher rate of pre-transplant chronic hepatitis C virus infection.
Further analysis showed significant independent predictors of PTMS were age, pre-transplant nonalcoholic fatty liver disease, BMI, diabetes, and triglycerides. Patients with PTMS also experienced more major vascular and cardiac events following their transplants than those without PTMS (15% versus 5%). "PTMS is associated with cardiovascular morbidity but not mortality, and it may be predicted by pre-transplantation conditions," concluded Professor Ben Ari.
In an editorial also published this month in Liver Transplantation, Michael Charlton, MD, FRCP, from the Mayo Clinic Transplant Center commented, "Professor Ben Ari and colleagues provide new evidence of the increasingly high prevalence and important associated outcomes of PTMS. Well designed, prospective studies are needed to validate these new observations and to establish optimal strategies for the diagnosis, prevention and management of post-transplant metabolic syndrome."
Source: Wiley-Blackwell
Soure
The natural history of interferon-alpha induced thyroiditis in chronic hepatitis C patients: A long term study
Published on: 2011-01-08
Autoimmune thyroid disease is a common complication of patients with chronic hepatitis C undergoing combination pegylated interferon-alpha and ribavirin treatment. A small proportion develops interferon-induced thyroiditis of which the long term natural history is unknown and how it compares with de novo thyroiditis.
The aim of the study is to determine the natural history of thyroid disease including antibody profile in this particular setting 36 months from the completion of therapy.
Methods: A cohort of 18 hepatitis C patients (mean age 45 +/- 8 years (standard deviation)) who developed exclusively thyroiditis in this setting was followed every 12 months after the completion of therapy for 36 months. Investigations included thyrotropin, free tetra-iodothyronine, free tri-iodothyronine levels and thyroid autoantibodies.
Results: None of the patients developed any long term thyroid disease.
Two patients had a prolonged hypothyroid phase of the thyroiditis early after the completion of treatment but recovered fully. The remaining 16 patients remained euthyroid.
Similarly, thyroid autoantibodies all declined and returned to reference range.
Conclusions: The long term natural history in this small series of interferon induced thyroiditis was benign. If a larger series confirms a similar outcome then there is no long term residual effect on thyroid function and follow-up testing would not be warranted.
Author: Huy TranTracey JonesElizabeth IannaGlenn Reeves
Credits/Source: Thyroid Research 2011, 4:2
Source
Autoimmune thyroid disease is a common complication of patients with chronic hepatitis C undergoing combination pegylated interferon-alpha and ribavirin treatment. A small proportion develops interferon-induced thyroiditis of which the long term natural history is unknown and how it compares with de novo thyroiditis.
The aim of the study is to determine the natural history of thyroid disease including antibody profile in this particular setting 36 months from the completion of therapy.
Methods: A cohort of 18 hepatitis C patients (mean age 45 +/- 8 years (standard deviation)) who developed exclusively thyroiditis in this setting was followed every 12 months after the completion of therapy for 36 months. Investigations included thyrotropin, free tetra-iodothyronine, free tri-iodothyronine levels and thyroid autoantibodies.
Results: None of the patients developed any long term thyroid disease.
Two patients had a prolonged hypothyroid phase of the thyroiditis early after the completion of treatment but recovered fully. The remaining 16 patients remained euthyroid.
Similarly, thyroid autoantibodies all declined and returned to reference range.
Conclusions: The long term natural history in this small series of interferon induced thyroiditis was benign. If a larger series confirms a similar outcome then there is no long term residual effect on thyroid function and follow-up testing would not be warranted.
Author: Huy TranTracey JonesElizabeth IannaGlenn Reeves
Credits/Source: Thyroid Research 2011, 4:2
Source
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