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Hepatitis C virus (HCV) infection is the most important liver disease (LD) after renal transplantation. Liver biopsy is the gold standard for the diagnosis and follow-up of LD. The aim of this retrospective study was to evaluate the correlation between values of Fibroscan (EchoSens, Paris, France), a new noninvasive method to assess liver fibrosis, liver biopsy, and clinical data among HCV-positive renal transplant patients. Twenty-four HCV/RNA-positive patients with a previous liver biopsy were selected to undergo Fibroscan (transient elastography) and a clinical evaluation of liver function. Fibroscan values were expressed in kilopascals (kPa). As 2 patients were eliminated due to obesity or ascites, we analyzed 22 patients. Thirteen patients (59%) with fibrosis F0-F1 (METAVIR score) by biopsy and normal liver function showed a mean Fibroscan score of 5.2 kPa (range, 2.3-6.8 kPa). Three patients (13.6%) exhibited F2 by biopsy and normal liver function with a mean Fibroscan score of 8.2 kPa (range, 7.3-8.9 kPa). Three patients (13.6%) with F3 by biopsy and abnormal liver function showed a high mean Fibroscan score of 10.9 kPa (range, 10.5-11.6 kPa). The last 3 patients (13.6%) with F4 (cirrhosis) by biopsy and abnormal clinical data showed the highest mean Fibroscan value of 14.2 kPa (range, 8.9-18 kPa). In conclusion, among renal transplant patients with HCV the values of Fibroscan seem to correlate with the degree of fibrosis by biopsy and with clinical liver function. Therefore, Fibroscan may be useful to follow patients with LD. However, these results should be analyzed with caution due to the small number of cases and retrospective nature of the study.
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PMID:Correlation between fibroscan, liver biopsy, and clinical liver function in patients with hepatitis C virus infection after renal transplantation. 1971 40

Obesity appears to be a risk factor for hepatic steatosis, which has been implicated in the development of hepatic fibrosis in patients with hepatitis C virus infection. We conducted the current study to examine whether obesity is associated with hepatic steatosis among patients with chronic hepatitis C identified from a population-based cohort. Study participants were persons with chronic hepatitis C who had had a liver biopsy, identified from a population-based study of persons with newly identified chronic liver disease conducted in gastroenterology practices. Data were collected through patient interviews, medical record abstraction, and review of previously performed liver biopsies. The outcome variable of interest was significant steatosis, defined as steatosis grade > or =2 determined from liver biopsy samples. Univariate and multivariate analyses were performed using logistic regression techniques. The analysis included 450 patients with chronic hepatitis C with available liver biopsy slides. Overall, only 15.8% of subjects had significant hepatic steatosis (grade > or =2), while 35.9% of obese subjects had significant steatosis. In multivariate analysis, significant fibrosis (defined as > or = grade 2) (odds ratio [OR], 3.43; 95% confidence interval [CI], 1.59-7.37), obesity (OR, 3.32; 95% CI, 1.84-5.98), genotype 3 (OR, 2.5; 95% CI, 1.09-5.75), and the presence of multiple metabolic comorbidities (OR, 1.91; 95% CI, 0.88-4.11) were independently associated with steatosis. In this unique United States cohort of patients with newly diagnosed chronic liver disease due to hepatitis C, obesity was independently associated with hepatic steatosis. The results of this study provide additional evidence that obesity worsens liver damage in patients with chronic hepatitis C, and suggest a role for weight loss as a treatment modality in these patients.
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PMID:Prevalence and predictors of hepatic steatosis in adults with newly diagnosed chronic liver disease due to hepatitis C. 1974 89

In recent decades, Diabetes Mellitus has become a severe and growing global public healthcare problem due to the increase of its prevalence, morbidity and mortality. Post-transplant diabetes mellitus (PTDM) is a complication which takes place after a solid organ transplant, and its incidence is widely variable, ranging from 2 to 53%. Some factors increase the risk of PTDM, such as age, ethnicity, cadaver-donor kidney presence of the hepatitis C virus and cytomegalovirus, overweight and obesity and the Immunosuppression scheme established in the immediate post-transplant period. High doses of tacrolimus and corticosteroid represent the highest risk for developing PTDM.Considering that the development of PTDM is associated with a higher risk of complications, such as infections and cardiovascular disease - thus representing a higher life threatening risk and a higher cost for the Health System - the relevance of identifying the risk factors and of the early diagnosis combined with appropriate therapy will be high for the follow up, and eventually resulting in the success of the procedure as far as patient survival and transplantation durability.
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PMID:Post-transplant diabetes mellitus. 1982 50

Hepatocellular carcinoma (HCC) is the most rapidly increasing cause of cancer death in the United States. Although many risk factors for HCC are well defined, including hepatitis B virus (HBV), hepatitis C virus (HCV), and alcohol, most series have indicated that 5% to 30% of patients with HCC lack a readily identifiable risk factor for their cancer. The majority of "cryptogenic" HCC in the United States is attributed to nonalcoholic fatty liver disease (NAFLD), a hepatic manifestation of the metabolic syndrome. The metabolic syndrome is a constellation of problems that includes insulin resistance, obesity, hypertension, and hyperlipidemia. Increasingly, components of the metabolic syndrome are being linked to various forms of cancer with respect to both increased risk of disease and worsened outcome. In this review, the authors focused on the relation between metabolic syndrome and HCC. They investigated the increased risks of HCC among individuals with features of metabolic syndrome, potentially worsened cancer outcomes in these patients, possible pathogenic mechanisms to explain these relations, and treatment options for those with NAFLD and its progressive counterpart, nonalcoholic steatohepatitis. It is predicted that metabolic syndrome will lead to large increases in the incidence of HCC over the next decades. A better understanding of the relation between these 2 diseases ultimately should lead to improved screening and treatment options for patients with HCC.
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PMID:Metabolic syndrome and hepatocellular carcinoma: two growing epidemics with a potential link. 1983 57

Viral hepatitis poses important problems for children. In preschoolers, hepatitis A virus (HAV) infection frequently causes acute liver failure. Vaccinating toddlers against HAV in countries with high endemicity is expected to decrease mortality. HAV vaccine demonstrates efficacy (comparable to immunoglobulin) as post-exposure prophylaxis. A recently developed vaccine against hepatitis E virus (HEV) may benefit fetal health, because pregnant women are most prone to acute liver failure as a result of HEV. Hepatitis B vaccine continues to demonstrate value and versatility for preventing serious liver disease. With chronic infection, undetectable levels of serum HBV DNA complement e-seroconversion as the preferred outcome measure; suppressed viral load correlates with long-term complications better than HBeAg status. Among Taiwanese children, low pretreatment HBV DNA (<2 x 10(8) copies/ml) strongly predicted response to interferon-alpha. Future paediatric studies must incorporate HBV DNA levels. The rationale for routine treatment of immunotolerant hepatitis B during childhood remains uncertain. Any treatment of chronic hepatitis B in childhood requires consideration of the risks and benefits. Childhood hepatitis C virus (HCV) infection results mainly from mother-to-infant transmission. Babies of HCV-infected women should be tested for serum HCV RNA at 1 month of age. If negative, confirmatory anti-HCV antibody testing may be performed between 12 and 15 months of age. Children with chronic hepatitis C may develop progressive fibrosis/cirrhosis, particularly in the setting of obesity and insulin resistance. Treatment of children chronically infected with genotype 2 or 3 is highly successful: combination therapy of pegylated interferon-alpha and ribavirin is well tolerated and superior to pegylated interferon-alpha alone.
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PMID:Current issues in the management of paediatric viral hepatitis. 1984 Feb 56

The hepatitis C virus (HCV) induces lipid accumulation in vitro and in vivo. The pathogenesis of steatosis is due to both viral and host factors. Viral steatosis is mostly reported in patients with genotype 3a, whereas metabolic steatosis is often associated with genotype 1 and metabolic syndrome. Several molecular mechanisms responsible for steatosis have been associated with the HCV core protein, which is able to induce gene expression and activity of sterol regulatory element binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor gamma (PPARgamma), increasing the transcription of genes involved in hepatic fatty acid synthesis. Steatosis has been also implicated in viral replication. In infected cells, HCV core protein is targeted to lipid droplets which serve as intracellular storage organelles. These studies have shown that lipid droplets are essential for virus assembly. Thus, HCV promotes steatosis as an efficient mechanism for stable viral replication. Chronic HCV infection can also induce insulin resistance. In patients with HCV, insulin resistance is more strongly associated with viral load than visceral obesity. HCV seems to lead to insulin resistance through interference of intracellular insulin signalling by HCV proteins, mainly, the serine phosphorylation of insulin receptor-1 (IRS-1) and impairment of the downstream Akt signalling pathway. The HCV core protein interferes with in vitro insulin signalling by genotype-specific mechanisms, where the role of suppressor of cytokine signal 7 (SOCS-7) in genotype 3a and mammalian target of rapamycin (mTOR) in genotype 1 in IRS-1 downregulation play key roles. Steatosis and insulin resistance have been associated with fibrosis progression and a reduced rate of sustained response to peginterferon plus ribavirin.
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PMID:Steatosis and insulin resistance in hepatitis C: a way out for the virus? 1985 93

1. Despite methodological problems in estimating the true incidence of new-onset diabetes (NODM), it is generally accepted that this is a common complication of liver transplantation (LT), with the mean reported incidence varying between 7% and 30%. 2. The main predictors of post-LT NODM are ethnicity, a family history of diabetes, age > 45 years, glucose intolerance prior to LT, central obesity, metabolic syndrome, use of corticosteroids over a long period, use of tacrolimus, and hepatitis C infection. 3. NODM is associated with impaired long-term graft function and reduced survival. Diabetes is among the main risk factors for coronary heart disease, cerebrovascular disease, and peripheral occlusive arterial disease in transplant recipients. 4. The management of NODM includes the therapeutic and preventive steps taken in patients with type 2 diabetes. Little information exists on the use of antidiabetic compounds in transplant recipients. Some studies have suggested that LT recipients with NODM may benefit from a conversion to cyclosporine through improved glucose metabolism.
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PMID:Long-term outcomes of liver transplantation: diabetes mellitus. 1987 23

1. Obesity is increasingly common among liver transplantation (LT) recipients and donors. Outcomes following LT for selected patients with class I-III obesity are similar to those for nonobese recipients. In patients who are otherwise satisfactory candidates for LT, a high body mass index, as long as it does not present a technical barrier, should not be considered to be an absolute contraindication to LT. 2. The most common causes of death beyond the first year of LT are, in descending order of frequency, graft failure (especially secondary to hepatitis C virus recurrence), malignancy, cardiovascular disease, infections, and renal failure. Metabolic syndrome is an important risk factor for each of these etiologies of posttransplant death. Posttransplant diabetes, posttransplant hypertension, and an original diagnosis of cryptogenic cirrhosis, which is commonly associated with metabolic syndrome, are all associated with an increased risk of post-LT mortality. Features of metabolic syndrome should be screened for and treated in LT recipients. 3. Because of the physiological mechanism of post-LT hypertension, which includes renal arteriolar constriction secondary to calcineurin inhibition, calcium channel blocking agents are a good pharmacological treatment modality and have been shown to be effective in renal protection in randomized controlled trials of posttransplant hypertension. 4. It is rare for dietary changes and weight reduction to result in normalization of the lipid profile. Statins should thus be initiated early in the course of management of post-LT dyslipidemia. Forty milligrams of simvastatin per day, 40 mg of atorvastatin per day, and 20 mg of pravastatin per day are reasonable starting doses for post-LT hypercholesterolemia. It is important to remember that the effects of statin therapy are additive to those of a controlled diet (eg, a Mediterranean diet rich in omega-3 fatty acids, fruits, vegetables, and dietary fiber). 5. Nonalcoholic steatohepatitis, an increasingly common etiology of cirrhosis and liver failure, recurs commonly after LT and may also arise de novo. Treatment should be directed at managing obesity and complications of metabolic syndrome. Optimal immunosuppression in patients with nonalcoholic steatohepatitis is still evolving but should include steroid minimization.
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PMID:Obesity, hyperlipidemia, and metabolic syndrome. 1987 24

With increasing survival after orthotopic liver transplantation (OLT), metabolic syndrome and its individual components, including diabetes mellitus, hypertension, dyslipidemia, and obesity, are increasingly being identified and contributing to cardiovascular complications and late morbidity and mortality. The prevalence of posttransplant metabolic syndrome (PTMS) and its individual components has been found to be higher post-OLT versus a comparable population without OLT. The development of nonalcoholic fatty liver disease (NAFLD) after liver transplantation for non-NAFLD cirrhosis is also being increasingly recognized. A number of predictors have been identified as potential risk factors related to these complications. The pretransplant risk factors include immunosuppression, a higher age at transplant, male gender, a history of smoking, the pretransplant body mass index, pre-OLT diabetes, the etiology of the underlying liver disease that resulted in OLT (hepatitis C, cryptogenic cirrhosis, or alcohol), an increased donor body mass index, and marital status. Although there is an increased risk of cardiovascular events, rejection, and infection among patients with PTMS, the overall impact on long-term survival and mortality remains inconclusive. Strategies to reduce the development of metabolic syndrome after transplantation should include lifestyle modifications involving alterations in diet and increased physical activity. Additional measures that may be potentially beneficial include the use of lipid-lowering agents, the optimal control of blood glucose, and the use of tacrolimus instead of cyclosporine.
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PMID:Posttransplant metabolic syndrome: an epidemic waiting to happen. 1993 36

A retrospective study was conducted to determine risk factors for the development of hypertension (HTN) and to describe the prevalence among long-term survivors of pediatric hematopoietic cell transplant (HCT). Records of 689 pediatric patients who survived 5 years or more after HCT, from 1969 to 2004, were reviewed for development of HTN. In children, HTN was defined as either a systolic or diastolic pressure > or =95th percentile according to age, sex, and height. In adults, HTN was defined as systolic pressures > or =140 mmHg and/or diastolic pressures > or =90 mmHg in nondiabetic adults and systolic pressures > or =130 and/or diastolic pressures > or =80 in diabetic adults. Multivariate Cox regression models were used to estimate the hazard ratio (HR) of risk factors associated with HTN. All patients included were off immunosuppressive therapy. Patients had been treated with total body irradiation (TBI) (n = 482, 70%) or non-TBI regimens (n = 207, 30%) followed by autologous (n = 87), related (n = 484), or unrelated donor HCT (n = 118). Median follow-up was 16 (range: 5-36) years. HTN developed in 120 patients with a 30-year cumulative incidence of 36%. Risk factors associated with HTN were acute kidney injury (AKI; doubling of baseline creatinine by day 100 after HCT) (HR = 2.5; 95% confidence interval (CI) 1.7-3.7, P < .0001), TBI in the preparative regimen (HR = 2.1; 95% CI 1.3-3.3, P = .001), donor type (autologous HR = 2.4; 95% CI 1.3-4.4 and unrelated donor HR = 1.8; 95% CI 1.0-3.2, P = .01), obesity (HR = 4.0; 95% CI 2.3-6.8, P < .0001), diabetes (HR = 6.7; 95% CI 3.9-11.0, P < 0.0001), and history of growth hormone therapy (HR = 1.6; 95% CI 1.0-2.5, P = .05). Patients with a positive history of hepatitis C infection were less likely to develop HTN (HR = 0.5; 95% CI 0.3-0.9, P = .009). Prevalence of HTN was 15% overall and among survivors 11-17 years and 18-39 years old, the prevalence was 10% and 14% or triple and double that of the general U.S. population, respectively. Pediatric HCT survivors are more likely to develop HTN than the general population and should be monitored for HTN throughout adulthood.
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PMID:Hypertension in long-term survivors of pediatric hematopoietic cell transplantation. 1996 45


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