Non-alcoholic fatty liver disease (NAFLD) is increasingly recognized as a significant liver disease, and it covers the disease spectrum from simple steatosis with a risk of development of non-alcoholic steatohepatitis (NASH) to fibrosis, subsequent cirrhosis, end-stage liver failure, and liver cancer with a potential need for liver transplantation. NAFLD and NASH are closely related to obesity, metabolic syndrome, and type 2 diabetes (T2D). The role of gut hormones, especially glucagon-like peptide 1 (GLP-1), is important in NAFLD. Bariatric surgery has the potential for inducing great weight loss and may improve the symptoms of metabolic syndrome and T2D. Recent data demonstrated significant effects of bariatric surgery on GLP-1 and other gut hormones and important lipid metabolic and inflammatory abnormalities in the pathophysiology of NAFLD. Therefore, bariatric surgery may reverse the pathological liver changes in NAFLD and NASH patients. In the present review, we describe NAFLD and NASH pathophysiology and the primary effects of bariatric surgery on metabolic pathways. We performed a systematic review of the beneficial and harmful effects and focused on changes in liver disease severity in NAFLD and NASH patients. The specific focus was liver histopathology as assessed by the invasive liver biopsy. Additionally, we reviewed several non-invasive methods used for the assessment of liver disease severity following bariatric surgery.

Background and Aims In 1984, Scheinberg and Sternlieb estimated the prevalence of Wilson’s disease to be 1:30,000 based on the limited available data. This suggested a large number of overlooked cases with potentially fatal consequences. The “Scheinberg‐Sternlieb Estimate” is still widely used, although more recent clinical and genetic studies of higher quality are now available. In the present study, we included these data to update the prevalence estimate. Approach and Results A MEDLINE Ovid, Science Citation Index Expanded, and PubMed systematic search for all relevant studies on the prevalence of Wilson’s disease was conducted. In total, 59 studies (50 clinical and 9 population‐based genetic) were included in the final analysis. We identified 4 recent clinical studies based on nationwide databases of high quality, providing prevalence estimates from 1:29,000 to 1:40,000. Higher frequency populations do exist because of frequent first‐cousin marriages and/or a higher mutation frequency. When calculating prevalence from the incidence related to number of births, estimates were 1:40,000‐1:50,000. Clinical screening studies, including examination for Kayser‐Fleischer rings or ceruloplasmin, did not improve these estimates because of insufficient sample size or selection biases. Population‐based genetic studies in US and UK populations were not in disagreement with the clinically based estimates. At the same time, studies from France and Sardinia suggested that the genetic prevalence may be 3‐4 times higher than the clinical disease prevalence. This raises the question whether the penetrance is indeed 100% as generally assumed. Conclusions The original prevalence estimate from 1984 of 1:30,000‐1:50,000 still appears valid, at least for the United States, Europe, and Asia. In some population‐based studies, the genetic prevalence was 3‐4 times higher than clinically based estimates. The question of penetrance needs further evaluation.

International studies suggesting that 20-37% of HIV-positive patients have diagnosable depression may underestimate the prevalence of this condition. The aim of this study was to investigate the prevalence of depression among HIV-positive patients in an out-patient clinic in Denmark and to detect factors of importance for the development of depression. MethodsIn 2005, a population of 205 HIV-positive patients was included in a questionnaire-based study. The Beck Depression Inventory II (BDI-II) was used to assess the prevalence and severity of depressive symptoms. Patients with a BDI score of 20 or above were offered a clinical evaluation by a consultant psychiatrist. ResultsSymptoms of depression (BDI414) were observed in 77 (38%) patients and symptoms of major depression (BDI 20) in 53 (26%). Eighteen patients subsequently started treatment with antidepressants. In a reduced logistic regression model, self-reported stress, loneliness, constant thoughts about HIV and being in a difficult financial situation were associated with risk of depression. Patients at risk of major depression were nearly six times more likely to have missed at least one dose of highly active antiretroviral therapy (HAART) in the 4 days prior to assessment (odds ratio 5.7, 95% confidence interval 1.7-18.6). There was a dose-response trend in relation to unsafe sex (P 5 0.03). ConclusionsThe study found that depression was under-diagnosed among HIV-positive patients and was associated with stress, loneliness, a difficult financial situation, low adherence and unsafe sex. Screening for depression should be conducted regularly to provide full evaluation and relevant psychiatric treatment. This is particularly important at the time of diagnosis and before initiating HAART.Keywords: adherence, AIDS, compliance, depression, HIV, psychiatry . A meta-analysis of data from 10 studies provided information on 2596 participants -primarily homosexual men -and found that HIV-positive patients were twice as likely to be diagnosed with a major depression compared to healthy individuals [2]. Several studies on HIV suggest that 20% to 37% of infected individuals may have a diagnosable depression [3][4][5][6]. The high prevalence of depression exists across countries despite cultural differences and differences in diagnostic criteria, measures used and respondent samples [6]. The current estimates may not reflect the true prevalence of depression; there is evidence that depression may be under-diagnosed among HIV patients [7]. Suffering from a mental disease is often perceived as shameful and may be neglected by both patients and health professionals. Living with two stigmatizing diseases -HIV and depression -is presumed to be important in the long-term prognosis of HIV patients and for their quality of life [8]. Together with HIV, the symptoms and diagnosis of depression are associated with poor adherence to antiretroviral medication regimens [9][10][11] Patients and methods Study participants Development of the questionnaireA focus-group interview was ...

Sofosbuvir‐based direct‐acting antiviral (DAA) therapy generally cures chronic hepatitis C (CHC) infections, however, the effects on the underlying liver disease and the potential rate of recovery are unclear. We aimed to investigate the effects of DAA therapy on liver inflammation, fibrosis, metabolic function and cognitive function and the time course in CHC patients with advanced liver disease. Seventy‐one CHC patients with advanced liver disease were studied before, during and one year after successful sofosbuvir‐based DAA therapy. Liver inflammation was assessed by plasma sCD163 and sMR levels (ELISA), fibrosis by liver stiffness (transient elastography), function by galactose elimination capacity (GEC) and cognitive performance by continuous reaction time (CRT). During DAA therapy, we observed a rapid sCD163 decline from baseline to end of treatment (6.9 vs 3.8 mg/L, P < .0001), whereas the change in sMR was more subtle (0.37 vs 0.30 mg/L, P < .0001). Liver stiffness decreased by 20% at end of treatment (17.8 vs 14.3 kPa, P < .0001), together suggesting rapid resolution of liver inflammation. One year after treatment, liver stiffness decreased by an additional 15% (P < .0001), suggestive of fibrosis regression. The GEC improved at follow‐up (all: 1.74 vs 1.98 mmol/min), mainly at 12 weeks post‐treatment, both in patients with cirrhosis (n = 56) and those with advanced liver fibrosis (n = 15) (P < .001). The CRT improved at one‐year follow‐up (1.86 vs 2.09, P = .04). In conclusion, successful DAA therapy of CHC proves beneficial in advanced liver disease, with an initial rapid resolution of liver inflammation and a subsequent gradual but steady improvement in liver fibrosis, metabolic liver function and reaction time.

Those with low CSE scores were more likely to report living secretly with HIV and to be depressed. Disclosing HIV may constitute a social stressor, and a lack of coping self-efficacy may increase the likelihood of non-disclosure and depression. Interventions that enhance self-efficacy may help in managing the demands of daily life with HIV, increase disclosure, and reduce depression.