Colleague's E-mail is Invalid. Your message has been successfully sent to your colleague. Save my selection. Prevalence and risk factors for hepatic steatosis HS in the human immunodeficiency virus HIV -positive population of western countries are controversially discussed and potentially confounded by coinfection with viral hepatitis. Aim of this study was to assess prevalence and factors associated with significant HS in HIV monoinfected patients.
CAP measures the degree of ultrasound kiver by hepatic fat at the central frequency of the FibroScan M probe, simultaneously with liver stiffness measurement. The liver in the acquired immunodeficiency syndrome: a clinical and histologic study. People with advanced liver damage are at greater risk for developing liver Nn latina gallery. The exact mechanism of PI-induced steatosus remains the subject of debate. Supplemental digital content is available for this article. Liver disease is a major cause of morbidity and mortality among people living with HIV. Liver fibrosis and fatty liver in Hiv and liver steatosis HIV-infected patients. In an animal model, selonsertib seemed effective in diminishing hepatic inflammation and fibrosis [ ]. Fibrosis — build-up of collagen and other fibrous scar tissue, leading ane a 'stiff' Hiv and liver steatosis. Int J Med Sci.
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Older age was a risk factor Doreen pond fucking fibrosis but not for steatosis. Device: Fibroscan. Then there is the often-overlooked fact that cosuming pot is, in fact, a form of smoking provided, of course, that individuals consume it through lighting up. A group of symptoms and diseases that together are characteristic of a specific condition. Ultrasonography is a sensitive, accurate, non-invasive screening tool to detect steatosis as this is steztosis always Hiv and liver steatosis in liver function tests. Any updates not saved will be lost. Liver disease is common among HIV-infected patients due to the shared routes of transmission Cum dodger HIV and viral Hiv and liver steatosis. FDA Resources. For general information, Learn About Clinical Studies. Join The Discussion. Ten Hiv and liver steatosis had type 2 diabetes. Blood samples should be taken every two weeks in the first two months to check liver function, then at the end of the third month, and then every three to four months if they are within normal limits. Liver toxicity becomes a more complicated problem when alcohol use or viral hepatitis have damaged the liver. This risk is related to CD4 count when starting treatment. People with moderate or worse fibrosis had significantly higher levels of inflammatory markers than people without fibrosis or with only mild fibrosis, including C-reactive protein, interleukin 6, leptin and adiponectin livdr hormones produced by adipose or fat tissue and a marker linked to activation of macrophages a type of immune system white blood cell.
During the 10 years between and , the prevalence rates for viral hepatitis decreased from
- Metabolic syndrome, type 2 diabetes and obesity are risk factors for the development of liver fibrosis and steatosis liver fat accumulation in people living with HIV, including those who do not have viral hepatitis co-infection, according to research presented at the 9th International AIDS Society Conference on HIV Science IAS last month in Paris.
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- Associated drugs: nevirapine Viramune , ritonavir Norvir , tipranavir Aptivus , efavirenz Sustiva.
Colleague's E-mail is Invalid. Your message has been successfully sent to your colleague. Save my selection. Prevalence and risk factors for hepatic steatosis HS in the human immunodeficiency virus HIV -positive population of western countries are controversially discussed and potentially confounded by coinfection with viral hepatitis. Aim of this study was to assess prevalence and factors associated with significant HS in HIV monoinfected patients. A total of HIV-infected patients monoinfected were included in this prospective, cross-sectional study.
All patients underwent CAP determination. Multivariable logistic regression analyses were performed to assess the factors associated with HS in this cohort. Significant HS was detected in monoinfected patients in the total cohort.
Interalia, age, gender, ethnicity, and metabolic factors were strongly associated with HS, while body mass index BMI , triglyceride, and glycated hemoglobin HbA1c levels were independently associated with significant HS. HS is highly prevalent among HIV monoinfected patients. Although metabolic risk factors, such as obesity and poorly controlled diabetes, are independently associated with HS in HIV monoinfected patients, cART and control of HIV seem to play an indirect role in the development of HS, probably through the return-to-health effect.
Availability of data and materials: The datasets are available from the corresponding author on reasonable request. Supplemental digital content is available for this article. The work cannot be changed in any way or used commercially without permission from the journal. Present day combined antiretroviral therapy cART , leading to permanent suppression of human immunodeficiency virus HIV replication, has dramatically improved survival of HIV-infected patients.
Chronic liver disease has emerged as an increasingly significant contributor to nonacquired immune deficiency syndrome related morbidity and mortality in the HIV-infected population. Little information is available on the prevalence and potential risk factors for liver steatosis among HIV monoinfected patients. With regard to risk factors promoting steatosis in HIV infection, little is known and this issue is controversially discussed. In HIV-positive population, the metabolic risk factors still play a role for the development of steatosis, the impact of long-term exposure to antiretroviral regimes for liver injury and specifically for steatosis has also been discussed.
This study aimed to examine in more detail the prevalence and risk factors for severe HS in a large cohort of HIV monoinfected patients from the Infectious Diseases outpatient clinic at Bonn University.
This cross-sectional prospective study included HIV-infected patients followed at the Infectious Diseases outpatient clinic at Bonn University. The use of anabolics or hormons was not reported by patients but would have exclusion criteria. To assess the potential effect of concomitant HCV or hepatitis B virus coinfection, as well as to minimize the potential effect of confounders, analyses were performed on the total study population and the group of HIV monoinfected patients Fig. Blood collection and controlled attenuation parameter CAP measurement were performed during a regular scheduled visit at our outpatient clinic.
Demographic and clinical characteristics as well as data on health trajectory of HIV infection and antiretroviral treatments were collected from the patient's health record and our department's database. Current comedication, alcohol consumption, and smoking status were recorded and the actual BMI was assessed.
CAP measures the degree of ultrasound attenuation by hepatic fat at the central frequency of the FibroScan M probe, simultaneously with liver stiffness measurement. Demographic, clinical, and laboratory characteristics stratified by severity of HS were compared.
Differences in continuous variables, expressed as medians, and 1st and 3rd quartiles were assessed using either nonparametric Mann—Whitney test or Kruskal—Wallis test. Categorical variables, expressed as absolute frequencies and percentages, were compared using Pearson chi squared test or Fisher exact tests. A correlation analysis estimated possible impacts on HS.
Uni- and multivariable analyses were performed using logistic and Cox-regression models. In total, patients were included in the study. The baseline characteristics of the study subjects are shown in Table 1.
As expected, patients with significant steatosis showed higher mean HbA1c levels 5. DM, gender, and ethnicity revealed a significant impact on HS Table 1.
Interestingly, apart from gender, ethnicity also revealed a significant difference in median CAP values Fig. Logistic regression analysis revealed that many demographic age, gender, and ethnicity , metabolic BMI, triglyceride, DM type 2, HbA1c, cholesterol, HDL, and LDL , and hepatic parameters aminotransferase and gamma-glutamyltransferase levels , but not time since HIV diagnosis, were significantly associated with significant HS.
In the current study, no other PIs nor other antiretroviral drug classes could be identified to have an impact on the severity of steatosis. Using CAP -derived data from a large and unselected real-life cohort, this cross-sectional study is likely to be more accurate than previous estimations. Although this study is not primarily designed to compare mono- and coinfected patients, we found evidence that many HIV-specific factors, which significantly correlate with CAP , are found only in the coinfected patients, such as transient elastography, aspartate aminotransferase to platelet ratio index score, HIV viral load, and duration of cART.
These factors are strongly associated with liver fibrosis and inflammation, which is another bias present in our previous studies. Other studies using liver biopsy, which is an invasive diagnostic tool and not applicable for screening purpose, hold a significant selection bias. Furthermore, hyperinsulinemia promotes the upregulation of de novo lipogenesis in the liver. Existing studies have found no relationship between HS and individual antiretroviral drugs.
Whether this is due to a direct drug effect or a secondary effect by the metabolic changes induced by PIs cannot be determined with certainty. Especially those with a lower nadir CD4 T-cell count, gained more lean mass and fat during the first 96 weeks of cART.
However, these were not independent associations but could predispose the patients to metabolic changes, which finally were independent and strongly associated with presence of HS. This is also supported by our previous data, showing that cART and control of HIV replication is protective for liver fibrosis and liver injury in HIV monoinfected patients.
This may be supported by the finding of a gender and ethnicity influence on CAP -value, despite the fact that these patient groups were randomly distributed among the population. The main limitations of this study are its cross-sectional design, which limits the ability to evaluate change in variables of interest over time, and the presence of a nonrandomized study population. Homeostasis model assessment index to quantify insulin resistance and dual-energy X-ray absorptiometry or magnetic resonance tomography imaging to quantify body composition changes were not available.
Alcohol consumption as well as anabolic use was self-reported by the patients, for example, binge drinking behavior may have been underestimated. No drug and anabolic screening tests were performed. Finally, while liver biopsy remains the gold standard for the assessment of HS, the acceptability and potential risks of biopsy make its application difficult for a large study population. In conclusion, we found that prevalence of HS in HIV-infected patients is higher than in the general population.
Overweight, dyslipidemia, and poorly controlled diabetes were independent factors for HS in HIV monoinfected patients. Suppression of viral replication might contribute to the development of steatosis. Controlling HIV replication might not condition liver disease by causing metabolic disorders, instead, this may be due to the return-to-health effect.
Study concept and design, acquisition of data, analysis and interpretation of data, drafting of the manuscript, statistical analysis: Raphael Mohr.
Acquisition of data, analysis and interpretation of data, drafting of the manuscript, statistical analysis: Christoph Boesecke. Acquisition of data, analysis and interpretation of data, critical revision of the manuscript regarding important intellectual content: Leona Dold. Acquisition of data, analysis and interpretation of data, critical revision of the manuscript regarding important intellectual content: Robert Schierwagen. CS: acquisition of data, analysis and interpretation of data, critical revision of the manuscript regarding important intellectual content: Carolynne Schwarze-Zander.
JCW: acquisition of data, analysis and interpretation of data, critical revision of the manuscript regarding important intellectual content: Jan-Christian Wasmuth. Acquisition of data, analysis and interpretation of data, critical revision of the manuscript regarding important intellectual content: Insa Weisensee.
Study concept and design, acquisition of data, analysis and interpretation of data, drafting of the manuscript, critical revision of the manuscript regarding important intellectual content, funding recipient, administrative, technical and material support, study supervision: Jonel Trebicka.
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Thought you might appreciate this item s I saw at Medicine. Send a copy to your email. Some error has occurred while processing your request. Please try after some time. JKR and JT shared last coauthorship. The authors have no conflicts of interest to disclose. Supplemental Digital Content is available for this article. Abstract 1 Introduction 2 Methods 2. Back to Top Article Outline.
Figure 1. Table 1. Table 2. Table 3. Figure 2. Table 4. Mortality in the highly active antiretroviral therapy era: changing causes of death and disease in the HIV outpatient study. J Acquir Immune Defic Syndr ;—
National Library of Medicine U. Methods: Patient number: Inclusion criteria: Age: years Males and females with HIV infection diagnosed by infection doctors Willing and able to comply with the study requirements Willing and able to provide written informed consent to participate in the study Exclusion criteria: Pregnancy Unable to complete the noninvasive procedure of VCTE and CAP Unwilling to provide written informed consent to participate in the study. Study Type :. This risk is related to CD4 count when starting treatment. Fibrosis occurs when scar tissue replaces normal liver cells known as hepatocytes.
Hiv and liver steatosis. Nevirapine
The term cirrhosis is often used in relation to the liver. A group of diseases characterized by high levels of blood sugar glucose. Type 1 diabetes occurs when the body fails to produce insulin, which is a hormone that regulates blood sugar. Type 2 diabetes occurs when the body either does not produce enough insulin or does not use insulin normally insulin resistance. Common symptoms of diabetes include frequent urination, unusual thirst and extreme hunger.
Some antiretroviral drugs may increase the risk of type 2 diabetes. Maud Lemoine of Imperial College London presented findings from a study of the association between metabolic syndrome and liver fibrosis in HIV-positive people without viral hepatitis known as HIV monoinfection.
Metabolic syndrome is a cluster of factors associated with elevated cardiovascular risk, including abdominal obesity, high blood pressure, abnormal blood lipid levels and high blood glucose, a sign of insulin resistance and type 2 diabetes. Fibrosis was assessed using transient elastography FibroScan , a non-invasive method of measuring liver 'stiffness' using sound waves; a stiffer liver indicates more extensive fibrosis.
Among participants with valid liver stiffness results, people with metabolic syndrome were matched by age and sex with people who did not.
The researchers found that participants with metabolic syndrome were significantly more likely to have liver fibrosis compared to those without it. People with moderate or worse fibrosis had significantly higher levels of inflammatory markers than those with absent or mild fibrosis stage F0 or F1 , including C-reactive protein, interleukin 6, leptin and adiponectin two hormones produced by adipose or fat tissue and a marker linked to macrophage activation a type of immune system white blood cell.
This was also the case when comparing people with and without cirrhosis. After adjusting for other factors, participants with metabolic syndrome were about twice as likely to have at least stage F2 fibrosis, about four times more likely to have at least stage F3 fibrosis and about eight times more likely to have cirrhosis.
Those with obesity were about three times more likely to have stage F2 or F3 fibrosis and about four times more likely to have cirrhosis. They suggested that adipose tissue, insulin resistance and macrophage activation "are probably key players" in the development of liver fibrosis in HIV-positive people without viral hepatitis.
These factors might include chronic inflammation and immune activation associated with HIV or use of hepatotoxic antiretrovirals. They had been on ART for a median of seven years and many had used older antiretrovirals associated with metabolic or liver-related side-effects. Women and men were equally likely to have fibrosis, but men were significantly more likely to have steatosis.
Older age was a risk factor for fibrosis, but not for steatosis. For steatosis, metabolic syndrome was associated with fourfold higher risk, obesity alone with almost elevenfold higher risk and type 2 diabetes with almost tenfold higher risk. Longer duration of ART use — especially older nucleoside reverse transcriptase inhibitors such as zidovudine Retrovir or stavudine Zerit — was associated with steatosis independently of metabolic factors, the researchers concluded.
They recommended that prevention and management of non-infectious conditions such as metabolic syndrome should be integrated into HIV care to decrease the burden of liver disease among people living with HIV.
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Warning You have reached the maximum number of saved studies Liver Steatosis and Stiffness in HIV The safety and scientific validity of this study is the responsibility of the study sponsor and investigators.
Listing a study does not mean it has been evaluated by the U. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details. Last Update Posted : August 21, See Contacts and Locations. Study Description. Background: With the advances in treatment and clinical care, individuals with human immunodeficiency virus HIV infection have experienced an increase in life expectancy.
Study design: This is a prospective observational study. Methods: Patient number: Inclusion criteria: Age: years Males and females with HIV infection diagnosed by infection doctors Willing and able to comply with the study requirements Willing and able to provide written informed consent to participate in the study Exclusion criteria: Pregnancy Unable to complete the noninvasive procedure of VCTE and CAP Unwilling to provide written informed consent to participate in the study.
FDA Resources. Intervention Details: Device: Fibroscan Fibroscan with controlled attenuation parameter and transient elastography. Outcome Measures. The liver fibrosis will be assessed by transient elastography at 6-month interval.
Eligibility Criteria. Information from the National Library of Medicine Choosing to participate in a study is an important personal decision. Inclusion Criteria: Age: years Males and females with HIV infection diagnosed by infection doctors Willing and able to comply with the study requirements Willing and able to provide written informed consent to participate in the study Exclusion Criteria: Pregnancy Unable to complete the noninvasive procedure of VCTE and CAP Unwilling to provide written informed consent to participate in the study.
HIV infection is a risk factor for liver fat accumulation | aidsmap
Infectious Diseases and Therapy. The burden of liver-related morbidity remains high among HIV-infected patients, despite advances in the treatment of HIV and viral hepatitis. The pathogenesis of NAFLD and the reasons for progression to non-alcoholic steatohepatitis NASH are still not fully elucidated, but insulin resistance, mitochondrial dysfunction and dyslipidemia seem to be the main drivers.
As ongoing HIV-related immune activation is associated with insulin resistance, early initiation of cART is needed to limit its duration. Patients at risk should therefore receive antiretroviral drugs with a more favorable metabolic profile. Since patients with NASH are at risk of developing liver cirrhosis and hepatocellular carcinoma, several non-antifibrotic and antifibrotic drugs are under investigation in clinical trials to broaden the therapeutic options.
Current guidelines recommend early initiation of cART that is less likely to induce insulin resistance, mitochondrial dysfunction and dyslipidemia. In the current era of combination antiretroviral therapy cART , the all-cause mortality in human immunodeficiency virus HIV -infected patients is low [ 1 ]. However, liver-related complications remain one of the major causes of mortality in this population [ 2 ]. Although viral hepatitis and excessive alcohol consumption are traditionally considered the most important causes of liver fibrosis and cirrhosis in HIV-infected patients, metabolic liver disease—mostly non-alcoholic fatty liver disease NAFLD —is increasingly recognized as an aetiological factor in the development of liver disease [ 2 , 3 , 4 , 5 ].
In fact, due to the introduction of effective therapies against viral hepatitis, it is likely that fatty liver disease will become the leading cause of liver cirrhosis in HIV-infected patients, as is already happening in the general population [ 6 ]. It should not be forgotten that NAFLD can coexist with other liver diseases, which will lead to faster progression of fibrosis towards end-stage liver disease.
Since the major risk factors for NAFLD—insulin resistance [ 8 , 9 ], mitochondrial dysfunction [ 10 ] and concurrent viral infections [ 11 ]—are highly prevalent in HIV-infected patients, this population is at risk for liver-related morbidity.
We also discuss the future with respect to novel antiretroviral medication and anti-NAFLD interventions. This article is based on previously conducted studies and does not contain any studies with human participants or animals performed by any of the authors. Guaraldi et al. Crum-Cianflone et al. Macias et al.
Nishijima et al. All HIV-infected patients that underwent ultrasound between Vuille-Lessard et al. Lemoine et al. Ingiliz et al. Sterling et al. Lombardi et al. Given its invasive nature with risks such as haemorrhagic complications and pain, liver biopsy is not useful as an epidemiological screening tool [ 28 ]. As a result, current cross-sectional epidemiological data are mainly based on surrogate markers such as imaging rather than on histopathological data.
Considering the higher sensitivity, lower costs and wide availability, ultrasound is preferred over CT-scanning for diagnosing NAFLD [ 29 ]. However, its sensitivity is limited in the setting of mild NAFLD and in morbidly obese patients [ 30 , 31 ]. Due to its wider availability and low risk for sampling error, magnetic resonance imaging proton density fat fraction MRI-PDFF is increasingly used in research.
In a recent review by Caussy et al. Considering the high costs and limited availability, MRI-based imaging is currently still not a useful screening tool and its use remains limited to research [ 32 ]. In , a new non-invasive tool for the detection of steatosis, called controlled attenuation parameter CAP , was introduced [ 33 ]. It is an addition to the Fibroscan Echosens, Paris, France and measures steatosis simultaneously with fibrosis.
CAP determines the total ultrasonic attenuation at a frequency of 3. In a meta-analysis by Wang et al. Using serum alanine aminotransferase ALT levels in addition to imaging to discriminate between steatosis and NASH turns out to be disappointing.
Several studies showed that a significant proportion of the patients with biopsy-proven NASH had normal ALT values, although some studies suggested that the common laboratory cut-off value for ALT was too high [ 38 , 39 , 40 ].
There are currently no guidelines that recommend universal screening for NAFLD in the general population or in specific subpopulations. Since the prevalence of NAFLD among HIV-infected patients with persistent liver enzyme elevations is high, ultrasound screening should also be considered in this population. NASH non-alcoholic steatohepatitis. As shown, there are four major hallmarks in the pathogenesis of NALFD—insulin resistance, dyslipidemia, hepatic accumulation and the microbiome—with a certain overlap between these factors.
As mentioned, genetics play an important role in the overall pathogenesis influencing most of these factors. The contributing factors are mentioned below the hallmarks. Risk factors more common in HIV-infected population are marked with an asterisk. Suggested mechanisms, like changes in intestinal permeability and production of microbe-derived metabolites, are more extensively addressed in the excellent recent reviews of Leung et al. Furthermore, there is strong evidence on the impact of hereditary component with polymorphisms for hepatic lipid regulation and insulin signalling pathways, in both the HIV-infected and general populations [ 57 , 58 ].
Although NAFLD is common in HIV-infected patients as a result of traditional risk factors, it is suggested that its exact aetiology may differ from the general population [ 59 ]. This phenomena has also been described in the setting of rheumatoid arthritis in which high levels of pro-inflammatory markers—e.
In this heterogeneous prospective cohort, there was a clear association between advanced HIV-infection—defined as low CD4 counts and detectable viral load—and IR, measured by fasting lipids, glucoses and insulin levels. This and other observations strongly suggest a link between chronic HIV-induced immune activation and IR with subsequent steatosis development [ 68 , 69 , 70 ]. In contrast to the limited number of studies on glucose haemostasis in HIV-positive patients, several studies have been performed on the occurrence of dyslipidemia—also associated with NAFLD [ 50 ].
A study in the early s established that untreated HIV-infected patients with advanced immunodeficiency have higher triglycerides and FFA levels compared to healthy controls [ 71 ]. In addition to hypertriglyceridemia, untreated HIV-infected patients have decreased high-density lipoprotein cholesterol and total cholesterol levels. These observations were confirmed in several other studies, although the mechanism of HIV-related dyslipidemia is poorly understood.
As the vast majority of HIV-infected patients treated with cART will reach virological suppression and near inhibition of immune activation, the impact of hypertriglyceridemia and IR caused by the virus itself will diminish. First, several antiretroviral drugs cause unfavorable metabolic changes such as dyslipidemia and insulin resistance [ 75 ].
Second, the use of certain antiretroviral drugs is associated with mitochondrial dysfunction. Especially, early-generation NRTIs are associated with insulin resistance and dyslipidemia [ 76 , 77 , 78 ]. The main driver for both metabolic disturbances is mitochondrial toxicity. The first reports of mitochondrial dysfunction in NRTIs were published in the early s, but this adverse event gained increasing attention after the introduction of combination therapy [ 79 , 80 , 81 ].
This leads to impairment of the oxidative phosphorylation and promotes the formation of reactive oxygen species which eventually damage the mtDNA even further, resulting in mitochondrial dysfunction [ 82 ]. First, both IR and dyslipidemia can be the result of mitochondrial dysfunction in the peripheral fat tissue [ 83 ]. Even though the mechanism is not exactly clear, mitochondrial dysfunction seems to induce adipocyte apoptosis, leading to peripheral lipodystrophy.
The clinical syndrome is characterized by the degeneration of peripheral fat tissue combined with metabolic changes such as IR and dyslipidemia [ 81 , 84 ].
In addition to peripheral effects, mitochondrial dysfunction also occurs in the liver. Hepatic mitochondria play an essential role in the oxidation of FFAs.
In the setting of mitochondrial dysfunction, mitochondria are unable to process this oxidation, leading to a local accumulation of triglycerides which is the hallmark of NAFLD [ 85 ].
Early-generation NRTIs are most commonly associated with mitochondrial dysfunction; especially stavudine, didanosine, zalcitabine and—to a lesser extent—zidovudine [ 86 ]. Modern NRTIs—e. Introduction of protease inhibitors PIs in broadened the possibilities in the treatment of HIV infection.
However, PIs display an unfavorable metabolic profile with an increased risk for insulin resistance and dyslipidemia. Especially, the early-generation PIs—e. Two animal studies showed that these PIs act as potent isoform-specific inhibitors of the transport function of the GLUT4-receptor, resulting in hyperglycemia and hyperinsulinemia [ 89 , 90 ]. Additional data suggested the ability to directly inhibit insulin secretion from the beta cells [ 91 , 92 ]. In contrast to early-generation PIs, current PIs like atazanavir and darunavir display a far more favorable profile with regard to IR [ 93 ].
Although the newer generation PIs seem to have little impact on the lipid levels in monotherapy, when combined with ritonavir or cobicistat as a pharmacological booster, these drugs still have an unfavorable lipid profile compared to most other classes of antiretroviral drugs [ 94 , 95 , 96 , 97 ].
The exact mechanism of PI-induced dyslipidaemia remains the subject of debate. Secondly, experimental research in mice showed that ritonavir inhibits the clearance of triglycerides from the circulation [ 99 ].
The amount of data describing the metabolic profile of the non-nucleoside reverse transcriptase inhibitors NNRTIs is limited compared to the number of studies for PI-based treatment. Rilpivirine and nevirapine have a more favorable profile compared to efavirenz [ , ]. Etravirine does not seem to influence lipid levels when compared with placebo [ ].
This new drug class is generally considered advantageous in respect with the metabolic profile. Data on entry-inhibitors e. The current literature suggests that these specific genotype 3 antigens induce upregulation of hepatic fatty acid synthesis [ , ]. When HCV genotype 3-infected patients achieve sustained viral response i.
Nowadays, HIV-patients grow old enough to be exposed to these traditional risk factors. Recent publications describe increases in median body-mass index BMI and the incidence of diabetes mellitus in the HIV-infected population, adding more risks for this population [ 14 , , ]. The impact of traditional risk factors was emphasized by the results of the meta-analysis of Maurice et al.
Weight loss is still the most important intervention in all patients [ , ]. Furthermore, excessive use of alcohol is discommended as alcohol itself can cause significant liver disease. Next to behavioural interventions, several medical treatments have been described to be effective [ 44 ]. These recommendations are mainly based on the study of Sanyal et al. The primary outcome was an improvement in histological features of NASH as a composite endpoint of standardized scores of steatosis, lobular inflammation, hepatocellular ballooning, and fibrosis.
In the trial of Sanyal et al. A major side effect of pioglitazone was weight gain [ ]. Furthermore, its use seems to be associated with the development of bladder cancer, although data are conflicting [ , ]. Other medical interventions, such as metformin, glucagon-like peptide-1 GLP-1 agonists and ursodeoxycholic acid are suggested as alternatives, but have not been proven effective and are therefore not recommended in current guidelines.
Bariatric surgery is another treatment option that has increasingly been recognized as a potential intervention for NAFLD [ ].