HIV: hepatic manifestations of HIV and antiretroviral therapy
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Mitochondrial toxicity
Liver disease
Etiology
Hepatitis B
Long-term alterations to body metabolism have become apparent with the prolonged use of antiretroviral nucleoside analogue reverse transcriptase inhibitors (NRTIs). The NRTIs differ in the mechanisms, potency and probably also tissue specificity of mitochondrial toxicity. One group of NRTIs, the so-called "d-drugs" (zalcitabine> didanosine>stavudine) are relatively strong inhibitors of g-polymerase and thus cause a time- and dose-dependent decrease in the intracellular levels of mitochondrial DNA (mtDNA). The most important target organs of d-drugs are the liver, skeletal muscle, peripheral nerves and probably also the subcutaneous adipose tissue of lipoatrophic subjects. Hyperlactataemia may be observed. Zidovudine is an inhibitor of the mitochondrial adenine nucleotide translocator, binds to adenylate kinase and may also be converted into stavudine triphosphate in vivo. Persistent hyperlactataemia, mtDNA depletion and isolated cases of mitochondrial encephalomyopathies have been observed in babies under perinatal exposure with zidovudine. Nucleotide analogues such as tenofovir are avidly taken up into renal tubular epithelia. Isolated cases of renal failure and Fanconi syndrome require further investigation. Mitochondrial toxicity cannot yet be adequately monitored and predicted. Drugs with potential additive or synergistic toxicity, such as valproate, should be used with caution. Didanosine interacts with allopurinol, hydroxyurea and ribavirin. In established mitochondrial toxicity, cessation of the offending NRTI remains the most effective therapeutic intervention because vitamin cocktails and l-carnitine have, at best, only a marginal effect.
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Didanosine
Stavudine
Zalcitabine
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Mitochondrial toxicity
Lactic acidosis
Lipodystrophy
Reverse-transcriptase inhibitor
Nucleoside analogue
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role in the disease development and progression.Our current knowledge of the natural history of NAFLD can be summarized as follows: elevated body mass index (BMI) plays a key role; simple steatosis NAFL (Fatty liver, FL) does not generally progress to Non-Alcoholic SteatoHepatitis (NASH); patients with NASH progress, in relatively many cases, to cirrhosis; older age and advanced fibrosis are risk factors for hepatocellular carcinoma (HCC) in NASH; up to a third of patients develop liver-related morbidity or mortality.It is extremely important that physicians diagnose NASH accurately and perform appropriate treatments, because it represents an illness mirroring a systemic process, and an adjunctive cardiovascular disease (CVD) risk [1] .A great deal of research highlight the need for surrogate serum markers for diagnosing NASH.Among them, serum cytokeratin 18 has captured certain interest [2] . COULD NAFLD BE CONSIDERED A FURTHER EXPRESSION OF METABOLIC SYNDROME?NAFLD and NASH are conditions gaining increasing recognition, obesity being (mainly of high grade) one of the more important risk factors.But, do other aspects of metabolic syndrome (MS) play a role?To answer this question, a prospective study was conducted in 127 consecutive obese patients (62% female, mean age 40 ± 11 years, mean BMI 42 ± 6 kg/m 2 ) undergoing gastric bypass over a 20-month period.The report highlighted that arterial hypertension was present in 52 patients (41%) and type 2 diabetes mellitus (DM) in 18 (14%).However, NAFLD was confirmed in 80 patients (63%).Of them, 47 (37%) had FL, and 33 (26%) had NASH.Cirrhosis was found in 2 patients corresponding to 1.6% of the total population.For multivariate analysis, elevated HOMA independently predicted only NASH, (OR 4.18, 95% Confidence Interval, CI, 1.39-12.49).That NAFLD was frequently found, it is easy to deduce that the NAFLD presence coupled with obesity (visceral) and hypertension could be used as criteria to label the patients with MS [3] .
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Objective To investigate the changes of serum vaspin levels in elderly type 2 diabetic patients with nonalcoholic fatty liver disease and its clinical significance.Methods The serum level of vaspin was measured in 44 elderly type 2 diabetic patients with nonalcoholic fatty liver disease(T2DM+ NAFLD group),40 elderly type 2 diabetic patients without nonalcoholic fatty liver disease(T2DM group), 40 elderly normal glucose tolerance patients with nonalcoholic fatty liver disease(NAFLD group) and 41 elderly normal glucose tolerance patients without nonalcoholic fatty liver disease(normal control,NC group) by enzyme-linked immunosorbent assay simultaneously.The visceral fat thickness(VFT) was measured with high freguency ultrasound.Results(1)The serum levels of vaspin in T2DM+NAFLD group,T2DM group and NAFLD group were significantly higher than those in NC group[(1.46±0.43, 1.03±0.27,0.76±0.28 vs 0.36±0.13) ng/ml,P0.01,P0.01,P0.05,respectively],respectively. (2)Multiple stepwise regression analysis showed FIns,VFT and HbA_1c level were independent foctors influensing vaspin level.Vaspin,VFT and TG were positively correlated with nonalcoholic fatty liver disease in elderly type 2 diabetes.Conclusions The change of serum vaspin level may partly play a role in the pathogenesis and development of elderly type 2 diabetes complicated nonalcoholic fatty liver disease.
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Liver disease
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Recent cross-sectional and randomized controlled studies of small sample sizes revealed that regular exercise is effective for improving nonalcoholic fatty liver disease. However, there has been no large-scale longitudinal study addressing the effect of regular exercise on remission of nonalcoholic fatty liver disease. Thus, we investigated the impact of exercise on the natural history of nonalcoholic fatty liver disease. We analyzed 1,010 (860 men and 150 women) Japanese participants who received health checkups repeatedly over 10 years by a historical cohort study and were diagnosed with nonalcoholic fatty liver disease at baseline. Regular exercise was defined as participating in any kind of sports at least once a week. Nonalcoholic fatty liver disease was diagnosed by ultrasonographic images. During 10 years of follow-up, remission of nonalcoholic fatty liver disease was observed in 46.0% (396/860) of men and 48.7% (73/150) of women. In men, the adjusted hazard ratio of regular exercise for remission of nonalcoholic fatty liver disease was 1.46 (95% confidence interval 1.10-1.95, p = 0.010). However, this was not significant in women. Exercise at least once a week is implicated in the remission of nonalcoholic fatty liver disease in men.
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Mitochondrial toxicity
Lipodystrophy
Lactic acidosis
Nucleoside analogue
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Objective To evaluate the role of serum retinol binding protein 4(RBP4) in patients with nonalcoholic fatty liver disease(NAFLD).Methods 62 patients with nonalcoholic fatty liver disease(NAFLD group) and 60 normal subjects(normal control group) were selected.The level of serum RBP4 was measured by ELISA.Fasting blood glucose(FBG),blood lipid(TC,TG,HDL-C,LDL-C),liver function(AST,ALT),and fasting insulin(FINS) were measured.Homeostasis model assessment of insulin resistance(HOMA-IR) were calculated as well.Results The levels of RBP4,FBG,TC,TG,LDL-C,FINS,ALT,AST and HOMA-IR were higher in NAFLD patients as compared to normal controls(P0.01).The levels of Serum RBP4 were positively correlated with FBG,TC,TG,FINS and HOMA-IR(r=0.329,0.298,0.261,0.219,0.378,P0.01).Conclusion RBP4 was involved in the development of nonalcoholic fatty liver disease.Thus,RBP4 may be used as a sensitive indicator for the pathogenesis and the development of NAFLD,which can assist in early diagnosis of the disease.
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THE AIM OF REVIEW: To verify the role of nutrition in development of Nonalcoholic Fatty Liver Disease in patients with metabolic syndrome.The article contains main conceptions of etiology and pathogenesis of Nonalcoholic Fatty Liver Disease. Spesial attention gives to the role of nutrition in development of this case. The are own dates presented, which shows relationship between degree of obesity, factual nutrition and expression of morphological changes in liver in patients with Nonalcoholic Fatty Liver Disease.Nutrition mistakes in patients with Nonalcoholic Fatty Liver Disease are: excess of energy, animal proteins and fats, deficit of nutrition fibres, carbohydrates, antioxidants, vitamins B1, B2, PP. The main directions of diet in patients with Nonalcoholic Fatty Liver Disease.
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