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1.
[Correction of dyslipidemia in patients with chronic hepatitis C, combined with diabetes type 2].
Derbak, M, Boldizhar, P
Georgian medical news. 2014;(226):25-31
Abstract
The article shows the results of treatment of 118 patients with chronic hepatitis C (CHC) which is associated with type 2 diabetes mellitus (DM). When planning therapeutic interventions in chronic hepatitis C in patients with diabetes, it is considered the presence of visceral obesit , dyslipidemia, and hepatic steatosis. The efficacy of different treatment regimens was studied. Found that the usage of ursodeoxycholic acid and ademetionin in HCV patients with diabetes type 2 receiving standard antiviral therapy (SAVT), significantly make a positive effect on the level of dyslipidemia. The normalization of lipid profile allows for a full course of SAVT, which reduces the frequency of relapse. It is also noted that the simultaneous use of ademetionin and ursodeoxycholic acid in treatment of chronic hepatitis C leads to a reduction of side effects of SAVT. Metabolic therapy may be recommended for patients with chronic hepatitis C in combination with type 2 diabetes in case of SAVT, and at its contraindications or intolerance.
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2.
Folic acid effects on s-adenosylmethionine, s-adenosylhomocysteine, and DNA methylation in patients with intermediate hyperhomocysteinemia.
Pizzolo, F, Blom, HJ, Choi, SW, Girelli, D, Guarini, P, Martinelli, N, Stanzial, AM, Corrocher, R, Olivieri, O, Friso, S
Journal of the American College of Nutrition. 2011;(1):11-8
Abstract
OBJECTIVE Folic acid (FA) supplementation decreases homocysteine (tHcy) levels. However, little is known about the effects of FA treatment on DNA methylation or plasma S-adenosylmethionine (AdoMet) and S-adenosylhomocysteine (AdoHcy) concentrations. The purpose of this study was to investigate the effects of FA supplementation on AdoMet, AdoHcy, and genomic DNA methylation in hyperhomocysteinemic subjects without end-stage renal disease. METHODS To evaluate the effects of 5 mg FA/d for 8 weeks, we recruited 7 hyperhomocysteinemic MTHFR677TT patients (tHcy >30 μmol/L) with normal renal function. RESULTS FA supplementation induced a decrease in tHcy (from 51.1 ± 21 at baseline to 26.1 ± 27 μmol/L after folate supplementation; p < 0.01). A parallel increase was seen in plasma AdoMet concentrations and the AdoMet/AdoHcy ratio (p < 0.05). However, FA supplementation had no effect on global DNA methylation levels in the present study. CONCLUSIONS Supraphysiologic FA supplementation can modulate biochemical markers in one-carbon metabolism such as tHcy, AdoMet, and the AdoMet/AdoHcy ratio in hyperhomocysteinemic subjects. However, the reduction in homocysteinemia and the increased availability of methyl compounds provided by vitamin supplementation may not be sufficient to affect genomic DNA methylation.
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3.
[The curative effects of transmetil on Amanita verna poisoning].
Wen, L, Liu, WW, Huang, JW, Yu, W
Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases. 2011;(2):134-6
Abstract
OBJECTIVE To observe the curative effects of transmetil on Amanita verna poisoning. METHODS Twelve cases with Amanita verna poisoning were reviewed. The patients were divided into 2 groups according to usage of transmetil: Group A was treated with traditional protocol (gastric lavage, catharsis, rehydration, diuresis, anti-infection and hemodialysis), Group B was treated with traditional protocol combined with transmetil. The liver function changes on the 1st, 3rd, 5th and 7th day after poisoning and the mortality were compared between 2 groups. RESULTS Two cases in group A (6 patients) died. The mortality of group A was 33.3%. The AST levels continued to increase on the 3rd and 5th day, but decreased on the 7th day. TBIL continued to increased on the 1st, 3rd, 5th and 7th day. None in group B died. The TBIL level dropped at 7 d 5 patients showed an increase in ALT at 7 d and 3 patients showed a decrease in AST at 7 d. CONCLUSION Transmetil may play an important role in reducing the mortality of Amanita verna poisoning.
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S-adenosyl methionine improves early viral responses and interferon-stimulated gene induction in hepatitis C nonresponders.
Feld, JJ, Modi, AA, El-Diwany, R, Rotman, Y, Thomas, E, Ahlenstiel, G, Titerence, R, Koh, C, Cherepanov, V, Heller, T, et al
Gastroenterology. 2011;(3):830-9
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Abstract
BACKGROUND & AIMS Less than half of patients infected with hepatitis C virus (HCV) achieve sustained viral clearance after pegylated interferon (peginterferon) and ribavirin therapy. S-adenosyl methionine (SAMe) improves interferon signaling in cell culture. We assessed the effect of SAMe on the kinetics of the early antiviral response and interferon signaling in nonresponders to previous antiviral therapy and investigated the mechanisms involved. METHODS Nonresponders with HCV genotype 1 were given peginterferon alfa-2a and ribavirin for 2 weeks (course A, baseline/control). After 1 month, patients received SAMe (1600 mg daily) for 2 weeks and then peginterferon and ribavirin for 48 weeks (course B; completed by 21 of 24 patients). Viral kinetics and interferon-stimulated gene (ISG) expression in peripheral blood mononuclear cells (PBMCs) were compared between courses. RESULTS The decrease in HCV RNA from 0 to 48 hours (phase 1) was similar with and without SAMe. However, the second phase slope of viral decline was improved with SAMe (course A, 0.11 ± 0.04 log(10) IU/mL/wk; course B, 0.27 ± 0.06; P = .009); 11 patients (53%) achieved an early virological response, and 10 (48%) had undetectable HCV RNA by week 24. Induction of ISGs in PBMCs was significantly greater during course B. In cultured cells, SAMe increased induction of ISGs and the antiviral effects of interferon by increasing STAT1 methylation, possibly affecting STAT1-DNA binding. CONCLUSIONS The addition of SAMe to peginterferon and ribavirin improves the early viral kinetics and increases ISG induction in nonresponders to previous therapy. SAMe might be a useful adjunct to peginterferon-based therapies in chronic HCV infection.
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S-adenosylmethionine and 5-methyltetrahydrofolate are associated with endothelial function after controlling for confounding by homocysteine: the Hoorn Study.
Spijkerman, AM, Smulders, YM, Kostense, PJ, Henry, RM, Becker, A, Teerlink, T, Jakobs, C, Dekker, JM, Nijpels, G, Heine, RJ, et al
Arteriosclerosis, thrombosis, and vascular biology. 2005;(4):778-84
Abstract
OBJECTIVE To explore to what extent homocysteine, S-adenosylmethionine (SAM), S-adenosylhomocysteine, total folate, 5-methyltetrahydrofolate (5-MTHF), vitamin B12, and vitamin B6 are associated with endothelium-dependent, flow-mediated vasodilation (FMD), and whether these associations are stronger in individuals with diabetes or other cardiovascular risk factors. METHODS AND RESULTS In this population-based study of 608 elderly people, FMD and endothelium-independent nitroglycerin-mediated dilation (NMD) were ultrasonically estimated from the brachial artery (absolute change in diameter [mum]). High SAM and low 5-MTHF were significantly associated with high and low FMD, respectively (linear regression coefficient, [95% confidence interval]): 48.57 microm (21.16; 75.98) and -32.15 microm (-59.09; -5.20), but high homocysteine was not (-15.11 microm (-42.99; 12.78). High SAM and low 5-MTHF were also significantly associated with high and low NMD, respectively. NMD explained the association of 5-MTHF with FMD but not of SAM. No interactions were observed for diabetes or cardiovascular risk factors. CONCLUSIONS In this elderly population, both SAM and 5-MTHF are associated with endothelial and smooth muscle cell function. The effect of homocysteine on endothelial function is relatively small compared with SAM and 5-MTHF. The relative impact of SAM, 5-MTHF, and homocysteine, and the mechanisms through which these moieties may affect endothelial and smooth muscle cell function need clarification.
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Relationship between S-adenosylmethionine, S-adenosylhomocysteine, asymmetric dimethylarginine, and endothelial function in healthy human subjects during experimental hyper- and hypohomocysteinemia.
Doshi, S, McDowell, I, Goodfellow, J, Stabler, S, Boger, R, Allen, R, Newcombe, R, Lewis, M, Moat, S
Metabolism: clinical and experimental. 2005;(3):351-60
Abstract
Experimental hyperhomocysteinemia after an oral methionine or homocysteine load is associated with impaired nitric oxide-dependent vasodilatation in healthy human beings. However, it remains unproven that this effect is mediated by elevations in plasma homocysteine. There is evidence that an increase in plasma homocysteine may increase the formation of asymmetric dimethylarginine (ADMA), an inhibitor of nitric oxide synthase. The methyl groups within ADMA are derived from the conversion of S -adenosylmethionine to S -adenosylhomocysteine intermediates in the methionine/homocysteine pathway. No previous study has assessed the role of methylation status, its impact on ADMA formation, and their association with endothelial function in healthy human beings. In a randomized, placebo-controlled, crossover study, 10 healthy subjects (mean age, 29.1 +/- 3.9 years) were administered an oral dose of methionine (0.1 g/kg), l -homocysteine (0.01 g/kg), N-acetylcysteine (NAC) (0.1 g/kg), or placebo. Endothelial function as assessed by flow-mediated dilatation (FMD) of the brachial artery was impaired after both the methionine and homocysteine load compared with placebo at 4 hours (36 +/- 15, 67 +/- 23 vs 219 +/- 26 microm, respectively, P < .001). N-Acetylcysteine had no effect on flow-mediated dilatation. Plasma total homocysteine was significantly elevated at 4 hours after methionine (23.1 +/- 6.2) and homocysteine (41.5 +/- 8.9) loading, but significantly reduced after NAC 2.4 +/- 0.6 vs 7.1 +/- 2.1 micromol/L in the placebo (P < .001). Plasma S-adenosylmethionine/S-adenosylhomocysteine ratio was significantly (P < .001) increased at 4 hours after methionine (10.9 +/- 0.7) compared with homocysteine (5.4 +/- 0.4), NAC (5.0 +/- 0.3), and placebo (6.0 +/- 0.5). Plasma ADMA concentrations were not altered by any intervention. Our results suggest that endothelial dysfunction due to methionine or homocysteine loading is not associated with an increase in plasma ADMA or a disruption in methylation status.
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[Efficacy of combined administration of ursodeoxycholic acid and hepthral in the treatment of primary biliary cirrhosis].
Avezov, SA, Mansurov, FKh
Klinicheskaia meditsina. 2004;(3):55-8
Abstract
The efficacy of ursodeoxycholic acid (UDCA) combined with s-adenosylmethionine (SAMe, heptral) and UDCA alone was studied in the treatment of 19 patients (age 36-57 years) with primary biliary cirrhosis (PBC). UDCA was given in a dose 10 mg/kg/day, heptral--in a dose 800-1600 mg/day. It was found that UDCA + SAMe treatment results in earlier and longer remission. Normalization of biochemical indicators of cholestase (levels of serum bilirubin, cholesterol, total bile acids, alkaline phosphatase, 5-nucleotidase and gamma-glutamyl transpeptidase) was recorded in 33% patients, cholestase diminished in the rest patients. Heptral potentiates cytoprotective and anticholestatic actions of UDCA but does not essentially influence its immunomodular and antiapoptotic effects.
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S-adenosylmethionine (SAM-e) for the treatment of depression in people living with HIV/AIDS.
Shippy, RA, Mendez, D, Jones, K, Cergnul, I, Karpiak, SE
BMC psychiatry. 2004;:38
Abstract
BACKGROUND This study reports on clinical data from an 8-week open-label study of 20 HIV-seropositive individuals, diagnosed with Major Depressive Disorder (DSM-IV), who were treated with SAM-e (S-Adenosylmethionine). SAM-e may be a treatment alternative for the management of depression in a population reluctant to add another "pill" or another set of related side effects to an already complex highly active antiretroviral therapy (HAART) regimen. METHODS The Hamilton Rating Scale for Depression (HAM-D) and the Beck Depression Inventory (BDI) were used to assess depressive symptomatology from 1,2,4,6 and 8 weeks after initiation of treatment with SAM-e. RESULTS Data show a significant acute reduction in depressive symptomatology, as measured by both the HAM-D and the BDI instruments. CONCLUSIONS SAM-e has a rapid effect evident as soon as week 1 (p < .001), with progressive decreases in depression symptom rating scores throughout the 8 week study.
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S-adenosylmethionine (AdoMet) supplementation for treatment of chemotherapy-induced liver injury.
Santini, D, Vincenzi, B, Massacesi, C, Picardi, A, Gentilucci, UV, Esposito, V, Liuzzi, G, La Cesa, A, Rocci, L, Marcucci, F, et al
Anticancer research. 2003;(6D):5173-9
Abstract
BACKGROUND Liver toxicity can be observed during treatment with most chemotherapic agents, and represents one of the principal causes of dose reduction or chemotherapy delays. S-Adenosylmethionine (AdoMet) plays a critical role in the synthesis of polyamines and provides cysteine for the production of glutathione (GSH), the major endogenous hepatoprotective agent. Our study was aimed at assessing the protective effect of AdoMet supplementation in cancer chemotherapy-induced liver toxicity. PATIENTS AND METHODS Fifty cancer patients who developed, for the first time, anticancer chemotherapy-induced liver toxicity were studied. Enrolled patients received oral AdoMet supplementation. RESULTS AST, ALT and LDH levels recorded at the moment of the recognition of liver toxicity were significantly reduced after one week of AdoMet therapy (respectively p: 0.009, 0.0005 and 0.012). AST, ALT and LDH decrease was confirmed after two weeks of treatment. Furthermore, the effect on these enzyme levels persisted in the following chemotherapy courses, permitting our patients to perform the scheduled chemotherapy courses with a minimal number of dose reductions or administration delays. The efficacy of AdoMet supplementation was not influenced by the presence of liver metastases, and no appreciable side-effects were recognized. CONCLUSION The results of our study clearly demonstrate a protective effect of AdoMet in cancer chemotherapy-induced liver toxicity. Further large phase III studies are required to assess the real clinical benefit associated with AdoMet supplementation.
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Plasma homocysteine and S-adenosylmethionine in erythrocytes as determinants of carotid intima-media thickness: different effects in diabetic and non-diabetic individuals. The Hoorn Study.
Becker, A, Henry, RM, Kostense, PJ, Jakobs, C, Teerlink, T, Zweegman, S, Dekker, JM, Nijpels, G, Heine, RJ, Bouter, LM, et al
Atherosclerosis. 2003;(2):323-30
Abstract
OBJECTIVE Hyperhomocysteinemia is a risk factor for atherothrombosis. Through unknown mechanisms, individuals with type 2 diabetes appear particularly susceptible. We determined whether components of homocysteine metabolism are associated with intima-media thickness in individuals with and without type 2 diabetes. METHODS AND RESULTS In a cross-sectional design, we studied 231 Caucasian individuals, 60.6% having type 2 diabetes. We measured fasting homocysteine, vitamin B6 and vitamin B12 in plasma, and folate, S-adenosylmethionine and S-adenosylhomocysteine in plasma and erythrocytes. A homocysteine concentration >12 micromol/l was associated with a greater intima-media thickness of +0.07 mm (95% CI, +0.01 to +0.13; P=0.03) among diabetic individuals and of -0.004 mm (95%CI, -0.08 to +0.07; P=0.92) among non-diabetic individuals. An erythrocyte S-adenosylmethionine concentration above >4000 nmol/l was associated with a smaller intima-media thickness of -0.04 mm (95%CI, -0.10 to +0.02; P=0.17) for diabetic individuals versus -0.12 mm (95%CI, -0.20 to -0.36; P=0.005) for non-diabetic individuals. CONCLUSIONS With regard to carotid intima-media thickness, individuals with diabetes appear more susceptible to the detrimental effects of homocysteine than non-diabetic individuals. In addition, diabetic individuals may lack the protective effect on the vascular wall conferred by high concentrations of S-adenosylmethionine. These findings may help explain why hyperhomocysteinemia is an especially strong risk factor for atherothrombosis among individuals with type 2 diabetes.