Zinc supplementation is associated with a reduction in serum markers of inflammation and oxidative stress in adults: A systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: Zinc (Zn) is a trace metal that is considered to have an impact on chronic inflammation. However, findings of clinical trials have been inconsistent. The present systematic review and meta-analysis aimed to provide a more robust examination of the evidence on the effectiveness of Zn supplements on markers of inflammation and oxidative stress. METHODS: A systematic search in PubMed, Scopus, Web of Science and Cochrane Library was undertaken to identify relevant randomized controlled trials (RCTs) assessing the impact of Zn on inflammation and oxidative stress until 17 August 2020. We applied a random-effects method to obtain effect sizes (ES) and 95% confidence intervals (CIs). Meta-regression was used to detect the potential source of between-study heterogeneity. RESULTS: Twenty-one eligible RCTs comprising 1321 participants were included in the meta-analysis. In comparison with the control groups, serum C-reactive protein (CRP) (ES = -0.92 mg/L, 95% CI = [-1.36, -0.48], P < 0.001, I2 = 90.2%), tumor necrosis factor-alpha (TNF-α) (ES = -0.49 pg/mL, 95% CI = [-084, -0.14], P = 0.006, I2 = 34.6%) and malondialdehyde (MDA) (ES = -0.42, 95% CI = [-083, -0.01], P = 0.04, I2 = 76.1%) were significantly reduced in the groups receiving Zn. Serum interleukin 6 (ES = -1.02 pg/mL, 95% CI = [-2.06, 0.02], P = 0.05, I2 = 92.3%) was marginally reduced following Zn supplementation. Moreover, treatment duration was found as the source of inter-study heterogeneity. CONCLUSION: This meta-analysis suggests that Zn supplements reduce serum concentrations of markers of inflammation and oxidation: CRP, TNF-α and MDA.

Thermovaccination - thermoheliox as a stimulator of the immune response. Kinetics of the synthesis of antibodies and C-reactive protein in coronavirus infection.

Clinical trials of thermoheliox application (inhalation with a high-temperature mixture of oxygen and helium, 90 °C) in the treatment of the acute phase of coronavirus infection were conducted. Dynamics of disease development in infected patients (PCR test for the virus) and, dynamics of changes in blood concentration of C-reactive protein, immunoglobulin M, specific immunoglobulin G were studied. High efficiency of thermoheliox in releasing the organism from the virus and stimulating the immune response (thermovaccination effect) was shown. The kinetic model of the process is proposed and analyzed.

Prototypic long pentraxin PTX3 is present in breast milk, spreads in tissues, and protects neonate mice from Pseudomonas aeruginosa lung infection.

Newborns and infants present a higher susceptibility to infection than adults, a vulnerability associated with deficiencies in both the innate and adaptive immune systems. Innate immune receptors are sensors involved in the recognition and elimination of microbes that play a pivotal role at the interface between innate and adaptive immunity. Pentraxin 3 (PTX3), the prototypic long pentraxin, is a soluble pattern recognition receptor involved in the initiation of protective responses against selected pathogens. Because neonates are generally resistant to these pathogens, we suspected that PTX3 may be provided by a maternal source during the early life times. We observed that human colostrum contains high levels of PTX3, and that mammary epithelial cell and CD11b(+) milk cells constitutively produce PTX3. Interestingly, PTX3 given orally to neonate mice was rapidly distributed in different organs, and PTX3 ingested during lactation was detected in neonates. Finally, we observed that orally administered PTX3 provided protection against Pseudomonas aeruginosa lung infection in neonate mice. Therefore, breastfeeding constitutes, during the early life times, an important source of PTX3, which actively participates in the protection of neonates against infections. In addition, these results suggest that PTX3 might represent a therapeutic tool for treating neonatal infections and support the view that breastfeeding has beneficial effects on the neonates' health.

Effects of magnoline on P-selectin's expression in diabetic rats and its reno-protection.

BACKGROUND AND OBJECTIVE: Magnoline is an active ingredient of magnolia fargesii with anti-inflammatory and anti-platelet effects. The objective is to explore the renoprotection of magnoline in diabetic rats and its effects on P-selectin. METHODS: Thirty-six rats were randomized into 4 groups-normal control group (C), diabetic group (D), small-dose magnoline treatment group (M1) and large-dose magnoline treatment group (M2) (n=9 in each group). Streptozotocin was selected to construct diabetic rat model, and group M1 and group M2 were treated with magnoline 0.5mg/Kg.d and 2mg/Kg.d respectively. Urinary albumin excretion rate, renal function, levels of P-selectin and TGF-ß1 were observed after 16 weeks. RESULTS: Levels of albuminuria and serum creatinine of group M1 (1078.9 ± 77.3µg/24h, 29.7 ± 3.9µmol/L) and M2 (852.9 ± 80.1µg/24h, 30.9 ± 2.9µmol/L) were lower than group D (1572.8 ± 176.2µg/24h, 39.4 ± 4.1µmol/L) (P <0.05). Serum levels of P-selectin in group M1 and M2 were lower than group D (P <0.05). The renal expression of P-selectin and TGF-ß1 in group M1 and M2 were significantly attenuated respectively. CONCLUSIONS: Magnoline has reno-protective effects on diabetic rats which may be related to the inhibition of P-selectin.

Association between prediagnostic biomarkers of inflammation and endothelial function and cancer risk: a nested case-control study.

Experimental and prevalent case-control studies suggest an association between biomarkers of inflammation, endothelial function, and adiposity and cancer risk, but results from prospective studies have been limited. The authors' objective was to prospectively examine the relations between these biomarkers and cancer risk. A nested case-control study was designed within the Supplémentation en Vitamines et Minéraux Antioxydants (SU.VI.MAX) Study, a nationwide French cohort study, to include all first primary incident cancers diagnosed between 1994 and 2007 (n = 512). Cases were matched with randomly selected controls (n = 1,024) on sex, age (in 2-year strata), body mass index (weight (kg)/height (m)(2); <25 vs. ≥25), and SU.VI.MAX intervention group. Conditional logistic regression was used to study the associations between prediagnostic levels of high-sensitivity C-reactive protein (hs-CRP), adiponectin, leptin, soluble intercellular adhesion molecule 1 (sICAM-1), soluble vascular cell adhesion molecule 1, soluble E-selectin, and monocyte chemoattractant protein 1 and cancer risk. All statistical tests were 2-sided. Plasma sICAM-1 level was positively associated with breast cancer risk (for quartile 4 vs. quartile 1, multivariate odds ratio (OR) = 1.86, 95% confidence interval (CI): 1.06, 3.26; P(trend) = 0.048). Plasma hs-CRP level was positively associated with prostate cancer risk (for quartile 4 vs. quartile 1, multivariate OR = 3.04, 95% CI: 1.28, 7.23; P(trend) = 0.03). These results suggest that prediagnostic hs-CRP and sICAM-1 levels are associated with increased prostate and breast cancer risk, respectively.

Epigallocatechin-3-gallate inhibits angiotensin II and interleukin-6-induced C-reactive protein production in macrophages.

BACKGROUND: Consumption of green tea has been associated with health benefits against multiple diseases including cardiovascular diseases. However, the action mechanisms of green tea and its major ingredient epigallocatechin-3-gallate (EGCG) against cardiovascular diseases are still unclear. Emerging evidence has suggested a common role for C-reactive protein (CRP) in the pathogenesis of inflammation and atherosclerosis. Therefore, the effect of EGCG on angiotensin II (Ang II)- and interleukin-6 (IL-6)-induced CRP production in U937 macrophages and the possible mechanisms were observed. METHODS: U937 macrophages were cultured, and Ang II and IL-6 were used as stimulants for generation of CRP. U937 macrophages were preincubated with EGCG at 1, 3, 10 µM for 1 h prior to the stimulation. mRNA expression and protein level were determined by RT-PCR and ELISA, respectively. ROS production was observed by a fluorescence microscope. RESULTS: Pretreatment of macrophages with EGCG prior to the stimulation concentration-dependently inhibited Ang II- and IL-6-induced expression of CRP both in protein and mRNA levels. Meanwhile, EGCG reduced Ang II- and IL-6-stimulated generation of ROS in macrophages. CONCLUSION: EGCG is able to inhibit Ang II- and IL-6-stimulated CRP expression in macrophages to produce an anti-inflammation by interfering with ROS generation. The finding is helpful to update understanding of anti-atherosclerotic effects of EGCG.

Characterization of rheumatoid arthritis subtypes using symptom profiles, clinical chemistry and metabolomics measurements.

OBJECTIVE: The aim is to characterize subgroups or phenotypes of rheumatoid arthritis (RA) patients using a systems biology approach. The discovery of subtypes of rheumatoid arthritis patients is an essential research area for the improvement of response to therapy and the development of personalized medicine strategies. METHODS: In this study, 39 RA patients are phenotyped using clinical chemistry measurements, urine and plasma metabolomics analysis and symptom profiles. In addition, a Chinese medicine expert classified each RA patient as a Cold or Heat type according to Chinese medicine theory. Multivariate data analysis techniques are employed to detect and validate biochemical and symptom relationships with the classification. RESULTS: The questionnaire items 'Red joints', 'Swollen joints', 'Warm joints' suggest differences in the level of inflammation between the groups although c-reactive protein (CRP) and rheumatoid factor (RHF) levels were equal. Multivariate analysis of the urine metabolomics data revealed that the levels of 11 acylcarnitines were lower in the Cold RA than in the Heat RA patients, suggesting differences in muscle breakdown. Additionally, higher dehydroepiandrosterone sulfate (DHEAS) levels in Heat patients compared to Cold patients were found suggesting that the Cold RA group has a more suppressed hypothalamic-pituitary-adrenal (HPA) axis function. CONCLUSION: Significant and relevant biochemical differences are found between Cold and Heat RA patients. Differences in immune function, HPA axis involvement and muscle breakdown point towards opportunities to tailor disease management strategies to each of the subgroups RA patient.

Mindfulness-Based Stress Reduction training reduces loneliness and pro-inflammatory gene expression in older adults: a small randomized controlled trial.

Lonely older adults have increased expression of pro-inflammatory genes as well as increased risk for morbidity and mortality. Previous behavioral treatments have attempted to reduce loneliness and its concomitant health risks, but have had limited success. The present study tested whether the 8-week Mindfulness-Based Stress Reduction (MBSR) program (compared to a Wait-List control group) reduces loneliness and downregulates loneliness-related pro-inflammatory gene expression in older adults (N = 40). Consistent with study predictions, mixed effect linear models indicated that the MBSR program reduced loneliness, compared to small increases in loneliness in the control group (treatment condition × time interaction: F(1,35) = 7.86, p = .008). Moreover, at baseline, there was an association between reported loneliness and upregulated pro-inflammatory NF-κB-related gene expression in circulating leukocytes, and MBSR downregulated this NF-κB-associated gene expression profile at post-treatment. Finally, there was a trend for MBSR to reduce C Reactive Protein (treatment condition × time interaction: (F(1,33) = 3.39, p = .075). This work provides an initial indication that MBSR may be a novel treatment approach for reducing loneliness and related pro-inflammatory gene expression in older adults.

Modulation of C-reactive protein and tumour necrosis factor-α in collagen-induced arthritis in Dark Agouti rats: impact of collagen concentration on severity of arthritis.

OBJECTIVES: The study investigated the effect of collagen-induced arthritis in Dark Agouti (DA) rats on the level of C-reactive protein and inflammatory cytokine tumour necrosis factor-alpha (TNF-α). SUBJECTS: Female Dark Agouti (DA) rats. METHODS: Three different dosages of (2 mg/kg of body weight, 3 mg/kg of body weight and 4 mg/kg of body weight) collagen and complete Freund's adjuvant suspension were tested. After 45 days, serum C-reactive protein, TNF-α, superoxide dismutase and total glutathione assays were done. Radiographic and histopathological changes in the joints were compared. RESULTS: All three groups showed signs of arthritic changes, confirmed by histopathological and radiographic changes. Severe arthritic changes were seen in the rats injected with 4 mg/kg of body weight of collagen. There was a significant increase in C-reactive protein, TNF-α, super oxide dismutase and total glutathione levels in the plasma in arthritis rats and the changes were more significant with 4 mg/kg of collagen. CONCLUSION: These results demonstrated that the optimal dose to inject to experimental animals in order to get server arthritic changes was 4 mg/kg of collagen with complete Freund's adjuvant suspension. Severe arthritis changes induced significant elevation in plasma C-reactive protein and TNF-α levels.

Nutritional compounds influence tissue factor expression and inflammation of chronic kidney disease patients in vitro.

OBJECTIVE: Nutritional compounds that potentially limit inflammation and tissue factor expression may decrease the progression of chronic kidney disease (CKD) and associated cardiovascular disease. This project aimed to determine the effect of curcumin, bovine colostrum, and fish oil on inflammatory cytokine and tissue factor procoagulant activity of peripheral blood mononuclear cells (PBMCs) from patients with CKD before dialysis. METHODS: Peripheral blood mononuclear cells from patients with CKD before dialysis (n = 13) and age- and sex-matched healthy controls (n = 12) were cultured alone and with low and high doses of the nutritional compounds for 24 h. Cells were cultured with and without lipopolysaccharide. Supernatants were analyzed for tumor necrosis factor-α, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1, IL-1ß, C-reactive protein, and tissue factor procoagulant activity. RESULTS: The production of C-reactive protein, monocyte chemoattractant protein-1, IL-6, and IL-1ß by PBMCs was inhibited by low- and high-dose fish oil in the CKD group (P < 0.05). Curcumin decreased secretion of IL-6 (P = 0.015) and IL-1 ß (P = 0.016). Curcumin was more effective than colostrum at decreasing the procoagulant activity of PBMCs in the CKD and control groups (P < 0.019). CONCLUSION: Fish oil decreased inflammatory cytokine secretion from CKD PBMCs. In addition, the beneficial effects of curcumin were demonstrated in decreasing inflammation in vitro, often to a similar magnitude as fish oil.

Effects of sodium thiosulfate on vascular calcification in end-stage renal disease: a pilot study of feasibility, safety and efficacy.

BACKGROUND AND OBJECTIVES: Vascular calcification is a major contributor to morbidity and mortality in hemodialysis. The objective of this pilot study was to determine the feasibility, safety and efficacy of sodium thiosulfate (STS) in the progression of vascular calcification in hemodialysis patients. METHODS: Chronic hemodialysis patients underwent a battery of cardiovascular tests. Those with coronary artery calcium (Agatston scores >50) received intravenous STS after each dialysis for 5 months (n = 22) and the tests were repeated. Changes in MDCT-determined calcification were assessed as the mean annualized rate of change in 3 vascular beds (coronary, thoracic and carotid arteries) and in L1-L2 vertebral bone density. RESULTS: Although individual analyses showed coronary artery calcification progression in 14/22 subjects, there was no progression in the mean annualized rate of change of vascular calcification in the entire group. The L1-L2 vertebral bone density showed no changes. There were no correlations between rates of progression of vascular calcification and phosphorus, fetuin or C-reactive protein levels. Changes in coronary artery calcification scores correlated with those of the thoracic aorta. CONCLUSION: STS treatment is feasible, appears safe and may decrease the rate of progression of vascular calcification in hemodialysis patients. A large, randomized, controlled trial is warranted.

Product-evaluation registry of Meriva®, a curcumin-phosphatidylcholine complex, for the complementary management of osteoarthritis.

AIM: A proprietary complex of curcumin with soy phosphatidylcholine (Meriva®, Indena SpA) was evaluated in a registry study to define its efficacy in 50 patients with osteoarthritis (OA) at dosages corresponding to 200 mg curcumin per diem. METHODS: OA signs/symptoms were evaluated by the WOMAC scores. Mobility was studied by walking performance (treadmill), and inflammatory status was assessed by measurements of C-reactive protein (CRP). RESULTS: After three months of treatment, the global WOMAC score decreased by 58% (P<0.05), walking distance in the treadmill test was prolonged from 76 m to 332 m (P<0.05), and CRP levels decreased from 168 +/- 18 to 11.3 +/-. 4.1 mg/L in the subpopulation with high CRP. In comparison, the control group experienced only a modest improvement in these parameters (2% in the WOMAC score, from 82 m to 129 m in the treadmill test, and from 175 +/- 12.3 to 112 +/- 22.2 mg/L in the CRP plasma concentration), while the treatment costs (use of anti-inflammatory drugs, treatment and hospitalization) were reduced significantly in the treatment group. CONCLUSION: These results show that Meriva® is clinically effective in the management and treatment of osteoarthritis and suggest that the increased stability and better absorption of curcumin induced by complexation with phospholipids have clinical relevance, setting the stage for larger and more prolonged studies.

The use of LeptiCore in reducing fat gain and managing weight loss in patients with metabolic syndrome.

BACKGROUND: LeptiCore is a proprietary combination of various ingredients which have been shown to have properties which could be beneficial to weight loss in obese and overweight human subjects. This study evaluates the effect of Lepticore on bodyweight as well as parameters associated with obesity and metabolic syndrome. METHODS: The study was an 8 week randomized, double-blind, placebo-controlled design involving 92 obese (mean BMI > 30 kg/m2) participants (37 males; 55 females; ages 19-52; mean age = 30.7). The participants were randomly divided into three groups: placebo (n = 30), LeptiCore formula A (low dose) (n = 31) and LeptiCore formula B (high dose) (n = 31). Capsules containing the placebo or active formulations were administered twice daily before meals with 300 ml of water. None of the participants followed any specific diet nor took any weight-reducing medications for the duration of the study. A total of 12 anthropomorphic and serological measurements were taken at the beginning of the study and after 2, 4, 6, and 8 weeks of treatment. RESULTS: Compared to the placebo group, the two active groups showed statistically significant differences on all 12 variables by week 8. These included four anthropomorphic variables (body weight, body fat, waist and hip size) and eight measures of serological levels (plasma total cholesterol, LDL, HDL, triglycerides, blood glucose, serotonin, leptin, C-reactive protein). The two active groups also showed significant intra-group differences on all 12 variables between study onset and week 8. CONCLUSION: The LeptiCore formulation at both the low and high dosages appears to be helpful in the management of fat gain and its related complications. The higher dosage resulted in significantly greater reductions in body weight and triglyceride, blood glucose, and C-reactive protein levels, as well as increased serotonin levels.

Cancer-induced cachexia: a guide for the oncologist.

Cancer-induced cachexia (CIC) is a paraneoplastic syndrome that may account for up to 20% of deaths in cancer patients. Cachexia includes distinct metabolic changes that are the result of an acute-phase response (APR) mounted by the host as a reaction to tumor cells. These changes include increased muscle proteolysis, increased fat lipolysis, and increased hepatic production of acute-phase proteins such as C-reactive protein and fibrinogen. This APR pathogenesis is an important consideration in trying to treat cachectic patients as most therapies do not target the APR and its subsequent metabolic effects. Although there is currently no cure for CIC, the oncologist frequently encounters cachectic patients in practice, and evidence-based management is needed. We review the current data for assessment of starvation and cachexia, providing guidelines for management that include serum markers and functional assessment. In addition, a review of current therapies is provided, including hypercaloric feeding and nutritional intervention to address starvation, as well as data on appetite stimulants such as corticosteroids and megestrol acetate. Experimental therapies are also discussed, including nonsteroidal antiinflammatory drugs, tumor necrosis factor alpha antagonists, tetrahydrocannabinol, growth hormone, ghrelin, oxandrolone, and omega-3 fatty acids.

Effect of a high dose of glucosamine on systemic and tissue inflammation in an experimental model of atherosclerosis aggravated by chronic arthritis.

Glucosamine sulfate (GS) is a glycosaminoglycan with anti-inflammatory and immunoregulatory properties. Here we set out to explore the effect of GS administration on markers of systemic and local inflammation in rabbits with atherosclerosis aggravated by chronic arthritis. Atherosclerosis was induced in rabbits by maintaining them on a hyperlipidemic diet after producing an endothelial lesion in the femoral arteries. Simultaneously, chronic arthritis was induced in these animals by repeated intra-articular injections of ovalbumin in previously immunized rabbits. A group of these rabbits was treated prophylactically with oral GS (500 mg.kg(-1).day(-1)), and, when the animals were killed, serum was extracted and peripheral blood mononuclear cells (PBMC) were isolated. Furthermore, the femoral arteries, thoracic aorta, and synovial membranes were examined in gene expression studies and histologically. GS administration reduced circulating levels of the C-reactive protein and of interleukin-6. GS also lowered nuclear factor-kappaB activation in PBMC, and it downregulated the expression of both the CCL2 (monocyte chemoattractant protein) and cyclooxygenase-2 genes in these cells. Lesions at the femoral wall were milder after GS treatment, as reflected by the intimal-to-media thickened ratio and the absence of aortic lesions. Indeed, GS also attenuated the histological lesions in synovial tissue. In a combined rabbit model of chronic arthritis and atherosclerosis, orally administered GS reduced the markers of inflammation in peripheral blood, as well as the femoral and synovial membrane lesions. GS also prevented the development of inflammation-associated aortic lesions. These results suggest an atheroprotective effect of GS.

Can endogenous lipid molecules serve as predictors and prognostic markers of coronary heart disease?

Dyslipidemia, and inflammatory markers: high-sensitivity C-reactive protein (hs-CRP), myeloperoxidase (MPO), lipoprotein associated phospholipase A2(Lp-PLA2), and lipid peroxides (LP) are insufficient to predict the onset, extent, and prognosis of CHD. Lipoxins (LXs), resolvins, and protectins are derived from omega-3 fatty acids: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and omega-6 arachidonic acid in the presence of aspirin; whereas nitrolipids are formed due to the interaction between polyunsaturated fatty acids and nitric oxide (NO). LXs, resolvins, protectins, and nitrolipids are endogenous anti-inflammatory lipid molecules that inhibit production of interleukin-6 (IL-6) and tumor necrosis factor- alpha (TNF-alpha), suppress free radical generation, enhance NO generation; and accelerate tissue repair. Thus, beneficial actions of EPA/DHA and aspirin in CHD could be attributed to the formation of LXs, resolvins, protectins, and nitrolipids and suggest that their plasma levels aid in the prediction and prognosis of CHD.

Beneficial effects of histidine and carnosine on ethanol-induced chronic liver injury.

Alleviative effects of histidine and carnosine in mice against ethanol-induced oxidative and inflammatory was examined. After chronic alcoholic liver injury was induced, histidine and carnosine at 0.5, 1, 2g/L were added to the drinking water for 3 weeks. Results showed that the post-intake of histidine or carnosine markedly decreased alanine aminotransferase and aspartate aminotransferase activities (P<0.05). Ethanol treatment increased malondialdehyde (MDA) level, decreased glutathione (GSH) content and catalase and glutathione peroxidase (GPX) activities, and increased cytochrome P450 2E1 (CYP2E1) activity in liver (P<0.05). The post-intake of histidine and carnosine significantly decreased MDA formations, increased GSH content, enhanced catalase and GPX activities, and suppressed CYP2E1 activity (P<0.05), in which the effects on catalase and CYP2E1 activities were dose-dependent (P<0.05). Ethanol treatment elevated hepatic levels of c-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) (P<0.05), the post-intake of histidine and carnosine significantly and dose-dependently diminished the release of CRP, IL-6, and TNF-alpha (P<0.05). Ethanol treatment caused down-regulation in both catalase and GPX mRNA expression, and up-regulated both IL-6 and TNF-alpha mRNA expression (P<0.05). Histidine and carnosine post-treatments significantly and dose-dependently upregulated catalase mRNA, and down-regulated mRNA expression of IL-6 and TNF-alpha (P<0.05). Based on the observed anti-oxidative and anti-inflammatory effects, the supplement of histidine or carnosine might be helpful for the treatment of chronic alcoholic liver injury.

Effects of L-carnitine infusions on inflammatory and nutritional markers in haemodialysis patients.

BACKGROUND: Carnitine loss through dialysis membranes is shown to be related to the lack of carnitine in long-term haemodialysis patients. It has been previously reported that haemodialysis patients might have benefited from carnitine supplementation. METHODS: A total of 21 chronic haemodialysis patients maintaining carnitine supplementation and 21 controls (haemodialysis patients not receiving carnitine) were included in the study. L-carnitine was used intravenously three times a week after each haemodialysis session, at a 20 mg/kg dose. C-reactive protein (CRP), lipid profile, transferrin, total protein and albumin levels were determined at baseline after 3 and 6 months of treatment, and compared with the control group. RESULTS: CRP levels were significantly decreased in carnitine group in contrast to the increase in the control group. Transferrin, total protein and albumin levels and body mass index (BMI) of the patients rose in the carnitine group. CONCLUSIONS: There was a significant benefit of L-carnitine on CRP, transferrin, total protein and albumin levels of the haemodialysis patients.