According to previous studies, the efficacy of xanthine oxidase inhibitors (XOIs) in patients with chronic heart failure (CHF) is still controversial. Therefore, the purpose of this study was to investigate the efficacy of XOIs in patients with CHF.

Up to July 2024, we searched PubMed, EMBASE, Medline, Web of Science, and Cochrane Library for studies on the efficacy of XOI in patients with CHF. The main results included all-cause mortality, cardiovascular (CV) mortality, and heart failure (HF) hospitalization rates. The results were evaluated by hazard ratio (HR) and 95% confidence interval (95% CI).

A total of eight studies were included in this meta-analysis, of which five were cohort studies and three were randomized controlled trials (RCTs). The total sample size was 301,345. The experimental group was exposed to allopurinol or hydroxypurinol. The all-cause mortality (HR = 1.26, 95% CI 1.05-1.51, p = 0.013) and CV mortality (HR = 1.58, 95% CI 1.17-2.14, p = 0.03) in the experimental group were higher than those in the control group. In terms of HF hospitalization, there was no difference between both groups (HR = 1.21, p = 0.292). Subgroup analysis showed that the CV hospitalization rate of the experimental group was higher than that of the control group, regardless of frequency and dose levels. The all-cause mortality in the low-dose group was higher than that in the control group (HR = 1.39, p = 0.033). The CV mortality of the low-dose group (HR = 1.55, p = 0.006) and the prevalent group (HR = 1.50, p = 0.042) was higher than that of the control group.

Purine XOI exposure may be unfavorable for the prognosis of CHF patients and is affected by the frequency and dose of use.

Serum uric acid (UA) has been associated with adverse outcomes in patients with heart failure. However, it remains inconclusive whether such association persists in patients with cardiorenal syndrome (CRS).

In a nationwide prospective cohort from China, 4907 adults hospitalized for heart failure were enrolled. Of them, 1284 had an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2 at admission were included in this study. The Cox regression model was employed to evaluate the relationship between UA levels and mortality, major cardiovascular events (MACE), and hospitalization for heart failure (HHF). Additionally, Harrell's concordance index was utilized to assess the incremental value of UA levels in predicting mortality.

During a median follow-up of 3.28 years, hyperuricemia was associated with a 27 % increased risk of all-cause mortality (HR 1.27, 95 % confidence interval [CI] 1.08-1.49) and a 36 % increased risk of cardiovascular mortality (HR 1.36, 95 % CI 1.11-1.65), regardless of patients' eGFR levels. This relationship remained consistent throughout the whole follow-up period. Hyperuricemia increased the risk of 3-month MACE by 39 % (HR 1.39, 95 % CI 1.03-1.88), 3-month HHF by 47 % (HR 1.47, 95 % CI 1.11-1.95), and 1-year MACE by 26 % (HR 1.26, 95 % CI 1.02-1.57). The additive effect of uric acid levels in predicting mortality was also confirmed.

Serum UA levels possess significant value in prognosis of mortality, MACE, and HHF among patients with CRS. These findings underscore the importance of monitoring serum UA in the management of patients with CRS, as UA may provide valuable insights into risk stratification.

Evidence on the longitudinal association of serum uric acid (SUA) with the risk of heart failure (HF) was limited and controversial. This study aimed to investigate the associations of cumulative SUA (cumSUA), incorporating its time course of accumulation, with the risk of HF.

This prospective study enrolled 54 606 participants from the Kailuan study. The magnitude of SUA accumulation was expressed as cumSUA, exposure duration, and cumulative burden from baseline to the third survey, with cumSUA, calculated by multiplying mean values between consecutive examinations by time intervals between visits, as the primary exposure.During a median follow-up of 10 years, 1260 cases of incident HF occurred. A higher risk of HF was observed in participants with the highest vs. the lowest quartile of cumSUA [adjusted hazard ratio (aHR), 1.54; 95% confidence interval (CI), 1.29-1.84], 6-year vs. 0-year exposure duration (aHR, 1.87; 95% CI, 1.43-2.45), cumulative burden >0 vs. = 0 (aHR, 1.55; 95 CI, 1.29-1.86), and those with a negative vs. positive SUA slope (aHR, 1.12; 95% CI, 1.02-1.25). When cumSUA was incorporated with its time course, those with cumSUA ≥median and a negative SUA slope had the highest risk of HF (aHR, 1.55; 95% CI, 1.29-1.86).

Incident HF risk was associated with the magnitude and time course of cumSUA accumulation. Early accumulation resulted in a greater risk of HF compared with later accumulation, indicating the importance of optimal SUA control earlier in life.

The most frequent consequence of elevated uric acid (UA) levels is the development of gout and urate kidney disease. Besides these effects, several studies have investigated the association between hyperuricemia and cardiovascular (CV) disease. High serum UA has been identified as an important determinant of all-cause and CV mortality and CV events (acute and chronic coronary syndrome, stroke and peripheral artery disease). Despite the high number of publications on this topic, there are two questions that are still unanswered: do we need a specific CV cut-off of serum UA to better refine the CV risk? Is urate lowering treatment (ULT) able to reduce CV risk in asymptomatic patients? In this review, we will focus on these two points.

Although no doubt exists that the relationship between CV events starts at lower levels than the actually used cut-off, different papers found dissimilar cut-offs. Furthermore, heterogeneity is present depending on the specific CV events evaluated and none of the found cut-off have been tested in external populations (in order to confirm its discriminatory capacity). Furthermore, only few randomized clinical trials on the role of hypouricemic agents in reducing the CV risk have been published giving heterogeneous results. The last published one (ALL-HEART) has strong limitations, that we will deeply discuss.

A definitive answer to the two questions is impossible with the actually published paper but, over identifying current gaps in knowledge we try to individuate how they can be overruled.

Biomarkers are critical for heart failure (HF) management by facilitating risk stratification, therapeutic decision-making, and monitoring treatment response. This prospective, single-center study aimed to assess predictors of death during one-year follow-up in patients with end-stage HF, with particular emphasis on the soluble suppression of tumorigenicity 2/left ventricular mass index (sST2/LVMI) ratio, modified Model for End-stage Liver Disease (modMELD), and Model for End-stage Liver Disease excluding INR (MELD-XI). This study comprised 429 consecutive patients with end-stage HF hospitalized between 2018 and 2023. The median age was 56.0 (50.0-60.0) years; and 89.2% were male. During the follow-up, 134 (31.2%) patients died. The area under the receiver operating characteristics (ROC) curves showed good predictive powers of sST2/LVMI-MELDXI (AUC: 0.90 [CI: 0.87-0.93]; specificity 85% and sensitivity 80%) and sST2/LVMI-modMELD (AUC: 0.92 [95% CI: 0.90-0.95]; specificity 92%, sensitivity 81%) for assessment of one-year mortality. In conclusion: the sST2/LVMI-modMELD and sST2/LVMI-MELD-XI ratios are independently related to one-year mortality in the analyzed group of patients. The prognostic power of these new models is significantly better than their individual components. This single-center study comprised a relatively small group of patients, so the prognostic value of these new models cannot be generalized to the entire HF population. Considering the limitations of this analysis, further randomized trials with a large cohort are necessary to confirm the utility of the new prognostic models in HF patients.

The prognostic value of the uric acid to albumin ratio (UAR) in heart failure (HF) remains underexplored. The objective of this research was to investigate the link between UAR and short-term outcomes in Chinese HF patients.

We analyzed data from 1893 HF patients, out of an initial cohort of 2008, who had available UAR measurements. The skewed distribution of UAR data was addressed by applying a Log-10 (lg) transformation and stratifying patients into three groups accordingly (low to high). The final outcome was identified as mortality or hospital readmission within 28 days. We employed restricted cubic spline analysis (RCS), Kaplan-Meier survival curves, and Cox proportional hazards models to evaluate the link between UAR and short-term outcomes.

Among 1893 patients with HF [≥ 70 years, 1,382 (73.0%); female, 1,100 (58.1%)], the incidence of 28-day outcome was 8.6%. The RCS analysis suggested a positive relationship between lg(UAR) and 28-day outcomes, with no evidence of nonlinearity (p = 0.008). The cumulative incidence of 28-day readmission/death indicated that patients in the tertile 3 faced a significantly elevated risk of adverse outcomes (p < 0.001). Cox proportional hazards models showed that an elevated UAR was associated with a greater likelihood of 28-day mortality or hospital readmission (HR = 2.433, 95% CI: 1.638-3.615, p < 0.001). Even after accounting for possible confounding variables, the result still existed (HR = 1.594, 95% CI: 1.032-2.462, p = 0.036). Moreover, the associations were consistent in various subgroups, and sensitivity analysis (all p > 0.05).

Increased UAR correlates with a heightened risk of short-term death or hospital readmission in Chinese individuals suffering from HF. Maintaining a relatively lower UAR could potentially improve the clinical prognosis for these patients.

Asymptomatic hyperuricemia is defined by serum uric acid levels above 6.2 mg/dl in women and 7 mg/dl in men. In the presence of monosodium urate crystal formation and articular inflammation, hyperuricemia may become symptomatic (namely nephrolithiasis and gout). Uric acid results from purine catabolism and is at the centre of a complex metabolic interplay that involves oxidative stress, inflammation, renin-angiotensin-aldosterone system (RAAS) activation and insulin resistance. Uric acid levels present a continuous relation with conditions like hypertension and chronic kidney disease (CKD) and are reported to have an impact on risk of cardiovascular events. However, whether elevated uric acid is a causal agent and thus a possible therapeutic target is still uncertain and matter of further investigation. Treating symptomatic hyperuricemia involves lowering uric acid drugs and controlling inflammation. Urate-lowering agents are well tolerated but show minimal impact on cardiovascular events in patients with gout. Use of direct-acting urate-lowering agents in asymptomatic hyperuricemia associated with cardiovascular diseases does not warrant a clear benefit, whereas addressing cardiovascular issues with guideline-recommended therapies lowers uric acid and reduces the occurrence of cardiovascular events. Regular assessment of uric acid and clinical symptoms is advised before starting and renewing a urate-lowering treatment.

Observational studies have established an association between serum uric acid and cardiovascular disease (CVD). However, these studies are susceptible to uncontrolled confounders and reverse causality bias. To overcome these challenges, we employed a two-sample Mendelian randomization (MR) approach to investigate the causal link between serum uric acid and CVD.

We utilized Genome-wide association study (GWAS) data for serum uric acid and six CVD: coronary artery disease (CAD), hypertension, myocardial infarction (MI), heart failure (HF), angina, and coronary heart disease (CHD). MR analyses employed inverse variance weighting (IVW), MR-Egger, weighted median, and weighted model. Sensitivity analyses were conducted to assess result reliability, including Cochrane's Q test, MR-Egger intercept, MR-PRESSO, and the leave-one-out approach.

IVW analysis revealed that a genetic predisposition to elevated serum uric acid levels significantly increases the risk of CVD, with higher odds ratios (ORs) observed for CAD (OR: 1.227; 95 % CI: 1.107-1.360, P = 0.0002), hypertension (OR: 1.318, 95 %CI: 1.184-1.466, P = 2.13E-06), MI (OR: 1.184, 95 %CI: 1.108-1.266, P = 2.13E-06), HF (OR: 1.158, 95 %CI: 1.066-1.258, P = 2.13E-06), angina (OR: 1.150, 95 %CI: 1.074-1.231, P = 0.0002) and CHD (OR: 1.170, 95 %CI: 1.072-1.276, P = 0.0005). Sensitivity analysis research results have robustness.

This MR study robustly demonstrates a significant causal relationship between genetically elevated serum uric acid and various cardiovascular diseases, suggesting that higher levels may enhance the risk of cardiovascular events. Consequently, patients with elevated uric acid levels warrant early and aggressive interventions to mitigate cardiovascular risks.

This study aimed to investigate the effect of tolvaptan on metabolism and electrolyte homeostasis in patients with heart failure (HF).

Literature databases, such as PubMed, EMBASE, the Cochrane Library, China National Knowledge Infrastructure, VIP, and WanFang Data, were systematically searched for relevant trials from inception to November 4, 2023. We used the fixed effect model to combine the effect sizes and used I2 to test heterogeneity. Funnel plots were plotted to assess publication bias.

16 studies were eligible for further analysis. No significant differences were identified in the incidence of hyperuricemia between the tolvaptan group and the placebo group (odds ratio (OR) = 1.23, 95% confidence interval (CI) = 0.97 to 1.55, p = 0.09). Tolvaptan decreased the levels of blood uric acid compared to traditional diuretics (mean difference (MD) = -82.8, 95% CI = -96.48 to -69.13, p < 0.00001). There was no significant difference in hypernatremia (OR = 1.62, 95% CI = 0.66 to 3.96, p = 0.29) and hyperkalemia (OR = 1.17, 95% CI = 0.93 to 1.48, p = 0.18) between the tolvaptan and control groups.

Tolvaptan reduced the level of blood uric acid compared to conventional diuretics, and could be used as a substitute for traditional diuretics for HF patients with a high risk of gout.

Patients with chronic heart failure (CHF) frequently develop hyperuricemia, an elevated serum uric acid level, associated with adverse outcomes. Dapagliflozin, a sodium-glucose cotransporter-2 inhibitor, demonstrates reduction in cardiovascular mortality and hospitalization in patients with CHF and ejection fraction (HFrEF), irrespective of diabetes. However, dapagliflozin's effect on the uric acid levels in patients with CHF and hyperuricemia remain unclear.

To investigate the effects of dapagliflozin on uric acid levels in CHF patients with hyperuricemia.

We conducted a randomized, double-blind, placebo-controlled trial in 200 patients with CHF and hyperuricemia, with HFrEF and serum uric acid levels ≥ 7 mg/dL (≥ 416 μmol/L). The participants were randomly assigned to receive a daily dose of 10 mg dapagliflozin or placebo for 24 months. The primary endpoint was the change in serum uric acid level from baseline to 24 months. Secondary endpoints included changes in left ventricular ejection fraction (LVEF), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and quality of life (QoL) scores, as well as the incidence of cardiovascular death and hospitalization for heart failure.

At 24 months, dapagliflozin significantly reduced serum uric acid levels by 1.2 mg/dL (71 μmol/L) compared with placebo (95%CI: -1.5 to -0.9; P < 0.001). Dapagliflozin also significantly improved LVEF by 3.5% (95%CI: 2.1-4.9; P < 0.001), NT-proBNP by 25% (95%CI: 18-32; P < 0.001), and QoL scores by 10 points (95%CI: 7-13; P < 0.001) and reduced the risk of cardiovascular death and hospitalization for heart failure by 35% (95%CI: 15-50; P = 0.002) compared with the placebo. Adverse events were similar between the two groups, except for a higher rate of genital infections in the dapagliflozin group (10% vs 2%, P = 0.01).

Dapagliflozin significantly lowered serum uric acid levels and improved the clinical outcomes in patients with CHF and hyperuricemia. Therefore, dapagliflozin may be a useful therapeutic option for this high-risk population.

This meta-analysis aimed to explore the association between serum uric acid levels and the efficacy of uric acid-lowering therapies on clinical outcomes among patients with heart failure with preserved ejection fraction (HFpEF).

A comprehensive literature search was conducted through October 21, 2023, across PubMed, Embase, Cochrane Library, and Web of Science databases. The pooled effect sizes were estimated and presented with their respective 95% confidence intervals (CI). Subgroup analyses were conducted based on various factors, including sample size (<1,000 vs. ≥1,000), follow-up duration (<2 years vs. ≥2 years), study quality (assessed by a score of <7 vs. ≥7), ethnicity (Non-Asian vs. Asian), study design (prospective vs. retrospective), type of heart failure (HF) (acute vs. chronic), presence of hyperuricemia (yes or no), left ventricular ejection fraction (LVEF) thresholds (≥45% vs. ≥50%), and the type of uric acid-lowering therapy (traditional vs. novel).

The analysis included a total of 12 studies. Elevated serum uric acid levels were significantly linked to an increased risk of all-cause mortality [relative risk (RR): 1.21, 95% CI: 1.06-1.37, P = 0.004] and cardiovascular (CV) mortality (RR: 1.71, 95% CI: 1.42-2.04, P < 0.001) in HFpEF patients. Subgroup analyses confirmed this association, particularly in non-Asian populations, those with chronic HFpEF, and studies with a follow-up duration of two years or more. Additionally, higher uric acid levels were associated with an increased risk of HF-related hospitalization [hazard ratio (HR): 1.61, 95% CI: 1.12-2.34, P = 0.011]. Regarding treatment, uric acid-lowering therapy did not show a significant effect on reducing mortality in HFpEF patients. However, it was associated with a decreased risk of hospitalization due to HF (RR: 0.85, 95% CI: 0.79-0.91, P < 0.001).

The findings of this study highlight the prognostic significance of serum uric acid levels in HFpEF and suggest that uric acid-lowering therapy may be beneficial in reducing the incidence of HF hospitalizations. Further research is warranted to elucidate the mechanisms by which uric acid-lowering therapy confers its potential benefits.

Recent studies have shown that increases in serum UA levels are associated with adverse clinical outcomes in patients with chronic heart failure (CHF); the aim of this study was to determine the relationship between serum uric acid and total diuretic dose received during hospitalization in hospitalized patients with acute exacerbation of heart failure. The main purpose of this study is to determine the role of uric acid as a biomarker that can be a substitute for pro-BNP in clinical evaluation and the need for diuretics in hospitalized patients with acute heart failure.

After approving the plan in the Research Council of the Heart Department and obtaining an ethical code from the Regional Committee on Research Ethics (Human Subjects Studies), the researcher referred to the archives of our center, the case of 100 patients diagnosed with acute heart failure. Cardiac patients were selected, and the information required for the study was collected using a pre-prepared data collection form, and the information was entered into SPSS software after categorization and appropriate analysis and statistical tests were performed on it. Were performed and in all statistical tests the statistical significance level was considered 0.05: RESULTS: 100 patients with acute heart failure were included in this study with a mean age of 63.43 ± 14.78 years. 66% of them were men. The mean dose of furosemide in these patients was 680.92 ± 377.47 mg and the mean serum uric acid level in these patients was 8.55 ± 2.50 mg / dL. In the study of the relationship between the variables, there was a significant relationship between the dose of furosemide received with the serum level of serum uric acid (P = 0.017, r = 0.248 and P = 0.009, r = -0.267, respectively). There is also a significant relationship between serum uric acid level and patient mortality (P = 0.013, r = 0.247). However this relationship lost its significance after multivariate analysis.

There is a significant relationship between serum uric acid level and diuretic use. However, in-hospital mortality is not related to uric acid levels at admission.

Vitamin D emerged as an important prognostic biomarker in heart failure (HF), with currently highly debated therapeutic implications. Several trials on vitamin D supplementation in HF showed improvements in left ventricular (LV) remodeling and function and health-related quality of life (HRQoL), which did not translate into mid- to long-term beneficial effects regarding physical performance and mortality. We addressed total 25-hydroxyvitamin D (25(OH)D), serum albumin, and uric acid (UA) levels, focusing mainly on vitamin D deficiency, as potential markers of LV systolic dysfunction in HF with reduced and mildly reduced ejection fraction (HFrEF, HFmrEF). Seventy patients with LVEF < 50% were comprehensively evaluated using ECG, echocardiography, lung ultrasound (LUS), blood sampling, and the six-minute walk test (6MWT). HRQoL was also assessed using the Minnesota Living with Heart Failure Questionnaire (MLHFQ). Statistically significant positive correlations were found between LVEF, 25(OH)D, serum UA, and albumin, respectively (p = 0.008, p = 0.009, and p = 0.001). Serum UA (7.4 ± 2.4 vs. 5.7 ± 2.1, p = 0.005), NT-proBNP levels (1090.4 (675.2-2664.9) vs. 759.0 (260.3-1474.8), p = 0.034), and MLHFQ scores (21.0 (14.0-47.0) vs. 14.5 (4.5-25.5), p = 0.012) were significantly higher, whereas 25(OH)D concentrations (17.6 (15.1-28.2) vs. 22.7 (19.5-33.8), p = 0.010) were lower in subjects with severely reduced LVEF. Also, 25(OH)D was independently associated with LVEF in univariate and multiple regression analysis, maintaining its significance even after adjusting for confounders such as age, NT-proBNP, the presence of chronic coronary syndrome, hypertension, and anemia. According to our current findings, 25(OH)D is closely associated with LVEF, further supporting the need to establish correct vitamin D supplementation schemes and dietary interventions in HF. The changes in LVEF, 25(OH)D, serum UA, and albumin levels in HFrEF and HFmrEF indicate a similar pathophysiological background.

Increased circulating uric acid (UA) concentration may disrupt cardiac function in heart failure patients, but the specific mechanism remains unclear. Here, we postulate that hyperuremia induces sterol regulatory element binding protein 1 (SREBP1), which in turn activate hepatic fatty acid biosynthesis response, leading to cardiac dysfunction.

Increased circulating uric acid was observed in heart failure patients and inversely correlated to cardiac function. Besides, uric acid correlated to circulating lipids profile based on metabolomics in heart failure patients. Using cultured human hepatoellular carcinomas (HepG2) and Tg(myl7:egfp) zebrafish, we demonstrated that UA regulated fatty acid synthase (FASN) via SREBP1 signaling pathway, leading to FFA accumulation and impaired energy metabolism, which could be rescued via SREBP1 knockdown. In ISO treated zebrafish, UA aggravated heart failure via increased cardiovascular cavity size, decreased heart beats, pericardial edema and long-stretched heart deformation.

Our findings suggest that UA-SREBP1-FASN signaling exacerbates cardiac dysfunction during FFA accumulation. Identification of this mechanism may help in treatment and prevention of heart failure.

Introduction: The study evaluated the selected appetite hormones (ghrelin, leptin) and inflammatory parameters (tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6)) in patients with urolithiasis, metabolic syndrome (MetS), and hyperuricemia. Materials: 57 patients with urolithiasis, MetS and hyperuricemia (UP group) and 29 healthy people as the control group (CG group) were recruited to the study. All persons were 22-60 age. Methods: After preliminary testing, the qualified participants were evaluated for fasting serum levels of ghrelin, leptin, IL-6, and TNF-α. Results: Our results revealed differences between average values of leptin (p = 0.045), ghrelin (p < 0.001), IL-6 (p < 0.001), and TNF-α (p < 0.001) in the studied groups. Moreover, in the UP group, significant correlations were found between ghrelin and leptin; between these hormones and IL-6, and between leptin and uric acid (UA). Besides, leptin concentration increased significantly along with the changes in the body mass index (BMI) categories in the UP group. Conclusions: This study showed that patients with urolithiasis, concomitant MetS, and high UA levels may have problems managing appetite hormones.

Previously, we have investigated the anti-tumor activity and mechanism through which dandelion acts against triple-negative breast cancer (TNBC). However, traditional Chinese medicine is mostly accepted as an adjunct therapy during chemotherapy in clinical practice. So far, little is known about the effects of dandelion in conjunction with chemotherapeutic drugs.

To investigate the effects of dandelion on the anti-tumor activity and cardiotoxicity of doxorubicin (DOX), and to further explore the molecular mechanisms through which these effects occur.

At the beginning of this study, dandelion was observed to alleviate DOX-induced cardiotoxicity and reduce the anti-tumor activity of DOX. Subsequently, we investigated whether the resistance to DOX mediated by P-glycoprotein was involved in the above effects.

The cardioprotective effect of dandelion was investigated on DOX-treated mice by histological analysis, myocardial enzyme assays, and an untargeted metabolomics study based on LC-Q-TOF/MS. TNBC cell lines and 4T1 tumor-bearing mice were employed to investigate the combined anti-tumor activity. Laser scanning confocal microscope and a flow cytometry analysis were employed to measure the intracellular accumulation of DOX. A specific, sensitive, and rapid LC-MS/MS method was developed to detect the efflux of DOX from cells. Expression of P-glycoprotein in mouse tumor and heart tissues was detected via Western blotting analysis.

Dandelion was found to significantly alleviate DOX-induced cardiotoxicity, as was evidenced by improved cardiomyocyte morphology, decreased LDH and CK-MB release, and adjusted metabolic biomarker levels. However, in vitro and in vivo studies showed that dandelion could reduce the anti-tumor activity of DOX. This counteraction was achieved by activating of the drug efflux transporter P-glycoprotein, thereby promoting the efflux of DOX from cells and reducing the intracellular accumulation of DOX. Moreover, the activation of P-glycoprotein by dandelion in mouse heart tissue was also observed, thus suggesting that the decrease of cardiac DOX accumulation plays an important role in the cardioprotective effect of dandelion.

Dandelion can activate the P-glycoprotein in heart and tumor tissues, which ameliorates DOX-induced cardiotoxicity but attenuates DOX cytotoxicity toward TNBC. Our findings have important implications for the correct clinical use of dandelion.