Elevated Uric Acid Concentrations Research Articles

Biomimetic Integrated Nanozyme for Flare and Recurrence of Gouty Arthritis

Flare and multiple recurrences pose significant challenges in gouty arthritis. Traditional treatments provide temporary relief from inflammation but fail to promptly alleviate patient pain or effectively prevent subsequent recurrences. It should also be noted that both anti-inflammation and metabolism of uric acid are necessary for gouty arthritis, calling for therapeutic systems to achieve these two goals simultaneously. In this study, we propose a biomimetic integrated nanozyme, HMPB-Pt@MM, comprising platinum nanozyme and hollow Prussian blue. It demonstrates anti-inflammatory properties by eliminating reactive oxygen species and reducing infiltration of inflammatory macrophages. Additionally, it rapidly targets inflamed ankles through the camouflage of macrophage membranes. Furthermore, HMPB-Pt@MM exhibits urate oxidase-like capabilities, continuously metabolizing locally elevated uric acid concentrations, ultimately inhibiting multiple recurrences of gouty arthritis. In summary, HMPB-Pt@MM integrates ROS clearance with uric acid metabolism, offering a promising platform for the treatment of gouty arthritis.

REVIEW OF THE PHYTOTHERAPY FOR NEPHROLITHIASIS

Nephrolithiasis (kidney stone) cases have a prevalence ranging from 1% to 13%. The disease not only hampers kidney function but also elevates the risk of chronic kidney diseases. The pathophysiology of nephrolithiasis is closely linked to elevated concentrations of calcium, oxalate, and/or uric acid in the urine. Pharmacotherapy to manage nephrolithiasis includes thiazide diuretics, allopurinol, citrate supplements, and alpha-blockers that have been prescribed to relieve symptoms. In addition, there is growing interest in exploring the potential of phytotherapy. This review aims to identify suitable phytotherapy approaches by examining relevant articles on nephrolithiasis. The research methodology involved searching PubMed articles using the keywords of (("Plant Extracts") AND ("Nephrolithiasis")) OR ("Ureterolithiasis"). The articles obtained from the initial search were n =123. 2 authors screened articles for their eligibility. The inclusion criteria were limited to articles written in English, topics related to nephrolithiasis and not other kidney diseases, the botanical names of the plants and the method of extraction are clearly described, complete studies with clear descriptions regarding the methods and results, not synthetic drugs, and not involving medical instruments or laser to remove the stones. Articles included in the review were n = 17. Water and hydro-alcohol were the solvents used to extract the plants. Twenty-two plants have confirmed their anti-nephrolithiasis activity, and nine articles described the assay by in vivo study, two by in vitro study, three by both in vitro and in vivo study, and only one article mentioned a study in humans by a randomized-control trial on a mixture of herbs. It is concluded that Rhizoma alismatis, Poria cocos, Polyporus umbellatus, Atractylodis macrocephalae, and Cinnamomi Cassiae prepared as a mixture in the Wu-Ling-San formula have a potential therapeutic effect on nephrolithiasis, as this formula has been studied in humans.

Evaluation of Macular and Optic Disc Radial Peripapillary Vessel Density Using Optical Coherence Tomography Angiography in Gout Patients.

In this cross-sectional study, optical coherence tomography angiography (OCT-A) findings were compared in patients with gout (n = 30) and healthy participants (n = 32). The superficial and deep vessel density variables measured using OCT-A were compared between the groups. The superficial foveal and perifoveal vessel densities of the patient group were lower than those of the healthy participants (p = 0.014 and p = 0.045, respectively). However, all superficial and parafoveal vessel densities were similar in both groups (p = 0.469 and p = 0.284, respectively). The deep capillary plexus density measurements of the whole-zone, foveal, parafoveal, and perifoveal vessel densities using OCT-A revealed no significant differences between the groups (p = 0.251, p = 0.074, p = 0.177, and p = 0.881, respectively). A higher serum uric acid (SUA) level was found to be independently associated with a decreased superficial capillary plexus density and an increased choriocapillary flow deficit in the study population. Men were less sensitive to high SUA levels than women. These findings suggest that an elevated uric acid concentration may play a role in the development and progression of cardiovascular disease through changes in the microvasculature, as shown by the OCT-A parameters.

Association between serum uric acid concentration and radiographic axial spondylarthritis: a cross-sectional study of 202 patients.

Association between serum uric acid concentration and radiographic axial spondylarthritis: a cross-sectional study of 202 patients.

Relationship Between Hyperuricemia-Waist Phenotype and Obstructive Sleep Apnea in Type 2 Diabetes Mellitus.

This study aimed to propose the hyperuricemia-waist (HUAW) phenotype and investigate the relationship between the HUAW phenotype and obstructive sleep apnea (OSA) in type 2 diabetes mellitus (T2DM). We enrolled 255 patients with T2DM (165 male and 90 female) from the First Hospital of Qinhuangdao. The sleep test was performed, and serum uric acid (UA) levels and waist circumference (WC) were calculated. The HUAW phenotype was defined as serum UA concentrations ≥420 μmol/L and WC ≥90 cm (male) and ≥85 cm (female).The participants were categorized into four phenotype groups based on the mentioned cutoffs: normal WC and normal UA concentrations (group A); normal WC and elevated UA concentrations (group B); enlarged WC and normal UA concentrations (group C); and enlarged WC and elevated UA concentrations (group D). Among these participants, 17.6% were characterized by the HUAW phenotype, 80.0% had OSA, and 47.0% had moderate-to-severe OSA. The prevalence of OSA was 43.4%, 71.4%, 89.7%, and 97.8% in groups A, B, C, and D, respectively. The prevalence of moderate-to-severe OSA was 7.5%, 28.6%, 56.9%, and 72.7% in groups A, B, C, and D, respectively. After adjusting for age, sex, duration of diabetes, glycosylated hemoglobin A1c, smoking, and drinking, the HUAW phenotype was found to be significantly associated with OSA and moderate-to-severe OSA. The present study proposed the HUAW phenotype and demonstrated that in T2DM, the HUAW phenotype was associated with OSA, especially with moderate-to-severe OSA. Unlike T2DM without the HUAW phenotype, T2DM with the HUAW phenotype showed a significantly higher prevalence of OSA, especially moderate-to-severe OSA. Thus, early sleep studies should be routinely examined in individuals with T2DM who display the HUAW phenotype.

Urate-Lowering Therapy Inhibits Thoracic Aortic Aneurysm and Dissection Formation in Mice.

Thoracic aortic aneurysm and dissection (TAAD) is a highly lethal vascular disease without effective drug therapy. Whether elevated serum concentrations of uric acid are involved in TAAD development remains unclear. Serum uric acid levels were detected in different TAAD mouse models and patients. The urate-lowering drug allopurinol was administered in the drinking water of TAAD mice. Adenine diet-induced mice were established to investigate the role of hyperuricemia in TAAD formation and RNA-sequencing of thoracic aortas from these mice was performed. We found serum uric acid levels were elevated in various mouse TAAD models, including mice fed a β-aminopropionitrile diet, Marfan mice with fibrillin-1 haploinsufficiency (Fbn1C1041G/+), and ApoE-/- mice infused with Ang II (angiotensin II), as well as in patients with TAAD. Administration of urate-lowering drug allopurinol in the drinking water significantly alleviated TAAD formation in β-aminopropionitrile-treated mice, Fbn1C1041G/+ mice, and Ang II-infused ApoE-/- mice. Moreover, an adenine diet was used to induce hyperuricemia in mice. Intriguingly, a 4-week adenine diet feeding directly induced TAAD formation characterized by increased maximal thoracic aortic diameters and severe elastin degradation, which were ameliorated by allopurinol. Unbiased RNA-sequencing in mouse thoracic aortas suggested that FcγR (Fc gamma receptor) was upregulated upon adenine diet, but reciprocally repressed by allopurinol. Mechanistically, hyperuricemia activated FcγR-mediated ERK1/2 (extracellular signal-regulated kinase 1/2) phosphorylation to induce macrophage inflammation and TAAD development, which was abrogated by allopurinol or FcγR deficiency. This study uncovered an important and previously unrecognized role of hyperuricemia in mediating the pathogenesis of TAAD, and uric acid-lowering drug may represent a promising therapeutic approach for TAAD.

Study on association between SLC2A9 rs3733591 and Gout susceptibility in 481 Vietnamese individuals

Gout is a common form of inflammatory arthritis that is strongly associated with elevated uric acid concentration in the blood. The development of the disease is not onlytriggered by environmental factors but also genetic variations. Previous studies demonstrated that the genetic associations with gout vary in different populations in the world. This study aimed to identify the relationship between SLC2A9 rs3733591and gout susceptibility in the Vietnamese population.Total DNAs were extracted from 481 blood samples including 160 patients with gout and 321 age-matched healthy controls. The genotyping of SLC2A9 rs3733591 was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Chi-squared test was used to test whether the genotypes frequencies of rs3733591 follow Hardy-Weinberg equilibrium (HWE) and to check its association with gout in three models (additive, recessive, dominant) and allele form. The result showed that SLC2A9 rs3733591 was in agreement with Hardy-Weinberg equilibrium (p>0.05). However, there was no association between the rs3733591 and gout in any tested models (p>0.05).This study will contribute to the genetic study of gout susceptibility in Vietnam.

Hyperuricemia-induced endothelial insulin resistance: the nitric oxide connection.

Hyperuricemia, defined as elevated serum concentrations of uric acid (UA) above 416µmol L-1, is related to the development of cardiometabolic disorders, probably via induction of endothelial dysfunction. Hyperuricemia causes endothelial dysfunction via induction of cell apoptosis, oxidative stress, and inflammation; however, it's interfering with insulin signaling and decreased endothelial nitric oxide (NO) availability, resulting in the development of endothelial insulin resistance, which seems to be a major underlying mechanism for hyperuricemia-induced endothelial dysfunction. Here, we elaborate on how hyperuricemia induces endothelial insulin resistance through the disruption of insulin-stimulated endothelial NO synthesis. High UA concentrations decrease insulin-induced NO synthesis within the endothelial cells by interfering with insulin signaling at either the receptor or post-receptor levels (i.e., proximal and distal steps). At the proximal post-receptor level, UA impairs the function of the insulin receptor substrate (IRS) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) in the insulin signaling pathway. At the distal level, high UA concentrations impair endothelial NO synthase (eNOS)-NO system by decreasing eNOS expression and activity as well as by direct inactivation of NO. Clinically, UA-induced endothelial insulin resistance is translated into impaired endothelial function, impaired NO-dependent vasodilation, and the development of systemic insulin resistance. UA-lowering drugs may improve endothelial function in subjects with hyperuricemia.

The role of oxidative stress on molybdenum enzymes and ischemic reperfusion injury in hyperuricaemic patients. An infrared spectroscopic study

Background and Aims: Hyperuricemia is a risk factor for the development of peripheral carotid and coronary vascular diseases. However, the mechanism of elevated uric acid concentration in biological systems is not yet clear.

Higher baseline uric acid concentration is associated with non-attainment of optimal blood pressure.

A significant relationship exists between elevated uric acid concentration and both prevalent and incident hypertension; however, data regarding the influence of higher uric acid concentration at baseline on blood pressure control by antihypertensive drugs is scarce. Thus, a prospective cohort study was performed. The study outcome was the non-attainment of optimal blood pressure (NOBP). NOBP level was defined according to the Japanese hypertension guideline. This study enrolled a Japanese community-based cohort (N = 8,664; age 65.5 ± 6.4 years; women, 55.0%) who were not using antihypertensive drugs on the first visit for a health check-up program but started using antihypertensive drug(s) on the next-year visit. The participants were classified into quartiles based basic uric acid concentration. Odds ratios (ORs) were calculated for NOBP as the primary outcome measure. Multivariable logistic analysis showed that quartile 4 was significantly associated with NOBP when quartile 1 was set as the reference (OR (95% confidence interval), 1.36 (1.16–1.59), p<0.01), adjusted for potential confounders, such as age, sex, body mass index, presence of diabetes/dyslipidemia/chronic kidney disease (CKD), history of cardiovascular disease, daily drinking, and current smoking. In the subgroup analysis of female participants and participants with diabetes and CKD, a significant association was observed between +1 mg/dL of uric acid and NOBP. Higher uric acid concentration at baseline was significantly associated with NOBP on the first use of antihypertensive drug(s).

Polyphenolic compounds of amla prevent oxidative stress and fibrosis in the kidney and heart of 2K1C rats.

Amla (Emblica officinalis Gaertn.) is a natural source of antioxidants and possesses valuable medicinal properties. However, the protective effect of amla in the kidney of two‐kidneys‐one‐clip (2K1C) rats has not been explained sufficiently. This study was performed to evaluate the renoprotective effect of amla fruit powder (2.5% W/W) supplementation in kidneys of 2K1C rats. 2K1C rats increased the remnant kidney wet weight and also increased plasma creatinine and uric acid concentration compared to the control. Amla supplementation ameliorates elevated creatinine and uric acid concentration in plasma of 2K1C rats. Various oxidative stress indicators such as malondialdehyde, nitric oxide (NO), and advanced protein oxidation product (APOP) were also increased in plasma, heart, and kidney tissues in 2K1C rats that were also significantly brought down to normal level by amla supplementation. Moreover, the inflammatory cells entry and fibrosis in the 2K1C rat's tissues were prevented by amla supplementation. These research results suggest that amla may restore plasma antioxidant capacities and prevents oxidative stress, inflammation, and fibrosis in 2K1C rats. Taken these results as a base, clinical supplementation of dried amla powder in diet or juice to the CKD patients would be beneficial.

Elevated Serum Uric Acid And Heart Failure In U.S. Adults: 2007-2016 NHANES

There is limited evidence examining the relationship between elevated serum uric acid (UA) concentration and heart failure (HF) in U.S. adults. PURPOSE: Examine the associations between elevated UA and HF using a nationally representative sample of U.S. adults. METHODS: The final sample with complete data for this analysis (N=17,412) included men and women aged ≥40 years who participated in the 2007-2016 National Health and Nutrition Examination Survey. Self-reported diagnosis of HF was assessed via interview. Elevated UA was defined as values >6.0 mg/dL for women and >7.2 mg/dL for men. Multivariable gender-stratified logistic regression was utilized to examine the odds of HF. RESULTS: The estimated prevalence of HF was 3.85% and 3.39% among men and women, respectively. Age adjusted analysis revealed significantly increased odds of HF in men (odds ratio [OR], 2.78; 95% confidence interval [CI] 2.09-3.71, P<0.01) and women (OR, 3.25; 95% CI 2.37-4.45, P<0.01) with elevated UA. Significance remained following adjustment for education, income, race, body mass index, alcohol consumption, hypertension, diabetes, physical activity, and creatinine in men (OR, 1.59; 95% CI 1.04-2.43 P=0.03) and women (OR, 2.03; 95% CI 1.33-3.08, P<0.01). CONCLUSIONS: In a representative sample of U.S. adults, having an elevated UA concentration was associated with significantly increased odds of HF when compared to adults with normal UA.

Hyperuricemia predicts adverse clinical outcomes after cardiac resynchronization therapy

Objectives: Changes in the levels of serum creatinine and N-terminal of prohormone brain natriuretic peptide (NT-proBNP) are useful risk markers after cardiac resynchronization therapy (CRT). The diagnostic value of changes in serum uric acid levels has been established in chronic heart failure, but no data are available on the prognostic value of hyperuricemia in a CRT population. Design: We measured markers of renal function [creatinine, blood urea nitrogen (BUN) and uric acid] and NT-proBNP levels of 129 heart failure patients undergoing CRT in a prospective, observational study. The 5-year all-cause mortality and the 6-month clinical response (≥ 15% increase in the left ventricular ejection fraction) were considered as study end points. Results: In multivariable analyses, the uric acid was found to be a statistically significant predictor of the outcome. Uric acid levels exceeding 386 mmol/L before CRT increased the chances of mortality [n = 55, hazard ratio = 2.39 (1.30-4.39), p < 0.01] and poor clinical response [n = 37, odds ratio = 2.89 (1.22-6.87), p = 0.01] independently of serum NT-proBNP and other factors. Conclusions: Elevated uric acid concentrations in patients with CRT are associated with an increased risk of mortality and poor clinical response independently of the NT-proBNP levels and other relevant clinical factors.

Correlation between Serum Uric Acid and HbA1c Levels in Patients with Type 2 Diabetes Mellitus

Background : Indonesia ranks fourth among countries with the highest number of diabetics. Increasing evidence suggests that hyperuricemia is an independent risk factor for impaired fasting glucose (IFG) and type 2 diabetes. Some observational studies have identified elevated uric acid concentration as a risk factor for diabetes, while others have found an inverse relationship. The present study was conducted to discover the strength and the direction of the correlation. Methods : This study was an analytical cross-sectional study conducted from May to October 2014. The study subjects were 56 medical records of new outpatients diagnosed with T2DM in the Internal Medicine Polyclinic who underwent laboratory examination at the Clinical Pathology Unit of Dr. Hasan Sadikin General Hospital, January-December 2013. Result : The correlation between HbA1c and uric acid levels on the whole subject revealed a weak but significant negative correlation (r=-0.354, p=0.007). There was an insignificant negative correlation in male subjects (r=-0.405, p=0.120); in female subjects (r=-0.319, p=0.05), the correlation was a weak but insignificant negative correlation. Conclusions : There is a weak correlation between HbA1c and uric acid levels in patients with Diabetes Mellitus type 2.

Salivary Biomarkers of Oxidative Stress in Children with Chronic Kidney Disease.

There are still missing non-invasive biomarkers of chronic kidney disease (CKD) in children. Therefore, the aim of the study was to evaluate oxidative stress indicators in the non-stimulated (NWS) and stimulated saliva (SWS) of CKD children (n = 25) and healthy controls (n = 25). Salivary antioxidants (catalase (CAT), peroxidase (Px), superoxide dismutase (SOD), uric acid (UA), reduced glutathione (GSH), albumin), redox status (total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI)), and oxidative damage products (advanced glycation end products (AGE), advanced oxidation protein products (AOPP), malondialdehyde (MDA)) were evaluated. We have demonstrated the significantly higher activity of SWS GPx and SOD, as well as elevated concentrations of UA and albumin in NWS and SWS of CKD children vs. the control group. TAC, TOS and OSI were significantly higher only in SWS, while oxidative damage products (AGE, AOPP and MDA) were significantly higher in both NWS and SWS of CKD children. ROC analysis showed a considerably high diagnostic value of AOPP in both NWS and SWS of CKD children compared to controls (AUC = 0.92; 0.98). CKD is responsible for disturbances in salivary antioxidant systems and oxidative damage to proteins and lipids. Salivary AOPP can be a potential biomarker of CKD in children.

Effect of fenofibrate on uric acid and gout in type 2 diabetes: a post-hoc analysis of the randomised, controlled FIELD study

Gout is a painful disorder and is common in type 2 diabetes. Fenofibrate lowers uric acid and reduces gout attacks in small, short-term studies. Whether fenofibrate produces sustained reductions in uric acid and gout attacks is unknown. In the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial, participants aged 50-75 years with type 2 diabetes were randomly assigned to receive either co-micronised fenofibrate 200 mg once per day or matching placebo for a median of 5 years follow-up. We did a post-hoc analysis of recorded on-study gout attacks and plasma uric acid concentrations according to treatment allocation. The outcomes of this analysis were change in uric acid concentrations and risk of on-study gout attacks. The FIELD study is registered with ISRCTN, number ISRCTN64783481. Between Feb 23, 1998, and Nov 3, 2000, 9795 patients were randomly assigned to fenofibrate (n=4895) or placebo (n=4900) in the FIELD study. Uric acid concentrations fell by 20·2% (95% CI 19·9-20·5) during the 6-week active fenofibrate run-in period immediately pre-randomisation (a reduction of 0·06 mmol/L or 1 mg/dL) and remained -20·1% (18·5-21·7, p<0·0001) lower in patients taking fenofibrate than in those on placebo in a random subset re-measured at 1 year. With placebo allocation, there were 151 (3%) first gout events over 5 years, compared with 81 (2%) among those allocated fenofibrate (HR with treatment 0·54, 95% CI 0·41-0·70; p<0·0001). In the placebo group, the cumulative proportion of patients with first gout events was 7·7% in patients with baseline uric acid concentration higher than 0·36 mmol/L and 13·9% in those with baseline uric acid concentration higher than 0·42 mmol/L, compared with 3·4% and 5·7%, respectively, in the fenofibrate group. Risk reductions were similar among men and women and those with dyslipidaemia, on diuretics, and with elevated uric acid concentrations. For participants with elevated baseline uric acid concentrations despite taking allopurinol at study entry, there was no heterogeneity of the treatment effect of fenofibrate on gout risk. Taking account of all gout events, fenofibrate treatment halved the risk (HR 0·48, 95% CI 0·37-0·60; p<0·0001) compared with placebo. Fenofibrate lowered uric acid concentrations by 20%, and almost halved first on-study gout events over 5 years of treatment. Fenofibrate could be a useful adjunct for preventing gout in diabetes. None.

Impact of Hyperuricemia on Long-term Outcomes of Kidney Transplantation: Analysis of the FAVORIT Study

Elevated uric acid concentration is associated with higher rates of cardiovascular (CV) morbidity and mortality in the general population. It is not known whether hyperuricemia increases the risk for CV death or transplant failure in kidney transplant recipients. Post hoc cohort analysis of the FAVORIT Study, a randomized controlled trial that examined the effect of homocysteine-lowering vitamins on CV disease in kidney transplantation. Adult recipients of kidney transplants in the United States, Canada, or Brazil participating in the FAVORIT Study, with hyperhomocysteinemia, stable kidney function, and no known history of CV disease. Uric acid concentration. The primary end point was a composite of CV events. Secondary end points were all-cause mortality and transplant failure. Risk factors included in statistical models were age, sex, race, country, treatment assignment, smoking history, body mass index, presence of diabetes mellitus, history of CV disease, blood pressure, estimated glomerular filtration rate (eGFR), donor type, transplant vintage, lipid concentrations, albumin-creatinine ratio, and uric acid concentration. Cox proportional hazards models were fit to examine the association of uric acid concentration with study end points after risk adjustment. 3,512 of 4,110 FAVORIT participants with baseline uric acid concentrations were studied. Median follow-up was 3.9 (IQR, 3.0-5.3) years. 503 patients had a primary CV event, 401 died, and 287 had transplant failure. In unadjusted analyses, uric acid concentration was significantly related to each outcome. Uric acid concentration was also strongly associated with eGFR. The relationship between uric acid concentration and study end points was no longer significant in fully adjusted multivariable models (P=0.5 for CV events; P=0.09 for death, and P=0.1 for transplant failure). Unknown use of uric acid-lowering agents among study participants. Following kidney transplantation, uric acid concentrations are not independently associated with CV events, mortality, or transplant failure. The strong association between uric acid concentrations with traditional risk factors and eGFR is a possible explanation.

Elevated uric acid and adenosine triphosphate concentrations in bronchoalveolar lavage fluid of eosinophilic pneumonia

BackgroundRecent evidence has suggested that the innate immune response may play a role in the development of eosinophilic airway inflammation. We previously reported that uric acid (UA) and adenosine triphosphate (ATP), two important damage-associated molecular pattern molecules (DAMPs), activate eosinophil functions, suggesting that these molecules may be involved in the development of eosinophilic airway inflammation. The objective of this study was to measure the concentrations of DAMPs including UA and ATP in the bronchoalveolar lavage fluid (BALF) of patients with eosinophilic pneumonia (EP). MethodsBAL was performed in patients with EP including acute and chronic eosinophilic pneumonia, and in patients with hypersensitivity pneumonia, and sarcoidosis. UA, ATP, and cytokine concentrations in the BALF were then measured. ResultsThe UA concentration was increased in the BALF of EP patients. UA concentrations correlated with eosinophil numbers, and with eosinophil-derived neurotoxin and interleukin (IL)-5 concentrations. Furthermore, the ATP concentration was increased in the BALF of EP patients and ATP concentrations correlated with UA concentrations. Moreover, IL-33 was increased in EP patients and IL-33 concentrations correlated with UA and ATP concentrations. ConclusionsThe UA and ATP concentration was increased in the BALF of EP patients. UA concentrations correlated with eosinophil numbers, and with ATP and IL-33 concentrations. Our findings suggest that DAMPs such as UA and ATP play a role in the pathogenesis of EP.

The Association Between Hyperuricemia in first Trimester and the Development of Gestational Diabetes

Objective: This study aimed to assess the accuracy of the elevation of serum uric acid in the first trimester as a predictive test for development of gestational diabetes mellitus. Patientsand methods: It was a prospective observational study included 200 pregnant patients who were regularly attending the out-patient clinic for routine antenatal care to find if the elevated first trimester uric acid is associated with development of GDM or not. Results: The risk of developing GDM was higher if first-trimester uric acid was &lt; 3.1 mg/dI. Women who developed GDM were significantly older when they compared to women who did not develop GDM [Normal with Mean + SD 24.53 + 4.40 years, Abnormal with Mean + SD 32.78 + 8.18 years, p-value 0.016]. It was found that, the mean BMI was significantly higher in women who developed GDM when compared to women who did not develop GDM [Normal 115 cases of total sample and no one developed GD with Mean + SD, 95.57 + 12.32, Overweight 59 cases, 56 cases (29.3%) were normal and 3 cases (33.3%) had GD with Mean + SD 106.29 + 26.62, Obese 26 cases, 20 cases (10.5%) were normal and 6 cases (66.7%) had GD with Mean + SD 124.27 + 39.78, p-value 0.000]. Conclusion: Elevated first-trimester uric acid concentration was correlated with an increased risk of developing GDM.

Serum uric acid concentrations are directly associated with the presence of benign multiple sclerosis.

It has been reported that patients with multiple sclerosis (MS) exhibit lower serum uric acid levels; however, the association between uric acid concentrations and benign MS (BMS) has not been assessed. Hence, the objective of the present study was to determine whether the serum concentrations of uric acid are associated with the presence of BMS. Men and non-pregnant women over 16years of age with diagnosis of MS were enrolled in a cross-sectional study. Expanded Disability Status Scale score<3, progression of disease ≤10years, diabetes, renal or hepatic diseases, gout, malignancy, alcohol intake, and treatment with thiazide diuretics and/or acetylsalicylic acid were exclusion criteria. According to subtype of disease, the eligible patients were allocated into groups with BMS and other varieties of MS. A logistic regression analysis was conducted in order to evaluate the association between serum concentrations of uric acid and BMS. A total of 106 patients were included, 39 in the group with BMS and 67 in the group with other varieties of MS. The logistic regression analysis adjusted by age, sex, and disease duration showed that increased concentrations of uric acid, indeed within the physiological levels, are significantly associated with the presence of BMS (OR=2.60; 95% CI: 1.55-4.38, p<0.001). The results of the present study suggest that elevated concentrations of uric acid, indeed within the physiological range, are likely linked to the presence of BMS.