Elevated Uric Acid Levels Research Articles

Uric acid plasma levels are associated with C-reactive protein concentrations and the extent of coronary artery lesions in patients with acute coronary syndromes.

Many studies have pointed out that inflammation plays a pivotal role in pathophysiology of acute coronary syndromes (ACS) because several inflammatory molecules impair the endothelial functions in the coronary circulation and promote atherothrombotic events. Recently, many clinical/experimental evidences indicate that elevated plasma levels of uric acid (UA) might be considered a risk factor for developing ACS. It has been reported that elevated UA doses impair physiologic functions of endothelial cells, shifting them toward a pro atherothrombotic phenotype. In the present manuscript, we investigated the relationship between UA plasma levels, inflammatory burden, and extension of coronary atherosclerotic disease in patients with ACS. Patients with a clinical presentation of ACS (ST-elevated and non-ST-elevated myocardial infarction) admitted to the Vanvitelli Catheterization Laboratory at Monaldi Hospital in 2019, before the COVID-19 pandemia, were retrospectively analyzed. Biochemical profile, type of ACS presentation, as well as extension of coronary atherosclerosis were assessed. A total of 132 ACS patients were included in the analysis, and grouped into 3 tertiles according to the UA values (UA < 4.72mg/dl, UA between 4.72 and 6.15mg/dl, and UA > 6.15mg/dl). Patients with UA plasma levels ≥ 6.15mg/dL showed higher levels of C-reactive protein (mean of 5.1mg/dL) as compared to patients with lower UA plasma levels. Moreover, the former group of patients showed higher levels of cardiac troponin and CPK, and presented more often with multivessel disease and complex coronary stenosis (type C of Ellis classification). Even though monocentric and with limited sample size, the present study shows that plasma levels of UA and hs-CRP are elevated in ACS patients and are associated with a more severe coronary disease, suggesting a potential role of UA in the pathophysiology of acute coronary events.

Purine-ifying uric acid by gut microbes

Elevated bloodstream levels of uric acid, a mammalian purine degradation product, are associated with several noncommunicable diseases. Recent studies by Kasahara etal. and Liu etal. define purine-degrading activities of the gut microbiota that lower bloodstream uric acid in atherosclerosis and gout disease models, establishing a novel microbial role in host health.

Risk due to Elevated Uric Acid Levels in Children With Henoch-Schonlein Purpura.

To compare uric acid levels in children with Henoch-Schonlein purpura (HSP)without nephritis and with renal damage, and at different pathological grades. A total of 451 children were enrolled in this study, including 64 with HSP without nephritis and 387 HSP with kidney damage. Age, gender, uric acid, urea, creatinine and cystatin C levels were reviewed. Pathological findings of those with renal impairment were also reviewed. Among the HSP children with renal damage, 44 were grade I, 167 were grade II and 176 were grade III. There were significant differences in age, uric acid, urea, creatinine and cystatin C levels between the two groups (p<0.05, all). Correlation analysis showed that uric acid levels in children with HSP without nephritis were positively correlated with urea and creatinine levels (p<0.05). Uric acid levels in HSP children with renal damage was positively correlated with age, urea, creatinine and cystatin C levels (p<0.05, all). Regression analysis found that, without adding any correction factors, there were significant differences in uric acid levels between the two groups; however, after adjusting for pathological grade, there was no longer a significant difference. There were significant differences of uric acid levels in children with HSP without nephritis and with renal impairment. Uric acid levels in the renal impairment group were significantly higher than that in the HSP without nephritis group. Uric acid levels were related to only the presence or absence of renal damage, not to the pathological grade.

Unveiling the Silent Danger of Childhood Obesity: Non-Invasive Biomarkers Such as Carotid Intima-Media Thickness, Arterial Stiffness Surrogate Markers, and Blood Pressure Are Useful in Detecting Early Vascular Alterations in Obese Children.

Obese children present a higher cardio-metabolic risk. Measuring vascular biomarkers that assess the evolution of arterial stiffness, subclinical atherosclerosis, and hypertension in such patients could be helpful in the long term. We studied 84 children, aged from 6 to 18 years: 50 obese subjects, versus 34 of normal weight. Clinical examination involved: BMI, waist circumference, waist-to-height ratio, and detection of the presence of acanthosis nigricans and irregular menstrual cycles (the latter in adolescent girls). The carotid intima-media thickness (CIMT) was measured with the Aixplorer MACH 30 echography device. The pulse wave velocity (PWV), augmentation index (AIx), and peripheral and central blood pressures (i.e., SBP, DBP, cSBP, cDBP, and cPP) were acquired through a Mobil-O-Graph device. Obese subjects underwent body composition analysis with a Tanita BC-418. Blood tests were: HOMA-IR, lipid panel, uric acid, and 25-OH vitamin D. All vascular biomarkers presented increased values in obese subjects versus controls. The following cut-off values were significant in detecting obesity: for PWV > 4.6 m/s, cSBP > 106 mmHg for the <12-year-olds, PWV > 4.5 m/s and cSBP > 115 mmHg for the 12-15-year-olds, and PWV > 5 m/s, cSBP > 123 mmHg for the >15-year-olds. AIx is higher in obese children, regardless of their insulin resistance status. Waist circumference and waist-to-height ratio correlate to all vascular parameters. HOMA-IR is an independent predictor for all vascular parameters except CIMT. Cut-off values for PWV of >4.8 m/s, SBP > 125 mmHg, and a cSBP > 117 mmHg predicted the presence of acanthosis nigricans. Obese girls with irregular menses displayed significantly higher PWV, SBP, and DPB. Elevated levels of uric acid, LDL-c, non-LDL-c, triglycerides, and transaminases, and low levels of HDL-c and 25-OH vitamin D correlated with higher arterial stiffness and CIMT values. We conclude that CIMT and the markers of arterial stiffness are useful in the early detection of vascular damage in obese children.

Investigation of the Inhibition Mechanism of Xanthine Oxidoreductase by Oxipurinol: A Computational Study.

Xanthine oxidoreductase (XOR) is an enzyme found in various organisms. It converts hypoxanthine to xanthine and urate, which are crucial steps in purine elimination in humans. Elevated uric acid levels can lead to conditions like gout and hyperuricemia. Therefore, there is significant interest in developing drugs that target XOR for treating these conditions and other diseases. Oxipurinol, an analogue of xanthine, is a well-known inhibitor of XOR. Crystallographic studies have revealed that oxipurinol directly binds to the molybdenum cofactor (MoCo) in XOR. However, the precise details of the inhibition mechanism are still unclear, which would be valuable for designing more effective drugs with similar inhibitory functions. In this study, molecular dynamics and quantum mechanics/molecular mechanics calculations are employed to investigate the inhibition mechanism of XOR by oxipurinol. The study examines the structural and dynamic effects of oxipurinol on the pre-catalytic structure of the metabolite-bound system. Our results provide insights on the reaction mechanism catalyzed by the MoCo center in the active site, which aligns well with experimental findings. Furthermore, the results provide insights into the residues surrounding the active site and propose an alternative mechanism for developing alternative covalent inhibitors.

Corn Silk Flavonoids Ameliorate Hyperuricemia via PI3K/AKT/NF-κB Pathway.

Hyperuricemia (HUA) is a widespread metabolic disease marked by an elevated level of uric acid, and is a risk factor for premature death. The protective effect of corn silk flavonoids (CSF) against HUA and its potential mechanisms were explored. Five important apoptosis and inflammation-related signaling pathways were identified by network pharmacological analysis. The CSF exhibited significant uric acid (UA)-lowering activity in vitro by decreasing xanthine oxidase (XOD) and increasing hypoxanthine-guanine phosphoribosyl transferase levels. In a potassium oxonate-induced HUA in vivo, CSF treatment effectively inhibited XOD activity and promoted UA excretion. Furthermore, it decreased the levels of TNF-α and IL-6 and restored pathological damage. In summary, CSF is a functional food component to improve HUA by reducing inflammation and apoptosis through the down-regulating PI3K/AKT/NF-κB pathway.

The role of uric acid in the development of infl ammation in kidney disease

Asymptomatic hyperuricemia is frequently seen in patients with kidney disease. A significant number of epidemiological studies suggest that elevated uric acid levels play a causal role in the development and progression of kidney disease. But whether hyperuricemia is simply the result of reduced renal excretion of uric acid or contributes to the progression of renal disease remains controversial. Over the past two decades, numerous experimental studies have expanded the knowledge of the biological effects of uric acid beyond its role in the development of gout. In particular, uric acid induces activation of the immune system and affects not only renal tissue cells but also endothelial cells. All this has led to the presentation of uric acid as a potential and modifying risk factor for kidney disease. This review examines the effects of uric acid on the immune system and further on renal tissue during inflammation.

Estradiol protects female mice from hyperuricemia induced by PCB138 exposure

Polychlorinated biphenyls (PCBs) are a type of persistent organic pollutant (POP). Our previous study demonstrated that exposure to 0.5–50 μg/kg bw PCB138 during postnatal days (PND) 3–21 led to elevated serum uric acid (UA) levels and kidney injury in adult male mice. Given that the prevalence of hyperuricemia (HUA) is significantly lower in women than in men, it is worth investigating whether POP-induced HUA and its secondary kidney injury have sexual dimorphism. Herein, we exposed female mice to 0.5–50 μg/kg bw PCB138 during PND 3–21, resulting in elevated serum UA levels, but without causing significant kidney damage. Concurrently, we found a negative correlation between serum 17β-estradiol (E2) and serum UA levels. We also observed down-regulation of estrogen receptor (ER) protein levels in the kidneys of the PCB138-exposed groups. Furthermore, our study showed that E2 rescued the increased UA level and cytotoxicity caused by HUA in human renal tubular epithelial (HK-2) cells. Collectively, our findings suggest that E2 likely plays a crucial protective role in PCB138-induced HUA and kidney injury in female mice. Our research highlights the existence of sexual dimorphism in kidney injury secondary to HUA induced by POPs, which could provide guidance for individuals of different genders in preventing kidney injury caused by environmental factors.

ANMCO statement: Uric acid and cardiovascular disease: evidence and therapeutic approach

Pathophysiologic processes promoted by uric acid, including inflammation and oxidative stress, play a key role in the pathogenesis of several cardiovascular diseases. Furthermore, a number of epidemiological studies have shown an association between uric acid plasma levels and multiple cardiovascular risk factors. This ANMCO statement provides an update on available evidence regarding the association between elevated plasma uric acid levels and cardiovascular disease risk and the safety and efficacy of uric acid lowering agents (allopurinol and febuxostat) used in patients with urate crystal deposits. In addition, it summarizes practical indications for the use of these drugs in at-risk patients or in patients with cardiovascular disease.

Incidence, clinical characteristics and prognosis of tumor lysis syndrome following B-cell maturation antigen-targeted chimeric antigen receptor-T cell therapy in relapsed/refractory multiple myeloma.

B-cell maturation antigen (BCMA)-targeted chimeric antigen receptor-T cell (CAR-T) therapy is used for refractory or relapsed multiple myeloma (r/r MM). However, CAR-T-related tumor lysis syndrome (TLS) has been observed. We aimed to elucidate the incidence, clinical and laboratory characteristics, and prognosis of CAR-T cell-related TLS. Patients (n=105) with r/r MM treated with BCMA-targeted CAR-T cell therapy were included. Patient characteristics, laboratory parameters, and clinical outcomes were assessed. Eighteen (17.1%) patients developed TLS after BCMA-targeted CAR-T cell therapy. The median time till TLS onset was 8 days. Patients with TLS had steep rise in uric acid (UA), creatinine, and lactate dehydrogenase (LDH) within 6 days following CAR-T cell infusion and presented earlier and persistent escalation of cytokines (C-reactive protein [CRP], interleukin-6 [IL-6], interferon-γ [IFN-γ], and ferritin levels). All 18 patients had cytokine release syndrome (CRS), of which 13 (72.2%) developed grade 3-4 CRS. Three of 18 patients (16.7%) developed immune effector cell-associated neurotoxicity syndrome (ICANS): two patients with grade 1 ICANS and one with grade 2 ICANS. TLS development had a negative effect on the objective response rate (77.8% in the TLS group vs. 95.4% in the non-TLS group, p<0.01). During the median follow-up of 15.1 months, the median PFS was poorer of patients with TLS (median: 3.4 months in the TLS group vs. 14.7 months in the non-TLS group, p<0.001, hazard ratio [HR]=3.5 [95% confidence interval [CI] 1.5-8.5]). Also, TLS development exhibited significant effects on OS (median: 5.0 months in the TLS group vs. 39.8 months in the non-TLS group, p<0.001, hazard ratio [HR]=3.7 [95% CI 1.3-10.3]). TLS was associated with a higher tumor burden, elevated baseline creatinine and UA levels, severe CRS, pronounced CAR-T cell expansion, and corticosteroid use. TLS is a frequently observed CAR-T therapy complication and negatively influences clinical response and prognosis. Close monitoring for TLS should be implemented during CAR-T cell therapy, especially for those at high TLS risk.

Impaired sensitivity to thyroid hormones is associated with hyperuricemia in a Chinese euthyroid population.

Impaired sensitivity to thyroid hormones has been reported as a common metabolic disorder, and it remains poorly understood whether it interplays with uric acid (UA) metabolism as an established risk factor for cardiovascular diseases (CVDs). We aimed to investigate the relationship between thyroid hormone sensitivity and elevated UA in a Chinese euthyroid population. A total of 15,955 euthyroid subjects were included in this study. Thyroid hormone sensitivity indices were calculated, including the thyroid feedback quantile-based index (TFQI), the Chinese-referenced parametric TFQI (PTFQI), the TSH index (TSHI), and the thyrotropin thyroxine resistance index (TT4RI), and the FT3/FT4 ratio. Linear and logistic regression analyses were performed to detect the association between thyroid hormone sensitivity and elevated UA. Subjects with reduced sensitivity to thyroid hormones had increased UA levels in both genders (p for trend < 0.001). Logistic and linear regression analyses showed that higher TFQI, PTFQI, TSHI, and TT4RI were positively associated with elevated UA levels, but negatively associated with the FT3/FT4 ratio. The odds ratio (OR) of the highest versus the first quartile of TFQI was 1.20 (1.05, 1.38) in men and 1.80 (1.46, 2.23) in women (p < 0.001). PTHQI, TSHI, and TT4RI obtained similar results in both genders. Conversely, the highest quartile of the FT3/FT4 ratio was negatively correlated with elevated UA levels [men: OR 0.78 (0.68,0.89), women: OR 0.66 (0.53,0.81)]. Impaired sensitivity to thyroid hormones was associated with elevated UA levels in euthyroid subjects. Our findings shed light on the role of thyroid hormone sensitivity in UA metabolism.

Role of serum uric acid in acute myocardial infarction as a prognostic marker, in a tertiary care center of South-Eastern Rajasthan

Abstract Introduction: Myocardial infarction (MI) is a leading cause of death worldwide, and myocardial cell death is associated with increased uric acid production. Therefore, in the underlying tissue death, the increased uric acid level can be used as a prognostic marker in MI, concerning Killip’s classification. Materials and Methods: Our study included 100 diagnosed cases of acute MI with 100 controls admitted to SRG Hospital, Jhalawar, Rajasthan, India. A meticulous clinical history and physical examination with special reference to the Killip class were carried out. All the routine investigations, including complete blood count, renal function test, liver function test, electrocardiogram, cardiac markers, and chest X-ray, were done on admission. Serum uric acid levels were measured on days 0, 3, and 7 of MI. Hyperuricemia is labeled in our study for males &gt;7 mg/dL and females &gt;5 mg/dL. Results: Our study included 63 males and 37 females as cases. On admission, we found statistically significant elevated levels of uric acid in patients with acute MI compared with controls. The higher Killip class patients had higher uric acid levels on days 0, 3, and 7, irrespective of their sex and history of hypertension and diabetes mellitus. During our study, four patients died within 5 days of admission and had higher serum uric acid levels, that is, &gt;7 mg/dL, and all of them were included in Killip class IV, irrespective of sex. Conclusion: Patients of acute MI with higher Killip class had elevated serum uric acid levels. The serum uric acid levels correlate with the Killip class and are an evident predictor of mortality and morbidity after acute MI.

Can We Take Hyperuricemia as a Cardiovascular Risk?

Study conducted for Gouty arthritis at Pan Pakistan level in 2017 showed mean Uric Acid levels of 6.11±1.7mg/dl with frequency of hyperuricemia of 39% and having 27.9% male and 49.35 women respectively.1 This type of arthritis results from monosodium urate crystal deposition in and around the joints affecting big toe around the joints of hands and feet. Gout has been shown to increase with age and associated with diabetes &amp; hypertension.2,3 It has also been shown that hyperuricemia may be tied to increased risk of cardiovascular disease mortality.4 Hyperuricemia has also shown to increase atherosclerosis by systemic inflammation and oxidative stress. It also causes endothelial dysfunction and oxidation of lipoproteins with formation of atherosclerotic plaques.5 Recent studies have shown hypertension, coronary artery disease, cardiovascular diseases, vascular dementia and preclampsia to be associated with high uric acid levels. The studies include Rotterdam (Serum Uric Acid Level and Myocardial infraction),2 PUMA study (Serum Uric Acid levels with cardiovascular events and deaths in hypertensive patients),6 PAMELA study (increased risk of cardiovascular deaths with increase of every 1mg /dl).4 Three important co-relation i.e. Hyperuricemia, atherosclerosis and heart failure need bit of understanding. In one study elevated uric acid levels (75.5mg/dl) in 90% of adolescents with essential hypertension7 and lower uric acid levels in teens with either white coat or secondary hypertension.7 Secondly association between increased uric acid levels and coronary artery calcification has shown an independent risk factor for subclinical atherosclerosis in young adults.8 Similar association was also seen in atherosclerotic vulnerable carotid plaque.9 Thirdly in cardiovascular health study incidence of heart failure was 21% with Chronic hyperuricemia and 18% without.10 For management of hyperuricemia (gout) multidisciplinary approach involving primary care physicians, rheumatologist and cardiologists might improve associated cardiovascular diseases other than primary pathology. Drugs like non-steroidal anti-inflammatory drug (NSAIDS), steroids &amp; colchicine may improve Gout but improvement in cardiovascular comorbids are questionable.11,12 Though different epidemiological studies have shown hyperuricemia as an independent risk factor for cardiovascular diseases and hypertension. Further studies are needed that my elucidate association of increased uric acid level with cardiovascular diseases. Multidisciplinary approach, awareness and counselling patient will hopefully prevent onset of heart disease and improve survival outcomes for gouty patients.

Clinical and diagnostic features of uncontrolled hypertension and including hypertensive crisis

Aim. To study clinical and diagnostic data, risk factors, the state of target organs damage (TOD) and prevalence of clinical associated conditions in patients with a hypertensive crisis and uncontrolled arterial hypertension.Materials and methods. The study included 297 patients hospitalized at the E.I. Chazov National Medical Research Center of Cardiology over the period from September 2019 to March 2022 with the presence of uncontrolled hypertension (blood pressure (BP) above 140/90 mm Hg while taking antihypertensive therapy). Patients were spread into two groups depending on the increase in the frequency of BP: group 1 (n=149) – uncontrolled hypertension with a hypertensive crisis (increase in BP 1 or more per week and/or the presence of severe clinical symptoms), and group 2 (n=148) – uncontrolled hypertension (increase in blood pressure more than 140/90 mm Hg less than 1 per week and/ or without severe clinical symptoms). The presence of risk factors in these groups was analyzed. At the baseline and after 12 months, the presence and severity of TOD (left ventricular mass index (LVMI), chronic kidney disease (CKD), severe retinopathy), history of/occurrence of clinical associated conditions were assessed.Results. There are significant elevated levels of uric acid, triglycerides, body mass index, heart rate, blood pressure indicators among the risk factors in the group of patients with hypertensive crisis. Patients in the group 1 showed higher rates of LVMI at the baseline and during follow-up for 12 months (baseline – 107±28 g/m2, after a year of follow-up 112±27 g/m2). The glomerular filtration rate (GFR) is lower in patients with hypertensive crisis (initially – 81.5±19.04 ml/min/1.73m2, after 12 months of observation 74.8±18.06 ml/min/1.73m2). There are significant differences in coronary artery disease, atherosclerosis of the brachiocephalic arteries, type 2 diabetes mellitus (DM 2) among clinical associated conditions. After 12 months of observation, acute cerebrovascular accident, coronary artery disease and diabetes occur more often in group 1.Conclusion. Uncontrolled hypertension with a hypertensive crisis manifestation is a release of hypertension associated with severe TOD and a high prevalence of clinical associated conditions.

Association between hyperuricemia and chronic kidney disease: a cross-sectional study in Bangladeshi adults

Background and aimsChronic kidney disease (CKD) is a public health concern worldwide and has been recognized as a significant risk factor for cardiovascular disease. The elevated level of uric acid (hyperuricemia) has been suggested to be associated with obesity, hypertension, cardiovascular disease and diabetes. However, there is limited information on the relationship between hyperuricemia and CKD. Therefore, this study aimed to estimate the prevalence of CKD and assess its relationship with hyperuricemia in Bangladeshi adults.MethodsIn this study, blood samples were collected from 545 participants (398 males and 147 females) aged ≥ 18 years. Biochemical parameters such as serum uric acid (SUA), lipid profile markers, glucose, creatinine and urea were measured by colorimetric methods. The estimated glomerular filtration rate (eGFR) and CKD were determined based on serum creatinine levels with existed formula. Multivariate logistic regression analysis was performed to evaluate the association between SUA and CKD.ResultsThe overall prevalence of CKD was 5.9% with 6.1% in males and 5.2% in females. Hyperuricemia was prevalent in 18.7% of participants with 23.2% in males and 14.6% in females. An increasing trend of CKD prevalence was observed with increasing age in the groups. The mean eGFR level was significantly lower in male (95.1 ± 31.8 ml/min/1.73m2) than in female (109.3 ± 77.4 ml/min/1.73m2) subjects (p < 0.01). The mean level of SUA was significantly higher (p < 0.01) in participants having CKD (7.1 ± 1.9 mg/dL) than in participants without CKD (5.7 ± 1.6 mg/dL). A decreasing trend for eGFR concentration and an increasing trend for CKD prevalence was observed across the SUA quartiles (p < 0.001). In regression analysis, a significant positive association was found between hyperuricemia and CKD.ConclusionThis study showed an independent association between hyperuricemia and CKD in Bangladeshi adults. Further mechanistic studies are needed to explore the potential link between hyperuricemia and CKD.

Alleviation of Hyperuricemia by Strictinin in AML12 Mouse Hepatocytes Treated with Xanthine and in Mice Treated with Potassium Oxonate

Hyperuricemia, an abnormally high level of blood uric acid, is a major risk factor for gout. Although xanthine oxidase inhibitors were clinically used to lower blood uric acid level, the concerned side effects restricted their utilization. In this study, strictinin, an abundant polyphenol in Pu'er tea, was evaluated for its preventive effects on hyperuricemia. The results showed that the xanthine oxidase activity, uric acid production, and inflammation in AML12 mouse hepatocytes treated with xanthine were significantly reduced by the supplementation of strictinin. Detailed analyses revealed that strictinin inhibited xanthine-induced NLRP3 inflammasome activation. Consistently, the elevated blood uric acid level and the enhanced xanthine oxidase activity in mice treated with potassium oxonate were effectively diminished by strictinin supplementation. Moreover, for the first time, strictinin was found to promote healthy gut microbiota. Overall, strictinin possesses a great potential to be utilized as a functional ingredient for the prevention of hyperuricemia.

Predictability of gestational diabetes mellitus using first trimester Serum uric acid levels

Introduction: For both mothers and fetuses, gestational diabetes mellitus (GDM) causes major morbidity and mortality in the Indian population. In pregnancy, serum uric acid levels are higher. Elevated first-trimester uric acid levels can be used to predict GDM. Study Design: In 1055 plasma samples taken at a mean gestational age of 9 ±2.1 weeks, uric acid was determined. The three-hour glucose tolerance test used to identify GDM as the main outcome. Results: The percentage of GDM was significantly high among the higher age group with 19.2% among 30-35 years of age and 25.8% among 35-40 years of age. With almost 35% of cases, GDM was most prevalent in the obese category. Among 348 patients with a confirmed family background of diabetes mellitus, 19.5% of pregnant women developed GDM. Uric acid levels were found significantly higher among GDM subjects both in first and second trimesters than in non-GDM subjects. Additionally, both normal and GDM individuals, serum uric acid levels were observed to be significantly greater in the second trimester than the first. Conclusion: First trimester hyperuricemia is linked to a higher chance of developing GDM.

A Study on Acute Myocardial Infarction and Its Prognostic Predictors.

Introduction Acute Myocardial Infarction (AMI) is a serious cardiac event characterized by the sudden death of heart muscle tissue due to the obstruction of blood flow to the heart. It is a leading cause of death and disability worldwide. The relationship between AMI and serum uric acid levels is an area of ongoing research. Serum uric acid is a byproduct of purine metabolism and is typically present in the blood at low levels. Elevated levels of uric acid have been linked to several cardiovascular risk factors, including hypertension, diabetes, and hyperlipidemia. This has led to the investigation of the relationship between uric acid levels and AMI. Materials and Methods In this study, 100 individuals who were presented with acute myocardial infarction were included. All patients were categorized into four Killip's classes based on history, clinical examination, and lab investigation. Subsequently, the four Killip's classes were co-related with the serum uric acid of the patient. Results Serum uric acid levels were high in males compared to females. serum uric acid levels were high in Killip's class III (7.24) and IV (7.57) compared to class I (4.48) and II (5.26). There was no significant correlation between serum uric acid and the co-morbidities like diabetes and hypertension, with a p-value of 0.48. Conclusion An increase in Killip Class is positively correlated with an increase in blood uric acid levels. Uric acid can therefore be utilized as a prognostic indicator in individuals who present with myocardial infarction.

Possible Colchicine Poisoning: Case Study

We have experienced a case of colchicine toxicity presenting with rapidly progressive gastrointestinal symptoms, hemodynamic instability, and multiple organ failure.&#x0D; An 86-year-old Japanese man presented to our hospital with subarachnoidal hemorrhage transferring from another hospital where he had been treated with colchicine 0.5 mg three times daily for an elevated uric acid level. During his admission, he had a nosocomial COVID-19 infection. Then, he developed loss of appetite, and significant diarrhea, which continued for two days. He then developed shock and hypoxia and was transferred to intensive care unit (ICU). The laboratory data revealed pancytopenia, acute kidney injury, lactic acidosis, marked coagulopathy, elevated troponin I, and C-reactive protein with poor cardiac function and hypotension refractory to vasopressors. Despite intensive care, he expired on 2nd day of ICU admission. Because his cardiac function was depressed from the beginning and was not respond to inotropic support, direct myocardial damage, rather than septic cardiomyopathy was suspected. We, therefore, emphasize that colchicine poisoning should be suspected in patients with access to the drug and the typical toxidrome.

Identification of end‐stage renal disease metabolic signatures from human perspiration

AbstractEnd‐stage renal disease (ESRD), characterized by cessation in kidney function, has been linked to severe metabolic disturbances, caused by the buildup of toxic solutes in blood. To remove these solutes, ESRD patients undergo dialysis. As a proof of concept, we tested whether ESRD‐related metabolic signatures can be detected in perspiration samples using a combined methodology. Our rapid methodology involves swabbing a glass slide across the patient's forehead, detecting the metabolites in the imprint using desorption electrospray ionization mass spectrometry, and identifying the key differences using machine learning methods. Based on collecting 42 healthy and 27 ESRD samples, we find saturated fatty acids are consistently suppressed in ESRD patients, with little change after dialysis. Moreover, our method enables the detection of uremic solutes, where we find elevated levels of uric acid (6.7 fold higher on average) that sharply decrease after dialysis. Beyond the study of individual metabolites, we find that a lasso model, which selects for 8 m/z fragments from 24,602 detected analytes, achieves area under the curve performance of 0.85 and 0.87 on training (n = 52) and validation sets (n = 17), respectively. Together, these results suggest that this methodology is promising for detecting signatures relevant for precision health.Key points Combines physical measurements with statistical analysis based on machine learning. Uses results to make medical predictions. Learns about biological pathways.