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Fukui S, Okada M, Shinozaki T, Asano T, Nakai T, Tamaki H, Kishimoto M, Hasegawa H, Matsuda T, Marrugo J, Tedeschi SK, Choi H, Solomon DH. Changes in alcohol intake and serum urate changes: longitudinal analyses of annual medical examination database. Ann Rheum Dis 2024; 83:1072-1081. [PMID: 38418204 PMCID: PMC11250628 DOI: 10.1136/ard-2023-225389] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/07/2023] [Accepted: 02/16/2024] [Indexed: 03/01/2024]
Abstract
INTRODUCTION Despite the established cross-sectional association between alcohol intake and serum urate (SU), its longitudinal association remains unknown. This study aimed to determine whether changes in alcohol intake have a clinically relevant association with SU change. METHOD We conducted retrospective analyses using systematically collected annual medical examination data from October 2012 to October 2022 in a Japanese preventive medicine centre. The exposure was changes in alcohol intake between two consecutive visits. The association of SU changes with alcohol intake changes was estimated by mixed-effect linear regression with adjustment for relevant covariates. RESULTS We analysed 63 486 participants (median age, 47.0 years; 55% women; 58.6% regular alcohol drinkers with a median of 1.4 drinks/day) with 370 572 visits. The median SU level was 5.3 mg/dL, and 506 (0.8%) participants had diagnoses of gout or hyperuricemia without medication use during the study period. Decreasing one daily alcohol intake had a clinically small association with SU changes (-0.019 (95% CI: -0.021 to -0.017) mg/dL). Beer had the largest association with SU (-0.036 (95% CI: -0.039 to -0.032) mg/dL for one beer decrease). Complete discontinuation of any alcohol from a mean of 0.8 drinks/day was associated with -0.056 mg/dL (95% CI: -0.068 to -0.043) decrease in SU; the association became larger in hyperuricemic participants (-0.110 mg/dL (95% CI: -0.154 to -0.066) for alcohol discontinuation from a mean of 1.0 drinks/day). CONCLUSIONS This study revealed changes in alcohol intake had small associations with SU change at the general Japanese population level. Complete discontinuation of alcohol in hyperuricemic participants had only modest improvement in SU.
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Affiliation(s)
- Sho Fukui
- Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA
- Immuno-Rheumatology Center, St. Luke's international Hospital, Tokyo, Japan
- Department of Emergency and General Medicine, Kyorin University School of Medicine, Tokyo, Japan
| | - Masato Okada
- Immuno-Rheumatology Center, St. Luke's international Hospital, Tokyo, Japan
| | - Tomohiro Shinozaki
- Department of Information and Computer Technology, Faculty of Engineering, Tokyo University of Science, Tokyo, Japan
| | - Takahiro Asano
- Immuno-Rheumatology Center, St. Luke's international Hospital, Tokyo, Japan
| | - Takehiro Nakai
- Immuno-Rheumatology Center, St. Luke's international Hospital, Tokyo, Japan
| | - Hiromichi Tamaki
- Immuno-Rheumatology Center, St. Luke's international Hospital, Tokyo, Japan
| | - Mitsumasa Kishimoto
- Immuno-Rheumatology Center, St. Luke's international Hospital, Tokyo, Japan
- Department of Nephrology and Rheumatology, Kyorin University School of Medicine, Tokyo, Japan
| | - Hiroshi Hasegawa
- Department of Emergency and General Medicine, Kyorin University School of Medicine, Tokyo, Japan
| | - Takeaki Matsuda
- Department of Emergency and General Medicine, Kyorin University School of Medicine, Tokyo, Japan
| | - Javier Marrugo
- Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA
| | - Sara K Tedeschi
- Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA
| | - Hyon Choi
- Arthritis Research Canada, Richmond, Virginia, Canada
- Division of Rheumatology, Harvard Medical School, Boston, Massachusetts, USA
| | - Daniel H Solomon
- Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA
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Cortese F, Scicchitano P, Cortese AM, Meliota G, Andriani A, Truncellito L, Calculli G, Giordano P, Ciccone MM. Uric Acid in Metabolic and Cerebrovascular Disorders: A Review. Curr Vasc Pharmacol 2020; 18:610-618. [PMID: 31845632 DOI: 10.2174/1570161118666191217123930] [Citation(s) in RCA: 16] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/09/2019] [Revised: 11/09/2019] [Accepted: 11/09/2019] [Indexed: 02/07/2023]
Abstract
BACKGROUND Several studies showed a close link between metabolic syndrome (MetS), type 2 diabetes (T2DM) and cerebrovascular diseases. There is considerable debate regarding the role of uric acid (UA) as a risk factor in these conditions. OBJECTIVE The aim of this narrative review is to discuss the links between UA, MetS, T2DM and cerebrovascular disease. METHODS An extensive review has been conducted based on the scientific literature published in English, and indexed in MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and Google Scholar from January to May 2019. Additional relevant studies published after the initial review were also considered during the period of June 2019-October 2019, during which, this manuscript was written. The Mesh Terms considered were: uric acid, antioxidant, oxidant, metabolic syndrome, diabetes, cerebrovascular diseases, stroke, haemorrhagic stroke, neurocognitive disorders, and their combinations. RESULTS The literature review shows a dose-dependent inflammatory action of UA, which occurs with serum concentrations >4 mg/dl (>0.24 mmol/l), representing one of the contributors to the chronic inflammatory process that underlies metabolic and cerebrovascular diseases. CONCLUSION UA, which is associated with arterial hypertension and cardiovascular diseases, represents one of the indicators of oxidative homeostasis. Increasing concentrations represent a status of active inflammation which is observed with metabolic and cerebrovascular diseases.
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Affiliation(s)
| | | | | | - Giovanni Meliota
- Cardiovascular Disease Section, Department of Organ Transplantation, University of Bari, Bari, Italy
| | - Andrea Andriani
- Cardiology Unit, Giovanni Paolo II Hospital, Policoro (MT), Italy
| | | | | | - Paola Giordano
- Department of Biomedical Science and Human Oncology, Pediatric Unit, University of Bari "Aldo Moro", Bari, Italy
| | - Marco M Ciccone
- Cardiovascular Disease Section, Department of Organ Transplantation, University of Bari, Bari, Italy
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Cortese F, Giordano P, Scicchitano P, Faienza MF, De Pergola G, Calculli G, Meliota G, Ciccone MM. Uric acid: from a biological advantage to a potential danger. A focus on cardiovascular effects. Vascul Pharmacol 2019; 120:106565. [PMID: 31152976 DOI: 10.1016/j.vph.2019.106565] [Citation(s) in RCA: 42] [Impact Index Per Article: 7.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/23/2019] [Revised: 05/26/2019] [Accepted: 05/27/2019] [Indexed: 02/07/2023]
Abstract
Non-communicable diseases represent nowadays the most common cause of death worldwide, having largely overcome infectious diseases. Among them, cardiovascular diseases constitute the majority. Given these premise, great efforts have been made by scientific societies to emphasize the fundamental role of cardiovascular prevention and risk factors control. In addition to classical cardiovascular risk factors such as smoking, arterial hypertension, hypercholesterolemia and male gender, new risk factors are emerging from international literature. Among them, uric acid is the protagonist. Several evidences show a direct role of hyperuricemia in the determinism of metabolic and vascular disorders. From the other hand, some researchers have demonstrated that uric acid is only a marker of cardiovascular damage and not a risk factor for its development. Aim of this review is to evaluate the scientific evidences on the role of uric acid in cardiovascular diseases in order to shed light on this confusing topic.
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Affiliation(s)
- Francesca Cortese
- Cardiological Unit, Cardiovascular Disease Section, Department of Organ Transplantation, University of Bari, Italy.
| | - Paola Giordano
- Department of Biomedicine and Human Oncology, Pediatric Section, University "A.Moro" of Bari, Bari, Italy
| | | | - Maria Felicia Faienza
- Department of Biomedicine and Human Oncology, Pediatric Section, University "A.Moro" of Bari, Bari, Italy
| | - Giovanni De Pergola
- Departmentof Biomedical Sciences and Human Oncology, Section of Internal Medicine and Clinical Oncology, University of Bari Aldo Moro, Bari, Italy
| | | | - Giovanni Meliota
- Cardiological Unit, Cardiovascular Disease Section, Department of Organ Transplantation, University of Bari, Italy
| | - Marco Matteo Ciccone
- Cardiological Unit, Cardiovascular Disease Section, Department of Organ Transplantation, University of Bari, Italy
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Johnson TA, Jinnah HA, Kamatani N. Shortage of Cellular ATP as a Cause of Diseases and Strategies to Enhance ATP. Front Pharmacol 2019; 10:98. [PMID: 30837873 PMCID: PMC6390775 DOI: 10.3389/fphar.2019.00098] [Citation(s) in RCA: 94] [Impact Index Per Article: 15.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/08/2018] [Accepted: 01/24/2019] [Indexed: 12/14/2022] Open
Abstract
Germline mutations in cellular-energy associated genes have been shown to lead to various monogenic disorders. Notably, mitochondrial disorders often impact skeletal muscle, brain, liver, heart, and kidneys, which are the body’s top energy-consuming organs. However, energy-related dysfunctions have not been widely seen as causes of common diseases, although evidence points to such a link for certain disorders. During acute energy consumption, like extreme exercise, cells increase the favorability of the adenylate kinase reaction 2-ADP -> ATP+AMP by AMP deaminase degrading AMP to IMP, which further degrades to inosine and then to purines hypoxanthine -> xanthine -> urate. Thus, increased blood urate levels may act as a barometer of extreme energy consumption. AMP deaminase deficient subjects experience some negative effects like decreased muscle power output, but also positive effects such as decreased diabetes and improved prognosis for chronic heart failure patients. That may reflect decreased energy consumption from maintaining the pool of IMP for salvage to AMP and then ATP, since de novo IMP synthesis requires burning seven ATPs. Similarly, beneficial effects have been seen in heart, skeletal muscle, or brain after treatment with allopurinol or febuxostat to inhibit xanthine oxidoreductase, which catalyzes hypoxanthine -> xanthine and xanthine -> urate reactions. Some disorders of those organs may reflect dysfunction in energy-consumption/production, and the observed beneficial effects related to reinforcement of ATP re-synthesis due to increased hypoxanthine levels in the blood and tissues. Recent clinical studies indicated that treatment with xanthine oxidoreductase inhibitors plus inosine had the strongest impact for increasing the pool of salvageable purines and leading to increased ATP levels in humans, thereby suggesting that this combination is more beneficial than a xanthine oxidoreductase inhibitor alone to treat disorders with ATP deficiency.
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Affiliation(s)
| | - H A Jinnah
- Departments of Neurology and Human Genetics, Emory University School of Medicine, Atlanta, GA, United States
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Fini MA, Gaydos J, McNally A, Karoor V, Burnham EL. Alcohol abuse is associated with enhanced pulmonary and systemic xanthine oxidoreductase activity. Am J Physiol Lung Cell Mol Physiol 2017; 313:L1047-L1057. [PMID: 28839105 PMCID: PMC5814699 DOI: 10.1152/ajplung.00570.2016] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/23/2016] [Revised: 08/17/2017] [Accepted: 08/17/2017] [Indexed: 01/05/2023] Open
Abstract
Acute respiratory distress syndrome (ARDS) is a common and devastating disorder. Alcohol use disorders (AUDs) increase ARDS risk and worsen outcomes through mechanisms that may include enhancement of pulmonary oxidative stress. Alcohol consumption increases activity of the enzyme xanthine oxidoreductase (XOR) that contributes to production of both reactive oxygen species (ROS) and uric acid, a damage-associated molecular pattern. These by-products have the potential to modulate proinflammatory pathways, such as those involving cyclooxygenase (COX)-2, and to activate the nucleotide-binding domain, leucine-rich-containing family, pyrin-domain containing-3 (NLRP3) inflammasome. We sought to determine if pulmonary and systemic XOR activity was altered by AUDs. Bronchoscopy with bronchoalveolar lavage (BAL) and blood sampling was performed in otherwise healthy human subjects with AUDs and controls. Uric acid in epithelial-lining fluid, derived from BAL, was substantially higher among individuals with AUDs and did not normalize after 7 days of abstinence; serum uric acid did not differ across groups. XOR enzyme activity in fresh BAL cells and serum was significantly increased in subjects with AUDs. XOR protein in BAL cells from AUD subjects was increased in parallel with COX-2 expression, and furthermore, mRNA expression of NLRP3 inflammasome components was sustained in LPS-stimulated BAL cells from AUD subjects in conjunction with increased IL-1β. Our data suggest that AUDs augment pulmonary and systemic XOR activity that may contribute to ROS and uric acid generation, promoting inflammation. Further investigations will be necessary to determine if XOR inhibition can mitigate alcohol-associated pulmonary oxidative stress, diminish inflammation, and improve ARDS outcomes.
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Affiliation(s)
- Mehdi A Fini
- Cardiovascular Pulmonary Research Laboratory, University of Colorado School of Medicine, Denver, Colorado; and
- Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado School of Medicine, Denver, Colorado
| | - Jeanette Gaydos
- Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado School of Medicine, Denver, Colorado
| | - Alicia McNally
- Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado School of Medicine, Denver, Colorado
| | - Vijaya Karoor
- Cardiovascular Pulmonary Research Laboratory, University of Colorado School of Medicine, Denver, Colorado; and
- Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado School of Medicine, Denver, Colorado
| | - Ellen L Burnham
- Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado School of Medicine, Denver, Colorado
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Malaguarnera G, Giordano M, Nunnari G, Bertino G, Malaguarnera M. Gut microbiota in alcoholic liver disease: Pathogenetic role and therapeutic perspectives. World J Gastroenterol 2014; 20:16639-16648. [PMID: 25469033 PMCID: PMC4248208 DOI: 10.3748/wjg.v20.i44.16639] [Citation(s) in RCA: 108] [Impact Index Per Article: 9.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/25/2014] [Revised: 06/04/2014] [Accepted: 07/11/2014] [Indexed: 02/06/2023] Open
Abstract
Alcoholic liver disease (ALD) is the commonest cause of cirrhosis in many Western countries and it has a high rate of morbidity and mortality. The pathogenesis is characterized by complex interactions between metabolic intermediates of alcohol. Bacterial intestinal flora is itself responsible for production of endogenous ethanol through the fermentation of carbohydrates. The intestinal metabolism of alcohol produces a high concentration of toxic acetaldehyde that modifies gut permeability and microbiota equilibrium. Furthermore it causes direct hepatocyte damage. In patients who consume alcohol over a long period, there is a modification of gut microbiota and, in particular, an increment of Gram negative bacteria. This causes endotoxemia and hyperactivation of the immune system. Endotoxin is a constituent of Gram negative bacteria cell walls. Two types of receptors, cluster of differentiation 14 and Toll-like receptors-4, present on Kupffer cells, recognize endotoxins. Several studies have demonstrated the importance of gut-liver axis and new treatments have been studied in recent years to reduce progression of ALD modifying gut microbiota. It has focused attention on antibiotics, prebiotics, probiotics and synbiotics.
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Sohrabvandi S, Mortazavian A, Rezaei K. Health-Related Aspects of Beer: A Review. INTERNATIONAL JOURNAL OF FOOD PROPERTIES 2012. [DOI: 10.1080/10942912.2010.487627] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 10/18/2022]
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Gaffo AL, Roseman JM, Jacobs DR, Lewis CE, Shikany JM, Mikuls TR, Jolly PE, Saag KG. Serum urate and its relationship with alcoholic beverage intake in men and women: findings from the Coronary Artery Risk Development in Young Adults (CARDIA) cohort. Ann Rheum Dis 2010; 69:1965-70. [PMID: 20525839 PMCID: PMC5404888 DOI: 10.1136/ard.2010.129429] [Citation(s) in RCA: 53] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/04/2022]
Abstract
OBJECTIVE To investigate if beer, liquor (spirits), wine and total alcohol intakes have different associations with serum urate (SU) concentrations at different ages in a cohort of young men and women. METHODS Data from 3123 participants at baseline and follow-up at 20 years were used, with balanced proportions of Caucasians and African Americans. The relationships of SU with categories of beer, liquor, wine and total alcohol intake referent to no intake were examined in sex-specific, cross-sectional analyses. RESULTS Mean age (SD) at the beginning of follow-up was 25.1 (3.6) years. Compared with non-drinkers, significant associations between higher SU concentrations and greater beer intake were observed among men and women, with more pronounced and consistent associations for women. An association between greater liquor intake and higher SU concentrations was only seen for men at the year 20 evaluation. Wine intake was not associated with SU in either sex and total alcohol was associated with higher SU concentrations in both men and women. The magnitude of the associations between alcoholic beverages intake and SU was modest (≤0.03 mg/dl/alcoholic beverage serving). CONCLUSION An association between higher SU concentrations and greater beer intake was consistent and pronounced among women, but also present in men. Despite the small magnitude of the increases in SU associated with alcohol intake, clinical implications in conditions such as cardiovascular disease and gout in young adults who are moderate and heavy drinkers cannot be ruled out.
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Affiliation(s)
- Angelo L Gaffo
- Birmingham Veterans Affairs Medical Center, University of Alabama at Birmingham, Birmingham, Alabama, USA
- Division of Rheumatology, University of Alabama at Birmingham, Birmingham, Alabama, USA
| | - Jeffrey M Roseman
- Department of Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama, USA
| | - David R Jacobs
- Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, USA
- Department of Nutrition, University of Oslo, Oslo, Norway
| | - Cora E Lewis
- Division of Preventive Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA
| | - James M Shikany
- Division of Preventive Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA
| | - Ted R Mikuls
- Section of Rheumatology and Clinical Immunology, University of Nebraska Medical Center, Omaha, Nebraska, USA
- Omaha Veterans Affairs Medical Center, Omaha, Nebraska, USA
| | - Pauline E Jolly
- Department of Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama, USA
| | - Kenneth G Saag
- Division of Rheumatology, University of Alabama at Birmingham, Birmingham, Alabama, USA
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Abstract
The aim of this article is to review the role of uric acid in the context of antioxidant effects of wine and its potential implication to human health. We described and discussed the mechanisms of increase in plasma antioxidant capacity after consumption of moderate amounts of wine. Because this effect is largely contributed by acute elevation in plasma uric acid, we paid special attention to wine constituents and metabolic processes that are likely to be involved in uric acid elevation.
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Affiliation(s)
- Mladen Boban
- Department of Pharmacology, University of Split School of Medicine, Soltanska 2, 21000 Split, Croatia.
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Kaneko K, Yamanobe T, Fujimori S. Determination of purine contents of alcoholic beverages using high performance liquid chromatography. Biomed Chromatogr 2009; 23:858-64. [DOI: 10.1002/bmc.1197] [Citation(s) in RCA: 33] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/10/2023]
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Inokuchi T, Ka T, Yamamoto A, Moriwaki Y, Takahashi S, Tsutsumi Z, Tamada D, Yamamoto T. RETRACTED: Effects of ethanol on monosodium urate crystal-induced inflammation. Cytokine 2008; 42:198-204. [PMID: 18282764 DOI: 10.1016/j.cyto.2008.01.001] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/10/2007] [Revised: 12/02/2007] [Accepted: 01/07/2008] [Indexed: 11/28/2022]
Abstract
This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal).
This article has been retracted at the request of the Editor-in-Chief.
Image duplication has been observed within Figure 3. The corresponding author has been asked to provide an acceptable explanation for this duplication but has not been able to do so, neither have the original source files been supplied.
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Affiliation(s)
- Taku Inokuchi
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, Mukogawa-cho 1-1, Nishinomiya, Hyogo 663-8501, Japan
| | - Tuneyoshi Ka
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, Mukogawa-cho 1-1, Nishinomiya, Hyogo 663-8501, Japan
| | - Asako Yamamoto
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, Mukogawa-cho 1-1, Nishinomiya, Hyogo 663-8501, Japan
| | - Yuji Moriwaki
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, Mukogawa-cho 1-1, Nishinomiya, Hyogo 663-8501, Japan
| | - Sumio Takahashi
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, Mukogawa-cho 1-1, Nishinomiya, Hyogo 663-8501, Japan
| | - Zenta Tsutsumi
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, Mukogawa-cho 1-1, Nishinomiya, Hyogo 663-8501, Japan
| | - Daisuke Tamada
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, Mukogawa-cho 1-1, Nishinomiya, Hyogo 663-8501, Japan
| | - Tetsuya Yamamoto
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, Mukogawa-cho 1-1, Nishinomiya, Hyogo 663-8501, Japan.
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Yamamoto T, Moriwaki Y, Takahashi S. Effect of ethanol on metabolism of purine bases (hypoxanthine, xanthine, and uric acid). Clin Chim Acta 2005; 356:35-57. [PMID: 15936302 DOI: 10.1016/j.cccn.2005.01.024] [Citation(s) in RCA: 112] [Impact Index Per Article: 5.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/13/2004] [Revised: 01/29/2005] [Accepted: 01/31/2005] [Indexed: 10/25/2022]
Abstract
There are many factors that contribute to hyperuricemia, including obesity, insulin resistance, alcohol consumption, diuretic use, hypertension, renal insufficiency, genetic makeup, etc. Of these, alcohol (ethanol) is the most important. Ethanol enhances adenine nucleotide degradation and increases lactic acid level in blood, leading to hyperuricemia. In beer, purines also contribute to an increase in plasma uric acid. Although rare, dehydration and ketoacidosis (due to ethanol ingestion) are associated with the ethanol-induced increase in serum uric acid levels. Ethanol also increases the plasma concentrations and urinary excretion of hypoxanthine and xanthine via the acceleration of adenine nucleotide degradation and a possible weak inhibition of xanthine dehydrogenase activity. Since many factors such as the ALDH2*1 gene and ADH2*2 gene, daily drinking habits, exercise, and dehydration enhance the increase in plasma concentration of uric acid induced by ethanol, it is important to pay attention to these factors, as well as ingested ethanol volume, type of alcoholic beverage, and the administration of anti-hyperuricemic agents, to prevent and treat ethanol-induced hyperuricemia.
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Affiliation(s)
- Tetsuya Yamamoto
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, Mukogawa-cho 1-1. Nishinomiya, Hyogo 663-8501, Japan.
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Yamamoto T, Moriwaki Y, Ka T, Takahashi S, Tsutsumi Z, Cheng J, Inokuchi T, Yamamoto A, Hada T. Effect of sauna bathing and beer ingestion on plasma concentrations of purine bases. Metabolism 2004; 53:772-6. [PMID: 15164327 DOI: 10.1016/j.metabol.2003.11.028] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/20/2022]
Abstract
To determine whether sauna bathing alone or in combination with beer ingestion increases the plasma concentration of uric acid, 5 healthy subjects were tested. Urine and plasma measurements were performed before and after each took a sauna bath, ingested beer, and ingested beer just after taking a sauna bath, with a 2-week interval between each activity. Sauna bathing alone increased the plasma concentrations of uric acid and oxypurines (hypoxanthine and xanthine), and decreased the urinary and fractional excretion of uric acid, while beer ingestion alone increased the plasma concentrations and urinary excretion of uric acid and oxypurines. A combination of both increased the plasma concentration of uric acid and oxypurines, and decreased the urinary and fractional excretion of uric acid, with an increase in the urinary excretion of oxypurines. The increase in plasma concentration of uric acid with the combination protocol was not synergistic as compared to the sum of the increases by each alone. Body weight, urine volume, and the urinary excretion of sodium and chloride via dehydration were decreased following sauna bathing alone. These results suggest that sauna bathing had a relationship with enhanced purine degradation and a decrease in the urinary excretion of uric acid, leading to an increase in the plasma concentration of uric acid. Further, we concluded that extracellular volume loss may affect the common renal transport pathway of uric acid and xanthine. Therefore, it is recommended that patients with gout refrain from drinking alcoholic beverages, including beer, after taking a sauna bath, since the increase in plasma concentration of uric acid following the combination of sauna bathing and beer ingestion was additive.
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Affiliation(s)
- Tetsuya Yamamoto
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, Hyogo, Japan
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Pritchard MH. Gout and pseudogout: crystal-induced arthropathies. CLINICS IN ENDOCRINOLOGY AND METABOLISM 1981; 10:141-61. [PMID: 7014045 DOI: 10.1016/s0300-595x(81)80042-4] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/23/2023]
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Hilton AM, Boyes BE, Smith PJ, Sharp J, Dymock IW. Liver disease in patients with joint symptoms. Ann Rheum Dis 1974; 33:540-7. [PMID: 4441132 PMCID: PMC1006322 DOI: 10.1136/ard.33.6.540] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/10/2023]
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Stevens HA. A multi-disciplinary catalogue of uric acid literature of interest to behavioural scientists. Percept Mot Skills 1973; 36:1007-20. [PMID: 4574303 DOI: 10.2466/pms.1973.36.3.1007] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/11/2023]
Abstract
The research on uric acid encompasses a large number of disciplines and their respective journals. This bibliography (1948 to 1972) was assembled to provide a co-ordinated reference to this source material for behavioural scientists.
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Isomäki H, Kreus KE. Serum and urinary uric acid in respiratory acidosis. Preliminary report. ACTA MEDICA SCANDINAVICA 1968; 184:293-6. [PMID: 5710036 DOI: 10.1111/j.0954-6820.1968.tb02460.x] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/16/2023]
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Evans JG, Prior IA, Harvey HP. Relation of serum uric acid to body bulk, haemoglobin, and alcohol intake in two South Pacific Polynesian populations. Ann Rheum Dis 1968; 27:319-25. [PMID: 5666671 PMCID: PMC1010452 DOI: 10.1136/ard.27.4.319] [Citation(s) in RCA: 35] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/16/2023]
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