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Gout: HELP
Articles from Pakistan
Based on 7 articles published since 2008
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These are the 7 published articles about Gout that originated from Pakistan during 2008-2019.
 
+ Citations + Abstracts
1 Review Comprehensive review on therapeutic strategies of gouty arthritis. 2014

Akram, Muhammad / Usmanghani, Khan / Ahmed, Iqbal / Azhar, Iqbal / Hamid, Abdul. ·Department of Eastern Medicine and Surgery, Faculty of Medical and Health Sciences, The University of Poonch, Rawalakot, Azad Jammu & Kashmir, Pakistan. · Faculty of Eastern Medicine and Surgery, Hamdard University Karachi Pakistan. · Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Baqai Medical University Karachi, Pakistan. · Department of Pharmacognosy, Faculty of Pharmacy, University of Karachi, Karachi. · Department of Horticulture, Faculty of Agriculture, The University of Poonch, Rawalakot, Azad Jammu & Kashmir, Pakistan. ·Pak J Pharm Sci · Pubmed #25176253.

ABSTRACT: Traditional medicines are practiced worldwide for treatment of gouty arthritis since ancient times. Herbs and plants always have been used in the treatment of different diseases such as gout. The present article deals with the therapeutic strategies and options for the cure of gouty arthritis. Bibliographic investigation was carried out by analyzing classical textbooks and peer reviewed papers, consulting worldwide accepted scientific databases. In this article a detailed introduction, classification, epidemiology, risk factors, symptoms, diagnosis and treatment of gout with reference to modern and Unani system of medicines have been discussed. It is also tried to provide a list of plants used in the treatment of gout along with their formulations used in Unani system of medicine. The herbs and formulations have been used in different systems of medicine particularly Unani system of medicines exhibit their powerful role in the management and cure of gout and arthritis. Most of herbs and plants have been chemically evaluated and some of them are in clinical trials. Their results are magnificent and considerable. However their mechanisms of actions are still on the way.

2 Article Interaction of the GCKR and A1CF loci with alcohol consumption to influence the risk of gout. 2017

Rasheed, Humaira / Stamp, Lisa K / Dalbeth, Nicola / Merriman, Tony R. ·Biochemistry Department, University of Otago, 710 Cumberland Street, Box 56, Dunedin, 9054, New Zealand. · University of Engineering and Technology, Lahore, Pakistan. · Department of Medicine, University of Otago, Christchurch, PO Box 4345, Christchurch, New Zealand. · Department of Medicine, University of Auckland, Auckland, New Zealand. · Biochemistry Department, University of Otago, 710 Cumberland Street, Box 56, Dunedin, 9054, New Zealand. tony.merriman@otago.ac.nz. ·Arthritis Res Ther · Pubmed #28679452.

ABSTRACT: BACKGROUND: Some gout-associated loci interact with dietary exposures to influence outcome. The aim of this study was to systematically investigate interactions between alcohol exposure and urate-associated loci in gout. METHODS: A total of 2792 New Zealand European and Polynesian (Māori or Pacific) people with or without gout were genotyped for 29 urate-associated genetic variants and tested for a departure from multiplicative interaction with alcohol exposure in the risk of gout. Publicly available data from 6892 European subjects were used to test for a departure from multiplicative interaction between specific loci and alcohol exposure for the risk of hyperuricemia (HU). Multivariate adjusted logistic and linear regression was done, including an interaction term. RESULTS: Interaction of any alcohol exposure with GCKR (rs780094) and A1CF (rs10821905) influenced the risk of gout in Europeans (interaction term 0.28, P = 1.5 × 10 CONCLUSIONS: These data support the hypothesis that alcohol influences the risk of gout via glucose and apolipoprotein metabolism. In the absence of alcohol exposure, genetic variants in the GCKR and A1CF genes have a stronger role in gout.

3 Article Burden of musculoskeletal disorders in the Eastern Mediterranean Region, 1990-2013: findings from the Global Burden of Disease Study 2013. 2017

Moradi-Lakeh, Maziar / Forouzanfar, Mohammad H / Vollset, Stein Emil / El Bcheraoui, Charbel / Daoud, Farah / Afshin, Ashkan / Charara, Raghid / Khalil, Ibrahim / Higashi, Hideki / Abd El Razek, Mohamed Magdy / Kiadaliri, Aliasghar Ahmad / Alam, Khurshid / Akseer, Nadia / Al-Hamad, Nawal / Ali, Raghib / AlMazroa, Mohammad AbdulAziz / Alomari, Mahmoud A / Al-Rabeeah, Abdullah A / Alsharif, Ubai / Altirkawi, Khalid A / Atique, Suleman / Badawi, Alaa / Barrero, Lope H / Basulaiman, Mohammed / Bazargan-Hejazi, Shahrzad / Bedi, Neeraj / Bensenor, Isabela M / Buchbinder, Rachelle / Danawi, Hadi / Dharmaratne, Samath D / Zannad, Faiez / Farvid, Maryam S / Fereshtehnejad, Seyed-Mohammad / Farzadfar, Farshad / Fischer, Florian / Gupta, Rahul / Hamadeh, Randah Ribhi / Hamidi, Samer / Horino, Masako / Hoy, Damian G / Hsairi, Mohamed / Husseini, Abdullatif / Javanbakht, Mehdi / Jonas, Jost B / Kasaeian, Amir / Khan, Ejaz Ahmad / Khubchandani, Jagdish / Knudsen, Ann Kristin / Kopec, Jacek A / Lunevicius, Raimundas / Abd El Razek, Hassan Magdy / Majeed, Azeem / Malekzadeh, Reza / Mate, Kedar / Mehari, Alem / Meltzer, Michele / Memish, Ziad A / Mirarefin, Mojde / Mohammed, Shafiu / Naheed, Aliya / Obermeyer, Carla Makhlouf / Oh, In-Hwan / Park, Eun-Kee / Peprah, Emmanuel Kwame / Pourmalek, Farshad / Qorbani, Mostafa / Rafay, Anwar / Rahimi-Movaghar, Vafa / Shiri, Rahman / Rahman, Sajjad Ur / Rai, Rajesh Kumar / Rana, Saleem M / Sepanlou, Sadaf G / Shaikh, Masood Ali / Shiue, Ivy / Sibai, Abla Mehio / Silva, Diego Augusto Santos / Singh, Jasvinder A / Skogen, Jens Christoffer / Terkawi, Abdullah Sulieman / Ukwaja, Kingsley N / Westerman, Ronny / Yonemoto, Naohiro / Yoon, Seok-Jun / Younis, Mustafa Z / Zaidi, Zoubida / Zaki, Maysaa El Sayed / Lim, Stephen S / Wang, Haidong / Vos, Theo / Naghavi, Mohsen / Lopez, Alan D / Murray, Christopher J L / Mokdad, Ali H. ·Institute for Health Metrics and Evaluation, University of Washington, Seattle, Washington, USA. · Department of Community Medicine, Preventive Medicine and Public Health Research Center, Iran University of Medical Sciences, Tehran, Iran. · Norwegian Institute of Public Health, Bergen, Norway. · Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway. · Japan International Cooperation Agency, Lusaka, Zambia. · Ophthalmology resident in Aswan University Hospital, Aswan, Egypt. · Clinical Epidemiology Unit, Department of Clinical Sciences Lund, Orthopedics, Lund University, Lund, Sweden. · Murdoch Childrens Research Institute, Melbourne, Victoria, Australia. · The University of Melbourne, Melbourne, Victoria, Australia. · The University of Sydney, Sydney, New South Wales, Australia. · Hospital for Sick Children, Toronto, Ontario, Canada. · University of Toronto, Toronto, Ontario, Canada. · Food and Nutrition Administration, Ministry of Health, Safat, Kuwait. · University of Oxford, Oxford, UK. · Saudi Ministry of Health, Riyadh, Saudi Arabia. · Division of Physical Therapy, Department of Rehabilitation Sciences, Faculty of Applied Medical Sciences, Jordan University of Science and Technology, Irbid, Jordan. · Charité Universitätsmedizin, Berlin, Germany. · King Saud University, Riyadh, Saudi Arabia. · Graduate Institute of Biomedical Informatics, Taipei Medical University, Taipei, Taiwan. · Public Health Agency of Canada, Toronto, Ontario, Canada. · Department of Industrial Engineering, School of Engineering, Pontificia Universidad Javeriana, Bogota, Colombia. · Charles R. Drew University of Medicine and Science, Los Angeles, California, USA. · David Geffen School of Medicine, University of California at Los Angeles (UCLA), California, USA. · College of Public Health and Tropical Medicine, Jazan, Saudi Arabia. · University of São Paulo, São Paulo, Brazil. · Monash Department of Clinical Epidemiology, Cabrini Institute, Melbourne, Victoria, Australia. · Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia. · Walden University, Minneapolis, Minnesota, USA. · Department of Community Medicine, Faculty of Medicine, University of Peradeniya, Peradeniya, Sri Lanka. · Clinical Investigation Centre INSERM (the National Institute for Health and Medical Research), Université de Lorraine, Vandoeuvre les Nancy, France. · Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA. · Harvard/MGH Center on Genomics, Vulnerable Populations, and Health Disparities, Mongan Institute for Health Policy, Massachusetts General Hospital, Boston, Massachusetts, USA. · Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institute, Stockholm, Sweden. · Non-Communicable Diseases Research Center, Endocrine and Metabolic Research Institute, Tehran University of Medical Sciences, Tehran, Iran. · Bielefeld University, Bielefeld, Germany. · West Virginia Bureau for Public Health, Charleston, West Virginia, USA. · Arabian Gulf University, Manama, Bahrain. · Hamdan Bin Mohammed Smart University, Dubai, United Arab Emirates. · Nevada Division of Behavior and Public Health, Carson City, Nevada, USA. · Fielding School of Public Health, University of California, Los Angeles, Los Angeles, California, USA. · Public Health Division, Secretariat of the Pacific Community, Noumea, New Caledonia. · Salah Azaiz Institute, Tunis, Tunisia. · Institute of Community and Public Health, Birzeit University, Birzeit, Palestine. · Health Economics Research Unit, University of Aberdeen, Aberdeen, UK. · Department of Ophthalmology, Medical Faculty Mannheim, Ruprecht-Karls-University Heidelberg, Mannheim, Germany. · Hematology-Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran. · Non-Communicable Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran. · Health Services Academy, Islamabad, Pakistan. · Ball State University, Muncie, Indiana, USA. · Department of Health Registries, Norwegian Institute of Public Health, Bergen, Norway. · University of British Columbia, Vancouver, British Columbia, Canada. · Aintree University Hospital National Health Service Foundation Trust, Liverpool, UK. · School of Medicine, University of Liverpool, Liverpool, UK. · Mansoura Faculty of Medicine, Mansoura, Egypt. · Imperial College London, London, UK. · Digestive Disease Research Institute, Tehran Universities of Medical Sciences, Tehran, Iran. · McGill University, Montreal, Quebec, Canada. · College of Medicine, Howard University, Washington DC, USA. · Thomas Jefferson University, Philadelphia, Pennsylvania, USA. · College of Medicine, Alfaisal University, Riyadh, Saudi Arabia. · Hunger Action Los Angeles, Los Angeles, California, USA. · Health Systems and Policy Research Unit, Ahmadu Bello University, Zaria, Nigeria. · Institute of Public Health, Heidelberg University, Heidelberg, Germany. · International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh. · Faculty of Health Sciences, Center for Research on Population and Health, American University of Beirut, Beirut, Lebanon. · Department of Preventive Medicine, School of Medicine, Kyung Hee University, Seoul, South Korea. · Department of Medical Humanities and Social Medicine, College of Medicine, Kosin University, Busan, South Korea. · National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA. · Noncommunicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran. · Contech International Health Consultants, Lahore, Pakistan. · Contech School of Public Health, Lahore, Pakistan. · Sina Trauma and Surgery Research Center, Tehran University of Medical Sciences, Tehran, Iran. · Finnish Institute of Occupational Health, Helsinki, Finland. · Sweidi Hospital, Riyadh, Saudi Arabia. · Society for Health and Demographic Surveillance, Suri, India. · Digestive Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran. · Independent Consultant, Karachi, Pakistan. · Faculty of Health and Life Sciences, Northumbria University, Newcastle upon Tyne, UK. · Alzheimer Scotland Dementia Research Centre, University of Edinburgh, Edinburgh, UK. · Department of Epidemiology & Population Health, Faculty of Health Sciences, American University of Beirut, Beirut, Lebanon. · Federal University of Santa Catarina, Florianópolis, Brazil. · University of Alabama at Birmingham, and Birmingham Veterans Affairs Medical Center, Birmingham, Alabama, USA. · Alcohol and Drug Research Western Norway, Stavanger University Hospital, Stavanger, Norway. · Department of Anesthesiology, University of Virginia, Charlottesville, Virginia, USA. · Outcomes Research Consortium, Cleveland Clinic, Cleveland, Ohio, USA. · Department of Anesthesiology, King Fahad Medical City, Riyadh, Saudi Arabia. · Department of Internal Medicine, Federal Teaching Hospital, Abakaliki, Nigeria. · Federal Institute for Population Research, Wiesbaden, Germany. · German National Cohort Consortium, Heidelberg, Germany. · Department of Biostatistics, School of Public Health, Kyoto University, Kyoto, Japan. · Department of Preventive Medicine, College of Medicine, Korea University, Seoul, South Korea. · Jackson State University, Jackson, Mississippi, USA. · University Hospital, Setif, Algeria. · Melbourne School of Population and Global Health, University of Melbourne, Melbourne, Victoria, Australia. ·Ann Rheum Dis · Pubmed #28209629.

ABSTRACT: OBJECTIVES: We used findings from the Global Burden of Disease Study 2013 to report the burden of musculoskeletal disorders in the Eastern Mediterranean Region (EMR). METHODS: The burden of musculoskeletal disorders was calculated for the EMR's 22 countries between 1990 and 2013. A systematic analysis was performed on mortality and morbidity data to estimate prevalence, death, years of live lost, years lived with disability and disability-adjusted life years (DALYs). RESULTS: For musculoskeletal disorders, the crude DALYs rate per 100 000 increased from 1297.1 (95% uncertainty interval (UI) 924.3-1703.4) in 1990 to 1606.0 (95% UI 1141.2-2130.4) in 2013. During 1990-2013, the total DALYs of musculoskeletal disorders increased by 105.2% in the EMR compared with a 58.0% increase in the rest of the world. The burden of musculoskeletal disorders as a proportion of total DALYs increased from 2.4% (95% UI 1.7-3.0) in 1990 to 4.7% (95% UI 3.6-5.8) in 2013. The range of point prevalence (per 1000) among the EMR countries was 28.2-136.0 for low back pain, 27.3-49.7 for neck pain, 9.7-37.3 for osteoarthritis (OA), 0.6-2.2 for rheumatoid arthritis and 0.1-0.8 for gout. Low back pain and neck pain had the highest burden in EMR countries. CONCLUSIONS: This study shows a high burden of musculoskeletal disorders, with a faster increase in EMR compared with the rest of the world. The reasons for this faster increase need to be explored. Our findings call for incorporating prevention and control programmes that should include improving health data, addressing risk factors, providing evidence-based care and community programmes to increase awareness.

4 Article Replication of association of the apolipoprotein A1-C3-A4 gene cluster with the risk of gout. 2016

Rasheed, Humaira / Phipps-Green, Amanda J / Topless, Ruth / Smith, Malcolm D / Hill, Catherine / Lester, Susan / Rischmueller, Maureen / Janssen, Matthijs / Jansen, Timothy L / Joosten, Leo A / Radstake, Timothy R / Riches, Philip L / Tausche, Anne-Kathrin / Lioté, Frederic / So, Alexander / van Rij, Andre / Jones, Gregory T / McCormick, Sally P / Harrison, Andrew A / Stamp, Lisa K / Dalbeth, Nicola / Merriman, Tony R. ·Department of Biochemistry, University of Otago, Dunedin, New Zealand Department of Chemistry, University of Engineering and Technology, Lahore, Pakistan. · Department of Biochemistry, University of Otago, Dunedin, New Zealand. · Department of Medicine, Flinders Medical Centre and Repatriation General Hospital, Adelaide. · Rheumatology Department, The Queen Elizabeth Hospital, Woodville South, SA, Australia. · Department of Rheumatology, Rijnstate Hospital, Arnhem. · Department of IQ HealthCare, VieCuri Medical Centre, Venlo. · Department of Internal Medicine and Radboud Institute of Molecular Life Science, Radboud University Medical Center, Nijmegen. · Department of Rheumatology and Clinical Immunology, Laboratory of Translational Immunology, University Medical Centre Utrecht, Utrecht, The Netherlands. · Rheumatic Diseases Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK. · Department of Rheumatology, University Clinic Carl-Gustav-Carus, Dresden, Germany. · INSERM, UMR-S 1132, Hospital Lariboisière University Paris Diderot (UFR de Médecine), Sorbonne Paris Cité, Paris, F-75205, France. · DAL, Service of Rheumatology, Laboratory of Rheumatology, University of Lausanne, CHUV, Nestlé 05-5029, Lausanne, Switzerland. · Department of Surgery, University of Otago, Dunedin. · Department of Medicine, University of Otago, Wellington. · Department of Medicine, University of Otago, Christchurch. · Department of Medicine, University of Auckland, Auckland, New Zealand. · Department of Biochemistry, University of Otago, Dunedin, New Zealand tony.merriman@otago.ac.nz. ·Rheumatology (Oxford) · Pubmed #27094595.

ABSTRACT: OBJECTIVE: Gout is associated with dyslipidaemia. Association of the apolipoprotein A1-C3-A4 gene cluster with gout has previously been reported in a small study. To investigate a possible causal role for this locus in gout, we tested the association of genetic variants from APOA1 (rs670) and APOC3 (rs5128) with gout. METHODS: We studied data for 2452 controls and 2690 clinically ascertained gout cases of European and New Zealand Polynesian (Māori and Pacific) ancestry. Data were also used from the publicly available Atherosclerosis Risk in Communities study (n = 5367) and the Framingham Heart Study (n = 2984). Multivariate adjusted logistic and linear regression was used to test the association of single-nucleotide polymorphisms with gout risk, serum urate, triglyceride and high-density lipoprotein cholesterol (HDL-C). RESULTS: In Polynesians, the T-allele of rs670 (APOA1) increased (odds ratio, OR = 1.53, P = 4.9 × 10(-6)) and the G-allele of rs5128 (APOC3) decreased the risk of gout (OR = 0.86, P = 0.026). In Europeans, there was a strong trend to a risk effect of the T-allele for rs670 (OR = 1.11, P = 0.055), with a significant protective effect of the G-allele for rs5128 being observed after adjustment for triglycerides and HDL-C (OR = 0.81, P = 0.039). The effect at rs5128 was specific to males in both Europeans and Polynesians. Association in Polynesians was independent of any effect of rs670 and rs5128 on triglyceride and HDL-C levels. There was no evidence for association of either single-nucleotide polymorphism with serum urate levels (P ⩾ 0.10). CONCLUSION: Our data, replicating a previous study, supports the hypothesis that the apolipoprotein A1-C3-A4 gene cluster plays a causal role in gout.

5 Article The Toll-Like Receptor 4 (TLR4) Variant rs2149356 and Risk of Gout in European and Polynesian Sample Sets. 2016

Rasheed, Humaira / McKinney, Cushla / Stamp, Lisa K / Dalbeth, Nicola / Topless, Ruth K / Day, Richard / Kannangara, Diluk / Williams, Kenneth / Smith, Malcolm / Janssen, Matthijs / Jansen, Tim L / Joosten, Leo A / Radstake, Timothy R / Riches, Philip L / Tausche, Anne-Kathrin / Lioté, Frederic / Lu, Leo / Stahl, Eli A / Choi, Hyon K / So, Alexander / Merriman, Tony R. ·Department of Biochemistry, University of Otago, Dunedin, New Zealand. · University of Engineering and Technology, Lahore, Pakistan. · Department of Medicine, University of Otago, Christchurch, Christchurch, New Zealand. · Department of Medicine, University of Auckland, Auckland, New Zealand. · School of Medical Sciences, University of New South Wales, Sydney, Australia. · Department of Clinical Pharmacology & Toxicology, St Vincent's Hospital, Sydney, Australia. · Department of Medicine, Flinders Medical Centre and Repatriation General Hospital, Adelaide, Australia. · Department of Rheumatology, Rijnstate Hospital, Arnhem, The Netherlands. · Department of IQ HealthCare, VieCuri Medical Centre, Venlo, The Netherlands. · Department of Internal Medicine and Radboud Institute of Molecular Life Science, Radboud University Medical Center, Nijmegen, The Netherlands. · Department of Rheumatology and Clinical Immunology, Laboratory of Translational Immunology, Department of Immunology, University Medical Centre Utrecht, Utrecht, The Netherlands. · Rheumatic Diseases Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom. · Department of Rheumatology, University Clinic "Carl-Gustav-Carus", Dresden, Germany. · INSERM, UMR-S 1132, Hospital Lariboisière, Paris, France. · University Paris Diderot (UFR de Médecine), Sorbonne Paris Cité, Paris, France. · Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States of America. · Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, United States of America. · DAL, Service of Rheumatology, Laboratory of Rheumatology, University of Lausanne, CHUV, Nestlé, Lausanne, Switzerland. ·PLoS One · Pubmed #26808548.

ABSTRACT: Deposition of crystallized monosodium urate (MSU) in joints as a result of hyperuricemia is a central risk factor for gout. However other factors must exist that control the progression from hyperuricaemia to gout. A previous genetic association study has implicated the toll-like receptor 4 (TLR4) which activates the NLRP3 inflammasome via the nuclear factor-κB signaling pathway upon stimulation by MSU crystals. The T-allele of single nucleotide polymorphism rs2149356 in TLR4 is a risk factor associated with gout in a Chinese study. Our aim was to replicate this observation in participants of European and New Zealand Polynesian (Māori and Pacific) ancestry. A total of 2250 clinically-ascertained prevalent gout cases and 13925 controls were used. Non-clinically-ascertained incident gout cases and controls from the Health Professional Follow-up (HPFS) and Nurses Health Studies (NHS) were also used. Genotypes were derived from genome-wide genotype data or directly obtained using Taqman. Logistic regression analysis was done including age, sex, diuretic exposure and ancestry as covariates as appropriate. The T-allele increased the risk of gout in the clinically-ascertained European samples (OR = 1.12, P = 0.012) and decreased the risk of gout in Polynesians (OR = 0.80, P = 0.011). There was no evidence for association in the HPFS or NHS sample sets. In conclusion TLR4 SNP rs2143956 associates with gout risk in prevalent clinically-ascertained gout in Europeans, in a direction consistent with previously published results in Han Chinese. However, with an opposite direction of association in Polynesians and no evidence for association in a non-clinically-ascertained incident gout cohort this variant should be analysed in other international gout genetic data sets to determine if there is genuine evidence for association.

6 Article In vitro xanthine oxidase inhibitory and in vivo hypouricemic activity of herbal coded formulation (Gouticin). 2014

Akram, Muhammad / Usmanghani, Khan / Ahmed, Iqbal / Azhar, Iqbal / Hamid, Abdul. ·Department of Eastern Medicine and Surgery, Faculty of Medical and Health Sciences, The University of Poonch, Rawalakot, Azad Jammu & Kashmir, Pakistan. · Faculty of Eastern Medicine and Surgery, Hamdard University Karachi, Pakistan. · Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Baqai Medical University, Karachi, Pakistan. · Department of Pharmacognosy, Faculty of Pharmacy, University of Karachi, Karachi, Pakistan. · Department of Horticulture, Faculty of Agriculture, The University of Poonch, Rawalakot, Azad Jammu & Kashmir, Pakistan. ·Pak J Pharm Sci · Pubmed #24811815.

ABSTRACT: Currently, natural products have been used in treating gouty arthritis and are recognized as xanthine oxidase inhibitors. Current study was designed to evaluate in vitro xanthine oxidase inhibitory potential of Gouticin and its ingredients extracts and in vivo hypouricemic activity of gouticin tablet 500 mg twice daily. Ethanol extracts of Gouticin and its ingredients were evaluated in vitro, at 200, 100, 50, 25 μ g/ml concentrations for xanthine oxidase inhibitory activity. IC(50) values of Gouticin and its ingredients were estimated. Further, in vivo therapeutic effect of Gouticin was investigated in comparison with allopathic medicine (Allopurinol) to treat gout. Total patients were 200 that were divided into test and control group. Herbal coded medicine (Gouticin) was given to test group and allopathic medicine allopurinol was administered to control group. In vitro, Gouticin has the highest percent inhibition at 96% followed by Allopurinol with 93% inhibition. In vivo study, mean serum uric acid level of patients was 4.62 mg/dl and 5.21mg/dl by use of Gouticin and Allopurinol at end of therapy. The study showed that herbal coded formulation gouticin and its ingredients are potential sources of natural xanthine oxidase inhibitors. Gouticin 500 mg twice daily is more effective than the allopurinol 300mg once daily in the management of gout.

7 Article Pharmacological basis for use of Pistacia integerrima leaves in hyperuricemia and gout. 2008

Ahmad, Naseem Saud / Farman, Muhammad / Najmi, Muzammil Hasan / Mian, Kouser Bashir / Hasan, Aurangzeb. ·College of Medical Sciences, National University of Sciences and Technology, Rawalpindi 46000, Pakistan. naseemsaud@yahoo.com ·J Ethnopharmacol · Pubmed #18420362.

ABSTRACT: ETHNOPHARMACOLOGICAL SIGNIFICANCE: Pistacia integerrima Stew ex. Brandis is an important component of commonly dispensed traditional dosage forms. We wished to determine whether polyphenolic constituents of this plant could be useful in oxidative stress and have potential to counter hyperuricemia. MATERIAL AND METHODS: Radical scavenging activity was determined by 1,1-diphenyl-2-picrylhydrazyl (DPPH) and xanthine oxidase (XO) inhibitory activity assay in vitro. Fructose (FRS) induced hyperuricemic animal model was used to asses the serum uric acid (UA) lowering effect by plant products. RESULTS: Ethyl acetate and n-BuOH fractions had the highest DPPH radical scavenging activity. Fifty percent inhibitory concentration (IC(50)) was 6 and 7.6 microg/ml respectively. It was less than quercetin (IC(50) 0.95 microg/ml) and ascorbic acid (IC(50) 1.76 microg/ml). Xanthine oxidase inhibitory activity was comparable between n-BuOH and EtOAc (IC(50) 19 and 20 microg/ml) extracts but less than quercetin (IC(50) 0.65 microg/ml) and allopurinol (IC(50) 0.10 microg/ml). The antioxidant activity as well as the inhibitory activity towards the enzyme XO by quercetin-3-O-beta-d-glucopyranoside (5), kaempferol-3-O-beta-d-glucopyranoside (6), quercetin-3-O-(6''-O-syringyl)-beta-d-glucopyranoside (7), kaempferol-3-O-(4''-O-galloyl)-alpha-l-arabinopyranoside (8), rutin (4) together with aglycons, quercetin (1), kaempferol (2) and apigenin (3) was promising to continue in vivo hypouricemic studies. Ethyl acetate extract had dose dependent UA lowering effect in hyperuricemic mice. This effect was comparable with quercetin but less than allopurinol. CONCLUSIONS: These findings are encouraging to plan clinical studies in hyperuricemic patients.