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Aluron (Allopurinol)
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Allopurinol

Aluron helps reduce urate levels in your blood (serum urate) and reduces gout attacks. Uric acid is a normal product of your metabolism and in the blood, uric acid becomes urate. When urate levels are high, crystals can form around joints causing inflammation, pain and damage. This is known as gout. To reduce gout attacks, it is important to keep your serum urate level below 0.36 mmol/L. When the serum urate is below 0.36mmol/L no new crystals form and crystals that are in your joints or skin can dissolve.

Other names for this medication:
Allopurinol, Zyloprim, Allosig, Allupol, Aloc, Alomaron, Alopron, Aluron, Darinol, Goutex, Llanol, Loric, Prodec, Puribel, Puricos, Purinase, Purinol, Talol, Tipuric, Uriprim, Zurim,

Similar Products:
Spiresis, Mosi, Mafena, Omnix, Celapram, Progen, Parocen, Lentizol, Citrex, Fungoral, Sipralexa, Risperidona, Carisoprodol, Teranex, Uprox, Aclav, Taxim, Salix, Puribel, Uritracin, Nefoxef, Simperten, Betamox, Gensia, Talopam, Grepid, Metformin, Coroval, Dafiro, Concor, Nateglinide, Loben, Clarimycin, Stresnil, Letop, Cymbalta, Indocin, Zafen, Amantan, Disipan, Liometacen, Epratenz, Fenox, Femoston, Azadose, Amlodipine,

Aluron is used to prevent or lower high uric acid levels in the blood. It is also used to prevent or lower excess uric acid levels caused by cancer medicines or in patients with kidney stones. A high uric acid level can cause gout or gouty arthritis (joint pain and inflammation). Aluron is a xanthine oxidase inhibitor that works by decreasing the uric acid produced by the body.

This medicine is available only with your doctor's prescription.

This product is available in the following dosage forms:

  • Tablet

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A gene responsible for cavernous malformations of the brain maps to chromosome 7q. Stat1 as a component of tumor necrosis factor alpha receptor 1-TRADD signaling complex to inhibit NF-kappaB activation. Immunolocalization and FM4-64 dye incubation experiments showed that DEK1 and CRINKLY4 (CR4), a receptor kinase implicated in aleurone cell fate specification, colocalized to plasma membrane and endosomes. XTC-1 level near 10.1 mg/m3 appeared to approximate to embryotropic activity threshold, but that near 1.3 mg/m3 is inactive. The characterization of thrombopoietin (TPO) and remarkable advancements in our understanding of the pathophysiology of ITP has led to the development of a new class of agents, the TPO-receptor agonists that have documented efficacy in the amelioration of thrombocytopenia and bleeding manifestations in chronic ITP.

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Different parts of morphologically heterogeneous astrocytic gliomas were microdissected, and direct DNA sequencing of p53 gene exons 5 through 8 was performed. Assessing the impact of educational intervention for improving management of malaria and other childhood illnesses in Kibaha District-Tanzania. In order to evaluate models to study the glycodynamics of bone cells, we examined primary human osteoblastic cells from osteoarthritis patients, and compared these to human osteosarcoma cells MG63 and SJSA-1. Several hypotheses concerning the role of main amino acids within the receptor protein are proposed based on the different properties of the receptors and comparison of sequences. Physical activity prescription: a critical opportunity to address a modifiable risk factor for the prevention and management of chronic disease: a position statement by the Canadian Academy of Sport and Exercise Medicine.

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Fifty years of the congress of neurological surgeons: foundations, objectives, and legacies. Critical-sized mandibular continuity defects were created in Macaca fascicularis locally implanted with absorbable collagen sponges (ACS) functionalized with chimeric anti-BMP-2 mAb or isotype control mAb. Causes or consequences of inflammation and pathological signs of Alzheimer disease. Teratogenic effects of DA-125, a new anthracycline anticancer agent, in rats.

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Regional distribution of beta-neo-endorphin in rat brain and pituitary. Comparing Rural and Urban Cervical and Breast Cancer Screening Rates in a Privately Insured Population. Local template switch events may have been neglected as an explanation for complex mutations because of biases in commonly used analyses. To remove genes from the epithelium at present requires epithelium to be transplanted from knockout donor mice, but this is a valuable extension of knockout technology, as (a) it creates knockout epithelium in a normal stromal and systemic environment, or vice versa, and (b) where the knockout mouse does not survive into adulthood, epithelium can be rescued from embryos after about 12 days of gestation, and grown to form mature mammary epithelium in a normal recipient mammary fat pad.

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