A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.
Agents that increase uric acid excretion by the kidney (URICOSURIC AGENTS), decrease uric acid production (antihyperuricemics), or alleviate the pain and inflammation of acute attacks of gout.
An iron-molybdenum flavoprotein containing FLAVIN-ADENINE DINUCLEOTIDE that oxidizes hypoxanthine, some other purines and pterins, and aldehydes. Deficiency of the enzyme, an autosomal recessive trait, causes xanthinuria.
A xanthine oxidase inhibitor.
Hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi.
An oxidation product, via XANTHINE OXIDASE, of oxypurines such as XANTHINE and HYPOXANTHINE. It is the final oxidation product of purine catabolism in humans and primates, whereas in most other mammals URATE OXIDASE further oxidizes it to ALLANTOIN.
Excessive URIC ACID or urate in blood as defined by its solubility in plasma at 37 degrees C; greater than 0.42mmol per liter (7.0mg/dL) in men or 0.36mmol per liter (6.0mg/dL) in women. This condition is caused by overproduction of uric acid or impaired renal clearance. Hyperuricemia can be acquired, drug-induced or genetically determined (LESCH-NYHAN SYNDROME). It is associated with HYPERTENSION and GOUT.
Gout suppressants that act directly on the renal tubule to increase the excretion of uric acid, thus reducing its concentrations in plasma.
A syndrome resulting from cytotoxic therapy, occurring generally in aggressive, rapidly proliferating lymphoproliferative disorders. It is characterized by combinations of hyperuricemia, lactic acidosis, hyperkalemia, hyperphosphatemia and hypocalcemia.
Drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways. (From AMA Drug Evaluations Annual, 1994, p2033)
An enzyme that catalyzes the conversion of urate and unidentified products. It is a copper protein. The initial products decompose to form allantoin. EC 1.7.3.3.
Purine bases related to hypoxanthine, an intermediate product of uric acid synthesis and a breakdown product of adenine catabolism.
A purine base found in most body tissues and fluids, certain plants, and some urinary calculi. It is an intermediate in the degradation of adenosine monophosphate to uric acid, being formed by oxidation of hypoxanthine. The methylated xanthine compounds caffeine, theobromine, and theophylline and their derivatives are used in medicine for their bronchodilator effects. (Dorland, 28th ed)
Substances that influence the course of a chemical reaction by ready combination with free radicals. Among other effects, this combining activity protects pancreatic islets against damage by cytokines and prevents myocardial and pulmonary perfusion injuries.
Purine bases found in body tissues and fluids and in some plants.
Uricosuric that acts by increasing uric acid clearance. It is used in the treatment of gout.
An enzyme that catalyzes the oxidation of XANTHINE in the presence of NAD+ to form URIC ACID and NADH. It acts also on a variety of other purines and aldehydes.
A purine and a reaction intermediate in the metabolism of adenosine and in the formation of nucleic acids by the salvage pathway.
Immunologically mediated adverse reactions to medicinal substances used legally or illegally.
Adverse cutaneous reactions caused by ingestion, parenteral use, or local application of a drug. These may assume various morphologic patterns and produce various types of lesions.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Substances that are destructive to protozoans.
The prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy.
Rare cutaneous eruption characterized by extensive KERATINOCYTE apoptosis resulting in skin detachment with mucosal involvement. It is often provoked by the use of drugs (e.g., antibiotics and anticonvulsants) or associated with PNEUMONIA, MYCOPLASMA. It is considered a continuum of Toxic Epidermal Necrolysis.

Reactive oxygen species play an important role in the activation of heat shock factor 1 in ischemic-reperfused heart. (1/630)

BACKGROUND: The myocardial protective role of heat shock protein (HSP) has been demonstrated. Recently, we reported that ischemia/reperfusion induced a significant activation of heat shock factor (HSF) 1 and an accumulation of mRNA for HSP70 and HSP90. We examined the role of reactive oxygen species (ROSs) in the induction of stress response in the ischemic-reperfused heart. METHODS AND RESULTS: Rat hearts were isolated and perfused with Krebs-Henseleit buffer by the Langendorff method. Whole-cell extracts were prepared for gel mobility shift assay using oligonucleotides containing the heat shock element. Induction of mRNA for HSP70 and HSP90 was examined by Northern blot analysis. Repetitive ischemia/reperfusion, which causes recurrent bursts of free radical generation, resulted in burst activation of HSF1, and this burst activation was significantly reduced with either allopurinol 1 mmol/L (an inhibitor of xanthine oxidase) or catalase 2x10(5) U/L (a scavenger of H2O2). Significant activation of HSF1 was observed on perfusion with buffer containing H2O2 150 micromol/L or xanthine 1 mmol/L plus xanthine oxidase 5 U/L. The accumulation of mRNA for HSP70 or HSP90 after repetitive ischemia/reperfusion was reduced with either allopurinol or catalase. CONCLUSIONS: Our findings demonstrate that ROSs play an important role in the activation of HSF1 and the accumulation of mRNA for HSP70 and HSP90 in the ischemic-reperfused heart.  (+info)

Acute vasoconstriction-induced insulin resistance in rat muscle in vivo. (2/630)

Insulin-mediated changes in blood flow are associated with altered blood flow distribution and increased capillary recruitment in skeletal muscle. Studies in perfused rat hindlimb have shown that muscle metabolism can be regulated by vasoactive agents that control blood flow distribution within the hindlimb. In the present study, the effects of a vasoconstrictive agent that has no direct effect on skeletal muscle metabolism but that alters perfusion distribution in rat hindlimb was investigated in vivo to determine its effects on insulin-mediated vascular action and glucose uptake. We measured the effects of alpha-methylserotonin (alpha-met5HT) on mean arterial blood pressure, heart rate, femoral blood flow, hindlimb vascular resistance, and glucose uptake in control and euglycemic insulin-clamped (10 mU x min(-1) x kg(-1)) anesthetized rats. Blood flow distribution within the hindlimb muscles was assessed by measuring the metabolism of 1-methylxanthine (1-MX), an exogenously added substrate for capillary xanthine oxidase. Alpha-met5HT (20 microg x min(-1) x kg(-1)) infusion alone increased mean arterial blood pressure by 25% and increased hindlimb vascular resistance but caused no change in femoral blood flow. These changes were associated with decreased hindlimb 1-MX metabolism indicating less capillary flow. Insulin infusion caused decreased hindlimb vascular resistance that was associated with increased femoral blood flow and 1-MX metabolism. Treatment with alpha-met5HT infusion commenced before insulin infusion prevented the increase in femoral blood flow and inhibited the stimulation of 1-MX metabolism. Alpha-met5HT infusion had no effect on hindlimb glucose uptake but markedly inhibited the insulin stimulation of glucose uptake (P < 0.05) and was associated with decreased glucose infusion rates to maintain euglycemia (P < 0.05). A significant correlation (P < 0.05) was observed between 1-MX metabolism and hindlimb glucose uptake but not between femoral blood flow and glucose uptake. The results indicate that in vivo, certain types of vasoconstriction in muscle such as elicited by 5HT2 agonists, which prevent normal insulin recruitment of capillary flow, cause impaired muscle glucose uptake. Moreover, if vasoconstriction of this kind results from stress-induced increase in sympathetic outflow, then this may provide a clue as to the link between hypertension and insulin resistance that is often observed in humans.  (+info)

The role of free serum tryptophan in the biphasic effect of acute ethanol administration on the concentrations of rat brain tryptophan, 5-hydroxytryptamine and 5-hydroxyindol-3-ylacetic acid. (3/630)

1. Acute administration of ethanol exerts a biphasic effect on the concentrations of rat brain tryptophan, 5-hydroxytryptamine and 5-hydroxyindol-3-ylacetic acid. Both effects are associated with corresponding changes in the availability of circulating free tryptophan. 2. The initial increases in the above concentrations are prevented by ergotamine, are unaltered by allopurinol and are potentiated by theophylline, whereas the later decreases are prevented by both ergotamine and allopurinol. 3. It is suggested that the initial enhancement by ethanol of brain tryptophan metabolism is caused by catecholamine-mediated lipolysis followed by displacement of protein-bound serum tryptophan, whereas the activation of liver tryptophaan pyrrolase, which is produced by the same mechanism, leads to the later decreases in the brain concentrations of tryptophan and its metabolites. 4. The initial effects of ethanol can be reproduced by an equicaloric dose of sucrose, and a comparison of the two treatments alone could therefore be misleading. 5. The effects of ethanol on liver and brain tryptophan metabolism have also been examined in mice, and a comparison of the results with those previously reported suggests that the ethanol effects are strain-dependent.  (+info)

Value of Western blotting in the clinical follow-up of canine leishmaniasis. (4/630)

Specific serum antibody levels in Leishmania infantum-infected dogs treated with a combination of glucantime and allopurinol were estimated by indirect immunofluorescence and Western blotting. The sensitivity of Western blot was greater than that obtained with immunofluorescence titration. In general, both diagnostic methods concurred with the post-treatment clinical status of the animals. Clinical improvement of successfully treated dogs was related to lower immunofluorescence titers and simpler and/or less reactive immunodetection patterns in Western blotting. The recognition, by infected dogs, of certain low molecular weight antigens, particularly one of approximately 26 kDa, was restricted to pretreatment samples and a single animal in relapse thus apparently constituting an active infection marker.  (+info)

Intravenous glycine improves survival in rat liver transplantation. (5/630)

In situ manipulation by touching, retracting, and moving liver lobes gently during harvest dramatically reduces survival after transplantation (P. Schemmer, R. Schoonhoven, J. A. Swenberg, H. Bunzendahl, and R. G. Thurman. Transplantation 65: 1015-1020, 1998). The development of harvest-dependent graft injury upon reperfusion can be prevented with GdCl3, a rare earth metal and Kupffer cell toxicant, but it cannot be used in clinical liver transplantation because of its potential toxicity. Thus the effect of glycine, which prevents activation of Kupffer cells, was assessed here. Minimal dissection of the liver for 12 min plus 13 min without manipulation had no effect on survival (100%). However, gentle manipulation decreased survival to 46% in the control group. Furthermore, serum transaminases and liver necrosis were elevated 4- to 12-fold 8 h after transplantation. After organ harvest, the rate of entry and exit of fluorescein dextran, a dye confined to the vascular space, was decreased about twofold, indicating disturbances in the hepatic microcirculation. Pimonidazole binding, which detects hypoxia, increased about twofold after organ manipulation, and Kupffer cells isolated from manipulated livers produced threefold more tumor necrosis factor-alpha after lipopolysaccharide than controls. Glycine given intravenously to the donor increased the serum glycine concentration about sevenfold and largely prevented the effect of gentle organ manipulation on all parameters studied. These data indicate for the first time that pretreatment of donors with intravenous glycine minimizes reperfusion injury due to organ manipulation during harvest and after liver transplantation.  (+info)

Tissue distribution and characteristics of xanthine oxidase and allopurinol oxidizing enzyme. (6/630)

Tissue distribution and levels of allopurinol oxidizing enzyme and xanthine oxidase with hypoxanthine as a substrate were compared with supernatant fractions from various tissues of mice and from liver of mice, rats, guinea pigs and rabbits. The allopurinol oxidizing enzyme activities in liver were quite different among the species and the sex difference of the enzyme activity only in mouse liver. In mice, the highest activity of allopurinol oxidizing enzyme was found in the liver with a trace value in lung, but the enzyme activity was not detected in brain, small intestine and kidney, while the highest activity of xanthine oxidase was detected in small intestine, lung, liver and kidney in that sequence. The allopurinol oxidizing enzyme activity in mouse liver supernatant fraction did not change after storage at -20 degrees C or dialysis against 0.1 M Tris-HCl containing 1.15% KCl, but the activity markedly decreased after dialysis against 0.1 M Tris-HCl. On the contrary, the xanthine oxidase was activated 2 to 3 times the usual activity after storage at -20 degrees C or dialysis of the enzyme preparation. These results indicated that allopurinol was hydroxylated to oxipurinol mainly by the enzyme which is not identical to xanthine oxidase in vivo. A possible role of aldehyde oxidase involved in the allopurinol oxidation in liver supernatant fraction was dicussed.  (+info)

Digestion and absorption of bovine milk xanthine oxidase and its role as an aldehyde oxidase. (7/630)

The effects of acidic and intestinal proteolytic environments on bovine milk xanthine oxidase (XO) activity were determined in order to evaluate the extent to which this enzyme was absorbed in biologically active form. The inhibition of XO by folic acid and the relative affinities of XO for the oxidation of palmitaldehyde, stearaldehyde, and xanthine were compared. The effects of acid and gastric juice on XO activity were measured by incubating purified enzyme, and non-purified enzyme (milk), in buffers ranging in pH from 2 to 9. Fresh gastric juice was also incubated with milk. Increasing amounts of the enzyme were inactivated as the pH of the incubation mixture was reduced below pH 6.5. Below pH 3.5, the enzyme was completely inactivated. Gastric juice, pH juice incubated with milk. Milk XO activity was reduced 36% when mild was incubated with an equal volume of gastric juice. Homogenized milk had 59% less XO activity compared with raw molk. Fresh raw milk XO, homogenized milk XO, and purified XO were equally susceptible to inactivation by acid or gastric juice. After incubation of milk with gastric juice, or gastric juice followed by pancreatin, XO activity was associated with a macromolecule of 300,000 daltons molecular weight and subunits containg activity were not found. It was estimated that 0.00008% of the XO in the intestine was absorbed. Both folic acid and allopurinol inhibited XO activity in vitro. Allopurinol was 3.5 times more potent an inhibitor than folic acid. A large excess of dietary folic acid did not reduce rat liver or intestinal XO activity in vivo. XO had a much greater affinity for xanthine than for palmitaldehyde or stearaldehyde substrates. It was estimated that of 100 mg of XO in fresh raw milk, 41 mg remained after homogenization, 27 mg entered the intestine and only 20 ng were absorbed as intact enzyme.  (+info)

Optimization of allopurinol challenge: sample purification, protein intake control, and the use of orotidine response as a discriminative variable improve performance of the test for diagnosing ornithine carbamoyltransferase deficiency. (8/630)

BACKGROUND: The diagnosis of heterozygosity for X-linked ornithine carbamoyltransferase (OCT) deficiency has usually been based on measurement of the increase of orotate and orotidine excretion after an allopurinol load. We examined the choices of analyte, cutoff, and test conditions to obtain maximal test accuracy. METHODS: Urine orotate/orotidine responses to allopurinol load in 37 children (13 OCT-deficient and 24 non-OCT-deficient) and 24 women (7 at risk for carrier status and 17 not related to OCT-deficient children) were analyzed by liquid chromatography after sample purification by anion-exchange chromatography. Diagnostic accuracy was evaluated by nonparametric ROC curves. RESULTS: Sample purification was necessary to prevent interferences. Orotate and orotidine excretion increased with increased protein intake during the test. At a cutoff of 8 mmol orotidine/mol creatinine, sensitivity was 1.0 and specificity was 0. 92 in mild forms of OCT deficiency. Results in monoplex carrier women may differ greatly from those expected because of the genetics of this deficiency. CONCLUSIONS: Standardization of protein intake is required in the allopurinol loading test. A negative response in the face of clinical suspicion should be followed with a repeat test during a protein intake not <2.5 g x kg-1 x day-1. Measurements of orotidine provide better clinical sensitivity than measurements of orotate.  (+info)

Allopurinol is a medication used to treat chronic gout and certain types of kidney stones. It works by reducing the production of uric acid in the body, which is the substance that can cause these conditions when it builds up in high levels. Allopurinol is a xanthine oxidase inhibitor, meaning it blocks an enzyme called xanthine oxidase from converting purines into uric acid. By doing this, allopurinol helps to lower the levels of uric acid in the body and prevent the formation of new kidney stones or gout attacks.

It is important to note that allopurinol can have side effects, including rash, stomach upset, and liver or kidney problems. It may also interact with other medications, so it is essential to inform your healthcare provider of any other drugs you are taking before starting allopurinol. Your healthcare provider will determine the appropriate dosage and monitoring schedule based on your individual needs and medical history.

Gout suppressants are a type of medication used to treat acute gout attacks and reduce the risk of future episodes. They work by decreasing the production of uric acid in the body or improving its elimination, thereby reducing the formation of uric acid crystals that cause inflammation and pain in the joints. Common examples of gout suppressants include:

1. Colchicine: This medication is often used to treat acute gout attacks by reducing inflammation and swelling in the affected joint. It should be taken as soon as possible after the onset of symptoms for best results.

2. Nonsteroidal anti-inflammatory drugs (NSAIDs): These medications, such as ibuprofen, naproxen, and celecoxib, can help alleviate pain and inflammation during an acute gout attack. They are usually more effective when taken at the first sign of an attack.

3. Corticosteroids: In some cases, corticosteroid medications like prednisone may be prescribed to treat severe gout attacks that do not respond to other treatments. These drugs can be administered orally or injected directly into the affected joint.

4. Allopurinol and febuxostat: These medications are called xanthine oxidase inhibitors, which reduce uric acid production in the body. They are typically used for chronic gout management to prevent future attacks and lower the risk of complications such as kidney stones and joint damage.

It is important to note that some gout suppressants may have side effects or interact with other medications, so it is crucial to discuss any concerns with a healthcare provider before starting treatment. Additionally, lifestyle changes such as maintaining a healthy weight, following a low-purine diet, and staying hydrated can help manage gout symptoms and lower the risk of future attacks.

Xanthine oxidase is an enzyme that catalyzes the oxidation of xanthine to uric acid, which is the last step in purine metabolism. It's a type of molybdenum-containing oxidoreductase that generates reactive oxygen species (ROS) during its reaction mechanism.

The enzyme exists in two interconvertible forms: an oxidized state and a reduced state. The oxidized form, called xanthine oxidase, reduces molecular oxygen to superoxide and hydrogen peroxide, while the reduced form, called xanthine dehydrogenase, reduces NAD+ to NADH.

Xanthine oxidase is found in various tissues, including the liver, intestines, and milk. An overproduction of uric acid due to increased activity of xanthine oxidase can lead to hyperuricemia, which may result in gout or kidney stones. Some medications and natural compounds are known to inhibit xanthine oxidase, such as allopurinol and febuxostat, which are used to treat gout and prevent the formation of uric acid stones in the kidneys.

Oxypurinol is not exactly a medical term itself, but it's the main metabolite (a substance that your body makes when it breaks down another substance) of allopurinol, which is a medication commonly used to treat gout and kidney stones. Allopurinol works by reducing the production of uric acid in your body, and oxypurinol helps to continue this effect even after the allopurinol has been metabolized.

So, in a broader medical context, you could define Oxypurinol as:

The primary active metabolite of allopurinol, a medication used to lower uric acid levels in the body, preventing gout attacks and kidney stone formation. Oxypurinol inhibits the enzyme xanthine oxidase, which is responsible for the production of uric acid, thereby reducing the risk of gout and kidney stones.

Gout is a type of inflammatory arthritis that occurs when urate crystals accumulate in and around the joints, causing sudden attacks of severe pain, swelling, redness, and tenderness. Urate crystals can form when there are high levels of uric acid in the blood. Uric acid is a waste product that is produced when the body breaks down purines, substances that are found naturally in certain foods, such as steak, organ meats, and seafood. Other foods also promote higher levels of uric acid, such as alcoholic beverages, especially beer, and drinks sweetened with fruit sugar (fructose).

Normally, uric acid dissolves in the blood and passes through the kidneys and out of the body in urine. But sometimes either the body produces too much uric acid or the kidneys excrete too little uric acid. When this happens, uric acid can build up, forming sharp, needle-like urate crystals in a joint or surrounding tissue that cause pain, inflammation and swelling.

Gout most commonly affects the big toe but can also occur in any joint in the body. The symptoms of gout are often acute, occurring suddenly without warning and frequently at night. The attacks are characterized by a rapid onset of pain, swelling, warmth, and redness in the affected joint. An attack of gout can be so painful that it wakes you up from sleep.

Over time, gout can cause permanent damage to the joints and surrounding tissue, resulting in chronic arthritis. If left untreated, gout also can lead to an accumulation of uric acid crystals in the kidneys, which can result in kidney stones.

Uric acid is a chemical compound that is formed when the body breaks down purines, which are substances that are found naturally in certain foods such as steak, organ meats and seafood, as well as in our own cells. After purines are broken down, they turn into uric acid and then get excreted from the body in the urine.

However, if there is too much uric acid in the body, it can lead to a condition called hyperuricemia. High levels of uric acid can cause gout, which is a type of arthritis that causes painful swelling and inflammation in the joints, especially in the big toe. Uric acid can also form crystals that can collect in the kidneys and lead to kidney stones.

It's important for individuals with gout or recurrent kidney stones to monitor their uric acid levels and follow a treatment plan prescribed by their healthcare provider, which may include medications to lower uric acid levels and dietary modifications.

Hyperuricemia is a medical condition characterized by an excessively high level of uric acid in the blood. Uric acid is a waste product that's produced when the body breaks down purines, which are substances found in certain foods and drinks, such as red meat, seafood, and alcoholic beverages. Normally, uric acid is dissolved in the blood and then excreted by the kidneys through urine. However, if there's too much uric acid in the body or if the kidneys can't eliminate it efficiently, it can build up in the blood, leading to hyperuricemia.

Mild cases of hyperuricemia may not cause any symptoms and may not require treatment. However, high levels of uric acid can lead to the formation of uric acid crystals, which can accumulate in the joints and tissues, causing inflammation and pain. This condition is known as gout. Hyperuricemia can also increase the risk of developing kidney stones and kidney disease.

Hyperuricemia can be caused by several factors, including a diet high in purines, genetic factors, kidney disease, certain medications, and conditions that cause rapid cell turnover, such as cancer or psoriasis. Treatment for hyperuricemia typically involves lifestyle changes, such as reducing the intake of purine-rich foods and beverages, maintaining a healthy weight, and staying hydrated. Medications may also be prescribed to lower uric acid levels in the blood and prevent gout attacks.

Uricosuric agents are a class of medications that work by increasing the excretion of uric acid through the kidneys, thereby reducing the levels of uric acid in the blood. This helps to prevent the formation of uric acid crystals, which can cause joint inflammation and damage leading to conditions such as gout.

Uricosuric agents achieve this effect by inhibiting the reabsorption of uric acid in the kidney tubules or by increasing its secretion into the urine. Examples of uricosuric agents include probenecid, sulfinpyrazone, and benzbromarone. These medications are typically used to manage chronic gout and hyperuricemia (elevated levels of uric acid in the blood). It is important to note that uricosuric agents may increase the risk of kidney stones due to increased excretion of uric acid in the urine, so it is essential to maintain adequate hydration while taking these medications.

Tumor Lysis Syndrome (TLS) is a metabolic complication that can occur following the rapid destruction of malignant cells, most commonly seen in hematologic malignancies such as acute leukemias and high-grade non-Hodgkin lymphomas. The rapid breakdown of these cancer cells releases a large amount of intracellular contents, including potassium, phosphorus, and nucleic acids, into the bloodstream.

This sudden influx of substances can lead to three major metabolic abnormalities: hyperkalemia (elevated potassium levels), hyperphosphatemia (elevated phosphate levels), and hypocalcemia (low calcium levels). Hyperuricemia (elevated uric acid levels) may also occur due to the breakdown of nucleic acids. These metabolic disturbances can cause various clinical manifestations, such as cardiac arrhythmias, seizures, renal failure, and even death if not promptly recognized and treated.

TLS is classified into two types: laboratory TLS (LTLS) and clinical TLS (CTLS). LTLS is defined by the presence of abnormal laboratory values without any related clinical symptoms, while CTLS is characterized by laboratory abnormalities accompanied by clinical signs or symptoms. Preventive measures, such as aggressive hydration, urinary alkalinization, and prophylactic medications to lower uric acid levels, are often employed in high-risk patients to prevent the development of TLS.

Antimetabolites are a class of drugs that interfere with the normal metabolic processes of cells, particularly those involved in DNA replication and cell division. They are commonly used as chemotherapeutic agents to treat various types of cancer because many cancer cells divide more rapidly than normal cells. Antimetabolites work by mimicking natural substances needed for cell growth and division, such as nucleotides or amino acids, and getting incorporated into the growing cells' DNA or protein structures, which ultimately leads to the termination of cell division and death of the cancer cells. Examples of antimetabolites include methotrexate, 5-fluorouracil, and capecitabine.

Urate oxidase, also known as uricase, is an enzyme that catalyzes the oxidation of uric acid to allantoin. This reaction is an essential part of purine metabolism in many organisms, as allantoin is more soluble and easier to excrete than uric acid. In humans, urate oxidase is non-functional due to mutations in the gene encoding it, which leads to the accumulation of uric acid and predisposes to gout and kidney stones. Urate oxidase is found in some bacteria, fungi, and plants, and can be used as a therapeutic agent in humans to lower serum uric acid levels in conditions such as tumor lysis syndrome and gout.

Hypoxanthine is not a medical condition but a purine base that is a component of many organic compounds, including nucleotides and nucleic acids, which are the building blocks of DNA and RNA. In the body, hypoxanthine is produced as a byproduct of normal cellular metabolism and is converted to xanthine and then uric acid, which is excreted in the urine.

However, abnormally high levels of hypoxanthine in the body can indicate tissue damage or disease. For example, during intense exercise or hypoxia (low oxygen levels), cells may break down ATP (adenosine triphosphate) rapidly, releasing large amounts of hypoxanthine. Similarly, in some genetic disorders such as Lesch-Nyhan syndrome, there is an accumulation of hypoxanthine due to a deficiency of the enzyme that converts it to xanthine. High levels of hypoxanthine can lead to the formation of kidney stones and other complications.

Xanthine is a purine base, which is a naturally occurring heterocyclic aromatic organic compound. It is formed in the body during the metabolism of purines, and it's a normal intermediate in the breakdown of nucleotides to uric acid. Xanthine is also found in various foods and beverages, such as coffee, tea, and chocolate. In the medical field, xanthine may refer to a class of drugs called xanthine derivatives, which include theophylline and caffeine, that act as bronchodilators and cardiac stimulants.

Free radical scavengers, also known as antioxidants, are substances that neutralize or stabilize free radicals. Free radicals are highly reactive atoms or molecules with unpaired electrons, capable of causing damage to cells and tissues in the body through a process called oxidative stress. Antioxidants donate an electron to the free radical, thereby neutralizing it and preventing it from causing further damage. They can be found naturally in foods such as fruits, vegetables, and nuts, or they can be synthesized and used as dietary supplements. Examples of antioxidants include vitamins C and E, beta-carotene, and selenium.

Xanthines are a type of natural alkaloids that are found in various plants, including tea leaves, cocoa beans, and mate. The most common xanthines are caffeine, theophylline, and theobromine. These compounds have stimulant effects on the central nervous system and are often used in medication to treat conditions such as asthma, bronchitis, and other respiratory issues.

Caffeine is the most widely consumed xanthine and is found in a variety of beverages like coffee, tea, and energy drinks. It works by blocking adenosine receptors in the brain, which can lead to increased alertness and reduced feelings of fatigue.

Theophylline is another xanthine that is used as a bronchodilator to treat asthma and other respiratory conditions. It works by relaxing smooth muscles in the airways, making it easier to breathe.

Theobromine is found in cocoa beans and is responsible for the stimulant effects of chocolate. While it has similar properties to caffeine and theophylline, it is less potent and has a milder effect on the body.

It's worth noting that while xanthines can have beneficial effects when used in moderation, they can also cause negative side effects such as insomnia, nervousness, and rapid heart rate if consumed in large quantities or over an extended period of time.

Benzbromarone is a medication that was previously used to treat gout and hyperuricemia (elevated levels of uric acid in the blood). It works by increasing the excretion of uric acid through the kidneys. However, due to concerns about its potential hepatotoxicity (liver toxicity), it is no longer widely used and has been discontinued or restricted in many countries.

The chemical structure of benzbromarone is characterized by a benzene ring substituted with bromine and a propylamino group, which is further substituted with a carbamoyl group. This gives the compound its unique properties as a uricosuric agent.

It's important to note that benzbromarone should only be used under the supervision of a healthcare professional, and patients should be closely monitored for signs of liver toxicity. Additionally, there are many alternative medications available to treat gout and hyperuricemia, so benzbromarone is typically reserved for use in specific cases where other treatments have failed or are contraindicated.

Xanthine dehydrogenase (XDH) is an enzyme involved in the metabolism of purines, which are nitrogen-containing compounds that form part of DNA and RNA. Specifically, XDH helps to break down xanthine and hypoxanthine into uric acid, a waste product that is excreted in the urine.

XDH can exist in two interconvertible forms: a dehydrogenase form (XDH) and an oxidase form (XO). In its dehydrogenase form, XDH uses NAD+ as an electron acceptor to convert xanthine into uric acid. However, when XDH is converted to its oxidase form (XO), it can use molecular oxygen as an electron acceptor instead, producing superoxide and hydrogen peroxide as byproducts. These reactive oxygen species can contribute to oxidative stress and tissue damage in the body.

Abnormal levels or activity of XDH have been implicated in various diseases, including gout, cardiovascular disease, and neurodegenerative disorders.

Hypoxanthine is a purine derivative and an intermediate in the metabolic pathways of nucleotide degradation, specifically adenosine to uric acid in humans. It is formed from the oxidation of xanthine by the enzyme xanthine oxidase. In the body, hypoxanthine is converted to xanthine and then to uric acid, which is excreted in the urine. Increased levels of hypoxanthine in the body can be indicative of various pathological conditions, including tissue hypoxia, ischemia, and necrosis.

Drug hypersensitivity is an abnormal immune response to a medication or its metabolites. It is a type of adverse drug reaction that occurs in susceptible individuals, characterized by the activation of the immune system leading to inflammation and tissue damage. This reaction can range from mild symptoms such as skin rashes, hives, and itching to more severe reactions like anaphylaxis, which can be life-threatening.

Drug hypersensitivity reactions can be classified into two main types: immediate (or IgE-mediated) and delayed (or non-IgE-mediated). Immediate reactions occur within minutes to a few hours after taking the medication and are mediated by the release of histamine and other inflammatory mediators from mast cells and basophils. Delayed reactions, on the other hand, can take several days to develop and are caused by T-cell activation and subsequent cytokine release.

Common drugs that can cause hypersensitivity reactions include antibiotics (such as penicillins and sulfonamides), nonsteroidal anti-inflammatory drugs (NSAIDs), monoclonal antibodies, and chemotherapeutic agents. It is important to note that previous exposure to a medication does not always guarantee the development of hypersensitivity reactions, as they can also occur after the first administration in some cases.

The diagnosis of drug hypersensitivity involves a thorough medical history, physical examination, and sometimes skin or laboratory tests. Treatment typically includes avoiding the offending medication and managing symptoms with antihistamines, corticosteroids, or other medications as needed. In severe cases, emergency medical care may be required to treat anaphylaxis or other life-threatening reactions.

A "drug eruption" is a general term used to describe an adverse skin reaction that occurs as a result of taking a medication. These reactions can vary in severity and appearance, and may include symptoms such as rash, hives, itching, redness, blistering, or peeling of the skin. In some cases, drug eruptions can also cause systemic symptoms such as fever, fatigue, or joint pain.

The exact mechanism by which drugs cause eruptions is not fully understood, but it is thought to involve an abnormal immune response to the medication. There are many different types of drug eruptions, including morphilliform rashes, urticaria (hives), fixed drug eruptions, and Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN), which is a severe and potentially life-threatening reaction.

If you suspect that you are experiencing a drug eruption, it is important to seek medical attention promptly. Your healthcare provider can help determine the cause of the reaction and recommend appropriate treatment. In some cases, it may be necessary to discontinue the medication causing the reaction and switch to an alternative therapy.

Enzyme inhibitors are substances that bind to an enzyme and decrease its activity, preventing it from catalyzing a chemical reaction in the body. They can work by several mechanisms, including blocking the active site where the substrate binds, or binding to another site on the enzyme to change its shape and prevent substrate binding. Enzyme inhibitors are often used as drugs to treat various medical conditions, such as high blood pressure, abnormal heart rhythms, and bacterial infections. They can also be found naturally in some foods and plants, and can be used in research to understand enzyme function and regulation.

Antiprotozoal agents are a type of medication used to treat protozoal infections, which are infections caused by microscopic single-celled organisms called protozoa. These agents work by either killing the protozoa or inhibiting their growth and reproduction. They can be administered through various routes, including oral, topical, and intravenous, depending on the type of infection and the severity of the illness.

Examples of antiprotozoal agents include:

* Metronidazole, tinidazole, and nitazoxanide for treating infections caused by Giardia lamblia and Entamoeba histolytica.
* Atovaquone, clindamycin, and pyrimethamine-sulfadoxine for treating malaria caused by Plasmodium falciparum or other Plasmodium species.
* Pentamidine and suramin for treating African trypanosomiasis (sleeping sickness) caused by Trypanosoma brucei gambiense or T. b. rhodesiense.
* Nitroimidazoles, such as benznidazole and nifurtimox, for treating Chagas disease caused by Trypanosoma cruzi.
* Sodium stibogluconate and paromomycin for treating leishmaniasis caused by Leishmania species.

Antiprotozoal agents can have side effects, ranging from mild to severe, depending on the drug and the individual patient's response. It is essential to follow the prescribing physician's instructions carefully when taking these medications and report any adverse reactions promptly.

Probenecid is a medication that is primarily used to treat gout and hyperuricemia (high levels of uric acid in the blood). It works by decreasing the production of uric acid in the body and increasing its excretion through the kidneys.

In medical terms, probenecid is a uricosuric agent, which means it increases the urinary excretion of urate, the salt form of uric acid. It does this by inhibiting the reabsorption of urate in the proximal tubules of the kidneys, thereby promoting its elimination in the urine.

Probenecid is also used in conjunction with certain antibiotics, such as penicillin and cephalosporins, to increase their concentration in the body by reducing their excretion by the kidneys. This is known as probenecid-antibiotic interaction.

It's important to note that probenecid should be used under the supervision of a healthcare provider, and its use may be contraindicated in certain medical conditions or in combination with specific medications.

Stevens-Johnson Syndrome (SJS) is a rare, serious and potentially life-threatening skin reaction that usually occurs as a reaction to medication but can also be caused by an infection. SJS is characterized by the detachment of the epidermis (top layer of the skin) from the dermis (the layer underneath). It primarily affects the mucous membranes, such as those lining the eyes, mouth, throat, and genitals, causing painful raw areas that are prone to infection.

SJS is considered a severe form of erythema multiforme (EM), another skin condition, but it's much more serious and can be fatal. The symptoms of SJS include flu-like symptoms such as fever, sore throat, and fatigue, followed by a red or purplish rash that spreads and blisters, eventually leading to the detachment of the top layer of skin.

The exact cause of Stevens-Johnson Syndrome is not always known, but it's often triggered by medications such as antibiotics, anti-convulsants, nonsteroidal anti-inflammatory drugs (NSAIDs), and antiretroviral drugs. Infections caused by herpes simplex virus or Mycoplasma pneumoniae can also trigger SJS.

Treatment for Stevens-Johnson Syndrome typically involves hospitalization, supportive care, wound care, and medication to manage pain and prevent infection. Discontinuing the offending medication is crucial in managing this condition. In severe cases, patients may require treatment in a burn unit or intensive care unit.

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"Allopurinol". MedlinePlus, National Library of Medicine, US National Institutes of Health. 2016. Retrieved 24 December 2016. " ... Medications that may contribute to the cure or amelioration of hyperuricosuria include allopurinol which acts by inhibiting ...
Jawad AS (June 1987). "Alternatives to allopurinol". Annals of the Rheumatic Diseases. 46 (6): 493. doi:10.1136/ard.46.6.493-a ... comparative enzyme inhibition and protein binding studies with allopurinol, oxipurinol and 6-mercaptopurine". British Journal ...
Jawad AS (June 1987). "Alternatives to allopurinol". Annals of the Rheumatic Diseases. 46 (6): 493. doi:10.1136/ard.46.6.493-a ... comparative enzyme inhibition and protein binding studies with allopurinol, oxipurinol and 6-mercaptopurine". British Journal ...
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However, they are already on allopurinol, continue it. Mcgill NW (2000). "Gout and other crystal-associated arthropathies". ... I put patients on famotidine 40 mg one tablet by mouth twice a day for 14 days Do not prescribe allopurinol for acute gout ...
Xanthine oxidase inhibitors, like allopurinol, can cause nephropathy. Additional possible cause of nephropathy is due to the ...
It is an active metabolite of allopurinol and it is cleared renally. In cases of renal disease, this metabolite will accumulate ... the chief metabolite of allopurinol". The American Journal of Medicine. 45 (1): 69-77. doi:10.1016/0002-9343(68)90008-9. PMID ...
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Xanthine oxidase inhibitors, including allopurinol, febuxostat and topiroxostat, decrease the production of uric acid, by ... Prognosis is good with regular consumption of allopurinol or febuxostat.[citation needed] Hypouricemia Hyperuricosuria ...
This has clinical relevance as it is agreed upon that prior to starting a medication such as allopurinol in a patient of ... Before treatment with allopurinol, the American College of Rheumatology guidelines for managing gout recommend HLA-B*58:01 ... Based on the Asian findings, similar studies in Europe showed 61% of allopurinol-induced SJS/TEN patients carried the HLA-B58 ( ... Wang CW, Dao RL, Chung WH (2016). "Immunopathogenesis and risk factors for allopurinol severe cutaneous adverse reactions". ...
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Porta C, Moroni M, Nastasi G (June 1994). "Allopurinol mouthwashes in the treatment of 5-fluorouracil-induced stomatitis". ... Fluorouracil's efficacy is decreased when used alongside allopurinol, which can be used to decrease fluorouracil induced ... stomatitis through use of allopurinol mouthwash. The dihydropyrimidine dehydrogenase (DPD) enzyme is responsible for the ...
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Wang CW, Dao RL, Chung WH (2016). "Immunopathogenesis and risk factors for allopurinol severe cutaneous adverse reactions". ...
01 and Stevens-Johnson syndrome/toxic epidermal necrolysis in patients taking allopurinol, and SLCO1B1 rs4149056 and myopathy ... ". "Annotation of CPIC Guideline for allopurinol and HLA-B". PharmGKB. "Annotation of CPIC Guideline for simvastatin and ...
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Low doses of allopurinol, though, have been shown to safely enhance the efficacy of azathioprine, especially in inflammatory ... Chocair P, Duley J, Simmonds HA, Cameron JS, Ianhez L, Arap S, Sabbaga E (July 1993). "Low-dose allopurinol plus azathioprine/ ... Sparrow MP, Hande SA, Friedman S, Lim WC, Reddy SI, Cao D, Hanauer SB (September 2005). "Allopurinol safely and effectively ... Sparrow MP, Hande SA, Friedman S, Cao D, Hanauer SB (February 2007). "Effect of allopurinol on clinical outcomes in ...
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  • Your doctor will probably start you on a low dose of allopurinol and gradually increase your dose, not more than once a week. (medlineplus.gov)
  • The usual dose for Allopurinol is between 50 to 800 mg every day, depending on a doctor's prescription. (rheuminfo.com)
  • Inform your doctor if you have diabetes or kidney dysfunction before taking Allopurinol as correction of your dose is needed. (austin-rhinoplasty.net)
  • The dose of oral mercaptopurine (Purinethol) and azathioprine (Imuran) should be reduced as Allopurinol increases their blood levels. (mgusa.shop)
  • The multiple regression analysis showed the change in serum urate level was significantly lower in male patients and in those with a lower baseline serum urate level, higher previous dose of allopurinol , lower dose of febuxostat and lower body surface area -unadjusted estimated glomerular filtration rate . (bvsalud.org)
  • In conclusion, it should be noted that the serum urate lowering efficacy of febuxostat may decrease in patients with a higher previous dose of allopurinol , renal impairment or male patients . (bvsalud.org)
  • Allopurinol may cause drowsiness. (californiapetpharmacy.com)
  • Continue giving allopurinol and talk to your veterinarian if your pet experiences upset stomach or diarrhea, dizziness or drowsiness or an acute attack of arthritis. (californiapetpharmacy.com)
  • Allopurinol may cause drowsiness, dizziness with sensations of spinning, or some problems with your coordination. (azurewebsites.net)
  • Allopurinol is in a class of medications called xanthine oxidase inhibitors. (medlineplus.gov)
  • Allopurinol belongs to a class of drugs called xanthine oxidase inhibitors which prevent the accumulation of uric acid. (californiapetpharmacy.com)
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  • Allopurinol cannot be used in patients with hypersensitivity to the medication, in individuals with a hepatic or renal disorders, primary hemochromatosis, asymptomatic hyperuricemia, acute gout, pregnancy, lactation. (austin-rhinoplasty.net)
  • If you come across a provider online offering Allopurinol or other pills without a prescription, you can be sure that it is a dubious and potentially dangerous provider. (austin-rhinoplasty.net)
  • Allopurinol is used to reduce urate formation in conditions where urate deposition has already occurred or is predictable. (wikipedia.org)
  • Allopurinol is used for the prevention of urate urinary stones by reducing the production of uric acid in your body. (californiapetpharmacy.com)
  • Allopurinol is a prescription medication used in dogs for the prevention of urate bladder stones. (californiapetpharmacy.com)
  • Drug interactions are extensive, and are as follows: Azathioprine and 6-mercaptopurine: Azathioprine is metabolised to 6-mercaptopurine which in turn is inactivated by the action of xanthine oxidase - the target of allopurinol. (wikipedia.org)
  • allopurinol increases levels of azathioprine by decreasing metabolism. (medscape.com)
  • Patients taking Allopurinol should not take azathioprine as the medications may interact. (rheuminfo.com)
  • Allopurinol is one of the drugs commonly known to cause Stevens-Johnson syndrome and toxic epidermal necrolysis, two life-threatening dermatological conditions. (wikipedia.org)
  • That applies to herbal medicines and diet, just as much as drugs such as allopurinol, Uloric, or any others. (goutpal.com)
  • May increase risk for allergic or hypersensitivity reactions to allopurinol Monitor for symptoms of hypersensitivty reactions if both drugs must be used together. (medscape.com)
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  • For people with frequent flares or chronic gout, doctors may recommend taking certain drugs like allopurinol, febuxostat, and pegloticase. (cdc.gov)
  • Do you choose Allopurinol or Uloric? (goutpal.com)
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  • May increase risk for allergic or hypersensitivity reactions to allopurinol. (medscape.com)
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  • Moreover, allopurinol can also cause peripheral neuritis in some patients, although this is a rare side effect. (wikipedia.org)
  • Does allopurinol improve major CV outcomes in patients with ischaemic heart disease? (escardio.org)
  • Patients were randomised 1:1 to receive allopurinol up-titrated to 600 mg daily plus usual care or usual care alone. (escardio.org)
  • Prof. Mackenzie summarises the findings by saying, "The ALL-HEART study has shown that allopurinol therapy does not improve major CV outcomes in patients with ischaemic heart disease. (escardio.org)
  • Allopurinol is already widely used in patients with gout to prevent acute flares, and many of these patients have co-existing ischaemic heart disease. (escardio.org)
  • The question of whether allopurinol might prevent CV events in people with heart disease but no clinical gout has been around for many years and we are pleased to have now definitively answered this question for patients and doctors in a robust study. (escardio.org)
  • If gout flares while taking Allopurinol, patients should see their doctor so that the flare can be treated with a different medicine. (rheuminfo.com)
  • Patients taking Allopurinol should have their blood tested occasionally, as advised by their doctor. (rheuminfo.com)
  • Patients taking Allopurinol are advised to avoid alcohol completely. (rheuminfo.com)
  • Patients taking Allopurinol should have their blood tested occasionally so their doctor can make sure that it isn't irritating their blood counts, liver, or kidneys. (rheuminfo.com)
  • Patients who become pregnant while taking Allopurinol should notify their doctor immediately. (rheuminfo.com)
  • Risk of skin rash increases in patients taking Allopurinol with penicillins. (mgusa.shop)
  • Previous Dosage of Allopurinol Is a Strong Determinant of Febuxostat Efficacy. (bvsalud.org)
  • Allopurinol attenuated the exercise-induced increase in oxidative stress, but it did not affect the elevated basal level of oxidative stress that was associated with aging. (cdc.gov)
  • tell your doctor and pharmacist what prescription and nonprescription medications, vitamins, nutritional supplements, and herbal products you are taking while you are taking allopurinol. (medlineplus.gov)
  • Be sure to check with your doctor or pharmacist before giving Allopurinol to a child or the elderly. (azurewebsites.net)
  • More rarely, allopurinol can also result in the depression of bone marrow elements, leading to cytopenias, as well as aplastic anemia. (wikipedia.org)
  • In rare cases Allopurinol can cause damage to nerve, kidney, and bone marrow as well as be a reason to a serious and even fatal allergic liver toxicity. (austin-rhinoplasty.net)
  • Allergic reaction - Allopurinol can sometimes cause an allergic reaction. (rheuminfo.com)
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  • Importantly, I should also review how all alternatives to allopurinol might affect cardiovascular events. (goutpal.com)
  • Meta-analytic evidence showed that adjunctive allopurinol was superior to placebo for acute mania (both with and without mixed features). (wikipedia.org)
  • Allopurinol has very high acute toxicity. (janusinfo.se)
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  • benazepril increases toxicity of allopurinol by unspecified interaction mechanism. (medscape.com)
  • captopril increases toxicity of allopurinol by Mechanism: unspecified interaction mechanism. (medscape.com)
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  • Skin rash - Allopurinol very rarely causes severe skin rashes. (rheuminfo.com)
  • Allopurinol has rare but potentially fatal adverse effects involving the skin. (wikipedia.org)
  • If you become pregnant while taking allopurinol, call your doctor. (medlineplus.gov)
  • Allopurinol is used to prevent gout attacks, not to treat them once they occur. (medlineplus.gov)
  • allopurinol increases levels of didanosine by unknown mechanism. (medscape.com)
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  • Allopurinol may increase the number of gout attacks during the first few months that you take it, although it will eventually prevent attacks. (medlineplus.gov)
  • Allopurinol has been tested as an augmentation strategy for the treatment of mania in bipolar disorder. (wikipedia.org)
  • The xanthine-oxidase inhibitor allopurinol reduces the formation of free radicals, thereby limiting the amount of hypoxia-reperfusion damage. (altmetric.com)
  • In case of suspected intra-uterine hypoxia, both animal and human studies suggest that maternal administration of allopurinol immediately prior to delivery reduces hypoxic-ischaemic encephalopathy. (altmetric.com)
  • Allopurinol reduces the body's production of uric acid by inhibiting an enzyme called xanthine oxidase. (rheuminfo.com)
  • allopurinol increases effects of protamine by decreasing metabolism. (medscape.com)
  • allopurinol increases levels of theophylline by decreasing metabolism. (medscape.com)
  • allopurinol increases effects of warfarin by anticoagulation. (medscape.com)
  • Another side effect of allopurinol is interstitial nephritis. (wikipedia.org)
  • Has anyone else found this as a side effect of drinking too much water, OR a side effect from allopurinol? (goutpal.com)