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.
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.
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 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.
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.
Gout suppressants that act directly on the renal tubule to increase the excretion of uric acid, thus reducing its concentrations in plasma.
A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.
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.
Arthritis, especially of the great toe, as a result of gout. Acute gouty arthritis often is precipitated by trauma, infection, surgery, etc. The initial attacks are usually monoarticular but later attacks are often polyarticular.
Uricosuric that acts by increasing uric acid clearance. It is used in the treatment of gout.
A glycosyl-phosphatidyl-inositol (GPI) - anchored membrane protein found on the thick ascending limb of the LOOP OF HENLE. The cleaved form of the protein is found abundantly in URINE.
Antagonist of urate oxidase.
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.
An inherited disorder transmitted as a sex-linked trait and caused by a deficiency of an enzyme of purine metabolism; HYPOXANTHINE PHOSPHORIBOSYLTRANSFERASE. Affected individuals are normal in the first year of life and then develop psychomotor retardation, extrapyramidal movement disorders, progressive spasticity, and seizures. Self-destructive behaviors such as biting of fingers and lips are seen frequently. Intellectual impairment may also occur but is typically not severe. Elevation of uric acid in the serum leads to the development of renal calculi and gouty arthritis. (Menkes, Textbook of Child Neurology, 5th ed, pp127)
Agents that inhibit SODIUM CHLORIDE SYMPORTERS. They act as DIURETICS. Excess use is associated with HYPOKALEMIA.
A cluster of metabolic risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components of metabolic syndrome X include excess ABDOMINAL FAT; atherogenic DYSLIPIDEMIA; HYPERTENSION; HYPERGLYCEMIA; INSULIN RESISTANCE; a proinflammatory state; and a prothrombotic (THROMBOSIS) state. (from AHA/NHLBI/ADA Conference Proceedings, Circulation 2004; 109:551-556)
The articulation between the head of one phalanx and the base of the one distal to it, in each toe.
The concept covering the physical and mental conditions of men.
I'm sorry for any confusion, but "Taiwan" is not a medical term and does not have a medical definition. It is a country located in East Asia. If you have any questions related to healthcare or medical terms, I would be happy to help with those!
Pathological processes of the KIDNEY or its component tissues.
Diseases that do not exhibit symptoms.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
A family of monosaccharide transport proteins characterized by 12 membrane spanning helices. They facilitate passive diffusion of GLUCOSE across the CELL MEMBRANE.
Inborn errors of purine-pyrimidine metabolism refer to genetic disorders resulting from defects in the enzymes responsible for the metabolic breakdown and synthesis of purines and pyrimidines, leading to the accumulation of toxic metabolites or deficiency of necessary nucleotides, causing various clinical manifestations such as neurological impairment, kidney problems, and developmental delays.
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.
A urea hydantoin that is found in URINE and PLANTS and is used in dermatological preparations.
A monosaccharide in sweet fruits and honey that is soluble in water, alcohol, or ether. It is used as a preservative and an intravenous infusion in parenteral feeding.
Foods made from SOYBEANS. Health benefits are ascribed to the high levels of DIETARY PROTEINS and ISOFLAVONES.
Proteins involved in the transport of organic anions. They play an important role in the elimination of a variety of endogenous substances, xenobiotics and their metabolites from the body.
A flavonol glycoside found in many plants, including BUCKWHEAT; TOBACCO; FORSYTHIA; HYDRANGEA; VIOLA, etc. It has been used therapeutically to decrease capillary fragility.
A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include ADENINE and GUANINE, constituents of nucleic acids, as well as many alkaloids such as CAFFEINE and THEOPHYLLINE. Uric acid is the metabolic end product of purine metabolism.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
A family of proteins involved in the transport of organic cations. They play an important role in the elimination of a variety of endogenous substances, xenobiotics, and their metabolites from the body.
An autosomal recessive disease in which gene expression of glucose-6-phosphatase is absent, resulting in hypoglycemia due to lack of glucose production. Accumulation of glycogen in liver and kidney leads to organomegaly, particularly massive hepatomegaly. Increased concentrations of lactic acid and hyperlipidemia appear in the plasma. Clinical gout often appears in early childhood.

Autosomal-dominant medullary cystic kidney disease type 1: clinical and molecular findings in six large Cypriot families. (1/362)

BACKGROUND: Autosomal-dominant medullary cystic kidney disease (ADMCKD), a hereditary chronic interstitial nephropathy, recently attracted attention because of the cloning or mapping of certain gene loci, namely NPHP1, NPHP2 and NPHP3 for familial juvenile nephronophthisis (NPH) and MCKD1 and MCKD2 for the adult form of medullary cystic kidney disease. Our aim was to present and discuss the clinical, biochemical, sonographic and histopathological findings in six large Cypriot families in whom molecular analysis has confirmed linkage to the MCKD1 locus on chromosome 1q21. METHODS: The clinical, biochemical, sonographic and histopathological findings in 186 members of six large Cypriot families with ADMCKD-1 are presented. Creatinine clearance was calculated according to the Cockroft-Gault formula and was corrected to a body surface area (BSA) of 1.73 m2. DNA linkage analysis was performed with previously identified flanking polymorphic markers. RESULTS: This disease is characterized by the absence of urinary findings in the vast majority of patients, leading to end-stage renal failure (ESRF) at a mean age of 53.7 years. Hypertension and hyperuricemia are common, especially in males, the former encountered more frequently in advanced chronic renal failure (CRF). Gout has been noted in a small percentage of male patients. Loss of urinary concentrating ability was not a prominent early feature of the disease, while severe natriuresis was observed in a few males toward ESRF. Renal cysts are mainly corticomedullary or medullary, and they are present in about 40.3% of patients and appear more frequently near ESRF. CONCLUSION: ADMCKD type 1 is a common cause of ESRF among our dialysis population. The disease is difficult to diagnose clinically, particularly in the early stage when renal cysts are not usually present, making them a weak diagnostic finding. A dominant pattern of inheritance and DNA linkage analysis are helpful in the diagnosis of this disease.  (+info)

Elevated serum leptin concentrations in women with hyperuricemia. (2/362)

The serum uric acid level has been said to be an independent predictor of cardiovascular disease death, mainly for women, and to be linked with the metabolic Syndrome X of insulin resistance, obesity, hypertension, and dyslipidemia. Recently, it has been suggested that the elevation of serum leptin, the ob gene product, may have a role in metabolic Syndrome X. Therefore, we studied the relationship of uric acid to leptin in 822 Japanese women in a cross-sectional manner. To estimate the effect of uric acid on the variables of metabolic Syndrome X, we calculated mean values of various components of the syndrome according to tertiles of uric acid (UA < 4.0 mg/dl, 4.0 < or = UA < 5.5, 5.5 < or = UA). Age, systolic and diastolic blood pressure (BP), body mass index (BMI), percent body fat mass (BFM), serum total cholesterol, triglyceride, atherogenic index, leptin, fasting immunoreactive insulin and homeostasis model assessment-ratio (HOMA-R: calculated insulin resistance) were significantly different across the uric acid tertiles with higher levels in the highest tertile in comparison to the first (ANOVA, p < 0.001, 0.001, 0.002, 0.001, 0.001, 0.025, 0.001, 0.001, 0.001, 0.001, 0.001, respectively), while high density lipoprotein cholesterol showed lower levels (p < 0.001). Serum leptin concentrations were also elevated in hyperuricemic women after adjusting for BMI or BFM (both p < 0.001), and were weakly correlated with serum uric acid concentrations (r = 0.22, p < 0.0001). BMI, HOMA-R, serum triglyceride, diastolic BP and age-adjusted serum leptin concentrations were calculated for each tertile of serum uric acid. Compared with the lowest tertile of uric acid level, BMI, HOMA-R, serum triglyceride, diastolic BP and age-adjusted leptin concentrations were higher in the highest tertile. In the stepwise regression analysis, serum leptin was the significant independent variable for uric acid values. These results indicate an independent relationship between leptin and uric acid, further supporting the involvement of leptin in metabolic Syndrome X.  (+info)

Acute myeloid leukemia complicated with staghorn calculus. (3/362)

An 11-year-old girl who presented with hyperleukocytosis accompanied by significant increases in serum uric acid and lactate dehydrogenase levels was discovered to be suffering from acute myeloid leukemia (AML). Subsequently a staghorn calculus was identified 22 months after the start of chemotherapy. The diagnosis of staghorn calculi was suggested by plain abdominal X-ray and ultrasonography. This paper describes the course of an adolescent patient with AML and focuses specifically upon her urological complications. To the best of our knowledge, this is the first reported pediatric case of AML complicated with staghorn calculi, which developed following repeated episodes of septicemia.  (+info)

A role for uric acid in the progression of renal disease. (4/362)

Hyperuricemia is associated with renal disease, but it is usually considered a marker of renal dysfunction rather than a risk factor for progression. Recent studies have reported that mild hyperuricemia in normal rats induced by the uricase inhibitor, oxonic acid (OA), results in hypertension, intrarenal vascular disease, and renal injury. This led to the hypothesis that uric acid may contribute to progressive renal disease. To examine the effect of hyperuricemia on renal disease progression, rats were fed 2% OA for 6 wk after 5/6 remnant kidney (RK) surgery with or without the xanthine oxidase inhibitor, allopurinol, or the uricosuric agent, benziodarone. Renal function and histologic studies were performed at 6 wk. Given observations that uric acid induces vascular disease, the effect of uric acid on vascular smooth muscle cells in culture was also examined. RK rats developed transient hyperuricemia (2.7 mg/dl at week 2), but then levels returned to baseline by week 6 (1.4 mg/dl). In contrast, RK+OA rats developed higher and more persistent hyperuricemia (6 wk, 3.2 mg/dl). Hyperuricemic rats demonstrated higher BP, greater proteinuria, and higher serum creatinine than RK rats. Hyperuricemic RK rats had more renal hypertrophy and greater glomerulosclerosis (24.2 +/- 2.5 versus 17.5 +/- 3.4%; P < 0.05) and interstitial fibrosis (1.89 +/- 0.45 versus 1.52 +/- 0.47; P < 0.05). Hyperuricemic rats developed vascular disease consisting of thickening of the preglomerular arteries with smooth muscle cell proliferation; these changes were significantly more severe than a historical RK group with similar BP. Allopurinol significantly reduced uric acid levels and blocked the renal functional and histologic changes. Benziodarone reduced uric acid levels less effectively and only partially improved BP and renal function, with minimal effect on the vascular changes. To better understand the mechanism for the vascular disease, the expression of COX-2 and renin were examined. Hyperuricemic rats showed increased renal renin and COX-2 expression, the latter especially in preglomerular arterial vessels. In in vitro studies, cultured vascular smooth muscle cells incubated with uric acid also generated COX-2 with time-dependent proliferation, which was prevented by either a COX-2 or TXA-2 receptor inhibitor. Hyperuricemia accelerates renal progression in the RK model via a mechanism linked to high systemic BP and COX-2-mediated, thromboxane-induced vascular disease. These studies provide direct evidence that uric acid may be a true mediator of renal disease and progression.  (+info)

Mutations of the UMOD gene are responsible for medullary cystic kidney disease 2 and familial juvenile hyperuricaemic nephropathy. (5/362)

INTRODUCTION: Medullary cystic kidney disease 2 (MCKD2) and familial juvenile hyperuricaemic nephropathy (FJHN) are both autosomal dominant renal diseases characterised by juvenile onset of hyperuricaemia, gout, and progressive renal failure. Clinical features of both conditions vary in presence and severity. Often definitive diagnosis is possible only after significant pathology has occurred. Genetic linkage studies have localised genes for both conditions to overlapping regions of chromosome 16p11-p13. These clinical and genetic findings suggest that these conditions may be allelic. AIM: To identify the gene and associated mutation(s) responsible for FJHN and MCKD2. METHODS: Two large, multigenerational families segregating FJHN were studied by genetic linkage and haplotype analyses to sublocalise the chromosome 16p FJHN gene locus. To permit refinement of the candidate interval and localisation of candidate genes, an integrated physical and genetic map of the candidate region was developed. DNA sequencing of candidate genes was performed to detect mutations in subjects affected with FJHN (three unrelated families) and MCKD2 (one family). RESULTS: We identified four novel uromodulin (UMOD) gene mutations that segregate with the disease phenotype in three families with FJHN and in one family with MCKD2. CONCLUSION: These data provide the first direct evidence that MCKD2 and FJHN arise from mutation of the UMOD gene and are allelic disorders. UMOD is a GPI anchored glycoprotein and the most abundant protein in normal urine. We postulate that mutation of UMOD disrupts the tertiary structure of UMOD and is responsible for the clinical changes of interstitial renal disease, polyuria, and hyperuricaemia found in MCKD2 and FJHN.  (+info)

Renal underexcretion of uric acid is present in patients with apparent high urinary uric acid output. (6/362)

OBJECTIVE: To compare renal handling of uric acid in patients with primary gout with that of a control group. METHODS: A case-control study of 100 patients with primary gout and 72 healthy controls was undertaken. Creatinine clearance, uric acid clearance, 24-hour uric acid urinary excretion, fractional excretion of uric acid, excretion of uric acid per volume of glomerular filtration, urinary uric acid to creatinine ratio, and glomerular uric acid filtered load were calculated using 24-hour urine samples. After treatment with allopurinol to achieve similar glomerular filtered load of uric acid, patients were again compared with controls. RESULTS: Patients with gout showed lower uric acid clearance, fractional excretion of uric acid, excretion of uric acid per volume of glomerular filtration, and urinary uric acid to creatinine ratio than controls at baseline, when patients showed hyperuricemia. Although the glomerular uric acid filtered load was much higher in patients with gout than controls, 24-hour uric acid excretion was not statistically different. After treatment with allopurinol, and achieving similar uric acid filtered loads, patients still showed lower figures than controls. When patients with 24-hour urinary uric acids levels >700 mg/day were compared with controls, they had lower uric acid clearance and fractional excretion of uric acid than controls, both at baseline and after achieving similar filtered loads with allopurinol therapy. CONCLUSIONS: Renal underexcretion is the main mechanism for the development of primary hyperuricemia in gout, but even patients showing apparent high 24-hour uric acid output show lower uric acid clearance than controls, indicating that relative, low-grade underexcretion of uric acid is at work.  (+info)

Long-term efficacy of hyperuricaemia treatment in renal transplant patients. (7/362)

BACKGROUND: Although hyperuricaemia and gout are frequently found in renal transplant recipients, little has been published on the efficacy of urate-lowering therapy (ULT) in this patient population. We therefore examine the effects of allopurinol and benziodarone therapy in a cohort of renal transplant patients. METHODS: We reviewed files from a cohort of 1328 patients that received renal transplantation. The selection criteria included: functioning allograft, hyperuricaemia for >12 months or gout, ULT lasting at least 1 year and at least two control measurements after the onset of ULT. Patients on azathioprine were treated with benziodarone to avoid azathioprine-allopurinol interactions. RESULTS: Two-hundred and seventy-nine patients fulfilled the criteria for review. They were treated with 289 courses of ULT: 100 with allopurinol (mean dose: 376 mg/day/dl/min of creatinine clearance) and 189 with benziodarone (mean dose: 73 mg/day). The mean follow-up was 38 months. Both drugs were effective for the control of hyperuricaemia, but benziodarone caused greater reductions in serum uric acid levels, especially when used at mean doses of >75 mg/day. Severe side effects were uncommon, in both the allopurinol and benziodarone groups. CONCLUSIONS: Both allopurinol and benziodarone were effective for the control of hyperuricaemia in renal transplantation. Benziodarone at doses >75 mg/day was more effective than allopurinol in reducing serum uric acid levels and also reduced the risk of azathioprine-allopurinol interactions.  (+info)

Fenofibrate enhances urate reduction in men treated with allopurinol for hyperuricaemia and gout. (8/362)

OBJECTIVE: To assess the short-term urate-lowering effect of fenofibrate in men on long-term allopurinol therapy for hyperuricaemia and gout. METHODS: Ten male patients (38-74 yr) with a history of chronic tophaceous or recurrent acute gout with hyperuricaemia and on established allopurinol at 300-900 mg/day for > or =3 months were studied in an open-crossover study of fenofibrate therapy. Allopurinol at the established dose was continued throughout the study. Clinical and biochemical assessments (serum urate and creatinine, 24-h urinary excretion of urate and creatinine, liver function tests, creatine kinase and fasting serum lipids) were undertaken at: (i) baseline, (ii) after 3 weeks of once-daily therapy with micronized fenofibrate (Lipantil Micro) at 200 mg and (iii) 3 weeks after fenofibrate was withdrawn. RESULTS: Fenofibrate was associated with a 19% reduction in serum urate after 3 weeks of treatment (mean+/-S.E. 0.37+/-0.04 vs 0.30+/-0.02 mM/l; P=0.004). The effect was reversed after a 3-week fenofibrate withdrawal period (0.30+/-0.02 vs 0.38+/-0.03 mM/l). There was a rise in uric acid clearance with fenofibrate treatment of 36% (7.2+/-0.9 vs 11.4+/-1.6 ml/min, normal range 6-11; P=0.006) without a significant change in creatinine clearance. Both total cholesterol and serum triglycerides were also reduced. No patient developed acute gout whilst taking fenofibrate. CONCLUSIONS: Fenofibrate has a rapid and reversible urate-lowering effect in patients with hyperuricaemia and gout on established allopurinol prophylaxis. Fenofibrate may be a potential new treatment for hyperuricaemia and the prevention of gout, particularly in patients with coexisting hyperlipidaemia or those resistant to conventional therapy for hyperuricaemia.  (+info)

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.

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.

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.

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.

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.

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.

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.

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.

Gouty arthritis is a type of inflammatory arthritis that occurs due to the buildup of uric acid crystals in the joints. Uric acid is a waste product that is formed when the body breaks down purines, which are substances found naturally in the body and in certain foods such as organ meats, anchovies, sardines, and beer.

In people with gouty arthritis, uric acid levels in the blood become elevated, leading to the formation of sharp, needle-like crystals that can accumulate in the joints, causing pain, inflammation, and swelling. The symptoms of gouty arthritis typically occur suddenly and may include:

* Intense pain in the affected joint, often occurring at night
* Redness, warmth, and swelling in the affected area
* Stiffness and limited mobility in the affected joint

The most commonly affected joint is the big toe, but gouty arthritis can also occur in other joints such as the ankles, knees, wrists, and fingers. Over time, repeated episodes of gouty arthritis can lead to joint damage and chronic pain. Treatment typically involves medications to reduce inflammation and manage pain, as well as lifestyle changes to lower uric acid levels in the body.

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.

Uromodulin, also known as Tamm-Horsfall protein, is a glycoprotein that is primarily produced in the thick ascending limb of the loop of Henle in the kidney. It is the most abundant protein found in normal urine. Uromodulin plays a role in the protection of the urinary tract by preventing the formation of calcium oxalate and brushite crystals, which can lead to kidney stones. Additionally, it has been implicated in various renal diseases, including chronic kidney disease and kidney transplant rejection.

I'm sorry for any confusion, but "Oxonic Acid" is not a recognized term in medical or clinical sciences. It is, however, a chemical compound with the formula C5H7NO5. It is a type of organic acid that is used in research and industrial settings, particularly as a precursor in the synthesis of other chemicals.

If you have any questions related to medical terminology or health-related topics, I would be happy to help answer them for you!

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.

Lesch-Nyhan Syndrome is a rare X-linked recessive genetic disorder caused by a deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRT). This leads to an accumulation of purines, which can result in neurological symptoms and self-injurious behaviors.

The main features of Lesch-Nyhan Syndrome include:

1. Neurological symptoms: These may include delayed development, choreoathetosis (involuntary movements), spasticity, and dystonia (sustained muscle contractions).
2. Self-injurious behaviors: Affected individuals often bite their lips, fingers, and inside of their cheeks, causing significant tissue damage.
3. Intellectual disability: Most individuals with Lesch-Nyhan Syndrome have moderate to severe intellectual disability.
4. Speech and language difficulties: Many affected individuals have difficulty speaking and understanding language.
5. Kidney problems: The accumulation of purines can lead to kidney stones and kidney failure in some cases.
6. Hyperuricemia: Elevated levels of uric acid in the blood (hyperuricemia) are a hallmark of Lesch-Nyhan Syndrome, which can lead to gout and joint damage.

Lesch-Nyhan Syndrome is typically diagnosed through genetic testing and enzyme assays. There is no cure for the disorder, but treatments may include medications to manage symptoms, behavioral interventions, and physical therapy.

Sodium chloride symporter inhibitors are a class of pharmaceutical agents that block the function of the sodium chloride symporter (NCC), which is a protein found in the kidney's distal convoluted tubule. The NCC is responsible for reabsorbing sodium and chloride ions from the filtrate back into the bloodstream, helping to regulate electrolyte balance and blood pressure.

Sodium chloride symporter inhibitors work by selectively binding to and blocking the NCC, preventing it from transporting sodium and chloride ions across the cell membrane. This leads to increased excretion of sodium and chloride in the urine, which can help lower blood pressure in patients with hypertension.

Examples of sodium chloride symporter inhibitors include thiazide diuretics such as hydrochlorothiazide and chlorthalidone, which have been used for many years to treat hypertension and edema associated with heart failure and liver cirrhosis. These medications work by reducing the amount of sodium and fluid in the body, which helps lower blood pressure and reduce swelling.

It's worth noting that while sodium chloride symporter inhibitors can be effective at treating hypertension, they can also cause side effects such as electrolyte imbalances, dehydration, and increased urination. As with any medication, it's important to use them under the guidance of a healthcare provider and to follow dosing instructions carefully.

Metabolic syndrome, also known as Syndrome X, is a cluster of conditions that increase the risk of heart disease, stroke, and diabetes. It is not a single disease but a group of risk factors that often co-occur. According to the American Heart Association and the National Heart, Lung, and Blood Institute, a person has metabolic syndrome if they have any three of the following five conditions:

1. Abdominal obesity (waist circumference of 40 inches or more in men, and 35 inches or more in women)
2. Triglyceride level of 150 milligrams per deciliter of blood (mg/dL) or greater
3. HDL cholesterol level of less than 40 mg/dL in men or less than 50 mg/dL in women
4. Systolic blood pressure of 130 millimeters of mercury (mmHg) or greater, or diastolic blood pressure of 85 mmHg or greater
5. Fasting glucose level of 100 mg/dL or greater

Metabolic syndrome is thought to be caused by a combination of genetic and lifestyle factors, such as physical inactivity and a diet high in refined carbohydrates and unhealthy fats. Treatment typically involves making lifestyle changes, such as eating a healthy diet, getting regular exercise, and losing weight if necessary. In some cases, medication may also be needed to manage individual components of the syndrome, such as high blood pressure or high cholesterol.

A toe joint, also known as a metatarsophalangeal (MTP) joint, is the articulation between the bones in the foot (metatarsals) and the bones in the toes (phalanges). There are five MTP joints in each foot, one for each toe except for the big toe, which has its own separate joint called the first metatarsophalangeal joint.

The MTP joints allow for movement and flexibility of the toes, enabling activities such as walking, running, and standing. Problems with these joints can lead to pain, stiffness, and difficulty moving, making it important to maintain their health and mobility through proper foot care and exercise.

"Men's Health" is not strictly defined in the medical field, but it generally refers to the branch of healthcare that focuses on the specific health concerns and needs of men. This can include issues related to reproductive health, sexual health, hormonal health, chronic conditions that disproportionately affect men (like heart disease and prostate cancer), mental health, and lifestyle factors that impact male health (such as diet, exercise, and stress management). It also promotes health education, prevention, and early detection of diseases and conditions that are common in men.

I'm sorry for any confusion, but "Taiwan" is not a medical term or concept. It is the name of an island nation located in East Asia. The official name of the country is the Republic of China (ROC). If you have any medical questions or inquiries, I would be happy to help answer those for you!

Kidney disease, also known as nephropathy or renal disease, refers to any functional or structural damage to the kidneys that impairs their ability to filter blood, regulate electrolytes, produce hormones, and maintain fluid balance. This damage can result from a wide range of causes, including diabetes, hypertension, glomerulonephritis, polycystic kidney disease, lupus, infections, drugs, toxins, and congenital or inherited disorders.

Depending on the severity and progression of the kidney damage, kidney diseases can be classified into two main categories: acute kidney injury (AKI) and chronic kidney disease (CKD). AKI is a sudden and often reversible loss of kidney function that occurs over hours to days, while CKD is a progressive and irreversible decline in kidney function that develops over months or years.

Symptoms of kidney diseases may include edema, proteinuria, hematuria, hypertension, electrolyte imbalances, metabolic acidosis, anemia, and decreased urine output. Treatment options depend on the underlying cause and severity of the disease and may include medications, dietary modifications, dialysis, or kidney transplantation.

The term "asymptomatic disease" refers to a medical condition or infection that does not cause any obvious symptoms in an affected individual. Some people with asymptomatic diseases may never develop any signs or symptoms throughout their lives, while others may eventually go on to develop symptoms at a later stage. In some cases, asymptomatic diseases may still be detected through medical testing or screening, even if the person feels completely well. A classic example of an asymptomatic disease is a person who has a positive blood test for a latent viral infection, such as HIV or HSV (herpes simplex virus), but does not have any symptoms related to the infection at that time.

Medical Definition:

"Risk factors" are any attribute, characteristic or exposure of an individual that increases the likelihood of developing a disease or injury. They can be divided into modifiable and non-modifiable risk factors. Modifiable risk factors are those that can be changed through lifestyle choices or medical treatment, while non-modifiable risk factors are inherent traits such as age, gender, or genetic predisposition. Examples of modifiable risk factors include smoking, alcohol consumption, physical inactivity, and unhealthy diet, while non-modifiable risk factors include age, sex, and family history. It is important to note that having a risk factor does not guarantee that a person will develop the disease, but rather indicates an increased susceptibility.

Glucose Transporter Proteins, Facilitative (GLUTs) are a group of membrane proteins that facilitate the passive transport of glucose and other simple sugars across the cell membrane. They are also known as solute carrier family 2 (SLC2A) members. These proteins play a crucial role in maintaining glucose homeostasis within the body by regulating the uptake of glucose into cells. Unlike active transport, facilitative diffusion does not require energy and occurs down its concentration gradient. Different GLUT isoforms have varying tissue distributions and substrate specificities, allowing them to respond to different physiological needs. For example, GLUT1 is widely expressed and is responsible for basal glucose uptake in most tissues, while GLUT4 is primarily found in insulin-sensitive tissues such as muscle and adipose tissue, where it mediates the increased glucose uptake in response to insulin signaling.

Inborn errors of purine-pyrimidine metabolism refer to genetic disorders that result in dysfunctional enzymes involved in the metabolic pathways of purines and pyrimidines. These are essential components of nucleotides, which in turn are building blocks of DNA and RNA.

Inherited as autosomal recessive or X-linked recessive traits, these disorders can lead to an accumulation of toxic metabolites, a deficiency of necessary compounds, or both. Clinical features vary widely depending on the specific enzyme defect but may include neurologic symptoms, kidney problems, gout, and/or immunodeficiency.

Examples of such disorders include Lesch-Nyhan syndrome (deficiency of hypoxanthine-guanine phosphoribosyltransferase), adenosine deaminase deficiency (leading to severe combined immunodeficiency), and orotic aciduria (due to defects in pyrimidine metabolism). Early diagnosis and management are crucial to improve outcomes.

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.

Allantoin is a naturally occurring substance that is found in some plants and animals, including humans. It is a white, crystalline powder that is only slightly soluble in water and more soluble in alcohol and ether. In the medical field, allantoin is often used as an ingredient in topical creams, ointments, and other products due to its ability to promote wound healing, skin soothing, and softening. It can also help to increase the water content of the extracellular matrix, which can be beneficial for dry or damaged skin. Allantoin has been shown to have anti-inflammatory properties, making it useful in the treatment of various skin conditions such as eczema, dermatitis, and sunburn. It is considered safe and non-irritating, making it a popular ingredient in many cosmetic and personal care products.

Fructose is a simple monosaccharide, also known as "fruit sugar." It is a naturally occurring carbohydrate that is found in fruits, vegetables, and honey. Fructose has the chemical formula C6H12O6 and is a hexose, or six-carbon sugar.

Fructose is absorbed directly into the bloodstream during digestion and is metabolized primarily in the liver. It is sweeter than other sugars such as glucose and sucrose (table sugar), which makes it a popular sweetener in many processed foods and beverages. However, consuming large amounts of fructose can have negative health effects, including increasing the risk of obesity, diabetes, and heart disease.

Soy foods are food products made from soybeans, which are a rich source of plant-based protein, fiber, and various beneficial compounds like isoflavones. Examples of soy foods include tofu, tempeh, soymilk, edamame (immature soybeans), soy flour, and textured vegetable protein (TVP). Soy products can be used as alternatives to animal-based proteins and can be incorporated into a variety of dishes, such as stir-fries, soups, smoothies, and baked goods. It's important to note that some people may have allergies to soy or sensitivities to its phytoestrogens, which can affect hormone balance in the body.

Organic anion transporters (OATs) are membrane transport proteins that are responsible for the cellular uptake and excretion of various organic anions, such as drugs, toxins, and endogenous metabolites. They are found in various tissues, including the kidney, liver, and brain, where they play important roles in the elimination and detoxification of xenobiotics and endogenous compounds.

In the kidney, OATs are located in the basolateral membrane of renal tubular epithelial cells and mediate the uptake of organic anions from the blood into the cells. From there, the anions can be further transported into the urine by other transporters located in the apical membrane. In the liver, OATs are expressed in the sinusoidal membrane of hepatocytes and facilitate the uptake of organic anions from the blood into the liver cells for metabolism and excretion.

There are several isoforms of OATs that have been identified, each with distinct substrate specificities and tissue distributions. Mutations in OAT genes can lead to various diseases, including renal tubular acidosis, hypercalciuria, and drug toxicity. Therefore, understanding the function and regulation of OATs is important for developing strategies to improve drug delivery and reduce adverse drug reactions.

Rutin is a flavonoid, a type of plant pigment that is found in various plants and foods including citrus fruits, buckwheat, and asparagus. It has antioxidant properties and is known to help strengthen blood vessels and reduce inflammation. In medical terms, rutin may be mentioned in the context of discussing treatments for conditions related to these effects, such as varicose veins or hemorrhoids. However, it's important to note that while rutin has potential health benefits, more research is needed to fully understand its effects and proper dosages.

Purines are heterocyclic aromatic organic compounds that consist of a pyrimidine ring fused to an imidazole ring. They are fundamental components of nucleotides, which are the building blocks of DNA and RNA. In the body, purines can be synthesized endogenously or obtained through dietary sources such as meat, seafood, and certain vegetables.

Once purines are metabolized, they are broken down into uric acid, which is excreted by the kidneys. Elevated levels of uric acid in the body can lead to the formation of uric acid crystals, resulting in conditions such as gout or kidney stones. Therefore, maintaining a balanced intake of purine-rich foods and ensuring proper kidney function are essential for overall health.

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

Organic cation transport proteins (OCTs) are a group of membrane transporters that facilitate the movement of organic cations across biological membranes. These transporters play an essential role in the absorption, distribution, and elimination of various endogenous and exogenous substances, including drugs and toxins.

There are four main types of OCTs, namely OCT1, OCT2, OCT3, and OCTN1 (also known as novel organic cation transporter 1 or OCT6). These proteins belong to the solute carrier (SLC) family, specifically SLC22A.

OCTs have a broad substrate specificity and can transport various organic cations, such as neurotransmitters (e.g., serotonin, dopamine, histamine), endogenous compounds (e.g., creatinine, choline), and drugs (e.g., metformin, quinidine, morphine). The transport process is typically sodium-independent and can occur in both directions, depending on the concentration gradient of the substrate.

OCTs are widely expressed in various tissues, including the liver, kidney, intestine, brain, heart, and placenta. Their expression patterns and functions vary among different OCT types, contributing to their diverse roles in physiology and pharmacology. Dysfunction of OCTs has been implicated in several diseases, such as drug toxicity, neurodegenerative disorders, and cancer.

In summary, organic cation transport proteins are membrane transporters that facilitate the movement of organic cations across biological membranes, playing crucial roles in the absorption, distribution, and elimination of various substances, including drugs and toxins.

Glycogen Storage Disease Type I (GSD I) is a rare inherited metabolic disorder caused by deficiency of the enzyme glucose-6-phosphatase, which is necessary for the liver to release glucose into the bloodstream. This leads to an accumulation of glycogen in the liver and abnormally low levels of glucose in the blood (hypoglycemia).

There are two main subtypes of GSD I: Type Ia and Type Ib. In Type Ia, there is a deficiency of both glucose-6-phosphatase enzyme activity in the liver, kidney, and intestine, leading to hepatomegaly (enlarged liver), hypoglycemia, lactic acidosis, hyperlipidemia, and growth retardation. Type Ib is characterized by a deficiency of glucose-6-phosphatase enzyme activity only in the neutrophils, leading to recurrent bacterial infections.

GSD I requires lifelong management with frequent feedings, high-carbohydrate diet, and avoidance of fasting to prevent hypoglycemia. In some cases, treatment with continuous cornstarch infusions or liver transplantation may be necessary.

Hyperuricaemia or hyperuricemia is an abnormally high level of uric acid in the blood. In the pH conditions of body fluid, uric ... Hyperuricemia can be detected using blood and urine tests.[citation needed] Medications used to treat hyperuricemia are divided ... Not all people with hyperuricemia develop gout. Many factors contribute to hyperuricemia, including genetics, insulin ... for hyperuricemia. Causes of hyperuricemia that are of mixed type have a dual action, both increasing production and decreasing ...
The definition was less than 0.14 mmol/L for women and less than 0.20 mmol/L in men.) Hyperuricemia Chizyński K, Rózycka M ( ... November 2005). "[Hyperuricemia]". Pol. Merkur. Lekarski (in Polish). 19 (113): 693-6. PMID 16498814. Ito O, Hasegawa Y, Sato K ... a condition normally associated with hyperuricemia. The reasons for this are unclear. Two kinds of genetic mutations are known ...
Excessive use of the myokinase reaction and purine nucleotide cycle leads to myogenic hyperuricemia. In muscle glycogenoses ( ... "Myogenic hyperuricemia. A common pathophysiologic feature of glycogenosis types III, V, and VII". The New England Journal of ...
July 1987). "Myogenic hyperuricemia. A common pathophysiologic feature of glycogenosis types III, V, and VII". The New England ... Glycogen Storage Disease Metabolic Myopathies Exercise intolerance § low ATP reservoir Myogenic hyperuricemia Purine nucleotide ...
Campion EW, Glynn RJ, DeLabry LO (March 1987). "Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study ...
July 1987). "Myogenic hyperuricemia. A common pathophysiologic feature of glycogenosis types III, V, and VII". The New England ... Mineo I, Tarui S (1995). "Myogenic hyperuricemia: what can we learn from metabolic myopathies?". Muscle & Nerve. Supplement. 3 ... hyperuricemia/gout (11.6%), gastrointestinal diseases (11.2%), neurological disease (10%), respiratory disease (9.5%), and ... GSD-V patients may experience myogenic hyperuricemia (exercise-induced accelerated breakdown of purine nucleotides in skeletal ...
Myogenic hyperuricemia, as a result of the Purine Nucleotide Cycle running when ATP reservoirs in muscle cells are low, is a ... Hyperuricemia (high levels of uric acid), which induces gout, has various potential origins: Diet may be a factor. High intake ... Hyperuricemia is associated with an increase in risk factors for cardiovascular disease. It is also possible that high levels ... ISBN 1-59377-192-4. Li, R.; Yu, K.; Li, C. (2018). "Dietary factors and risk of gout and hyperuricemia: a meta-analysis and ...
July 1987). "Myogenic hyperuricemia. A common pathophysiologic feature of glycogenosis types III, V, and VII". The New England ... Mineo I, Tarui S (1995). "Myogenic hyperuricemia: what can we learn from metabolic myopathies?". Muscle & Nerve. Supplement. 3 ... known as myogenic hyperuricemia. AMP → IMP → Inosine → Hypoxanthine → Xanthine → Uric acid. Unfortunately, the studies on PGM1- ... so it is currently unknown definitively whether PGM1-CDG individuals also experience myogenic hyperuricemia. PGM1, PGM2, PGM3, ...
ATP), resulting in exercise-induced excessive AMP buildup in muscle, and subsequent exercise-induced hyperuricemia (myogenic ... In these metabolic myopathies, myogenic hyperuricemia is exercise-induced; inosine, hypoxanthine and uric acid increase in ... Uric Acid Myogenic hyperuricemia, as a result of the purine nucleotide cycle running when ATP reservoirs in muscle cells are ... "Myogenic Hyperuricemia". New England Journal of Medicine. 317 (2): 75-80. doi:10.1056/NEJM198707093170203. ISSN 0028-4793. PMID ...
Associated conditions include hyperuricemia; fatty liver (especially in concurrent obesity) progressing to nonalcoholic fatty ... In 1921, Joslin first reported the association of diabetes with hypertension and hyperuricemia. In 1923, Kylin reported ... Kylin E (1923). "[Studies of the hypertension-hyperglycemia-hyperuricemia syndrome]". Zentralbl Inn Med (in German). 44: 105- ... hyperuricemia, and hepatic steatosis when describing the additive effects of risk factors on atherosclerosis. The same year, ...
Hyperuricemia is a classic feature of gout, but nearly half of the time gout occurs without hyperuricemia and most people with ... Hyperuricemia is defined as a plasma urate level greater than 420 μmol/L (7.0 mg/dl) in males and 360 μmol/L (6.0 mg/dl) in ... Hyperuricemia may be induced by excessive use of Vitamin D supplements. Levels of serum uric acid have been positively ... The risk, however, varies depending on the degree of hyperuricemia. When levels are between 415 and 530 μmol/L (7 and 8.9 mg/dl ...
Figg WD (February 1990). "Cyclosporine-induced hyperuricemia and gout". The New England Journal of Medicine. 322 (5): 334-336. ...
Jiménez RT, Puig JG (2012). "Purine Metabolism in the Pathogenesis of Hyperuricemia and Inborn Errors of Purine Metabolism ... "Primary Metabolic and Renal Hyperuricemia". Genetic Diseases of the Kidney. pp. 651-660. doi:10.1016/b978-0-12-449851-8.00038-3 ...
"Gout, Hyperuricemia & Chronic Kidney Disease". The National Kidney Foundation. 24 December 2015. Retrieved 24 November 2017. " ...
... is used to treat chronic gout and hyperuricemia. Febuxostat is typically recommended only for people who cannot ... Febuxostat for the management of hyperuricaemia in people with gout (TA164) Chapter 4. Consideration of the evidence Archived ... for Hyperuricemia and Gout". American Family Physician. 81 (10): 1287. Retrieved 15 April 2020. Portal: Medicine (Webarchive ... Receives FDA Approval for the Chronic Management of Hyperuricemia in Patients with Gout Teijin. January 21, 2011 Press release ...
Long-standing hyperuricemia can cause deposition of monosodium urate crystals in or around joints, resulting in an arthritic ... The build up of uric acid causing high amount of uric acid in blood, is a condition called hyperuricemia. ... Bardin T, Richette P (March 2014). "Definition of hyperuricemia and gouty conditions". Current Opinion in Rheumatology. 26 (2 ...
Signs include hyperkalemia, hyperuricemia, and hyperphosphatemia. TLS is very serious and can lead to death if it is not ...
Mutations in the gene lead to hyperuricemia. At least 67 disease-causing mutations in this gene have been discovered: Some men ...
Hyperuricemia in Dalmatians (as in all breeds) is inherited, but unlike other breeds, the normal gene for a uric acid ... Hyperuricemia in Dalmatians responds to treatment with orgotein, the veterinary formulation of the antioxidant enzyme ... Dalmatians' livers have trouble breaking down uric acid, which can build up in the blood serum (hyperuricemia) causing gout. ... Therefore, there is no possibility of eliminating hyperuricemia among pure-bred Dalmatians. The only possible solution to this ...
Schepers GW (1981). "Benzbromarone therapy in hyperuricaemia; comparison with allopurinol and probenecid". The Journal of ... a review of its pharmacological properties and therapeutic use in gout and hyperuricaemia". Drugs. 14 (5): 349-66. doi:10.2165/ ... "Efficacy of allopurinol and benzbromarone for the control of hyperuricaemia. A pathogenic approach to the treatment of primary ... experience with benzbromarone in the management of gout and hyperuricaemia" (PDF). South African Medical Journal = Suid- ...
Solak, Yalcin; Karagoz, Ali; Atalay, Huseyin (October 2010). "Sugar-sweetened soda consumption, hyperuricemia, and kidney ...
SPATA16 Glomerulocystic kidney disease with hyperuricemia and isosthenuria; 609886; UMOD Glomerulopathy with fibronectin ...
Overdoses have been associated with hematuria and hyperuricemia. Rifapentine should be avoided in patients with an allergy to ...
"OMIM Entry - # 613845 - HYPERURICEMIA, PULMONARY HYPERTENSION, RENAL FAILURE, AND ALKALOSIS SYNDROME; HUPRAS". www.omim.org. ... "Orphanet: Hyperuricemia pulmonary hypertension renal failure alkalosis syndrome". www.orpha.net. Retrieved 20 January 2017. " ... The acronym stands for Hyperuricemia, Pulmonary hypertension, Renal failure in infancy and Alkalosis. And it's due to mutations ... "Mutations in the Mitochondrial Seryl-tRNA Synthetase Cause Hyperuricemia, Pulmonary Hypertension, Renal Failure in Infancy and ...
Lee SJ, Terkeltaub RA (June 2006). "New developments in clinically relevant mechanisms and treatment of hyperuricemia". Curr ... Ben Salem, C.; Slim, Raoudha; Fathallah, Neila; Hmouda, Houssem (2016). "Drug-induced hyperuricaemia and gout". Rheumatology. ... "Effect on serum uric acid levels of drugs prescribed for indications other than treating hyperuricaemia". Curr. Pharm. Des. 11 ... but are contraindicated in persons with conditions including hyperuricemia and gout. Uricosuria Hamada T, Ichida K, Hosoyamada ...
... also can lead to gout caused by hyperuricemia. Hyperglycemia is also a common side effect.[citation needed] The ...
2006). "Dose Adjustment of Allopurinol According to Creatinine Clearance Does not Provide Adequate Control of Hyperuricemia in ... Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. (2012) This is part 1 of ... Part 1: Systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia". Arthritis Care & Research. ... Dose adjustment of allopurinol according to creatinine clearance does not provide adequate control of hyperuricemia in patients ...
It is primarily used in treating gout and hyperuricemia. Probenecid was developed as an alternative to caronamide to ... Probenecid is primarily used to treat gout and hyperuricemia. Probenecid is sometimes used to increase the concentration of ...
Hyperuricemia Medication~medication at eMedicine "Acetazolamide: mechanism of action". www.openanesthesia.org. Retrieved 2017- ...
It is also associated with glucose intolerance and hyperuricemia.[citation needed] In medicine, combined hyperlipidemia (or - ...
Hyperuricaemia or hyperuricemia is an abnormally high level of uric acid in the blood. In the pH conditions of body fluid, uric ... Hyperuricemia can be detected using blood and urine tests.[citation needed] Medications used to treat hyperuricemia are divided ... Not all people with hyperuricemia develop gout. Many factors contribute to hyperuricemia, including genetics, insulin ... for hyperuricemia. Causes of hyperuricemia that are of mixed type have a dual action, both increasing production and decreasing ...
For years, hyperuricemia has been identified with or thought to be the same as gout, but uric acid has now been identified as a ... certain pathophysiologic aspects of hyperuricemia are still not clearly understood. ... encoded search term (Hyperuricemia) and Hyperuricemia What to Read Next on Medscape ... While decreased urate filtration may not cause primary hyperuricemia, it can contribute to the hyperuricemia of kidney ...
To determine if hyperuricemia and gouty arthritis are independent risk factors for acute myocardial infarction (MI) and, if so ... Hyperuricemia is well known to be an independent risk factor for atherosclerotic diseases in general ([7]), and since chronic ... We used data from the MRFIT to test the following hypotheses: that hyperuricemia is an independent risk factor for acute MI, ... The caricature of the typical patient with hyperuricemia is an obese middle-aged man with hypertension, diabetes mellitus, and ...
Duzallo has received FDA approval as a once-daily oral treatment for hyperuricemia associated with gout in patients who have ... Duzallo is the first drug that combines the current standard of care for the treatment of hyperuricemia associated with gout- ... Duzallo Gains FDA Nod for Hyperuricemia in Uncontrolled Gout. August 22, 2017. Article ... "This represents an important and needed new option in the treatment of hyperuricemia." ...
Hyperuricemia - Pipeline Review, H1 2016 - New Market Study Published. Hyperuricemia - Pipeline Review, H1 2016 - New Market ... Global Markets Directs, Hyperuricemia - Pipeline Review, H1 2016, provides an overview of the Hyperuricemia pipeline ... The report reviews latest news related to pipeline therapeutics for Hyperuricemia About Fast Market Research Fast Market ... The report assesses Hyperuricemia therapeutics based on drug target, mechanism of action (MoA), route of administration (RoA) ...
Hyperuricaemia in patients with right or left heart failure. MM Hoeper, JM Hohlfeld, H Fabel ... Hyperuricaemia in patients with right or left heart failure Message Subject (Your Name) has sent you a message from European ...
How should hyperuricemia be treated in a patient with allopurinol hypersensitivity?. Stefan D. Monev, MD ... How should hyperuricemia be treated in a patient with allopurinol hypersensitivity? Message Subject (Your Name) has sent you a ...
Drugs Causing Hyperuricemia[2] (click image for list). Your Drug Induced Hyperuricemia and Gout. Drugs for conditions other ... Drug Induced Hyperuricemia and Gout References. *Pearson, Norma Lynn. "Hyperuricemia and Gout: Some Medications can ... Drug Induced Hyperuricemia and Gout. GoutPal Facts For Secondary Gout. September 23, 2020 December 15, 2012 ... Drug Induced Hyperuricemia and Gout Related Topics. Please remember: to find more related pages that are relevant to you, use ...
A new study suggests that weekend catch-up sleep may minimize the risk of hyperuricemia in postmenopausal women. Study results ... including hyperuricemia (elevated serum uric acid), which can often lead to gout and other life-threatening conditions such as ... Hyperuricemia is most often associated with gout, an increasingly common form of arthritis characterized by severe pain, ... The prevalence of hyperuricemia increases with age in all populations and especially in women after menopause. Thats because, ...
... a Treatment for Hyperuricemia and Gout, in China is posted. ... In addition, hyperuricemia is known to be associated with ... 1 For the estimated data regarding the number of patients with hyperuricemia as well as the number of patients with gout:. * * ... Data of morbidity prevalence rate - Rui Liu et al., Prevalence of Hyperuricemia and Gout in Mainland China from 2000 to 2014: A ... Dotinurad is a treatment for gout and hyperuricemia created by FUJI YAKUHIN CO., LTD. Dotinurad selectively inhibits URAT1 and ...
This cross-sectional study of 42 332 Han Chinese from southwestern China investigated the combined effect of hyperuricaemia and ... While hyperuricaemia and overweight/obesity can act alone to increase the prevalence of hypertension, few studies have examined ... Background: While hyperuricaemia and overweight/obesity can act alone to increase the prevalence of hypertension, few studies ... Conclusion: Co-occurrence of hyperuricaemia and overweight/obesity increases risk of hypertension more than either morbidity on ...
1989) Management of hyperuricemia. in Arthritis and allied conditions. ed McCarthy DJ (Lee and Febiger, Philadelphia), 11th ed. ... 1989) Clinical gout and the pathogenesis of hyperuricemia. in Arthritis and allied conditions. ed McCarty DJ (Lee and Febiger, ... 1990) Strategies and controversies in the treatment of gout and hyperuricemia. Baillieres Clin Rheumatol 4:177-183, . ... Although most standard sources of information recommend uricosurics to correct hyperuricaemia in underexcretors,5-8 ,29 ,30this ...
Instead, 9 of the 14 patients presented with hyperuricemia, including the 3 probands. The age at onset of hyperuricemia in the ... Heteroplasmic and homoplasmic m.616T,C in mitochondria tRNAPhe promote isolated chronic kidney disease and hyperuricemia. ... Routine blood tests revealed renal insufficiency (serum creatinine [Scr], 257 μmol/L; CCR 10.8 mL/min), hyperuricemia (serum ... and hyperuricemia at age 12 during a routine physical examination. The Scr of proband 3 was 108.0 μmol/L and the serum uric ...
Participants aged , 50 years who sleep less than 4 hours a day have a higher risk of hypertension and hyperuricemia than those ... This study revealed that short sleep duration is associated with an increased risk of hyperuricemia and hypertension. Patients ... Previous studies have reported that sleep duration may increase the risk of hypertension and hyperuricemia. However, the ... We aimed to assess the association between sleep duration, hypertension, and hyperuricemia in a population-based cross- ...
Hyperuricaemia as a cause of acute renal failure complicating cardiopulmonary bypass surgery. ... Hyperuricaemia as a cause of acute renal failure complicating cardiopulmonary bypass surgery. ...
The OR (95% CI) for the risk of developing hyperuricemia was 1.56(1.05-2.32) at the cumulative dust exposure of ≥ 30.02 (mg/m3/ ... Interventions for shift work, heat and dust may help to reduce the incidence rate of hyperuricemia and improve the health of ... The case group consisted of a total of 641 cases of hyperuricemia identified during the study period, while 641 non- ... The incidence rate of hyperuricemia among workers in the steel company was 17.30%, with an incidence density of 81.32/1,000 ...
Therapeutic Efficacy of Allopurinol in Mania Associated With Hyperuricemia Journal Articles ...
For years, hyperuricemia has been identified with or thought to be the same as gout, but uric acid has now been identified as a ... certain pathophysiologic aspects of hyperuricemia are still not clearly understood. ... encoded search term (Hyperuricemia) and Hyperuricemia What to Read Next on Medscape ... Hyperuricemia Differential Diagnoses. Updated: Feb 22, 2016 * Author: Yasir Qazi, MD; Chief Editor: Vecihi Batuman, MD, FACP, ...
Hyperuricemia and Progression of CKD in Children and Adolescents: The Chronic Kidney Disease in Children (CKiD) Cohort Study. ... "Hyperuricemia" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... Hyperuricemia can be acquired, drug-induced or genetically determined (LESCH-NYHAN SYNDROME). It is associated with ... This graph shows the total number of publications written about "Hyperuricemia" by people in this website by year, and whether ...
Jeyaruban, A., Hoy, W., Cameron, A., Healy, H., Wang, Z., Zhang, J., and Mallett, A. (2021) Hyperuricaemia, gout and ... Conclusion Hyperuricaemia seemed to be independently associated with faster CKD progression or renal death. This was not ... Introduction There is scant data on the role of hyperuricaemia, gout and allopurinol treatment in chronic kidney disease (CKD ... These data suggest that hyperuricaemia is likely the effect and not the cause of CKD or CKD progression. ...
Hyperuricemia has been recently identified as a factor of progression of CKD. Identifying factors associated with hyperuricemia ... In this sample of non-dialysed CKD patients in Cameroon, about 7 out of 10 had hyperuricemia. Hyperuricemia was independently ... We sought to determine the prevalence and factors associated with hyperuricemia in non-dialysed CKD adult patients in Cameroon ... Sixty-nine (67%) had hyperuricemia. Patients age (OR: 1.08, 95% CI: 1.03-1.13), estimated glomerular filtration rate (OR: 0.94 ...
Elitek 2020 U.S. PROMOTIONAL AUDIT REPORT Published July 2021 • 19 Pages The 5 Key Questions Addressed by this Report:... ...
Liya M. B. Pillai,DieticianGout is a condition in which the level of uric acid in our body increases gradually.[...]
Prevalence of Diabetes in Patients with Hyperuricemia and Gout: A Systematic Review and Meta-analysi… ... The chemistry, processing, and preclinical anti-hyperuricemia potential of tea: a comprehensive revi… ... A wide-range UAC sensor for the classification of hyperuricemia in spot samples. ...
Hyperuricemia was defined as uric acid levels ≥ 7.0 mg/dL in men and ≥ 5.8 mg/dL in women. The association of ... In women, the OR for hyperuricemia for those who consume >1.0- < 3.0 SB/day was 1.33 (95% CI; 1.04-1.70) and 1.35 (95% CI ... The odds ratios (OR) for hyperuricemia in men who consume 0.5-1 SB/day was 1.59 (95% CI; 1.05-2.40) and 2.29 (95% CI; 1.55-3.38 ... Men and women with high SB consumption and a body mass index (BMI) ≥ 25 Kg/m2 had greater risk for hyperuricemia than men and ...
Hyperuricemia is a condition that forms when there is an excess level of uric acid in the blood. It isnt dangerous on its own ... Hyperuricemia isnt dangerous on its own and rarely produces symptoms. However, hyperuricemia can lead to gout, which is when ... You can prevent hyperuricemia by keeping your uric acid levels low. Ways to achieve this include eating a diet low in purines ( ... Hyperuricemia is a condition that forms when there is an excess level of uric acid in the blood. ...
Mutations in the SLC2A9 gene cause hyperuricosuria and hyperuricemia in the dog. PLoS Genet 4:e1000246, 2008. Pubmed reference ...
What is Hyperuricemia?. October 10, 2023. by Steve Hyperuricemia is just a fancy medical term for "high amount of uric acid in ... Hyperuricemia is often associated with a condition called gout, which is a form of arthritis. When uric acid levels are too ... Hyperuricemia can also be linked to other health problems, including kidney stones and certain kidney diseases. In some cases, ... Treatment for Hyperuricemia often involves managing the underlying causes and may include lifestyle changes, dietary ...
Primary hyperuricemia can be aggravated by poor dietary habits.. Secondary hyperuricemia [4] * Decreased uric acid excretion: ... Hyperuricemia. *Can be idiopathic (primary hyperuricemia) or secondary to insufficient excretion or increased production of ... Acute gout flare: often elevated (hyperuricemia) ; may also be normal or low ... Primary hyperuricemia. *Idiopathic extracellular supersaturation of uric acid. *No history of comorbidities or medications that ...
If you are suffering from hyperuricemia, bordfreesupply.com can provide you with the drugs and medications you need to manage ... Hyperuricemia is a medical condition in which the body has too much uric acid in the blood. It can lead to painful and ... What is hyperuricemia? cause of hyperuricemia? Hyperuricemia occurs when the blood has a high level of ... Hyperuricemia is a medical condition in which the body has too much uric acid in the blood. It can lead to painful and ...
  • Dotinurad is a treatment for gout and hyperuricemia created by FUJI YAKUHIN CO., LTD. Dotinurad selectively inhibits URAT1 and has a small effect on other transporters, so it reduces serum uric acid levels at lower doses. (eisai.com)
  • You can prevent hyperuricemia by keeping your uric acid levels low. (footfiles.com)
  • If you suspect you have Hyperuricemia or are experiencing symptoms related to high uric acid levels, it's essential to consult a healthcare professional for a proper diagnosis and guidance on appropriate management. (goutreference.com)
  • It is typically associated with hyperuricemia , but can also occur if uric acid levels are normal. (amboss.com)
  • Gout is primarily associated with high Uric Acid levels in blood (Hyperuricemia) that causes joints pain or arthritic symptoms. (ayurvedic-herbalist.com)
  • High Uric Acid levels in blood or Hyperuricemia is the universal factor present in Gout. (ayurvedic-herbalist.com)
  • Background: Hyperuricemia belongs to metabolic syndromes where increased uric acid levels are identified in the blood serum. (currentmedicinalchemistry.com)
  • While decreased urate filtration may not cause primary hyperuricemia, it can contribute to the hyperuricemia of kidney insufficiency. (medscape.com)
  • Desideri G, Puig JG, Richette P. The management of hyperuricemia with urate deposition. (medscape.com)
  • The management of chronic gout includes lifestyle modifications and urate-lowering medications (e.g., allopurinol ) to control hyperuricemia . (amboss.com)
  • Tophi are deposits of solid urate crystals that elicit a foreign body reaction of mononuclear cells with granuloma formation, this occurs after longstanding severe hyperuricemia. (med2date.com)
  • We tested this hypothesis in a bi-racial cohort of younger African-American and white men and women.Methods: Data from 5,049 participants at the Coronary Artery Risk Development in Young Adults (CARDIA) cohort baseline (1985 to1986) and follow-up for up to 20 years of individuals without hyperuricemia (defined as a serum urate of 6.8 mg/dL or more) at baseline were utilized. (umn.edu)
  • We determined associations between race, serum urate and the development of hyperuricemia in sex-specific cross-sectional and longitudinal analyses. (umn.edu)
  • African-American women developed a significantly increased risk of hyperuricemia when compared to white women (HR = 2.31 (1.34 to 3.99)).Conclusions: Young African-American men and women had lower concentrations of serum urate than whites. (umn.edu)
  • Duzallo is not recommended for treatment of patients with asymptomatic hyperuricemia. (hcplive.com)
  • Decreased renal excretion and/or increased production of uric acid leads to hyperuricemia , which is commonly asymptomatic but also predisposes to gout . (amboss.com)
  • When high blood uric acid is present without causing any symptoms, it is simply called Silent or Asymptomatic Hyperuricemia . (ayurvedic-herbalist.com)
  • Asymptomatic hyperuricemia is a concept associated with laboratory evidence of elevated serum uric acid without clinical disease known to be caused by hyperuricemia. (medicsciences.com)
  • Some people with hyperuricemia do not develop gout (known as asymptomatic hyperuricemia). (holisticlivingannex.com)
  • Nevertheless, do not take asymptomatic hyperuricemia lightly as it is still considered a precursor state to the development of gout. (holisticlivingannex.com)
  • See "Asymptomatic hyperuricemia" . (medilib.ir)
  • Duzallo has received FDA approval as a once-daily oral treatment for hyperuricemia associated with gout in patients who have not achieved target serum uric acid (sUA) levels with a medically appropriate daily dose of allopurinol alone, Ironwood Pharmaceuticals, Inc. announced in a press release . (hcplive.com)
  • Duzallo is the first drug that combines the current standard of care for the treatment of hyperuricemia associated with gout-allopurinol-with the most recent FDA-approved treatment for this condition, lesinurad, the company stated. (hcplive.com)
  • How should hyperuricemia be treated in a patient with allopurinol hypersensitivity? (ccjm.org)
  • Efficacy of allopurinol and benzbromarone for the control of hyperuricaemia. (bmj.com)
  • Introduction There is scant data on the role of hyperuricaemia, gout and allopurinol treatment in chronic kidney disease (CKD). (edu.au)
  • Therefore, our aim is to investigate the possible associations between hyperuricaemia, gout, prescription of allopurinol and renal outcomes in patients with CKD. (edu.au)
  • 0.36 mmol/L. Association of delta estimated glomerular filtration rate (eGFR) with gout, allopurinol treatment and hyperuricaemia were analysed. (edu.au)
  • Proportion of patients with gout, hyperuricaemia and allopurinol treatment increased with advanced CKD stages. (edu.au)
  • A suggested approach to lowering the risk of hyperuricemia is adequate sleep duration that unfortunately becomes more of a challenge during the postmenopausal phase. (medicalxpress.com)
  • In this latest study involving nearly 1,900 participants, the researchers hypothesized that weekend catch-up sleep could be a solution to making up for lost sleep during the week and effectively lowering the risk of hyperuricemia in postmenopausal women, who often struggle to get sufficient sleep. (medicalxpress.com)
  • Hyperuricemia may be the result of increased production of uric acid, decreased excretion of uric acid, or both increased production and reduced excretion. (wikipedia.org)
  • Causes of hyperuricemia can be classified into three functional types: increased production of uric acid, decreased excretion of uric acid, and mixed type. (wikipedia.org)
  • The principal drugs that contribute to hyperuricemia by decreased excretion are the primary antiuricosurics. (wikipedia.org)
  • Hyperuricemia may occur because of decreased excretion (underexcretors), increased production (overproducers), or a combination of those two mechanisms. (medscape.com)
  • INTRODUCTION - Reduced uric acid excretion can occur after kidney transplantation, leading to hyperuricemia and, in some cases, gout [ 1-4 ]. (medilib.ir)
  • One man was affected by hyperuricemia, two had proteinuria, three had high excretion of beta-2-microglobulin and one had low urinary acidifying ability. (cdc.gov)
  • Decreased renal excretion is by far the most common cause of hyperuricemia. (msdmanuals.com)
  • This represents an important and needed new option in the treatment of hyperuricemia. (hcplive.com)
  • On the other hand new evidence regarding the benefits of treatment of hyperuricemia cannot be ignored. (medicsciences.com)
  • Previous studies have reported that sleep duration may increase the risk of hypertension and hyperuricemia. (ndhu.edu.tw)
  • We investigated whether sleep duration was independently associated with hypertension and hyperuricemia. (ndhu.edu.tw)
  • We aimed to assess the association between sleep duration, hypertension, and hyperuricemia in a population-based cross-sectional study. (ndhu.edu.tw)
  • There were excellent response rates to sleep duration associated with hypertension and hyperuricemia questions and measurements representative sample of Taiwan population. (ndhu.edu.tw)
  • The independent risk relationship between hyperuricemia and acute MI is confirmed. (natap.org)
  • The relationship between hyperuricemia and gout is however, unclear. (holisticlivingannex.com)
  • Development of gout - which is a painful, short-term disorder - is the most common consequence of hyperuricemia, which causes deposition of uric acid crystals usually in joints of the extremities, but may also induce formation of kidney stones, another painful disorder. (wikipedia.org)
  • The prevalence of hyperuricemia increases with age in all populations and especially in women after menopause. (medicalxpress.com)
  • Study results suggest that weekend catch-up sleep is linked with a lower prevalence of hyperuricemia in postmenopausal women with insufficient sleep. (medicalxpress.com)
  • This study shows that weekend catch-up sleep of just 1 to 2 hours was linked with a lower prevalence of hyperuricemia in postmenopausal women with insufficient sleep. (medicalxpress.com)
  • While hyperuricaemia and overweight/obesity can act alone to increase the prevalence of hypertension, few studies have examined their combined effect. (uwi.edu)
  • We sought to determine the prevalence and factors associated with hyperuricemia in non-dialysed CKD adult patients in Cameroon. (biomedcentral.com)
  • Although hyperuricemia is a recognised feature of CKD, studies evaluating its prevalence in CKD are relatively sparse in SSA. (biomedcentral.com)
  • We therefore sought to determine the prevalence and factors associated with hyperuricemia in non-dialysed adult CKD patients in Cameroon, in order to generate findings that would help determine interventions to reduce CKD mortality, particularly in resources limited countries. (biomedcentral.com)
  • Prevalence of hyperuricaemia in an Eastern Chinese population:a cross-sectional study [J]. BMJ Open, 2020, 10(5):e035614. (magtech.com.cn)
  • Unless high blood levels of uric acid are determined in a clinical laboratory, hyperuricemia may not cause noticeable symptoms in most people. (wikipedia.org)
  • Foods high in the purines adenine and hypoxanthine may aggravate symptoms of hyperuricemia. (wikipedia.org)
  • Hyperuricemia isn't dangerous on its own and rarely produces symptoms. (footfiles.com)
  • People who have hyperuricemia but do not have gout symptoms do not need medical treatment. (cdc.gov)
  • Primary hyperuricemia can be aggravated by poor dietary habits. (amboss.com)
  • That's because, according to previous studies, hyperuricemia is inversely related to estrogen levels. (medicalxpress.com)
  • In some studies hyperuricemia is present in 40 to 60% of subjects with untreated hypertension. (cmeindia.in)
  • Several studies have shown that too little or too much sleep is related to poor health problems such as hyperuricemia, hyperlipidemia, hypertension, type 2 diabetes, obesity, cardiovascular disease, and even mortality. (medicalxpress.com)
  • This cross-sectional study of 42 332 Han Chinese from southwestern China investigated the combined effect of hyperuricaemia and overweight/obesity on risk of hypertension in the entire sample as well as in different genders and age groups. (uwi.edu)
  • Similarly, the increase in hypertension risk in the presence of both hyperuricaemia and overweight/obesity (OR = 6.777, 95%CI 6.133, 7.489) was significantly greater than the increase in the presence of hyperuricaemia alone (OR = 3.168, 95%CI 2.705, 3.711) or overweight/obesity alone (OR = 3.693, 95% CI 3.503, 3.893). (uwi.edu)
  • Co-occurrence of hyperuricaemia and overweight/obesity increases risk of hypertension more than either morbidity on its own, and this risk differential is significantly greater in women than men. (uwi.edu)
  • Shiraishi H, Une H. The effect of the interaction between obesity and drinking on hyperuricemia in Japanese male office workers. (medscape.com)
  • Factors that can contribute to Hyperuricemia include a diet rich in purine-containing foods, obesity, excessive alcohol consumption, certain medications, and genetic factors. (goutreference.com)
  • In a study of over 2500 people resident in Taiwan, a blood lead level exceeding 7.5 microg/dL (a small elevation) had odds ratios of 1.92 (95% CI: 1.18-3.10) for renal dysfunction and 2.72 (95% CI: 1.64-4.52) for hyperuricemia. (wikipedia.org)
  • To determine if hyperuricemia and gouty arthritis are independent risk factors for acute myocardial infarction (MI) and, if so, whether they are independent of renal function, diuretic use, metabolic syndrome, and other established risk factors. (natap.org)
  • Hyperuricaemia as a cause of acute renal failure complicating cardiopulmonary bypass surgery. (bmj.com)
  • Reappraisal of the pathogenesis and consequences of hyperuricemia in hypertension, cardiovascular disease, and renal disease. (medscape.com)
  • Conclusion Hyperuricaemia seemed to be independently associated with faster CKD progression or renal death. (edu.au)
  • Hyperuricemia in CKD has been mostly attributed to declining renal function [ 28 ]. (biomedcentral.com)
  • Hyperuricemia is most often associated with gout, an increasingly common form of arthritis characterized by severe pain , redness, and tenderness in joints. (medicalxpress.com)
  • Hyperuricemia and Progression of CKD in Children and Adolescents: The Chronic Kidney Disease in Children (CKiD) Cohort Study. (childrensmercy.org)
  • The observation that longstanding hyperuricemia is associated with chronic tubulointerstitial disease and intrarenal vaso-constriction raised the hypothesis that hyperuricemia might contribute to chronic CSA nephropathy. (ewha.ac.kr)
  • Hyperuricemia and risk of stroke: a systematic review and meta-analysis. (medscape.com)
  • 13. What a systematic review and meta-analysis 0n Hyperuricemia and incident hypertension tells? (cmeindia.in)
  • Fewer studies have examined the risk of hyperuricemia and gout in patients receiving tacrolimus and/or mycophenolate mofetil, which have largely replaced the use of cyclosporine and azathioprine , respectively. (medilib.ir)
  • Myogenic hyperuricemia, as a result of the myokinase (adenylate kinase) reaction and the Purine Nucleotide Cycle running when ATP reservoirs in muscle cells are low (ADP>ATP), is a common pathophysiologic feature of glycogenoses such as GSD-III, GSD-V and GSD-VII, as they are metabolic myopathies which impair the ability of ATP (energy) production for the muscle cells to use. (wikipedia.org)
  • For years, hyperuricemia has been identified with or thought to be the same as gout, but uric acid has now been identified as a marker for a number of metabolic and hemodynamic abnormalities. (medscape.com)
  • Hyperuricemia is the second most common metabolic disease after diabetes mellitus in China. (eisai.com)
  • In addition, hyperuricemia is known to be associated with various diseases in the urinary system, endocrine system, metabolic system, cardio-cerebrovascular system etc., including gout. (eisai.com)
  • Hyperuricemia cosegregating with osteogenesis imperfecta has been shown to be associated with a mutation in GPATCH8 using exome sequencing A ketogenic diet impairs the ability of the kidney to excrete uric acid, due to competition for transport between uric acid and ketones. (wikipedia.org)
  • Elevated blood lead is significantly correlated with both impaired kidney function and hyperuricemia (although the causal relationship among these correlations is not known). (wikipedia.org)
  • Hyperuricemia can also be linked to other health problems, including kidney stones and certain kidney diseases. (goutreference.com)
  • EPIDEMIOLOGY AND RISK FACTORS - Hyperuricemia and gout are common in kidney transplant recipients, particularly in those receiving the calcineurin inhibitor cyclosporine to prevent graft rejection [ 1,2,5-15 ]. (medilib.ir)
  • In one study of kidney transplant recipients, the incidence of hyperuricemia was 84 percent in those treated with cyclosporine and prednisone versus 30 percent in those treated with azathioprine and prednisone [ 1 ]. (medilib.ir)
  • In one study of 121 kidney transplant recipients treated with a tacrolimus- and mycophenolate-based regimen, the incidence of hyperuricemia at one year posttransplant was 38 percent [ 9 ]. (medilib.ir)
  • Concurrent diuretic use, kidney function impairment due to rejection, higher body mass index, older age, and male sex are other risk factors for hyperuricemia and gout [ 2,11 ]. (medilib.ir)
  • However, in clinical practice, raised serum uric acid level in CKD is associated with a combination of several other factors, as not every CKD patient presents with hyperuricemia. (biomedcentral.com)
  • Methods: Authors have performed a thorough literature research from 2010-2023 using keywords such as hyperuricemia, gout, diagnosis, guidelines, drug delivery and clinical trials. (currentmedicinalchemistry.com)
  • Hyperuricemia as a risk factor for cardiovascular disease: clinical review. (bvsalud.org)
  • These data suggest that hyperuricaemia is likely the effect and not the cause of CKD or CKD progression. (edu.au)
  • Hyperuricemia has been recently identified as a factor of progression of CKD. (biomedcentral.com)
  • Correlation analysis of hyperuricemia with dietary vitamin D intake inmale youngsters[J]. Chinese Journal of Child Health Care, 2021, 29(6): 609-613. (magtech.com.cn)
  • Association between low dietary zinc and hyperuricaemia in middle-aged and older males in China: a cross-sectional study. (medscape.com)
  • Association between Dietary Zinc Intake and Hyperuricemia among Adults in the United States. (qxmd.com)
  • We aim to explore the associations between dietary zinc intake and hyperuricemia (HU) in United States (US) adults. (qxmd.com)
  • Additionally, the report provides an overview of key players involved in therapeutic development for Hyperuricemia and features dormant and discontinued projects. (clickpress.com)
  • Dotinurad is a new therapeutic agent for gout and hyperuricemia discovered by FUJI YAKUHIN. (eisai.com)
  • Dalbeth N, Merriman T. Crystal ball gazing: new therapeutic targets for hyperuricaemia and gout. (medscape.com)
  • Hyperuricaemia or hyperuricemia is an abnormally high level of uric acid in the blood. (wikipedia.org)
  • Sleep deprivation, especially common during postmenopause, has been linked with a number of health problems, including hyperuricemia (elevated serum uric acid), which can often lead to gout and other life-threatening conditions such as heart disease. (medicalxpress.com)
  • However, hyperuricemia can lead to gout, which is when needle-like crystals of uric acid begin to deposit themselves into the body's joints, tendons and tissue. (footfiles.com)
  • The caricature of the typical patient with hyperuricemia is an obese middle-aged man with hypertension, diabetes mellitus, and hyperlipidemia who is given to excessive drinking. (natap.org)
  • Hyperuricemia and Gout: Some Medications can 'Precipitate'Gout. (goutpal.com)
  • If you are suffering from hyperuricemia, bordfreesupply.com can provide you with the drugs and medications you need to manage your condition. (borderfreesupply.com)
  • Changing or stopping medications associated with hyperuricemia (like diuretics) may also help. (cdc.gov)
  • The report provides comprehensive information on the therapeutics under development for Hyperuricemia, complete with analysis by stage of development, drug target, mechanism of action (MoA), route of administration (RoA) and molecule type. (clickpress.com)
  • Global Markets Direct's, 'Hyperuricemia - Pipeline Review, H1 2016', provides an overview of the Hyperuricemia pipeline landscape. (clickpress.com)
  • Hyperuricemia does not always cause gout. (cdc.gov)
  • Missense mutations in UMOD cause tubulointerstitial nephropathy with hyperuricemia , previously named MCKD type 2 or juvenile hyperuricemic nephropathy type 1. (medscape.com)
  • Sweetened beverage consumption and the risk of hyperuricemia in Mexican adults: a cross-sectional study. (medscape.com)
  • Finally, enhanced reabsorption of uric acid distal to the site of secretion is the mechanism thought to be responsible for the hyperuricemia observed with diuretic therapy and diabetes insipidus. (medscape.com)
  • Carotid-femoral pulse wave velocity (CF-PWV) was significantly higher in hypertension subjects with hyperuricemia compared to hypertension without hyperuricemia subjects, and serum uric acid was an independent associating factor of CF-PWV. (cmeindia.in)
  • During longitudinal follow-up, African-American women had a significantly increased risk of developing hyperuricemia when compared with white women, a difference that was not observed in men. (umn.edu)
  • Hyperuricemia was an independent risk factor for acute MI in the multivariable regression models, with an odds ratio (OR) of 1.11 (95% confidence interval [95% CI] 1.08-1.15, P (natap.org)
  • In separate analyses, a relationship between gout and the risk of acute MI was evident among those with and without those hyperuricemia. (natap.org)
  • Avoid alcohol as it is known to precipitate acute gout attacks and also affects uric acid metabolism that can cause hyperuricemia. (holisticlivingannex.com)
  • By identifying patients who are at higher risk for hyperuricemia , pharmacists can monitor patients when suspected agents are added to their regimen. (goutpal.com)
  • A new study suggests that weekend catch-up sleep may minimize the risk of hyperuricemia in postmenopausal women. (medicalxpress.com)
  • This study revealed that short sleep duration is associated with an increased risk of hyperuricemia and hypertension. (ndhu.edu.tw)
  • Besides, the risk of hyperuricemia in females who slept for more than 8 hours was 1.019 times that of those who slept for 7 hours. (ndhu.edu.tw)
  • As already mentioned earlier, hyperuricemia may indicate an increased risk of gout. (holisticlivingannex.com)
  • Conclusion: Hyperuricemia is associated with an increased risk for incident hypertension, independent of traditional hypertension risk factors. (cmeindia.in)
  • Hyperuricemia increased the relative risk of hypertension by approximately 30% in men under 60 and by 2.6-fold in women under 40. (cmeindia.in)
  • However, there is controversy about whether hyperuricemia is an independent risk factor for developing cardiovascular disease . (bvsalud.org)
  • Hyperuricemia frequently complicates cyclosporine (CSA) therapy. (ewha.ac.kr)
  • To answer this question, we performed a recent literature review of relevant published material to assess the association of hyperuricemia with four major cardiovascular diseases hypertension , coronary heart disease , heart failure and atrial fibrillation . (bvsalud.org)
  • Association between Dietary Magnesium Intake and Hyperuricemia. (medscape.com)
  • Objective To analyze the correlations of hyperuricemia (HU) with dietary vitamin D intake in male youngsters, in order to provide new preventive method to male youngsters with HU. (magtech.com.cn)
  • Dietary education is important for patients with hyperuricemia. (medscape.com)
  • Furthermore, it is estimated that currently in China, the number of patients with hyperuricemia is approximately 190 million and the number of patients with gout is approximately 16 million. (eisai.com)
  • Following commercialization, Eisai will aim to contribute to patients with hyperuricemia that is unmet medical needs by utilizing the knowledge and networks that Eisai has cultivated through its China business. (eisai.com)
  • Through the development and commercialization of dotinurad, Eisai and FUJI YAKUHIN will provide new treatment options for hyperuricemia and gout in China and contribute to improving the quality of life of patients. (eisai.com)
  • Identifying factors associated with hyperuricemia in CKD patients would help determine interventions to reduce CKD mortality, particularly in resources limited countries. (biomedcentral.com)
  • In this sample of non-dialysed CKD patients in Cameroon, about 7 out of 10 had hyperuricemia. (biomedcentral.com)
  • In CKD patients, factors associated with hyperuricemia have not been fully elucidated. (biomedcentral.com)
  • It is used by patients in gout and hyperuricemia, and their family members, friends, nurses, and related medical staff. (guidelines-registry.cn)
  • La greffe rénale n?est pas encore pratiquée en RDC, ce qui oblige les patients à se faire opérer à l?étranger. (bvsalud.org)
  • Nous avons colligé les dossiers des patients qui ont bénéficié d?une greffe rénale à l?étranger (86% en Inde) et dont le suivi post-greffe a été effectué dans les hôpitaux de Kinshasa entre 2000 et 2017. (bvsalud.org)
  • 0nze patients (38%) ont été repris en dialyse. (bvsalud.org)
  • Nonobstant un faible échantillonnage, ces donnent révèlent une moins bonne survie des greffons après la transplantation rénale chez les patients suivis à Kinshasa, notamment lorsque la prise en charge n?est pas faite en milieu spécialisé. (bvsalud.org)
  • Conclusion: The available drugs and dosage forms are limited, and therefore, scientific society should focus on the development of more efficient drug delivery systems for hyperuricemia and gout management. (currentmedicinalchemistry.com)
  • The greater the degree and duration of hyperuricemia, the greater is the likelihood that gout will develop. (msdmanuals.com)
  • Hyperferritinemia and hyperuricemia may be associated with liver function abnormality in obese adolescents. (medscape.com)
  • Further studies are required to identify the causal relationships between sleep recovery and hyperuricemia in postmenopausal women. (medicalxpress.com)
  • CSA treated rats developed mild hyperuricemia with arteriolar hyalinosis, tubular injury and striped interstitial fibrosis. (ewha.ac.kr)
  • The effect of hyperuricemia on CSA nephropathy was determined by blocking the hepatic enzyme uricase with oxonic acid (CSA-OA). (ewha.ac.kr)
  • Results: In this article, authors have summarized the pathogenesis, diagnosis and updated guidelines for gout and hyperuricemia management. (currentmedicinalchemistry.com)
  • citation needed] A purine-rich diet is a common but minor cause of hyperuricemia. (wikipedia.org)
  • Diet alone generally is not sufficient to cause hyperuricemia (see Gout). (wikipedia.org)