A high blood uric acid level is known as hyperuricemia. Anything above the typical maximum limit of 6.8 mg/dL is regarded as saturated, & symptoms may appear. Increased uric acid generation, reduced uric acid excretion, or a mixture of both mechanisms are to blame for this excessive level.
Accelerated purine breakdown, high cell turnover stages (such as rhabdomyolysis, hemolysis, & tumor lysis), and reduced excretion are further signs of elevated uric acid (renal insufficiency & metabolic acidosis). Nephrolithiasis and gout can result from hyperuricemia. Additionally, it has been linked to conditions including diabetes mellitus, metabolic syndrome, heart disease, & chronic kidney disease as indicators.
Epidemiology
25 percent of the total hospitalized patients and up to 21% of the general population are thought to have symptomless hyperuricemia. Gout, which affects 3.9% of Americans, is the most typical side effect of hyperuricemia.
Anatomy
Pathophysiology
Purine degradation yields uric acid (2,6,8 trioxypurine-C5H4N4O3). Urate, an ionized form of uric acid, circulates at the physiological pH of 7.4, which is normal. Although the liver is where purine metabolism primarily takes place, it can also be created in any other tissue that has xanthine oxidase (intestines). Uric acid is primarily eliminated in the kidneys, with the gut receiving around one-third of it. 90% of it is reabsorbed after being filtered and secreted in the kidneys.
Due to the activity of uricase, other mammals have lower levels of uric acid. This enzyme changes urate into allantoin’s more water-soluble molecule. A small percentage of cases of hyperuricemia are brought on by ureate synthesis, which is exacerbated by purine-rich meals, endogenous urea generation, and excessive cell breakdown. All meats, but especially organ meats (kidneys, liver, “sweet bread”), game meats, as well as some seafood, are high in purine (herring, anchovies, scallops). Purine-rich beer also raises uric acid levels by reducing renal excretion.
Phosphoribosylpyrophosphate (PRPP) synthetase activity, as well as a malfunction in the regulating enzyme HPRT (hypoxanthine phosphoribosyltransferase), can speed up endogenous production of the purine. Rhabdomyolysis, hemolysis, & tumor lysis are examples of conditions characterized by increased cell turnover or breakdown that can also serve as a purine source and raise urate production. Ninety percent of people have hyperuricemia as a result of ureate excretion, which mostly takes place in the kidneys.
Reduced glomerular filtration, reduced tubular secretion, and increased tubular reabsorption all appear to contribute to underexcretion. Hyperuricemia can be brought on by a short-term or long-term reduction in glomerular filtration. uric acid transporter 1 (URAT1) regulates the proximal tubular reuptake of uric acid. Organic acids like lactate & acetoacetate, as well as beta-hydroxybutyrate, drugs like ethambutol, niacin, pyrazinamide, & chemotherapy, & reduced extracellular fluid capacity that cause hyperuricemia, can all enhance this transport.
Etiology
Overproduction of Urate
Diet high in purines
Purine metabolism error: PRPP (phosphoribosylpyrophosphate synthetase overactivity), HPRT (hypoxanthine phosphoribosyltransferase deficiency).
Exercise, polycythemia vera, myeloproliferative disorders, Paget disease, tumor lysis, psoriasis, hemolysis, & rhabdomyolysis are all conditions that cause cell turnover or breakdown.
The majority of patients have no symptoms, and no distinct physical findings are observed. Symptomatic manifestations could take the following forms:
The affected joint in acute gouty arthritis is often heated, swollen, erythematous, & excruciatingly painful.
The helix and antihelix of the ear, the ulnar surface of the forearm, the olecranon bursa, or other tissues may develop tophi in people with persistent gouty arthritis.
Patients with uric acid nephrolithiasis may exhibit stomach or flank soreness.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Since the majority of individuals never get nephrolithiasis or gout, they do not require medical treatment for hyperuricemia. The benefits of commencing medicine are outweighed by the unneeded expense and risk of side effects. Only people receiving cytolytic treatment for malignancy who are asymptomatic should take urea-lowering drugs to avoid tumor lysis syndrome.
Urate-lowering drugs:
Probenecid: increases uric acid output and is used as a second-line treatment for gout.
Allopurinol: inhibitors of xanthine oxidase, utilized as a preventative measure against gouty arthritis, hyperuricemia, nephrolithiasis, and caused by chemotherapy
Rasburicase:Recombinant uricase prevents chemo-related hyperuricemia by converting uric acid to allantoin, which is significantly more water soluble and easily eliminated from the kidneys.
Indicated for Hyperuricemia Secondary to Chemotherapy:
0.2 mg/kg IV dose given over 30 minutes daily 5 days
Note:
When children and adults with leukaemia, lymphoma, and solid tumour malignancies are getting anticancer therapy, which is anticipated to cause tumour lysis and a subsequent rise in plasma uric acid levels, this medication is indicated for the initial management of uric acid levels in the blood
Indicated for Hyperuricemia Secondary to Chemotherapy:
Age: > 1 month
0.2 mg/kg IV dose given over 30 minutes daily 5 days
Note:
When children and adults with leukaemia, lymphoma, and solid tumour malignancies are getting anticancer therapy, which is anticipated to cause tumour lysis and a subsequent rise in plasma uric acid levels, this medication is indicated for the initial management of uric acid levels in the blood
A high blood uric acid level is known as hyperuricemia. Anything above the typical maximum limit of 6.8 mg/dL is regarded as saturated, & symptoms may appear. Increased uric acid generation, reduced uric acid excretion, or a mixture of both mechanisms are to blame for this excessive level.
Accelerated purine breakdown, high cell turnover stages (such as rhabdomyolysis, hemolysis, & tumor lysis), and reduced excretion are further signs of elevated uric acid (renal insufficiency & metabolic acidosis). Nephrolithiasis and gout can result from hyperuricemia. Additionally, it has been linked to conditions including diabetes mellitus, metabolic syndrome, heart disease, & chronic kidney disease as indicators.
25 percent of the total hospitalized patients and up to 21% of the general population are thought to have symptomless hyperuricemia. Gout, which affects 3.9% of Americans, is the most typical side effect of hyperuricemia.
Purine degradation yields uric acid (2,6,8 trioxypurine-C5H4N4O3). Urate, an ionized form of uric acid, circulates at the physiological pH of 7.4, which is normal. Although the liver is where purine metabolism primarily takes place, it can also be created in any other tissue that has xanthine oxidase (intestines). Uric acid is primarily eliminated in the kidneys, with the gut receiving around one-third of it. 90% of it is reabsorbed after being filtered and secreted in the kidneys.
Due to the activity of uricase, other mammals have lower levels of uric acid. This enzyme changes urate into allantoin’s more water-soluble molecule. A small percentage of cases of hyperuricemia are brought on by ureate synthesis, which is exacerbated by purine-rich meals, endogenous urea generation, and excessive cell breakdown. All meats, but especially organ meats (kidneys, liver, “sweet bread”), game meats, as well as some seafood, are high in purine (herring, anchovies, scallops). Purine-rich beer also raises uric acid levels by reducing renal excretion.
Phosphoribosylpyrophosphate (PRPP) synthetase activity, as well as a malfunction in the regulating enzyme HPRT (hypoxanthine phosphoribosyltransferase), can speed up endogenous production of the purine. Rhabdomyolysis, hemolysis, & tumor lysis are examples of conditions characterized by increased cell turnover or breakdown that can also serve as a purine source and raise urate production. Ninety percent of people have hyperuricemia as a result of ureate excretion, which mostly takes place in the kidneys.
Reduced glomerular filtration, reduced tubular secretion, and increased tubular reabsorption all appear to contribute to underexcretion. Hyperuricemia can be brought on by a short-term or long-term reduction in glomerular filtration. uric acid transporter 1 (URAT1) regulates the proximal tubular reuptake of uric acid. Organic acids like lactate & acetoacetate, as well as beta-hydroxybutyrate, drugs like ethambutol, niacin, pyrazinamide, & chemotherapy, & reduced extracellular fluid capacity that cause hyperuricemia, can all enhance this transport.
Overproduction of Urate
Diet high in purines
Purine metabolism error: PRPP (phosphoribosylpyrophosphate synthetase overactivity), HPRT (hypoxanthine phosphoribosyltransferase deficiency).
Exercise, polycythemia vera, myeloproliferative disorders, Paget disease, tumor lysis, psoriasis, hemolysis, & rhabdomyolysis are all conditions that cause cell turnover or breakdown.
The majority of patients have no symptoms, and no distinct physical findings are observed. Symptomatic manifestations could take the following forms:
The affected joint in acute gouty arthritis is often heated, swollen, erythematous, & excruciatingly painful.
The helix and antihelix of the ear, the ulnar surface of the forearm, the olecranon bursa, or other tissues may develop tophi in people with persistent gouty arthritis.
Patients with uric acid nephrolithiasis may exhibit stomach or flank soreness.
Since the majority of individuals never get nephrolithiasis or gout, they do not require medical treatment for hyperuricemia. The benefits of commencing medicine are outweighed by the unneeded expense and risk of side effects. Only people receiving cytolytic treatment for malignancy who are asymptomatic should take urea-lowering drugs to avoid tumor lysis syndrome.
Urate-lowering drugs:
Probenecid: increases uric acid output and is used as a second-line treatment for gout.
Allopurinol: inhibitors of xanthine oxidase, utilized as a preventative measure against gouty arthritis, hyperuricemia, nephrolithiasis, and caused by chemotherapy
Rasburicase:Recombinant uricase prevents chemo-related hyperuricemia by converting uric acid to allantoin, which is significantly more water soluble and easily eliminated from the kidneys.
Indicated for Hyperuricemia Secondary to Chemotherapy:
0.2 mg/kg IV dose given over 30 minutes daily 5 days
Note:
When children and adults with leukaemia, lymphoma, and solid tumour malignancies are getting anticancer therapy, which is anticipated to cause tumour lysis and a subsequent rise in plasma uric acid levels, this medication is indicated for the initial management of uric acid levels in the blood
Indicated for Hyperuricemia Secondary to Chemotherapy:
Age: > 1 month
0.2 mg/kg IV dose given over 30 minutes daily 5 days
Note:
When children and adults with leukaemia, lymphoma, and solid tumour malignancies are getting anticancer therapy, which is anticipated to cause tumour lysis and a subsequent rise in plasma uric acid levels, this medication is indicated for the initial management of uric acid levels in the blood
A high blood uric acid level is known as hyperuricemia. Anything above the typical maximum limit of 6.8 mg/dL is regarded as saturated, & symptoms may appear. Increased uric acid generation, reduced uric acid excretion, or a mixture of both mechanisms are to blame for this excessive level.
Accelerated purine breakdown, high cell turnover stages (such as rhabdomyolysis, hemolysis, & tumor lysis), and reduced excretion are further signs of elevated uric acid (renal insufficiency & metabolic acidosis). Nephrolithiasis and gout can result from hyperuricemia. Additionally, it has been linked to conditions including diabetes mellitus, metabolic syndrome, heart disease, & chronic kidney disease as indicators.
25 percent of the total hospitalized patients and up to 21% of the general population are thought to have symptomless hyperuricemia. Gout, which affects 3.9% of Americans, is the most typical side effect of hyperuricemia.
Purine degradation yields uric acid (2,6,8 trioxypurine-C5H4N4O3). Urate, an ionized form of uric acid, circulates at the physiological pH of 7.4, which is normal. Although the liver is where purine metabolism primarily takes place, it can also be created in any other tissue that has xanthine oxidase (intestines). Uric acid is primarily eliminated in the kidneys, with the gut receiving around one-third of it. 90% of it is reabsorbed after being filtered and secreted in the kidneys.
Due to the activity of uricase, other mammals have lower levels of uric acid. This enzyme changes urate into allantoin’s more water-soluble molecule. A small percentage of cases of hyperuricemia are brought on by ureate synthesis, which is exacerbated by purine-rich meals, endogenous urea generation, and excessive cell breakdown. All meats, but especially organ meats (kidneys, liver, “sweet bread”), game meats, as well as some seafood, are high in purine (herring, anchovies, scallops). Purine-rich beer also raises uric acid levels by reducing renal excretion.
Phosphoribosylpyrophosphate (PRPP) synthetase activity, as well as a malfunction in the regulating enzyme HPRT (hypoxanthine phosphoribosyltransferase), can speed up endogenous production of the purine. Rhabdomyolysis, hemolysis, & tumor lysis are examples of conditions characterized by increased cell turnover or breakdown that can also serve as a purine source and raise urate production. Ninety percent of people have hyperuricemia as a result of ureate excretion, which mostly takes place in the kidneys.
Reduced glomerular filtration, reduced tubular secretion, and increased tubular reabsorption all appear to contribute to underexcretion. Hyperuricemia can be brought on by a short-term or long-term reduction in glomerular filtration. uric acid transporter 1 (URAT1) regulates the proximal tubular reuptake of uric acid. Organic acids like lactate & acetoacetate, as well as beta-hydroxybutyrate, drugs like ethambutol, niacin, pyrazinamide, & chemotherapy, & reduced extracellular fluid capacity that cause hyperuricemia, can all enhance this transport.
Overproduction of Urate
Diet high in purines
Purine metabolism error: PRPP (phosphoribosylpyrophosphate synthetase overactivity), HPRT (hypoxanthine phosphoribosyltransferase deficiency).
Exercise, polycythemia vera, myeloproliferative disorders, Paget disease, tumor lysis, psoriasis, hemolysis, & rhabdomyolysis are all conditions that cause cell turnover or breakdown.
The majority of patients have no symptoms, and no distinct physical findings are observed. Symptomatic manifestations could take the following forms:
The affected joint in acute gouty arthritis is often heated, swollen, erythematous, & excruciatingly painful.
The helix and antihelix of the ear, the ulnar surface of the forearm, the olecranon bursa, or other tissues may develop tophi in people with persistent gouty arthritis.
Patients with uric acid nephrolithiasis may exhibit stomach or flank soreness.
Since the majority of individuals never get nephrolithiasis or gout, they do not require medical treatment for hyperuricemia. The benefits of commencing medicine are outweighed by the unneeded expense and risk of side effects. Only people receiving cytolytic treatment for malignancy who are asymptomatic should take urea-lowering drugs to avoid tumor lysis syndrome.
Urate-lowering drugs:
Probenecid: increases uric acid output and is used as a second-line treatment for gout.
Allopurinol: inhibitors of xanthine oxidase, utilized as a preventative measure against gouty arthritis, hyperuricemia, nephrolithiasis, and caused by chemotherapy
Rasburicase:Recombinant uricase prevents chemo-related hyperuricemia by converting uric acid to allantoin, which is significantly more water soluble and easily eliminated from the kidneys.
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