Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P47989 (
xanthine oxidase
)
8,633
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Serum
xanthine oxidase
activity was measured by a radiochemical method in 137 consecutive patients with jaundice of varying etiology and in 40 non-jaundiced patients with liver or other disease. Serum
xanthine oxidase
was markedly increased, up to 50 times the upper normal limit (mean + 2 S.D.), in 32 out of 34 patients with infectious hepatitis. A slight elevation of serum
xanthine oxidase
, up to twice the upper normal limit, was found in 2 out of 49 patients with extrahepatic obstructive jaundice and in 4 out of 20 patients with
chronic renal failure
. In comparison to serum glutamic-oxaloacetic transaminase and lactate dehydrogenase serum
xanthine oxidase
appeared to be the more sensitive and specific indicator of acute hepatocellular damage.
...
PMID:Serum xanthine oxidase in jaundice. 118 Oct 72
The rise in plasma uric acid (UA) in
chronic renal failure
(
CRF
) is quite limited. This may be due to either increased extrarenal excretion, diminished biosynthesis, and/or enhanced degradation of uric acid. The intestinal flux studies revealed a striking modification of urate transport from no net flux to a net secretory flux in the jejunum and from a basal net absorptive to a net secretory flux in the colon of
CRF
animals. In addition,
CRF
animals showed a marked reduction in hepatic, renal, and enteric tissue
xanthine oxidase
activity and no significant change in tissue uricase activity. The correction of anemia with erythropoietin did not significantly alter the plasma concentration or urinary excretion of urate. Thus, enhanced enteric excretion and depressed production of uric acid (reduced
xanthine oxidase
activity) may account for the lack of significant hyperuricemia in
CRF
.
...
PMID:Effect of chronic experimental renal insufficiency on urate metabolism. 858 4
Derangements of the three endothelium-related vasodilator systems (prostaglandins, endothelium-derived hyperpolarizing factor(s) and nitric oxide) cause the endothelial dysfunction observed in hypertension. Free radical-induced nitric oxide degradation plays a crucial role in hypertension. An increase in superoxide producing enzymes such as NAD(P)H oxidase and
xanthine oxidase
has been demonstrated. Superoxide dismutase may correct endothelial dysfunction in vitro and superoxide dismutase mimetics can lower blood pressure in experimental animals. Antioxidant agents and
xanthine oxidase
-inhibiting compounds have been used in humans. In addition, the synthesis of vasoconstrictor peroxides derived from the activity of cyclooxygenase in the endothelium and the vascular smooth muscle is stimulated by the OH. radical. Hydrogen peroxide levels are augmented in hypertension, but its role is unclear because recent investigations have shown that this substance may act as a hyperpolarizing factor. It is thought that the therapeutic benefit of anti-hypertensive drugs, such as calcium antagonists and angiotensin-converting enzyme inhibitors, could be in part due to an inhibition of free radical production. A role of superoxide in the endothelial dysfunction and hypertension of
chronic renal failure
has also been suggested by recent animal experiments.
...
PMID:Oxygen species in the microvascular environment: regulation of vascular tone and the development of hypertension. 1181 69
Gouty arthritis is a metabolic disorder associated with hyperuricemia. Despite the development of novel pharmacotherapies, some hyperuricemia patients are drug refractory and develop gout. A 74-year-old man with frequent gouty attacks and
chronic renal failure
presented with asymmetrical polyarthritis affecting multiple joints. The diagnosis of gout was confirmed based on the presence of monosodium urate crystals in the patient's right wrist. The administration of systemic corticosteroids relieved the joint inflammation and pain; however, the urate level increased to 28 mg/dL and the gout attacks recurred. Combined allopurinol, febuxostat, and benzbromarone therapy reduced the urate level to <6 mg/dL, and the attacks gradually declined. This is the first report of two
xanthine oxidase
inhibitors being used to treat refractory gout.
...
PMID:Successful treatment of refractory gout using combined therapy consisting of febuxostat and allopurinol in a patient with chronic renal failure. 2463 32