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allopurinol/nekrosis
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Allopurinol protects the bowel from necrosis caused by indomethacin and temporary intestinal ischemia in mice.
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The present study was undertaken to evaluate if allopurinol administration protects mice from bowel necrosis caused by temporary intestinal ischemia followed by indomethacin (INDO). We have previously reported that ischemia (15-minute occlusion of superior mesenteric vessels) followed by intravenous
[Fatal liver necrosis due to allopurinol].
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Allopurinol hypersensitivity syndrome (AHS) is a severe reaction which is potentially lethal. Exanthematous rash, fever, eosinophilia, and other severe reactions such as toxic epidermal necrolysis, acute vasculitis, and severe hepatic and renal dysfunctions are manifestations of this syndrome. The
Influence of allopurinol plus verapamil treatment on myocardial tissue necrosis during permanent coronary occlusion in canine hearts with small infarcts.
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We previously showed that combined treatment with allopurinol plus verapamil had a salutary effect on tissue necrosis during 24-h permanent coronary occlusion. The present study was undertaken to determine whether cardioprotection with allopurinol plus verapamil as compared with either allopurinol
[Hypersensitivity syndrome caused by allopurinol. A case of massive hepatic necrosis].
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Adverse drug reactions have a wide variety of clinical manifestations mainly related to the affected organ. The skin is one of the most common organs involved due to the visibility of the lesions to the observer. These untoward drug cutaneous responses may mimic any known dermatosis, and may be a
The effects of allopurinol and superoxide dismutase in a rat model of skin flap necrosis.
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Oxygen-free radicals have been implicated as mediators of ischemic damage in a number of tissues, including heart, kidney, small intestine, and skin. Superoxide dismutase, a free radical scavenger, and allopurinol, an inhibitor of xanthine oxidase (a catalyst in the formation of superoxide) have
The inhibitory effects of allopurinol on the production and cytotoxicity of tumor necrosis factor.
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Allopurinol, a xanthine oxidase inhibitor, impaired the cytotoxic effect of human recombinant tumor necrosis factor (TNF) against WEHI cells. Actinomycin D abolished the inhibition of cytotoxicity by allopurinol. Allopurinol also exerted an inhibitory effect on the production of TNF by human
[Role of allopurinol and rofecoxib in agranulocytosis and acute tubular necrosis].
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OBJECTIVE
To report the case of a patient who developed a life-threatening agranulocytosis and acute tubular necrosis after the administration of allopurinol and rofecoxib.
METHODS
After minor surgery, a 70-year-old male underwent a routine blood test which encountered: anemia, leucopenia,
Anti-gout agent allopurinol exerts cytotoxicity to human hormone-refractory prostate cancer cells in combination with tumor necrosis factor-related apoptosis-inducing ligand.
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Allopurinol has been used for the treatment of gout and conditions associated with hyperuricemia for several decades. We explored the potential of allopurinol on cancer treatment. Allopurinol did not expose cytotoxicity as a single treatment in human hormone refractory prostate cancer cell lines,
Massive hepatic necrosis in a patient receiving allopurinol.
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Massive hepatic necrosis in a patient receiving allopurinol concomitant medication.
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Acute renal failure and liver necrosis associated to allopurinol therapy.
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Allopurinol and N-acetylcysteine avoid 60% of intestinal necrosis in an ischemia-reperfusion experimental model.
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Effect of mannitol, dextran (macrodex), allopurinol, and methylprednisolone on the morphology of the proximal tubule of the rat kidney made ischemic in vivo.
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Rats were anesthetized and their lift kidneys were made ischemic for 1 h by clamping of the aorta just above the left renal artery. Mannitol (2.5 g/kg), Dextran 70 (0.6 g/kg), methylprednisolone (50 and 100 mg/kg), and allopurinol (100 mg/kg body weight) were administered before, during, or after
Protective effects of allopurinol against acute liver damage and cirrhosis induced by carbon tetrachloride: modulation of NF-κB, cytokine production and oxidative stress.
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BACKGROUND
The aim of this work was to evaluate the hepatoprotective ability of allopurinol to prevent the liver injury induced by carbon tetrachloride (CCl(4)).
METHODS
Acute liver damage was induced with CCl(4) (4g/kg, by gavage); allopurinol (50mg/kg, by gavage) was given 1h before and 1h after
Allopurinol potentiates the hepatoprotective effect of metformin and vitamin E in fructose-induced fatty liver in rats.
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