Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diuretics can result in various undesired biochemical changes, such as impotence, skin rashes, nausea, dizziness and lethargy as well as subjective side effects. The side effects are mostly predictable, their effects depending on both the circulatory blood volume and on the transport of water and solute in the renal tubules. Two of the commonest side effects are mild hypovolaemia, when any diuretic is used, and mild hypokalaemia when the non-potassium-sparing diuretics, such as thiazides and frusemide are used. Its occurrence is dose dependent and can be corrected by potassium supplements, but potassium-retaining diuretics, which also correct the often associated fall in serum magnesium, are preferable. Many reports link hypokalaemia with cardiac arrhythmias, but some dispute this association in the absence of the concomitant use of digoxin. Hyponatraemia rarely occurs, but can be life threatening. Calcium excretion is markedly reduced, but unlike other electrolyte disturbances from diuretics, this may be valuable: some suggest diuretics have an anti-osteoporotic action. Diuretics increase glucose and insulin resistance and should be used sparingly in diabetics. They rarely cause a non-ketotic hyperosmolar coma. Urate is raised, but clinical gout is not common. Cholesterol elevation has been reported in some studies, but long-term studies indicate that lipid changes are minor. Other rare side effects are not predictable from their pharmacological actions and these include the occurrence of skin rashes, thrombocytopenia, pancreatitis and interstitial nephritis; and ototoxicity from frusemide.
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PMID:Adverse reactions to diuretics. 148 14

During Ramadan, Moslems are required strictly to avoid fluids and nourishment from dawn to sunset. Heat stress during such abstinence represents a substantial health hazard. In the Federal Republic of Germany (FRG) where numerous Moslems, particularly of Turkish origin, perform heat work and other heavy labour, we observed moderate to severe health disturbances in such labourers during Ramadan, e.g.: tachycardia, severe headaches, dizziness, nausea, vomiting and circulatory collapse. The severe dehydration of these workers was demonstrated by substantial increases in their hematocrit, serum protein, urea, creatinine, uric acid and electrolyte imbalance. Because of the evidence of the substantial health hazard to Islamic workers in such situations, we have strongly urged employers to refrain from assigning Islamic workers to heat work or heavy daytime work during Ramadan; we have therefore limited systematic studies of health problems during Ramadan to persons performing only moderate work. Even under these conditions signs of dehydration were found in the 32 labourers monitored. Some of these labourers also had to interrupt their observance of Ramadan due to health problems, e.g.: acute gout due to serum uric acid increase, or circulatory insufficiency. In light of the observed potentially harmful pathophysiological effects, the danger of dehydration of Islamic workers due to heat work during Ramadan should be taken very seriously.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The health risks of occupational stress in islamic industrial workers during the Ramadan fasting period. 181 40

A patient with gout and schizophrenia is described who during a schizophrenic paroxysm with paranoid-hypochondriac-hallucinatory syndrome attempted to commit suicide and took 200 tablets milurit (20 g). He developed the picture of acute intoxication with nausea, vomiting, profuse diarrhea, abdominal pain, flushing, temperature, collapse manifestations, hepatomegaly, direct hyperbilirubinemia, elevated transaminase, leukopenia, accelerated ESR. After reanimation and infusion therapy, the patient recovered within 4 days and 2 weeks later all blood indices reached the limits of the norm.
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PMID:[Acute allopurinol (milurit) poisoning]. 402 4

The authors carried out an open noncomparative study to evaluate the anti-inflammatory therapeutic activity of piroxicam in 40 adult patients suffering from acute gout. The patients ranged in age from 28 to 68 years (the average age was 51.6 years) overall, 21 men and 19 women participated in the trial. All of the patients had their disease for more than one year and they were receiving treatment with Benziodarone, 100 mg per day when the drug was discontinued from clinical use in Brazil. All of these patients subsequently experienced aggravation of their disease and had an acute attack of gout. Each patient was given piroxicam, 40 mg, in a single dose on the first day and two divided doses of 20 mg for the following five days. The affected joints were: elbow, knee, ankle and hallux. Severity of pain at rest, severity of pain on movement, tenderness, swelling, redness, heat and restriction of movement were evaluated. By the sixth day of the trial, good or total remission was observed in all patients. Overall evaluation of efficacy showed excellent and good results in 81.6% of the patients. Tolerability was excellent and good in 92.5%. All adverse reactions that occurred during the use of piroxicam therapy were noted. Five patients showed mild side effects, such as pyrosis, nausea and headache, and two patients had severe side effects (skin rash, gastric disturbance) that necessitated withdrawal from therapy. Finally, statistical analysis demonstrates that piroxicam is highly efficacious in the treatment of acute gout.
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PMID:Use of piroxicam in the treatment of acute gout. 686 11

Dyslipidaemia may be treated with a number of safe and effective pharmacological agents that target specific lipid disorders through a variety of mechanisms. The bile-acid sequestrants--cholestyramine and colestipol--primarily decrease LDL cholesterol by binding bile acids, thereby decreasing intrahepatic cholesterol, and by increasing the activity of LDL receptors. Nicotinic acid lowers LDL cholesterol and triglyceride by decreasing VLDL synthesis and by decreasing free fatty acid mobilization from peripheral adipocytes. The HMG-CoA reductase inhibitors--fluvastatin, lovastatin, pravastatin and simvastatin--lower LDL cholesterol by partially inhibiting HMG-CoA reductase (the rate-limiting enzyme of cholesterol biosynthesis) and by increasing the activity of LDL receptors. The fibric-acid derivatives--bezafibrate, ciprofibrate, clofibrate, fenofibrate and gemfibrozil--primarily decrease triglyceride by increasing lipoprotein lipase activity and by decreasing the release of free fatty acids from peripheral adipose tissue. Probucol decreases LDL cholesterol by increasing non-receptor-mediated LDL clearance; as an anti-oxidant, probucol also decreases LDL oxidation; oxidized LDL which is thought to lead to atherogenesis. Although these agents have been proven safe in clinical trials, like any drug, they carry the risk for adverse effects. The bile-acid sequestrants may cause constipation, reflux oesophagitis, and dyspepsia, and may bind coadministered medications such as digitalis glycosides, beta blockers, warfarin, and exogenous thyroid hormone. Nicotinic acid use is commonly associated with flushing and pruritus and may also cause non-specific gastrointestinal complaints, hepatotoxicity (hepatic necrosis, hepatitis, or elevated liver enzymes), gout, myolysis, decreased glucose tolerance and increased fasting glucose levels, and ophthalmological complications including decreased visual acuity, toxic amblyopia, and cystic maculopathy. The HMG-CoA reductase inhibitors may produce liver enzyme elevations, creatine kinase elevations and rhabdomyolysis. The combination of a reductase inhibitor and a fibrate increases the risk for rhabdomyolysis. Possible adverse effects of the fibric-acid derivatives include abdominal discomfort, nausea, flatulence, increased lithogenicity of bile, liver enzyme elevations and creatine kinase elevations. Probucol may increase the QTc interval and may cause non-specific gastrointestinal complaints.
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PMID:Currently available hypolipidaemic drugs and future therapeutic developments. 859 27

Although intoxications with colchicine, the alkaloid of Colchicum autumnale (meadow saffron), are well known, in most cases the intoxications are evoked by oral or parenteral preparations traditionally used as medication against gout. The accidental ingestion of Colchicum autumnale, on the other hand, is a rare event and has to our knowledge only twice been described in detail. We report a further case in which two persons confused this highly poisonous plant with wild garlic (Allium ursinum), a popular spice in the Central European cuisine. While one person merely complained about a 3-day episode of nausea, vomiting and watery diarrhea, the second person died of multi-organ system derangements 48 h after the ingestion of the colchicum leaves. At autopsy hemorrhagic lung oedema, hypocellular bonemarrow, centrilobular fatty necrosis of the liver and necrosis of the proximal convoluted tubuli of the kidneys were observed. A colchicine concentration of 7.5 micrograms/ml was found in the bile whereas no substance was detected in the postmortem blood.
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PMID:Colchicine poisoning by accidental ingestion of meadow saffron (Colchicum autumnale): pathological and medicolegal aspects. 1068 67

A clinical evaluation of phenylbutazone and Butapyrin(R) (a mixture of phenylbutazone and aminopyrine) was made in 409 patients who had a variety of rheumatic diseases. Preliminary European claims were substantiated.In gout a specific favorable effect was brought about by phenylbutazone alone. Effects equivalent to the previously reported favorable response to Butapyrin (Irgapyrin) were observed when its constituent phenylbutazone was used alone. The drug had a suppressive effect in a high percentage of patients with rheumatoid arthritis, ankylosing spondylitis, arthritis with psoriasis and mixed arthritis (rheumatoid arthritis plus osteoarthritis). Favorable effect in peritendinitis of the shoulders, osteoporosis of the spine and acute lumbosacral strain also was noted. Toxicity resulted in discontinuance of medication in 10 per cent of patients with each drug. Manifestations of toxicity generally included fluid retention, nausea and rash, but there were several instances of transitory leukopenia and anemia. There was one instance of agranulocytosis with Butapyrin but none with phenylbutazone.dagger Aggravation of peptic ulcer occurred in ten patients with hemorrhage in two. Generally the toxicity was of a low order as compared with that of other drugs having an antirheumatic effect.
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PMID:Phenylbutazone (butazolidin) and butapyrin; a study of clinical effects in arthritis and gout. 1300 82

A 37-year-old black woman with nephritis secondary to systemic lupus erythematosus, steroid-induced diabetes mellitus, and hypertension presented with fever, nausea, vomiting, and right upper quadrant abdominal pain with distension. Abdominal computed tomography (CT) scan revealed a colonic mass, and CT- guided fine-needle aspiration demonstrated birefringent crystalline material. After several weeks of antibiotic therapy, the patient underwent laparoscopic examination followed by extended right hemicolectomy for a large mass in the subserosa of the transverse colon. Pathological examination of this mass revealed it to be a gouty tophus. To our knowledge, no case of tophaceous gout presenting as an intestinal mass has previously been reported.
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PMID:Intestinal pseudotumorous gouty nodulosis: a colonic tophus without manifestation of gouty arthritis. 1525 57

(1) Febuxostat is a selective inhibitor of xanthine oxidase. Its use in the management of hyperuricemia and gout is being studied. (2) In a 52-week, phase III randomized clinical trial, febuxostat was superior to allopurinol for lowering uric acid levels. Its efficacy in preventing gout attacks was similar to that of allopurinol. Despite a similar rate of adverse effects, individuals on febuxostat were more likely to stop treatment than those on allopurinol. (3) The most commonly observed adverse effects with febuxostat include liver function test abnormalities, diarrhea, headache, nausea, vomiting, abdominal pain, and dizziness. (4) Given that renal dysfunction is a risk factor for hyperuricemia and gout, the safety and efficacy of febuxostat in this population should be considered, but only limited data are available. (5) The diffusion of febuxostat may be limited by its price relative to that of allopurinol, regardless of whether febuxostat proves to have advantages in specific populations.
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PMID:Febuxostat for prevention of gout attacks. 1695 89

Febuxostat is a new non-purine xanthine oxidase inhibitor that is more potent than allopurinol 300 mg daily. In two Phase III trials, significantly more febuxostat-treated gout patients met the primary endpoint [serum urate (sUA) <6 mg/dl (<360 mumol/l) at the last three visits] (48 and 53% with 80 mg; 65 and 62% with 120 mg), compared with those receiving allopurinol 300 mg (22 and 21%; P < 0.001 in both studies). Febuxostat was more effective than allopurinol in the subset with impaired renal function; no dose adjustment is required in mild-to-moderate renal impairment. Long-term extension studies confirmed the efficacy and tolerability of febuxostat. In patients who achieved the sUA target of 6 mg/dl (360 mumol/l), the incidence of gout flares fell steadily and tophi resolved in many patients. The incidence of adverse events such as dizziness, diarrhoea, headache and nausea with febuxostat was similar to allopurinol. The incidence of cardiovascular side-effects (Antiplatelet Trialists Collaboration events) was numerically higher with febuxostat than with allopurinol, but this was not statistically significant. Co-administration of febuxostat with AZA or 6-mercaptopurine is not recommended. Prophylaxis (colchicine and/or NSAIDs) against acute attacks should be used for at least the first 6 months, since early mobilization flares were observed in the clinical trials. In conclusion, febuxostat is more effective than allopurinol 300 mg daily in reducing sUA levels <6 mg/dl (360 mumol/l), the target recommended by EULAR, and offers a new option for the long-term treatment of gout.
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PMID:Febuxostat: a new treatment for hyperuricaemia in gout. 1944 78


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