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At least 235 records · Page 13Linked to original sources
PubMed1990

Gout and hyperuricemia.

The prevalence of gout in the United States has been rising steadily for the past two decades. Hyperuricemia is considered a necessary but not sufficient precondition for gout. Known risk factors for gout include male sex, hypertension, renal insufficiency, obesity/weight gain, diuretic use, lead exposure, and family history. The association of gout and hyperuricemia with coronary artery disease is controversial. Current evidence from the Framingham Study suggests that gout is in fact an independent risk factor for CHD. These data suggest that patients with gout should be screened for modifiable risk factors for CHD, and that early intervention in such patients may be worthwhile. Finally, the effect of AHU as risk factor for CHD remains unclear but is probably a weak one.

Gout↗
PubMed1990

[Clinical studies on hyperuricemia and gout after transplantation].

We performed renal transplantation on 67 patients (living 37, cadaver 30) between November 1975 and December 1987. Twenty-seven of the 67 patients had hyperuricemia (serum uric acid: male greater than or equal to 8.0 mg/dl, female greater than or equal to 7.0 mg/dl) and 2 of them had episodes of gout. However, there was no correlation between serum creatinine and uric acid in 27 hyperuricemic patients. Twelve of 27 hyperuricemic patients were treated with either allopurinol or benzbromarone. These therapies were effective for 9 of them and serum uric acid level controlled well. One of 2 gouty patients developed gout 4 years after cadaveric renal transplantation. She was treated with anodyne and benzbromarone for gout. These treatments were effective and she has been in good condition. We consider it necessary to treat hyperuricemia after renal transplantation and to control serum uric acid well.

Adult↗
PubMed1978

[Effect of halofenate on triglyceride and uric acid levels, coagulation and platelet behaviour in patients with hyperlipoproteinemia type IV and hyperuricemia (author's transl)].

From experimental work, an influence of a drug with hypolipidemic and hypouricemic acition on blood coagulability and platelet function may be expected. Consequently, if these effects were demonstrable in man the drug could be assumed to reduce the tendency to develop thrombosis and atherosclerosis in patients with hyperlipidemia and hyperuricemia. In the study reported, the effect of 2-acetamidoethyl-(p-chlorophenyl)-(m-trifluoro-methylphenoxy)-acetate (halofenate) was investigated in 14 patients suffering from hyperlipoproteinemia type IV and hyperuricemia. Platelet aggregation and adhesiveness, plasma levels of triglycerides, cholesterol, uric acid, and clotting factors were regularly examined during a three-month double blind trial. While uric acid and triglyceride levels decreased, no influence of the drug treatment could be observed on platelet function and blood coagulability by the laboratory methods used.

Adult↗
PubMed1990

Obesity, hypertension, hyperuricemia and diabetes mellitus among the Cree and Inuit of northern Québec.

In the last thirty years, sociocultural and political changes have profoundly affected the way of life of the Cree and Inuit of Northern Québec. Their health status profile has also changed. This study presents the main results of a health survey performed among the Cree and Inuit in 1982-1984 by a multidisciplinary team. Obesity, arterial hypertension, hyperuricemia and diabetes mellitus while almost unknown in the past, have now been added to the list of Cree and Inuit health problems. Crees have the highest risk for obesity, hypertension and diabetes mellitus. Hyperuricemia for unknown reasons seems more prevalent among the Inuit. Our findings suggest that further in-depth studies of chronic conditions in these communities are needed.

Adolescent↗
PubMed1990

[Lipid peroxidation and hyperuricemia in patients with ischemic heart disease].

Lipid peroxidation, activity of the enzymatic link of the antioxidative system, and parameters of the lipid system were studied in 62 patients with coronary heart disease (27 patients with hyperuricemia and 35 subjects with normal uric acid levels) in relation to blood uric acid concentrations. The levels of uric acid, malonic dialdehyde, total lipids, total cholesterol, beta-lipoprotein cholesterol, triglycerides were measured and the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were evaluated. In the patients there was an increase in lipid peroxidation and lipid composition changes which were more drastically marked in hyperuricemia.

Adult↗
PubMed1989

[The role of homeostatic function of the kidneys in the development of hyperuricemia].

The content of uric acid in blood plasma has been determined and its relation with the homeostatic renal function has been studied in CHD and hypertensive patients. The attenuation of renal filtration processes has been revealed in a half of the 117 patients. The CHD patients have showed a significant relation between the levels of uric acid and protein in blood. There is an immediate correlation between the uric acid content and alpha 2-globulins in patients with CHD and hyperuricemia. It has been suggested that the development of hyperuricemia in CHD patients is dut to the mechanism of disturbances in binding of uric acid to transport blood proteins.

Adult↗
PubMed1989

Differences in urate metabolism between normouricemia and hyperuricemia in coronary heart disease in man.

We examined hyperuricemia in patients with coronary heart disease. In 85 patients with coronary sclerosis confirmed by coronary angiography, the serum urate level (6.08 +/- 1.60 mg/dL) was not different from that in subjects with normal coronary arteries (6.47 +/- 1.69 mg/dL). The incidence of hyperuricemia in patients with coronary sclerosis was 26%, and was significantly correlated with diuretics, obesity and hypertriglyceridemia, but not with hypertension or hypercholesterolemia. To elucidate the mechanism of urate metabolism in coronary sclerosis, we separated coronary sclerosis patients without complicating factors into hyperuricemics and normouricemics, and studied urate metabolism in comparison with subjects with normal coronary arteries. We found that normouricemics with coronary sclerosis had decreases in the filtered urate load and urate clearance with a normal urate-creatinine clearance ratio. Hyperuricemics with coronary sclerosis had decreases in urate clearance and urate-creatinine clearance ratios, but the filtered urate load was similar to that in normouricemics. It is suggested that in coronary sclerosis patients, normouricemics had a low glomerular filtration of urate with normal tubular urate transport, whereas hyperuricemics had enhanced tubular reabsorption of urate without any difference of urate filtration from normouricemics.

Coronary Disease↗
PubMedDate not supplied

[Hyperuricemia as a risk factor].

Many stress situations such as physical exertion, overheating, alcohol abuse, poisoning with lead, etc. are accompanied by a higher level of uric acid. The question up till what moment hyperuricemia is considered compensatory and under what effect it changes to a pathological state still remains unsolved. Proceeding from the literature data and the results of their own research the authors confirm the importance of regarding hyperuricemia as a risk factor since it is a biochemical marker not only of the disease of the joints but also of the cardio-vascular pathology and other states.

Aged↗
PubMed1988

[Hyperuricemia as a risk factor of nephropathy in gout].

Among 196 patients with primary gout examined in hospital or earlier stable or transient hyperuricemia was noted in 160 (81.6%). These patients were entered into the study group. The control group included 36 persons in whom the level of blood uric acid did not exceed normal values. The familial pattern of disease was established in the patients of the study group. Urolithic, proteinuric and hypertensive types of nephropathy as well as chronic renal insufficiency were more frequently observed in hyperuricemia patients. Alongside with severe tubular, interstitial and vascular changes, glomeruli in the form of mesangioproliferative or mesangiocapillary glomerulonephritis were regularly involved in the pathological process. In the rest of the patients vascular lesions were less marked and less frequent, renal glomerular changes reminded the picture of mesangioproliferative glomerulonephritis only; urolithiasis in them took a more favorable course. Thus, a high level of blood uric acid is one of the risk factors of renal affection in gout determining in many ways prognosis of disease.

Adult↗
PubMed1988

Integrity of the blood-aqueous barrier in hyperuricemia.

Neither the origin nor the role of high levels of uric acid, found in the aqueous humor of some human glaucomatous eyes, is known. A model of hyperuricemia in the rat was evaluated for its contribution to urate levels in the aqueous humor. Epinephrine-induced hyperuricemia in male rats was shown to increase mean serum urate levels from 1.2 mg/dL to 6.7 mg/dL. Female rats were shown to have a lower uric acid baseline and a lower absolute hyperuricemic level than males. The mean aqueous-humor urate levels were increased from 0.06 mg/dL to 0.33 mg/dL for male rats. In our studies, the blood-aqueous barrier effectively prevented equilibration between the systemic and ocular compartments. The increased aqueous-humor uric acid levels in glaucoma may arise from intraocular mechanisms.

Animals↗
PubMed1986

[Hyperuricemia: explain, ignore or treat?].

Human purin metabolism is summarized briefly and the terms primary and secondary gout are defined. Asymptomatic hyperuricemia as a risk factor for gout, urate nephropathy and ischemic heart disease is discussed. Treatment modalities of hyperuricemia are presented.

Coronary Disease↗
PubMedDate not supplied

[Differentiated dietotherapy of patients with obesity and hyperuricemia].

Asymptomatic hyperuricemia was recognized in 344 patients with obesity. The use of low-calorie diets led to a reduction in the body weight and made purine metabolism more normal. The correcting effect was most remarkable with the use of low-caloric diets with a low purine content. Inasmuch hyperuricemia of long standing plays an important role in the development of podarga, atherosclerosis, it is recommended that obese patients should be treated with the diets with a low content of food purines.

Adolescent↗
PubMed1984

[How to treat hyperuricemia?].

Among a normal population, 21.5% of men have a blood level of uric acid above 6.8 mg%. Half of these subjects also present concomitant elevation of at least one other biological parameter. Clinically they differ from normo-uricemic subjects by weight, level of blood pressure and a trend to diabetes. From the recent literature it appears that hyperuricemia by itself does not constitute a risk factor as far as renal and vascular diseases are concerned. However, prevalence of gouty arthritis and urinary stones correlates with the blood uric acid level. Therefore, treatment of asymptomatic hyperuricemia must be avoided, and side effects of the drugs weighed. Acceptable indications for treatment are frequent attacks of urolithiasis or arthritis poorly tolerated by the patients.

Arthritis, Rheumatoid↗
PubMed1984

An approach to hyperuricemia and gout.

Arthrocentesis and patient and family histories make gout relatively easy to diagnose. The next step is to distinguish between primary and secondary hyperuricemia. Hyperuricemia results from either impaired renal excretion or excessive production of uric acid--or both. Determining the cause guides the choice of therapy.

Allopurinol↗
PubMed1980

Familial hyperuricemia and renal disease.

Information on a familial syndrome of hyperuricemia and renal disease with or without gout was obtained on 33 of 41 blood relatives: Nine had renal disease; abnormalities of the urinary sediments were minimal; serum uric acid levels were elevated in seven and were not measured in two. Hyperuricemia was noted in three additional family members without evidence of renal disease. Goulty arthritis (three patients) did not precede renal disease. One individual had hyperuricosuria. The following erythrocyte purine enzyme levels were normal: adenine phosphoribosyltransferase, hypoxanthine-guanine phosphoribosyltransferase, phosphoribosylpyrophosphate, synthetase, adenosine deaminiase, and purine nucleoside phosphorylase. Renal biopsy specimens showed focal global and segmental sclerosis of glomeruli, occasional hypercellularity, foci of atrophic tubules, chronic interstitial inflammation, and folding and wrinkling of glomerular basement membrane without electron-dense deposits. There were no immunofluorescent abnormalities.

Arthritis↗
PubMedDate not supplied

[Gout and hyperuricemia in Tananarive (Madagascar) (author's transl)].

Review of 41 cases observed in "Girard et Robic hospital", Tananarive (35 cases of plain articular gout either acute or chronic, and 6 cases of latent hyperuricemia).--Gout and hyperuricemia are frequently observed within Malagasy high-lands Merina population.--Women and even, in exceptional cases, children may be affected. A responsible hereditary factor is probably associated with the side effects of food habits (diet rich in rice, local vegetables, zebu meat and pork; beverages are not abundant).

Age Factors↗
PubMed1995

[Persistent granulocytosis and hyperuricemia after a single G-CSF injection (Filgrastim) in treatment of chemotherapy-induced myelosuppression in metastatic breast carcinoma].

We report about a patient with metastatic breast cancer treated with chemotherapy regime (CMF), who developed a febril leukopenia as well as a hyperuricemia. A single subcutaneous application of 300 micrograms Filgrastim led to a severe overstimulation with leukocytosis of max. 50,000 for about 8 days and hyperuricemia.

Aged↗
PubMedDate not supplied

[The correction of hyperuricemia in patients with different forms of nephrolithiasis using allopurinol and Allomaron].

Metabolic status was assessed in 48 patients with nephrolithiasis followed-up for 4 years. Allopurinol and allomaron-treated patients were examined biochemically by 17 parameters of the blood and urine. The effects of the drugs were compared. It is concluded that in hyperuricemia up to 0.37 +/- 0.02 mmol/l allomaron is more effective (1--2 pills a day). In higher hyperuricemia allopurinol is preferable (4 pills a day). Allomaron can be also used (1--2 pills a day) under the control of urinalysis.

Adult↗