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At least 343 records · Page 19Linked to original sources
PubMed1981

Hyperuricemia and gout: an update.

Gout may be a primary or a secondary disorder. In both types of gout, overproduction or underexcretion of uric acid, or a combination of these abnormalities, may be the underlying mechanism. Controversy exists over the need for treatment of asymptomatic hyperuricemia. Treatment of tophi requires use of both uricosurics and allopurinol. A xanthine oxidase inhibitor is the drug of choice for patients with uric acid stones and for those with renal insufficiency.

Allopurinol↗
PubMed1981

[Tienilic acid, hyperuricemia and kidney function].

Tienilic acid (Diflurex) was given to 10 patients with secondary hyperuricemia following hydrochlorothiazide or furosemide administration. Eight of these 10 patients suffered acute worsening of renal function reflected in a significant increase in plasma creatinine. Plasma urates fell in all patients. Plasma creatinine returned to pretreatment levels in all patients within 4 to 15 days. Extreme caution should be exercised in prescribing tienilic acid to hyperuricemic patients, in view of the significant risk of reversible renal impairment.

Aged↗
PubMedDate not supplied

[Xeroradiography in comparison to roentgen studies in gout, hyperuricemia and dyspurinia].

In 24 patients with gout and in 15 patients with clinical oligo- and polyarthritic syndromes associated with hyperuricemia and dyspurinia xeroradiographic examinations of the clinically affected joints and soft tissues were carried out. In 32 cases comparisons were made with the classic x-ray examinations. In most cases the findings correlated, particularly the rarifaction of the bone structure including cystic changes of fingers and toes. In advanced cases, particularly in the hallux, erosions occurred and at the same time the changes in the soft tissues were recorded. Cystic changes in the larger bones were better estimated by the classical x-ray examinations. The soft tissues are shown better xeroradiographically. Xeroradiography has the advantage that it can record the structure of bones and soft tissue at the same time.

Adult↗
PubMed1980

[Clinical biochemical changes in ischemic heart disease: hyperuricemia as a risk factor].

One hundred and sixty patients with IHD were examined--73 males and 87 females, average age for males--58.58 +/- 12.69 and for females--59.65 +/- 7.76. Elevated levels of uric acid were found in 51.5 per cent. The correlation analysis showed a positive correlation dependence between total fats and uric acid, between cholesterol and uric acid as well as between total protein and uric acid and reverse dependence between uric acid and alpha 2-globulines, beta and gamma globuline fractions. The results from the investigations carried out provided grounds to admit hyperuricemia to be one of the risk factors of IHD.

Blood Glucose↗
PubMed1980

Atraumatic avascular necrosis of the talus associated with hyperuricemia.

Although the presence of hyperuricemia and avascular necrosis of the hip is well documented, a similar association in the talus seems not to have been previously reported. The clinical and radiographic findings were confirmed by the histologic alterations in bone structure. Successful arthrodesis of the destroyed left ankle joint was accomplished by iliac bone graft.

Black People↗
PubMed1980

[Mechanism of fasting hyperuricemia].

The authors followed up 73 obese patients submitted to fasting for 7 days; 46 of them took nos drugs (control subjects); the others took daily 100 to 200 mg of benzbromarone. The average serum uric acid of the controls rose from 49.37 mg to 90.52 mg per litre. Their uric acid clearance during the week of fasting fell to 4.67 ml per minute. The uric acid turnover was multiplied by two and the mixable pool by 3.5. These results that the hyperuricemia of fasting is due both to a fall in uric acid clearance and increased catabolism of cellular nucleic acid.

Adolescent↗
PubMed1995

Body mass index and hyperuricemia differences between aboriginal and non-aboriginal children in Taiwan.

To explore the relationship between the body mass index (BMI) and uric acid in different races before growing up into adulthood, we selected a total of 1236 five to 14 year-old children in the period from March to December 1994. The children originated from three Aboriginal tribes (the Bunun, and the Paiwan tribes--classified as South-Aborigines and Atayal tribe as North-Aborigines) and two non-Aboriginal tribes (Fukein-Taiwanese and Hakka), all of whom are from the following four countries: Chien-Shih, Sandimen, Gaushuh and Sanmin. The results showed that the percentage of hyperuricemia (> or = 7.5 mg/dl) was 28.5% (352/1236) and of obesity (BMI > or = 22 kg/m2) was 9.5% (118/1236). Increased uric acid concentration was found to be related to age, sex, BMI, race, triglyceride (TG) and cholesterol levels in both the primary analysis and after the adjusted logistic regression model. Obesity did not vary with sex (OR = 1.0; 95% CI = 0.7-1.5), or with Aborigines in north Taiwan as compared with non-Aborigines (OR = 1.0, 95% CI = 0.6-1.6), but the logistic regression model adjusted for age indicated large BMI values for children with high serum uric acid concentration, triglyceride levels and the Aborigines who originated from south Taiwan. It was concluded from this study that both of the North-Aborigines and South-Aborigines made an important influence on serum uric acid concentration in children, especially the South-Aborigines made difference to BMI as compared with non-Aborigines and North-Aborigines.

Adolescent↗
PubMed1975

[Physical and mental fatigue of probable hyperuricemia origin].

A blood uric acid analysis has been effected on 193 Iranians of the intellectual group aged from 25 to 60, of which the normal average rate for 99 women and 94 men of a normal state are (47.5 +/- 2.73) and (53.62 +/- 2.73) respectively. After having controlled the uricemia of these subjects during a period of three years in the three states of healthiness, fatigue or physical strains and sickness, we have been able to note that during physical fatigue and intellectual strains the uricemia presents an augmentation notable as in the case of the sicknesses. Taking into consideration the hyperuricemia resulting from fatigue and strains, it may be noteworthy to be taken into consideration by the clinical laboratories and the physicians as well.

Adult↗
PubMed1976

[Treatment of hyperlipemia and hyperuricemia with 2-acetamidoethyl-(4-chlorophenyl)-(3-trifluoromethylphenoxy)-acetate (halofenate), a derivative of clofibrate].

23 patients with hyperlipidemia and hyperuricemia received acetamidoethyl-(4-chlorophenyl)-(trifluoromethylphenoxy)-acetate (halofenate), a clofibrate derivative, and probenecid or probenecid and placebo over 36 weeks following a placebo period of 6 weeks. Halofenate compared with probenecid lowered elevated serum uric acid levels satisfactorily to a therapeutic level between 5 and 6 mg/100 ml. Serum triglyceride levels were not always lowered sufficiently, serum cholesterol levels were not influenced.

Cholesterol↗
PubMed1994

[Clinical significance of hyperuricemia in psoriasis].

After analysis of 1146 psoriasis patients, high incidence of asymptomatic hyperuricemia (18.8%) and elevated average levels of uric acid in these patients' blood were confirmed (346.8 +/- 2.4 mumol/l). More severe forms of uric acid disbolism lead to aggravated skin affections (psoriatic erythrodermia, exudative psoriasis), arthritis, occur in familial predisposition to psoriasis. Advanced psoriasis patients are at risk to develop apparent gout.

Case-Control Studies↗
PubMed1994

[Hyperuricemia].

Uric acid is formed by catabolism of purine nucleotides. Approximately 25% is excreted through the intestines and the rest through the kidneys. A little less than 5% of the population in western industrialised countries have hyperuricaemia, primarily men and postmenopausal women. Hyperuricaemia is in most cases caused by reduced renal excretion, which may be idiopathic with otherwise normal renal function. But the condition is often associated with hypertension, nephropathy and treatment with diuretics and certain other drugs. Hyperuricaemia due to increased purine metabolism is seen in malignant haematological diseases, other conditions with increased cellular turnover and during initiation of chemotherapy in malignant diseases. Moreover hyperuricaemia is associated with some metabolic disturbances and risk factors of atherosclerotic cardiovascular disease including hypertension, overweight, insulin resistance and hyperlipidaemia. Hyperuricaemia is rarely caused by constitutional enzymatic abnormalities influencing purine metabolism. In most cases hyperuricaemia is asymptomatic. It may though be complicated by gout, urolithiasis and possibly gouty nephropathy. The risk of complications is correlated to the degree and duration of hyperuricemia. Consequently, measures to affect predisposing and associated conditions should be taken including weight reduction, physical exercise and diet guidance, treatment of hypertension and possibly changes in medication. Urate lowering drug treatment is normally not indicated in asymptomatic hyperuricaemic individuals.

Gout↗
PubMed1996

[How to select and use urate lowering agents for hyperuricemia].

Two classes of urate lowering agents, i.e. uricosuric agents and allopurinol, are available for the treatment of hyperuricemia. To prevent the formation of urinary urate stones and possible damage to liver function, it is recommended to use uricosuric agents in those patients with underexcretion of urate, and allopurinol in those with overproduction. Urinary uric acid/creatinine ratio is a convenient index to determine these phenotypes. These agents should be started to prescribe from the minimal dose to prevent the gouty arthritis which is easily evoked in the first several months after the introduction of these agents. An uric acid level between 5.0 and 6.4 mg/dl had minimal occurence of gouty attack during the first six months of the drug therapy.

Allopurinol↗
PubMed1996

[Hyperuricemia and insulin resistance].

Hyperuricemia is often associated with obesity, hypertension and dyslipidemia, and is thought to be a risk factor for cardiovascular disease, thereby making resemblance to the insulin resistance syndrome. Our data showed a low, but significant correlation between serum uric acid concentration and the degree of insulin resistance (GIR) estimated by euglycemic hyperinsulinemic clamp method in 67 subjects with combined normal glucose tolerance and IGT(r = -0.278, p < 0.05). Plasma HDL-C and TG levels were also correlated with uric acid levels. One hundred sixty NIDDM patients who had undergone the clamp study were stratified into 5 groups according to the serum uric acid level. In the top quintile (UA : 7.8 +/- 0.8 mg/dl), BMI, male prevalence, plasma TG, HDL-C, fasting IRI, and total IRI response(0 + 60 + 120 min) during meal tolerance test were significantly higher, while age and GIR value tended to be lower without significance compared with those in the bottom quintile (UA : 3.4 +/- 0.5 mg/dl). These results, which are in agreement with the previous studies, support the notion that elevated serum uric acid is a feature of insulin resistance syndrome.

Cardiovascular Diseases↗
PubMedDate not supplied

[Globulinopathy and hyperuricemia].

Investigation of the locomotor system of 20 patients is reported. One patient with arthrosis of the hip joint and concomitant osteonecroses had a myeloma. In 5 RA patients the manifestations of secondary amyloidosis are described. Among the patients with monoclonal gamma globulinemia two had polyarthritis and RA could not be excluded in one of them, one had arthritis of the ankle and foot joints, and one had a vasculitis characteristic of polyarteritis nodosa. Among those with polyclonal immunoglobulinemia one had RA, two had arthrosis of knees and hips, and two had ankylosing spondylitis. Furthermore four patients with alpha2-hyperglobulinemia which is important in evaluation of the alpha2-globulin peak in amyloidosis, are described. Three patients had cryoglobulinemia. In 10 patients hyperuricemia was found repeatedly (by the uricase method). Consequently in these diseases it is necessary to search clinically for crystal induced synovitides and arthropathies. The classification of globulinopathies and the method of their determination is indicated and particular investigations are recommended for such diseases, where the activity of the joint process does not correlate with laboratory findings.

Adolescent↗
PubMed1996

[Lipoprotein profile in patients with isolated hyperuricemia].

There have been described abnormalities in the lipoprotein profile of hyperuricemic patients, it has not been clarified wether these abnormalities are due to the hyperuricemia or to the hyperlipidemia often associated to these patients. Our aim is to study the apolipoprotein profile in hyperuricemic patients without hyperlipidemia compared to a control population. 30 hyperuricemic patients and 26 healthy controls. Measurements were of blood uric acid, total cholesterol, total triglycerides, creatinine, HDL-C, and VLDL cholesterol, triglyceride, Apo B, Apo CII and Apo CIII (1 and 2). Uric acid clearance and fractionated excretion were measured in 24 h. urine samples. No significant differences were found between hyperuricemic and control patients in cholesterol, triglycerides and apo B in VLDL, or LDL and HDL cholesterol. The levels of apo B, Apo AI levels and apo CIII/apo CII were similar in the hyperuricemic and controls. There are two types of hyperuricemic patients, one group associated to hyperlipidemia and would be included in the X Syndrome. The other group not associated to other metabolic abnormalities. Is important to distinguish between these two groups to define the prognosis of a given patient because the greater cardiovascular risk linked hyperuricemic patients could be related to the association to others cardiovascular risks factors.

Apolipoproteins↗
PubMedDate not supplied

[Severe acute hepatitis due to allopurinol in a patient with asymptomatic hyperuricemia and kidney failure. A review of the literature and an analysis of the risk factors].

The case of a 39-year-old female with mild renal failure and asymptomatic hyperuricemia who developed generalized exanthema, fever and eosinophilia followed by progressive jaundice and worsening of renal function 19 days after the initiation of treatment with alopurinol (300 mg/day) is reported. Liver biopsy showed a combination of mixed inflammatory infiltrate with abundant eosinophils and periportal necrosis and bridging, together with cholestasis and moderate steatosis. A review of the literature is made providing detailed analysis of other cases with preexisting renal failure and the role of renal dysfunction as a risk factor is discussed.

Acute Disease↗
PubMed1998

Reversible renal insufficiency, hyperuricemia and gouty arthritis in a case of hypothyroidism.

We present the case of a young man with 3-month history of generalized weakness and lethargy, constipation, weight gain, and swelling in the lower extremities. He was found to have an elevated serum creatinine of 203 mumol/l (2.3 mg/dl), markedly elevated TSH, severe hypercholesterolemia, hyperuricemia, a 24-hour urine creatinine excretion rate of 16.8 mmol/d (1.9 g/d), a creatinine clearance of 58 ml/min, and a uric acid excretion rate of 4.2 mmol/d (700 mg/d). With the impression of primary hypothyroidism, the patient was started on levothyroxine supplementation at which point he developed a classic gouty arthritis of right first metatarsophalangial joint. Six weeks after thyroid replacement therapy his serum creatinine had declined to 124 mumol/l (1.4 mg/dl), and 24-hour urine creatinine excretion rate declined to 11.5 mmol/d (1.3 g/d) with an estimated creatinine clearance rate of 65 ml/min. This was accompanied by reduction in serum uric acid and cholesterol levels, and a decline in uric acid excretion rate. Eighteen months later his creatinine had further declined to 88.4 mumol/l (1.0 mg/dl).

Adult↗
PubMed2004

Pyrazinamide induced hyperuricemia in patients taking anti-tuberculous therapy.

OBJECTIVE: To record the effect of pyrazinamide on uric acid in patients of tuberculosis. DESIGN: Descriptive and observational study. PLACE AND DURATION OF STUDY: Chandka Medical College Hospital, Larkana from February 2000 to January 2003. PATIENTS AND METHODS: All patients receiving anti-tuberculosis drugs with pyrazinamide were included. Serum uric acid levels were monitored at weeks 0, 2, 8 and 12 of therapy. Serum creatinine was done at weeks 0, 8 and 12. RESULTS: Results were reported on 216 patients. Mean uric acid and creatinine levels at the start of therapy, i.e., week '0' were 5.07 -/+ 0.57 mg/dl and 0.87 -/+ 0.11 mg/dl respectively. The results show significant increase in uric acid levels from week '0' to week '2', at the end of week '8', the levels remained elevated and there was no statistical significant difference from that at week '2'. The uric acid levels reduced at week '12' after pyrazinamide was stopped and the difference was significant. Despite that renal function steadily improved with the treatment of tuberculosis to the extent that comparable pre-treatment values were obtained at the end of treatment. CONCLUSION: Anti-tuberculous therapy with pyrazinamide affects the uric acid levels early. This change is reversible after the withdrawal of the agent.

Adult↗