PubMed HealthSearch

SEARCH · PubMed Health

Results for “primary gout”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Efficacy and Safety of Ultra-Low Starting Dose Febuxostat Titration in Male Patients With Primary Gout.

BACKGROUND: Since gout is a common metabolic arthritis caused by urate crystal deposition, urate-lowering therapy (ULT) is clearly indicated, but the initiation of ULT frequently causes paradoxical acute flares that in turn impair patient adherence. OBJECTIVE: This study sought to assess the effectiveness and safety of an ultra-low-dose initiation strategy for febuxostat (10&#x2009;mg/day) compared to the standard starting dose (20&#x2009;mg/day) in reducing initiation-related flares while maintaining long-term urate control. METHODS: 120 male patients with primary gout presenting with acute arthritis were randomly assigned to initiate febuxostat at 10&#x2009;mg/day (Group A) or 20&#x2009;mg/day (Group B), with protocol-mandated biweekly titration. The primary outcomes were gout flare frequency over 24&#x2009;weeks (assessed using Poisson regression), serum uric acid (SUA) target attainment, and the incidence of adverse events. RESULTS: Although both groups achieved comparable target SUA levels by week 24, Group A demonstrated a significantly lower overall flare incidence (36.7% vs. 70.0%; p&#x2009;<&#x2009;0.001), along with a greater percentage of flare-free patients (70.0% vs. 46.7%; p&#x2009;=&#x2009;0.016). Multivariable Poisson regression revealed that Group B had an approximately twofold higher risk of flares compared to Group A (Incidence Rate Ratio&#x2009;=&#x2009;1.95; p&#x2009;=&#x2009;0.012), with obese patients deriving the most pronounced benefit from the ultra-low-dose approach. To avert one additional flare, the calculated number needed to treat was 4.3. Additionally, the occurrence of clinically significant liver injury (ALT/AST >&#x2009;3&#xd7; ULN) was low in both groups, with 3.3% in Group A and 1.7% in Group B. Multivariable regression analysis confirmed that LDL-C is an independent predictor of ALT (&#x3b2;&#x2009;=&#x2009;12.90, p&#x2009;=&#x2009;0.009), while febuxostat dosage was not linked to hepatotoxicity. CONCLUSION: Initiating febuxostat at a dose of 10&#x2009;mg/day with gradual titration demonstrates a superior safety profile by effectively reducing early acute flares without compromising long-term urate control, which is particularly advantageous for high-risk cohorts, including obese patients.

Humans

Enzyme defect in primary gout.

The rate-limiting step in the degradation of adenine nucleotides in the liver is the conversion of adenosine monophosphate (A.M.P.) to inosine monophosphate by A.M.P. deaminase, which is normally 95% inhibited. When the inhibition is released, uric acid is formed in large excess, and the biosynthesis of purines is increased. We therefore propose that congenital hyperuricaemia is caused by the presence of an abnormal A.M.P. deaminase, which is less sensitive to its physiological inhibitors. Verification of the hypothesis depends upon the availability of liver tissue from patients with congenital hyperuricaemia for kinetic analysis of A.M.P. deaminase. A call for collaboration is addressed to the medical community.

AMP Deaminase

Secondary hypertriglyceridemia and hyperlipoproteinemia in patients with primary asymptomatic gout.

We carefully selected 30 men with primary gout, rendered asymptomatic by therapy, to examine the frequency and type of hyperlipidemia and hyperlipoproteinemia, with the objective of determining whether serum uric acid, alcohol intake, liver function, kidney function, and (or) drugs were participating in the secondary lipid disorder. Sixty-one age- and sex-matched men were used as controls. About 73% of the gout patients had hypertriglyceridemia, 1.6-fold the frequency found in the control group. Types IV and IIb lipoprotein electrophoretic patterns were most prevalent in the gout group. Neither alcohol intake nor hyperuricemia, per se, seems to be the cause of the lipid and lipoprotein disorder and cannot be related to liver or kidney dysfunctions. Obesity was the major underlying factor associated with the lipidemia. The study suggests that diet and, possibly, defective clearance of triglycerides may be etiologic factors associated with the abnormal serum triacylglycerol (triglyceride) and lipoprotein concentrations in these individuals.

Blood Chemical Analysis

Normal activity of metabolic pathways involved in the formation and utilization of phosphoribosylpyrophosphate in erythrocytes of patients with primary metabolic gout.

The activity of metabolic pathways involved in the formation and utilization of phosphoribosylpyrophosphate (PRPP) was studied in. The erythrocytes of 34 patients with idiopathic metabolic gout. The activities of the oxidative pentose shunt, of the hypoxanthine-guanine and adenine phosphoribosyltransferases (HGPRT, APRT) and of PRPP synthetase, as well as the rates of PRPP generation and of adenine incorporation into nucleotides were found to be normal in the erythrocytes of all these patients. Four patients with metabolic gout due to enzymatic abnormalities, two relatives with partial deficiency of HGPRT and two relatives with mutant feedback-resistant PRPP synthetase, were studied for comparison. The significance of the results is discussed in relation to postulated mechanisms for purine overproduction in metabolic gout.

Adenine Phosphoribosyltransferase

Erythrocyte adenosine kinase activity in gout.

Erythrocyte adenosine kinase (AK) (EC 2.7.1.20) and guanosine monophosphate (GMP) reductase (EC 1.6.6.8) were measured in healthy male controls and primary gout subjects. Adenosine kinase activity in 19 controls and 26 gouty subjects was 0.717 +/- 0.176 and 0.615 +/- 0.128 nmol/mg protein/h, respectively. The difference was statistically significant (p less than 0.05). GMP reductase activity in 39 controls and 46 gouty subjects was 30.90 +/- 6.28 and 33.43 +/- 7.97 mumol/mg protein/h, respectively, without statistically significant difference.

Adult

Prevalence and incidence of the diagnosis of gout in Great Britain.

A study in gout of the incidence of diagnosis from 1971 to 1975 and of the prevalence at 31 December 1975 was carried out in a representative general practice sample comprising 64 practices and a population numbering 1 in 145 of the total population of Great Britain. The results show an annual incidence in Great Britain from 1971 to 1975 varying from 0.25 to 0.35 per 1000 and an overall prevalence at 31 December 1975 of 2.6 per 1000. The prevalence in England was found to be significantly greater than in the rest of Great Britain and that in Wales to be significantly greater than in Scotland. In 10% of the cases the gout was believed to be secondary, with induction by diuretics being the most frequent cause. The prevalence of primary gout was estimated to be 2.3 per 1000.

Adolescent

Renal function in gout. V. Factors influencing the renal hemodynamics.

Renal hemodynamics as measured by inulin clearance (Cinulin) and para-aminohippurate clearance (CPAH) was evaluated in 149 patients with primary gout over intervals of two to 22 years. In over 30 per cent of the patients plasma urate was greater than 10 mg/dl and urinary uric acid greater than 800 mg/min. A linear trend in decreasing frequency of hyperuricemia and excessive uricosuria is significantly related to the patient's age at the onset of gout. Group I consisted of 84 patients with uncomplicated gout in both clearance studies. Cinulin and CPAH were somewhat lower in patients larger than or equal to 50 years of age with longer duration of gout. Further reduction in clearances was minimal at the second clearance study in intervals of approximately 10 years. Group II included 27 patients who had no associated disease at the time of the first clearance study but in whom associated disease had developed by the time of the second clearance study. A striking reduction in Cinulin and CPAH was noted, especially in those 50 years old or above. There were 38 patients in group III with associated diseases at the time of both clearance studies. They had lower Cinulin and CPAH at the time of the first study, particularly the older patients. Further reduction during the second study was less striking than that in group II. Analyses of variance suggest that various coexisting vascular diseases with associated nephropathy have the most significant impact on the status of renal function in gout, with aging the second most important and duration of gout, the third.

Adult

The hypotriglyceridemic effect of chenodeoxycholic acid in type IV hyperlipemia.

The effect of chenodeoxycholic acid on the fasting serum triglycerides was studied in 30 patients with type IV hyperlipemia and in 20 patients with primary gout and associated endogenous hypertriglyceridemia, the triglycerides being determined before treatment and at monthly intervals for three months. Chenodeoxycholic acid treatment resulted in a significant lowering of the serum triglycerides in both groups of patients. The drug was well tolerated and there were no undesirable side-effects. Although the mechanism of action is still not known, the drug is thought to reduce triglyceride synthesis in the liver. Chenodeoxycholic acid appears to be electively indicated in type IV hyperlipemia treatment.

Adult

Uricosuric therapy and urate solubility in blood and urine.

In most patients with primary gout hyperuricaemia results from a renal defect in tubular uric acid secretion. An increased endogenous purine biosynthesis is observed in only 2% of all patients with gout. Secondary hyperuricaemai results either from an increased breakdown of endogenous nucleic acids as in polycythaemia or from a decreased renal excretion of uric acid due to drug treatment, renal insufficiency or metabolic disturbances. Hyperuricaemia may be defined either in statistical terms from epidemiological studies of normal and gouty populations or from physicochemical properties of urate. Monosodium urate and uric acid are soluble in water to the extent of 6.32 mmol/l and 0.39 mmol/l respectively. In human plasma saturation of monosodium urate occurs at a concentration of about 0.42 mmol/l. The solubility of uric acid and urate in urine is more complicated as it is affected by changes in pH and salt concentration. Uricosuric drugs decrease serum uric acid concentration by enhancing the renal excretion of uric acid. Effects and side effects of uricosuric therapy are discussed.

Gout

Treatment of acute gouty arthritis with proquazone and indomethacin. A comparative, double-blind trial.

Eighteen patients (11 men and 7 women) suffering from primary or secondary gout, were treated with either proquazone or indomethacin for acute attacks in a double-blind study. There were 9 patients in each treatment group. A marked improvement of clinical symptoms appeared in 2-3 days. In the proquazone group, complete remission was achieved in 6 patients, a good result in one, and a slight improvement in one patient, whereas one patient did not respond to treatment. The corresponding figures for the indomethacin group were 4 cases with complete remission, 4 with a good result, and one not responding to treatment. A significant decrease in s-uric acid values was noted in the proquazone group. In this group too, mild gastrointestinal symptoms appeared in 2 patients.

Acute Disease

[Value and significance of the immunologic determination of various serum sialoglycoproteins in rheumatic diseases of inflammatory nature].

A statistical method was used in the evaluation of alpha-1-antitrypsin, acid alpha-1-glycoprotein, and haptoglobin in patients with rheumatic fever, rheumatoid arthritis, gout, periarthritis, arthrosis with inflammation, and primary arthrosis. A highly significant increase was noted in rheumatic fever and rheumatoid arthritis, less so in arthrosis with inflammation and acute gout, while increases were poorly significant for periarthritis and not significant for primary arthrosis. It can be concluded that the determination of these serum sialoglycoproteins serves to distinguish inflammatory and degenerative rheumatism. Haptoglobin proved the most sensitive of the three. Moreover, there was a distinct correlation between ESR and the three indices. It is felt that sialoglycoproteins act as an indirect pointer to acute inflammation, since their degree of increase is related to the formation of inflammatory proteases.

Adolescent

[Relationship between avascular necrosis and lipid and purine metabolisms].

The serum levels of uric acid, triglycerides, cholesterol, and lipoproteins were determined in 35 patients suffering from primary avascular necrosis. The results were compared with those of a control group and with those of patients suffering from gout. The frequency distribution of the results in the three groups was of the log-normal type and statistical calculations were made on logarithmic transformations of the serum values. In comparison with the control group, significant increases in the levels of triglycerides, cholesterol, pre-beta-lipoproteins, and uric acid were observed in patients presenting an avascular necrosis. No significant differences were observed between these patients and patients with gout in the levels of lipids and lipoproteins. Uricaemia was higher in the gout patients. Contrary to observations made on the gout patients, there was no correlation in the avascular necrosis patients between the uric acid level and the serum levels of lipids or lipoproteins. In an earlier study the authors put forward an hypothesis according to which the close relationship between the lipid and purine metabolisms in gout patients was due to a genetic linkage based on a common enzyme defect, which directly affected the two metabolisms. In avascular necrosis there is no common enzyme defect; the initial event is a disturbance in the lipid metabolism. The authors conclude with data which tend to show that the bone necrosis observed in patients using steroids or alcohol is not directly induced by these substances, but that once again the initial event is a disturbance in the lipid metabolism.

Adrenal Cortex Hormones

Postoperative complications and outcomes after surgical treatment for tophaceous gout: A systematic review and meta-analysis.

BACKGROUND: Surgical treatment remains necessary for selected patients with tophaceous gout, particularly when mechanical limitation, nerve compression, ulceration, infection, deformity, or failure of conservative treatment is present. However, postoperative outcomes after surgery for tophaceous gout have not been comprehensively quantified. This systematic review and meta-analysis evaluated postoperative complication profiles and recurrence burden after surgical treatment for tophaceous gout. METHODS: A systematic search of PubMed, Embase, Web of Science, and the Cochrane Library was conducted from database inception to March 25, 2026. Original studies reporting postoperative outcomes after surgical treatment for tophaceous gout were included. Pooled event rates with 95% confidence intervals (CIs) were calculated using a random-effects single-arm meta-analytic approach. Primary outcomes were postoperative infection, delayed wound healing, and recurrence. Secondary outcomes were reoperation, amputation, and overall complications. Functional outcomes were summarized descriptively. RESULTS: 18 retrospective studies were included. The pooled postoperative infection rate was 11.3% (95% CI 8.0%-15.7%), delayed wound healing 9.9% (95% CI 5.1%-18.2%), and recurrence 8.5% (95% CI 4.7%-14.9%). Secondary pooled rates were 9.7% (95% CI 5.5%-16.7%) for reoperation, 3.7% (95% CI 2.0%-6.8%) for amputation, and 24.0% (95% CI 14.0%-38.1%) for overall complications. Significant subgroup differences were identified only for infection according to anatomic site and intervention type. Sensitivity analyses showed that pooled estimates were robust. The certainty of evidence was very low for all outcomes. CONCLUSIONS: Surgical treatment for tophaceous gout is associated with measurable postoperative risks, particularly infection and overall complications. These findings support careful perioperative counseling, structured postoperative surveillance, integrated long-term urate-lowering management, and more standardized reporting of perioperative risk factors and postoperative outcomes in future surgical studies of tophaceous gout.

Humans

[Physiopathological bases for a rational therapy of gout].

Rational therapy of gout must be correlated with the two basic aetiopathogenetic factors, i.e. metabolic error and the inflammatory dysreactive moment. Due to its different action mechanism, the former is responsible for the typing of adult primary hyperuricaemia: a) hyperincorporating and hyperescretory forms; b) normo-incorporating and relatively or absolutely hypoexcretory forms; c) hyperincorporating and hyposcretory forms. It would be a mistake to treat the condition chemically without knowing the physiopathology of the metabolic error. On the basis of a preliminary typing assessment, rational chemical correction of the metabolic error in gout cases can be achieved with drugs that block the enhanced endogenous synthesis of uric acid (allopurinol, etc.) or correct the metabolite renal excretion defect. Therapy of the dysreactive-inflammatory component should involve non-steroid anti-inflammatory drugs. The disadvantages of using cortisones in gout treatment are stressed.

Allopurinol

Rheumatologic conditions of the wrist.

With the exception of the arthritis associated with rubella, acute wrist conditions have no pathognomonic physical findings. The primary physician can diagnose and treat the majority of wrist problems presented. Referral to a rheumatologist is necessary only when confronted with an anxious patient or an individual having persistent wrist pain and swelling of obscure etiology. This article focuses on rheumatologic problems of the wrist that are most likely to come to the attention of the primary physician.

Acute Disease