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Gout - Diuretics - Glucosamine - Diuretics: Cause of gout? Glucosamine: Can it worsen gout symptoms? Choi HK effet, Atkinson DiuretcKarlson EWAnti-cancer habits G. Obesity, Weight Sugar alternatives for weight loss, Hypertension, Diuretic Use, and Risk Diuretic effect on gout Diurstic in Men : The Health Professionals Follow-up Study. Arch Intern Med. Background Limited prospective information exists on the relation between obesity and weight change and the risk of gout. Similarly, both hypertension and diuretic use have been considered risk factors for gout; however, their independent contributions have not been established prospectively.Diuretic effect on gout -
Hyperuricaemia, or the increase in serum urate SU levels, is a necessary condition for the development of gout.
Thus, disorders that impair the glomerular filtration of uric acid such as renal failure or interfere with its tubular transport such as insulin-resistant states or drugs would contribute to the development of hyperuricaemia and gout. As a result of this link, renal failure and diuretics are commonly seen in patients with gout [ 7 ].
Chronic kidney disease CKD has an impact on gout management by limiting the dosage or hampering the use of urate-lowering drugs ULD , colchicine, and non-steroidal anti-inflammatory agents [ 8 ]. The frequent prescription of diuretics might also impact outcomes in these patients [ 9 ].
Diuretics both loop agents and thiazides can increase SU levels but also interfere with allopurinol, enhancing the renal clearance of its active metabolite oxypurinol and increasing the dose needed to ensure effectiveness [ 10 ].
This would also apply to advanced heart failure or hypertension, where diuretics are often used. Febuxostat is used even in patients with advanced CKD based on its hepatic metabolism, though whether diuretics modify its urate-lowering effect is unknown. If not, its use would be preferential in patients with CKD or heart failure who are on diuretics, especially when diuretics cannot be discontinued.
In this context, there is a need to determine the impact of diuretics on gout management in clinical practice, especially after the incorporation of new ULD and treat-to-target strategies [ 11 ].
This knowledge could inform management plans for patients with gout who are taking diuretics, helping to achieve suitable SU reductions that ensure the cure of the disease. The aim of the present study was to assess the impact of diuretic therapy on the response to ULD in patients with gout, according to the type of drug prescribed.
We performed a retrospective analysis on an inception cohort in the Rheumatology Unit of the Hospital General Universitario de Alicante Spain. The characteristics of the cohort have been described elsewhere [ 12 ].
Briefly, recruited patients are those presenting to the unit for the first time with crystal-proven gout without having received previous specialised care. The study period for the present work was January to July We excluded patients without SU results during follow up.
Our primary outcome variable was the maximum dose of ULD prescribed, as we considered this the best indicator of the potential influence of covariables - such as diuretics - in achieving proper SU reduction and the recommended SU targets [ 5 ] for managing patients with gout. The primary explanatory variable was the use and dosage of diuretic therapy, specifically loop agents furosemide, torasemide and thiazides, both at baseline and after achieving maximal dose of ULD.
We also recorded the reason for prescribing diuretics hypertension, heart failure, CKD, others, or mixed. Other explanatory variables were demographic age, sex ; clinical hypertension, diabetes mellitus, dyslipidaemia, smoking, cardiovascular disease ; anthropometric data weight, height, body mass index BMI ; laboratory measurements estimated glomerular filtration rate eGFR , according to the Chronic Kidney Disease Epidemiology Collaboration CKD-EPI formula [ 13 ] at baseline and after maximal dose of ULD; and gout-related data years since first attack, numbers of attacks suffered, number of involved joints, joint pattern at presentation monoarticular, oligoarticular, polyarticular , tophi, and type of ULD employed and prior usage.
We performed a descriptive analysis of the sample, expressing continuous variables as means standard deviation SD or medians interquartile range [IQR , depending on the data distribution, and we expressed qualitative variables as frequencies and percentages.
Based on clinical experience, we deemed a unified analysis of the use of diuretics inappropriate, as the patients eligible in clinics for certain ULDs allopurinol, febuxostat, benzbromarone are usually very heterogeneous, as are their pharmacodynamics and kinetics.
We considered that a patient was on diuretics when being treated at the moment of maximal dosage of ULD for at least a week, to avoid bias due to diuretic start or discontinuation during follow up. Manifest variability in the type and dosage of diuretics precluded subgroup analyses.
In the case of significant results in the univariable analysis, we built a linear regression model for the primary outcome maximal dose of ULD prescribed to adjust for potential confounders age, sex, hypertension, diabetes mellitus, dyslipidaemia, tobacco use, cardiovascular disease, BMI, baseline SU levels and eGFR, and final eGFR.
All statistical analyses were performed using SPSS Of patients enrolled in the inception cohort, follow-up data were available for patients General baseline characteristics are shown in Table 1 ; these are typical of patients with gout seen in specialised clinical practice. Median disease duration at enrolment was 4 years IQR 0—10 , with a median of 4 reported flares IQR 2—10 having involved a median of 3 joints IQR 2.
At presentation, Tophi were recorded in At baseline, patients More patients were taking thiazides than loop agents When the maximal dose of ULD was reached, 90 patients were on diuretics At this time point, more patients were taking loop diuretics than thiazides The supplementary material describes dosage at both time points Additional file 1 : Table S1.
With regard to ULDs, patients Table 1 compares baseline characteristics according to ULD treatment: the febuxostat group was significantly older, included more women, and had a higher prevalence of hypertension, CKD, and cardiovascular disease.
On the other hand, there were fewer smokers, and their blood tests revealed higher levels of SU and lower eGFR. Given the significant heterogeneity, we did not pool groups but report results separately according to type of ULD. Despite higher final SU levels in those taking diuretics compared to those who were not, the average SU reduction was similar between subgroups.
The maximum doses of allopurinol were comparable between subgroups, though they tended to be lower in those on diuretics and especially in those on diuretic combination; there was no difference between thiazides and loop agents Additional file 1 : Table S2. Table 3 shows the results of patients on febuxostat.
Of the 33 patients, 19 Two patients We did not observe significant differences in the reduction of SU levels or the achievement of the different SU targets. The present study assessed the impact of diuretics in managing gout in an inception cohort of patients in specialised care.
This issue is a subject of debate in the literature, with conflicting data in the case of allopurinol [ 10 , 14 ], but we did not observe any significant effect of diuretics on the achievement of SU targets or on the maximum doses prescribed in patients on allopurinol or febuxostat.
Diuretics, especially loop agents and thiazides, are extensively used in clinical practice and are often essential for managing potentially life-threating disorders such as heart or kidney failure. Diuretic-induced hyperuricaemia is a well-established secondary effect and derives from impaired SU excretion due to reducing extracellular volume [ 15 ] and interactions with renal urate transport at the proximal convoluted tubule [ 16 ].
Diuretics are common in patients with gout, who tend to be older and suffer from a number of comorbidities [ 17 ]. However, whether the development of gout relates to the diuretic-induced hyperuricaemia or is attributable to the underlying disease is still unclear [ 18 ].
The dosage of allopurinol needed to achieve SU targets varies widely between patients, depending on variables such as kidney function, body size, or genetic factors influencing tubular reabsorption [ 19 ]. However, in our adjusted analysis there were no differences in allopurinol dosage based on concomitant diuretic therapy.
Wright et al. analysed data from five clinical trials, while here patients were recruited in a clinical practice setting, which is often more complex due to the prevalence of comorbidities.
Loop diuretics and thiazides were analysed together in both studies, with no stratification according to dosage in the present study due to the risk of an underpowered analysis. For furosemide, some authors have suggested that allopurinol interferes with down-regulation of xanthine oxidase, explaining higher dosage requirements [ 20 ], but this hypothesis has not been fully confirmed [ 21 ].
In contrast, no authors have observed significant interactions with thiazides [ 22 , 23 ]. Further studies should assess the existence of a differential effect in allopurinol dosage between types of diuretics.
Regarding the impact of diuretics on the effect of febuxostat, hydrochlorothiazide showed no significant clinical interaction [ 24 ], and we did not identify any studies assessing loop agents from the current literature.
The present study showed no differences in dosage or achievement of SU targets based on the use of diuretics. These findings - the first to come from clinical practice - would lend support to the use of febuxostat in this setting.
However, they should be interpreted with caution, as our sample included few participants taking this drug, and moreover, febuxostat is only marketed in Europe as 80 mg and mg tablets thus limiting its dosage, unlike allopurinol.
Larger studies are needed to corroborate our results. Almost a quarter of the patients in the study sample had their diuretics discontinued during follow up. Although this treatment strategy is in line with recommendations from the European League Against Rheumatism EULAR [ 5 ], these were based on low-quality evidence, and our results do not support this course of action, at least in the case of urate-lowering therapy.
Nevertheless, the approach may be of interest when the patient reaches persistent normouricaemia and there is a clinical presumption of complete removal of crystal deposits.
ULD dose reduction or discontinuation should aim to maintain uricaemia below its saturation point to prevent new crystal formation [ 25 ]. At this point, the absence of factors contributing to hyperuricaemia, such as diuretics, is desirable. However, this research question, while of active interest, was beyond the scope of the present study.
The main strength of this study is its structured assessment of outcomes in a cohort of patients with crystal-proven gout. We analysed a significant sample size of more than patients treated with allopurinol, compared to patients included in the study by Wright et al.
Furthermore, we considered several covariates, adjusting the analysis to reinforce the robustness of the results. Regarding the limitations, these mainly relate to the cohort study design and include the absence of random sampling and allocation to ULDs or diuretics, along with the impossibility of modifications to the treatment regimens by researchers.
We did not undertake a differential analysis on the type of diuretic, owing to small numbers in the subgroups. Although the results are comparable with current evidence, this should be properly assessed in the future. The effect of diuretics on the duration of achieving the recommended SU targets could provide an additional idea of their impact on management; unfortunately, this issue could not be assessed in the present study as records review focused on the time of maximum dose of ULD prescribed - the primary study outcome.
We did not assess safety. Both loop agents and thiazides are diuretics that are commonly prescribed in patients with gout and have often been associated with impaired response to allopurinol and refractoriness, prompting recommendations for their discontinuation when possible.
However, the results of the present study do not support prior observations related to the achievement of SU targets or the necessary ULD dosage, while they are in keeping with those recently reported by Kannangara et al.
These findings require further confirmation through prospective, intervention studies. Roddy E, Choi HK. Epidemiology of gout. Rheum Dis Clin N Am. Article Google Scholar. Scire CA, Manara M, Cimmino MA, et al. Gout impacts on function and health-related quality of life beyond associated risk factors and medical conditions: results from the KING observational study of the Italian Society for Rheumatology SIR.
Arthritis Res Ther. Clarson LE, Chandrate P, Hider SL, et al. Increased cardiovascular mortality associated with gout: a systematic review and meta-analysis.
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BMJ Open. Richette P, Doherty M, Pascual E, et al. Ann Rheum Dis. Pascual E, Perdiguero M. Gout, diuretics and the kidney. Richette P, Clerson P, Perissin L, Flipo RM, Bardin T. Revisiting comorbidities in gout: a cluster analysis.
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BMC Med. Wright DF, Duffull SB, Merriman TR, Dalbeth N, Barclay ML, Stamp LK. Predicting allopurinol response in patients with gout.
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Levey AS, Stevens LA, Schmid CH, Zhang YL, Castro AF 3rd, Feldman HI, et al. A new equation to estimate glomerular filtration rate. Ann Int Med. Kannangara DRW, Graham GG, Wright DFB, et al. Individualising the dose of allopurinol in patients with gout.
Weinman EJ, Eknoyan G, Suki WN. The influence of the extracellular fluid volume on the tubular reabsorption of uric acid. J Clin Invest. McAdams-DeMarco MA, Maynard JW, Baer AN, et al. A urate gene-by-diuretic interaction and gout risk in participants with hypertension: results from the ARIC study.
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Sodium lactate solution has many advantages and appears promising for resuscitation of critically ill patients [ 72 ]. However, high dose lactate infusion may induce hyperuricaemia by decreasing urinary excretion and the fractional clearance of uric acid [ 73 ].
Lactate interacts with URAT1 [ 25 ]. This latter is an important transporter of urate reabsorption in exchange for lactate at the apical membrane of the proximal tubules. Therefore, lactate stimulates urate uptake, leading to hyperuricaemia.
In addition, lactate may also interfere with organ anion transporters OAT4 and OAT10 Fig. Testosterone replacement therapy TRT , used for patients with female to male gender identity disorder, increases uric acid level in a dose-dependent manner.
In a recent study, the rates of serum uric acid increase after 3 months of TRT intramuscular injection of testosterone enanthate were 29 and Testosterone-induced gout has also been reported [ 76 ].
Testosterone treatment leads to increased serum uric acid levels and reduced renal excretion of uric acid [ 77 ]. The serum uric acid elevation may be also, at least partially, attributed to an increase in muscle mass during the early phase of TRT [ 75 ].
In addition to the drugs listed above, many miscellaneous agents may induce hyperuricaemia and gout Table 2 [ 79—88 ]. T able 2 Miscellaneous drugs inducing hyperuricaemia and their suggested mechanism.
Although, there are no published guidelines on how to prevent drug-induced hyperuricaemia, patients receiving drugs known to induce hyperuricaemia should be encouraged to maintain adequate hydration and have their uric acid levels routinely monitored. These patients should also be monitored for symptoms that might precede the onset of gout.
Approximately two out of three patients with drug-induced hyperuricaemia will remain asymptomatic [ 24 ]. In drug-induced asymptomatic hyperuricaemia, especially with diuretics, treatment to control serum uric acid levels is rarely required.
However, gouty episodes in patients with a personal or family history of established gout may be aggravated by diuretic therapy in hypertensive patients. When gout develops the decision to continue therapy needs to be individualized, and so too does a decision to initiate allopurinol or a uricosuric drug [ 7 ].
In drug-induced symptomatic hyperuricaemia and gout, management includes the identification of offending drugs and the institution of appropriate anti-hyperuricaemic agents. Withdrawal of the offending drug should be based on an assessment of the benefit—risk ratio. When alternative therapy is available, the offending drug may be replaced by a drug that does not cause hyperuricaemia.
However, in certain cases, the offending drug is necessary. For example, the use of low-dose aspirin for prevention of cardiovascular disease should not be suspended for patients with gout. Close monitoring of serum uric acid when an individual is taking low-dose aspirin may help to avoid the risk of gout attacks.
However, allopurinol or uricosuric agents may be necessary in some cases of aspirin-induced gout [ 54 ]. In hypertensive patients controlled on one or two medications with acute thiazide-induced gout, the reduction of the dose of thiazide rather than its discontinuation is an appropriate option because drug-induced hyperuricaemia is dose-related [ 8 ].
In hypertensive patients controlled on three or more medications thiazide continuation with dose reduction or pharmacological anti-hyperuricaemic therapy, that is, allopurinol, should be considered. Treatment of ciclosporin-induced acute attacks may be difficult since interactions with NSAIDs may lead to enhanced renal toxicity.
Colchicine, if prescribed in these acute attacks, should also be used cautiously and the dose reduced. Corticosteroids are an effective alternative to colchicine. In patients who develop ciclosporin-induced hyperuricaemia and gouty arthritis with tophi, benzbromarone, a uricosuric agent, may be useful.
It should be initiated at a low dose and gradually increased, and liver function should be monitored closely. Allopurinol is also a useful alternative in these patients. Interestingly, the normalization of uric acid levels by allopurinol or benzbromarone reduced the tubulointerstitial disease and arteriolar hyalinosis induced by ciclosporin [ 89 ].
Ciclosporin and tacrolimus withdrawal may be considered for transplant patients with recurrent, severe gout that cannot be managed safely or effectively [ 90 ]. The cornerstone management of TLS is prevention. Prevention strategies may also include hydration plus allopurinol or rasburicase for intermediate-risk patients, and close monitoring for low-risk patients [ 91 ].
For nicotinic acid-induced hyperuricaemia, allopurinol is usually used when therapy is indicated. Nicotinic acid inhibits the effect of uricosuric drugs such as sulfinpyrazone and the latter should be avoided. Pyrazinamide-induced hyperuricaemia can be managed by observation and does not require withdrawal of treatment.
It can be also controlled with allopurinol. However, paradoxical increase in uric acid level with allopurinol use in pyrazinamide-induced hyperuricaemia has been reported [ 92 ].
Allopurinol was shown to increase plasma concentrations of pyrazinoic acid, which is directly responsible for the inhibition of renal urate secretion [ 92 , 93 ]. Aspirin may prevent hyperuricaemia and the arthralgia associated with pyrazinamide therapy.
Hyperuricaemia due to ethambutol was reversed with probenicid, sulfinpyrazone or allopurinol. The latter, increases the serum level of theophylline and therefore the serum level of theophylline should be carefully monitored when allopurinol is added to a hyperuricaemic patient who is under this treatment [ 94 ].
However, benzbromarone and probenecid do not seem to interfere with the theophylline serum level. In conclusion, drug-induced hyperuricaemia and gout present an emergent and increasingly prevalent problem in clinical practice. Drugs raise serum uric acid level by various mechanisms.
Patients receiving these drugs should be encouraged to maintain adequate hydration and have their uric acid levels monitored. Funding : No specific funding was received from any funding bodies in the public, commercial or not-for-profit sectors to carry out the work described in this article.
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Diuetic pathogenesis, epidemiology, and Diuretic effect on gout overview of Diuretic effect on gout Duretic diuretic-induced hyperuricemia and gout are efvect in Weight gain challenges topic. The pathophysiology, clinical manifestations, diagnosis, and treatment of gout flares as well as the prevention of gout flares are discussed separately:. To continue reading this article, you must sign in. For more information or to purchase a personal subscription, click below on the option that best describes you:. Why UpToDate?
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