
Gout And Diabetes
Tweet Gout is a form of arthritis (inflammation of joints) caused by high levels of uric acid. Gout can be a painful condition but one that can be managed to reduce the frequency at which gout attacks occur. Gout is known to affect around 1 in 100 people in the UK and is around four times more common in men than in women. Research shows that people with gout are significantly more likely to develop type 2 diabetes than people without gout. Gout and diabetes A number of research papers have shown associations between gout and type 2 diabetes including a study from Harvard Medical School, published in 2014, which showed gout to be associated with a 70 increased risk of developing type 2 diabetes. A common medication for treating gout, allopurinol, has shown promise for reducing thickening of heart muscle and is currently undergoing testing as a possible medication for reducing risk of diabetic nephropathy (kidney disease). Symptoms of gout Gout is characterised by swelling of joints. The base of the big toe is most commonly affected by gout. More than one joint may be affected by gout in some people. Symptoms can come on quickly, with swelling occurring within a few hours. The swollen joint can be very painful and sensitive to touch. During swelling, skin covering the joint may typically turn red and shiny in appearance. The swelling and symptoms may occur for several days if not treated. Once the inflammation has subsided, the skin on the joint may become itchy and flaky. Causes of gout Gout occurs if high levels of uric acid in the blood leads to crystals of sodium urate forming in and around the joints. If these crystals spill into the joint space, this can cause the joint to become inflamed. Risk factors High levels of uric acid are more likely to build if you have an Continue reading >>
![[effect Of Metformin On The Clinical Course Of Gout And Insulin Resistance].](https://diabetestalk.net/images/.jpg)
[effect Of Metformin On The Clinical Course Of Gout And Insulin Resistance].
Abstract The aim of this prospective study was to evaluate results of metformin (MF) therapy during 1 year of uric acid (UA) metabolism and the clinical course of gout with insulin resistance (IR). The study included 30 patients (28 men and 2 women) of mean age 51 yr and duration of he disease 4-11 yr. IR was diagnosed based on the HOMA index. INCLUSION CRITERIA: the absence of anti-gout therapy, normal renal and hepatic function, abstinence. The patients were given 1500 mg MF/day. The measured parameters included anthropometric and clinical characteristics, 24 hour AP, plasma UA, glucose, insulin, urea, creatinine, ALT, AST, lipid spectrum at the first and subsequent visits. UA clearance and excreted UA fraction were calculated. UA level decreased from 569 +/- 109.5 to 442.8 +/-107.4 mcmol/l (p < 0.01) after 12 months of MF therapy. Normouricemia ( < 360 mcmol/l) was achieved in 11 patients. Fasting insulin level dropped by 35% (from 23.9 to 15.9 mcU/ml, p < 0.01), HOMA index from 6.5 to 3. 7(p < 0.01). Serum glucose, cholesterol, triglycerides, and LDL cholesterol decreased while HDL cholesterol increased. Parameters of renal UA regulation and anthropometry remained unaltered. MF therapy resulted in a decrease of serum UA, insulin, and the degree of IR. The hypouricemic effect of MF was unrelated to renal UA excretion, reduced AP and body weight. It is hypothesized that MF reduces production of UA in patients with gout due to inhibition of synthesis of free fatty acids. Continue reading >>

Gout: Never Have An Attack Again
Gout is a condition that commonly effects both men and women as they age, especially this time of year during the holidays when we all tend to over-indulge in rich foods and alcohol. And now the good news: you never have to suffer from gout again. What it is, and how your other doctor treats it Gout is the deposition of uric acid crystals in joints, most commonly the big toe, and can be debilitating due to the extreme pain it can cause. Uric acid is a breakdown product of purines (see below for the list of foods that contain high levels) and is broken down by an enzyme called xanthine oxidase. Allopurinol is a typical drug used in the treatment of gout as it blocks the action of xanthine oxidase, thereby decreasing the amount of uric acid crystals being produced. NSAID’s are often used for pain management, as is colchicine, for their anti-inflammatory effects. How you can treat it, naturally Even if you do some of the following, you will decrease the severity and frequency of your attacks. Lifestyle Lose some weight and improve your blood pressure – hyperuricemia (elevated levels of uric acid in blood) is associated with abdominal obesity and hypertension Improve your blood lipid and glucose levels- hyperuricemia is also associated with dyslipidemia and insulin resistance. If you’re on a lipid medication (most commonly a statin), or a prescription for type II diabetes (most commonly metformin), then there’s work to be done Diet Increase water intake – not only will this decrease uric acid levels, but it will help with your blood pressure as well Increase consumption of cherries or unsweetened cherry juice – consuming the equivalent 6 cups of cherries daily can reduce your uric acid levels to normal in 3 months Eliminate alcohol – this does not go over well Continue reading >>
![[use Of Metformin (siofor) In Patients With Gout And Insulin Resistance (pilot 6-month Results)].](https://diabetestalk.net/images/.jpg)
[use Of Metformin (siofor) In Patients With Gout And Insulin Resistance (pilot 6-month Results)].
Abstract AIM: To evaluate metformin efficacy and safety in patients with gout and insulin resistance (IR). MATERIAL AND METHODS: The trial included 26 patients with gout (criteria of the American collage of rheumatologists) and IR (index HOMA). The inclusion criteria were the following: absence of antigout therapy, normal hepatic and renal function, rejection of alcohol. The drug dose was 1500 mg/day. The study was made of anthropometric and clinical characteristics, 24-h blood pressure monitoring, blood tests for uric acid, glucose, insulin, urea, creatinin, alaninaminotransferase, aspartataminotransferase, lipid spectrum at the first and further visits. RESULTS: A 6-month metformin therapy significantly changed the levels of glucose, insulin, HDLP and LDLP cholesterol, uric acid, HOMA index. Normouricemia was achieved in 11 patients, a significant lowering of uric acid--in 12 patients. The number of affected joints in 23 patients reduced from 4 (1-5) to 1 (0-2), p < 0.01. Seven patients with achieved normouricemia had no arthritis attacks. In 3 of 10 patients with chronic arthritis joint inflammation persisted. Six patients had dyspepsia during the first week of therapy, 1 patient discontinued the drug because of persistent diarrhea. CONCLUSION: Metformin therapy is safe. It reduces IR. The principal result of the study was lowering of uric acid and attenuation of the articular syndrome. Continue reading >>

Use Of Metformin (siofor®) In Patients With Gout And Insulin Resistance (pilot 6-month Results)
Abstract To evaluate metformin efficacy and safety in patients with gout and insulin resistance (IR). The trial included 26 patients with gout (criteria of the American collage of rheumatologists) and IR (index HOMA). The inclusion criteria were the following: absence of antigout therapy, normal hepatic and renal function, rejection of alcohol. The drug dose was 1500 mg/day. The study was made of anthropometric and clinical characteristics, 24-h blood pressure monitoring, blood tests for uric acid, glucose, insulin, urea, creatinin, alaninaminotransferase, aspartataminotransferase, lipid spectrum at the first and further visits. A 6-month metformin therapy significantly changed the levels of glucose, insulin, HDLP and LDLP cholesterol, uric acid, HOMA index. Normouricemia was achieved in 11 patients, a significant lowering of uric acid--in 12 patients. The number of affected joints in 23 patients reduced from 4 (1-5) to 1 (0-2), p < 0.01. Seven patients with achieved normouricemia had no arthritis attacks. In 3 of 10 patients with chronic arthritis joint inflammation persisted. Six patients had dyspepsia during the first week of therapy, 1 patient discontinued the drug because of persistent diarrhea. Metformin therapy is safe. It reduces IR. The principal result of the study was lowering of uric acid and attenuation of the articular syndrome. Continue reading >>

Effect Of Diacerein As An Add-on To Metformin In Patients With Type 2 Diabetes Mellitus And Inadequate Glycemic Control
Objective To evaluate the effect of diacerein as an add-on to metformin in patients with type 2 diabetes mellitus (T2DM) and inadequate glycemic control. Materials and methods A randomized, double-blind, placebo-controlled clinical trial was carried out on 12 patients with T2DM and inadequate glycemic control [glycated hemoglobin A1c (A1C) ≥ 7%] with metformin as monotherapy (≥ 1500 mg per day) for at least the previous 90 days. Fasting and postprandial glucose were measured before and after the pharmacological intervention. A1C, lipid profile, creatinine and uric acid were also evaluated. After randomization, all patients continued with their dose of metformin. Six subjects received placebo and the other six volunteers took diacerein. Data were tested using the Wilcoxon signed-rank, Mann-Whitney U and chi-square tests. The Institutional Ethics Committee approved the study protocol. Results After 90 days of diacerein as an add-on to metformin, there was a significant decrease in fasting glucose (196 ± 79 vs. 149 ± 70 mg/dL, p < 0.05), postprandial glucose (262 ± 99 vs. 187 ± 70 mg/dlL, p < 0.05) and A1C (8.4 ± 2.0 vs. 6.7 ± 1.7 %, p < 0.05). Conclusions Diacerein as an add-on to metformin in patients with T2DM improved their glycemic control. Key words: Diacerein; metformin; glycemic control; type 2 diabetes mellitus Continue reading >>

Starlix Side Effects Center
Starlix (nateglinide) is an oral diabetes medicine used together with diet and exercise to treat type 2 (non-insulin dependent) diabetes. Other diabetes medicines are sometimes used in combination with Starlix if needed. Starlix is available in generic form. Common side effects of Starlix include: weight gain, sneezing, cough, cold or flu symptoms, diarrhea, nausea, dizziness, or joint pain or stiffness. Starlix can cause low blood sugar (hypoglycemia). Tell your doctor if you have symptoms of low blood sugar such as: chills, dizziness, drowsiness, shaking, fast heartbeat, weakness, headache, tingling of the hands or feet, or hunger. Tell your doctor if you have serious side effects of Starlix including: The recommended starting and maintenance dose of Starlix, alone or in combination with metformin or a thiazolidinedione, is 120 mg three times daily before meals. Hyperglycemia (high blood sugar) may result if you take Starlix with drugs that raise blood sugar, such as: isoniazid, diuretics (water pills), steroids, phenothiazines, thyroid medicine, birth control pills and other hormones, seizure medicines, and diet pills, or medicines to treat asthma, colds or allergies. Hypoglycemia (low blood sugar) may result if you take Starlix with drugs that lower blood sugar, such as: non-steroidal anti-inflammatory drugs (NSAIDs), aspirin or other salicylates, sulfa drugs, monoamine oxidase inhibitors (MAOIs), beta-blockers, or probenecid. Tell your doctor all medications you use. During pregnancy, Starlix should be used only when prescribed. Pregnancy may cause or worsen diabetes. Discuss a plan with your doctor to manage blood sugar while pregnant. Your doctor may change diabetes treatment during your pregnancy. It is not known if this drug passes into breast milk. Consult you Continue reading >>

Irq J Pharm Vol. Ù¡ù¡, No. Ù¢ù Ù¡ù¡ ,ù¡
Effects of glibenclamide and metformin on serum uric acid level in patients with type Ù¢ diabetes mellitus Najlaa Saadi Ismail Department of Pharmacology, Mosul College of Medicine, University of Mosul Received Accepted Ù£Ù .١١.٢٠١٠١٣.Ù§.Ù¢Ù Ù¡Ù ABSTRACT Objectives: To assess the effect of glibenclamide and metformin on serum uric acid level in patients with type Ù¢ diabetes. Study design: Case control study. Subjects and Methods: This study was conducted from March Ù¢Ù Ù Ù© to January Ù¢Ù Ù¡Ù . Fasting blood sugar and serum uric acid level were measured in patients suffering from type- Ù¢ diabetes mellitus who were referred to Al-Wafa Diabetic Center in Mosul City. Group ٣٢ :Ù¡ patients on glibenclamide therapy, group ٤٢ :Ù¢ patients on metformin therapy and group ٤٢ :Ù£ patients on combination therapy, group ٣٢ :Ù¤ patients on restricted diet, and ٢٣ apparently healthy volunteers, were taken as a control group. Results: The study showed a significant increase in the serum uric acid level of the diabetic patients as compared with the control. Glibenclamide and/or metformin showed no significant difference in the serum uric acid level in patients with type Ù¢ diabetes mellitus. Conclusion: Glibenclamide and/or metformin had no significant effect on serum uric acid level in patients with type Ù¢ diabetes mellitus. Keywords: Uric acid, hyperuricemia, type Ù¢ diabetes mellitus, glibenclamide, metformin. الخالصة Ù‰ وميتÙورمين ال عقار رتاثي لدراسة :Ø§Ù‡Ø¯Ø§Ù Ø§Ù„Ø¨ØØ« ÙŠ مصل المرضى مستوى Ø¹Ù‚Ø§Ø Continue reading >>

Effect Of Combined Resveratrol Plus Metformin Therapy In Db/db Diabetic Mice
Abstract The prevalence of Type 2 Diabetes mellitus in the world is associated with other conditions that trigger metabolic syndrome. Although there are several studies on benefits of resveratrol, few have assessed in combination of metformin. The aim of this study was to investigate at the effects of combined therapy (metformin/resveratrol) on body weight gain, biochemical clinical findings, liver and renal function of db/db diabetic mice. Diabetic mice were treated whit resveratrol (20 mg/kg/day), metformin (150 mg/kg/day) and combined therapy for 5 weeks. Histopathological tissues analyses and biochemical parameters (glucose, insulin, triglycerides and cholesterol), functional liver enzymes (AP, AST and GGT) and renal parameters (urea and uric acid) were examined. Our results clearly showed that combined therapy of resveratrol and metformin therapy reduced obesity, glucose and triglyceride levels, as well as improving renal function and partially improving liver function in diabetic mice. The combined therapy may enhance remedial effects in diabetic patients and also in other metabolic disorders as such as metabolic syndrome. Support or Funding Information CONACYT-PEI Mexico for its financial support (Project 231344). Continue reading >>

What Is It?
What Is It? Gout is a disorder characterized by too much uric acid in the blood and tissues. In gout, crystals of uric acid are deposited in the joints, where they cause a type of arthritis called gouty arthritis. These same crystals can also deposit in the kidneys, where they can cause kidney stones. There are three main causes of the high levels of uric acid that lead to gout: A diet rich in chemicals called purines, because purines are broken down by the body into uric acid. Foods that contain high levels of purines include anchovies; nuts; and organ foods such as liver, kidney and sweetbreads. High production of uric acid by the body. This can happen for unknown reasons. It can also occur in certain inherited genetic metabolic disorders, leukemia and during chemotherapy for cancer. The kidneys do not excrete enough uric acid. This can be caused by kidney disease, starvation and alcohol use, especially binge drinking. This also can occur in people taking medications called diuretics (such as hydrochlorothiazide or furosemide). Obesity or sudden weight gain can cause high uric acid levels because the body's tissues break down more purines. In some people, gout is caused by a combination of these factors. People with a family history of gout are more likely to develop the condition. About 90% of patients with gout are men older than 40. Gout is quite rare in younger women; when women develop gout, they are usually post-menopausal. Symptoms The first attack of gouty arthritis usually involves only one joint, most commonly the big toe. However, it can affect other joints, such as a knee, ankle, wrist, foot or finger. In gouty arthritis, the joint can become red, swollen and extremely tender to the touch. Typically, even a bed sheet brushing against the joint will trigger Continue reading >>

Metformin Activates Amp-kinase Through Inhibition Of Amp Deaminase
Abstract The mechanism for how metformin activates AMPK (AMP activated kinase) was investigated in isolated skeletal muscle L6 cells. A widely held notion is that inhibition of the mitochondrial respiratory chain is central to the mechanism. We also considered other proposals for metformin action. As metabolic pathway markers, we focused on glucose transport and fatty acid oxidation. We also confirmed metformin actions on other metabolic processes in L6 cells. Metformin stimulated both glucose transport and fatty acid oxidation. The mitochondrial Complex I inhibitor rotenone also stimulated glucose transport but it inhibited fatty acid oxidation, independently of metformin. The peroxynitrite generator 3-morpholinosydnonimine stimulated glucose transport, but inhibited fatty acid oxidation. Addition of the nitric oxide precursor arginine to cells did not affect glucose transport. These studies differentiate metformin from inhibition of mitochondrial respiration and from active nitrogen species. Knockout of adenylate kinase also failed to affect metformin stimulation of glucose transport. Hence, any means of increase in ADP appears not to be involved in the metformin mechanism. Knockout of LKB1, an upstream kinase and AMPK activator, did not affect metformin action. Having ruled out existing proposals, we suggest a new one: metformin might increase AMP through inhibition of AMP deaminase (AMPD). We found that metformin inhibited purified AMP deaminase activity. Furthermore, a known inhibitor of AMPD stimulated glucose uptake and fatty acid oxidation. Both metformin and the AMPD inhibitor suppressed ammonia accumulation by the cells. Knockout of AMPD obviated metformin stimulation of glucose transport. We conclude that AMPD inhibition is the mechanism of metformin action. Continue reading >>

Have High Uric Acid ( Value= 8) Since Dec'12 , While The Fasting, Pp Values Are Under Control. Request Suggestions To Avoid Medicine
Have been on metformin for 8 years ( 500mg tablet after Breakfast and repeat after dinner) Started Ecospirin AV 75mg given family history of CAD Metformin is an oral diabetes medicine that helps control blood sugar levels. Metformin is for people with type 2 diabetes. Metformin is sometimes used in combination with insulin or other medications, but it is not for treating type 1 diabetes. This is a side effect of your drug which has resulted in high uric acid levels. Ask your doctor for any other alternative which is suitable as per your diabetic history . for lowering Uric Acid levels you may take chandraprabhavati tablets 3 times a days and also take Sansamani vati or Giloy Ghanvati . This will also helpful to you in lowering suger level. take sansamni vati with with cold water (Avoid refrigerator water) . Monitor your diabetes regularly. Continue reading >>

Metformin And Blood Uric Acid Increased - From Fda Reports
Blood uric acid increased is found among people who take Metformin, especially for people who are male, 60+ old , have been taking the drug for 1 - 2 years, also take medication Allopurinol, and have High blood pressure. This review analyzes which people have Blood uric acid increased with Metformin. It is created by eHealthMe based on reports of 199,020 people who have side effects when taking Metformin from FDA , and is updated regularly. What to expect? If you take Metformin and have Blood uric acid increased, find out what symptoms you could have in 1 year or longer. You are not alone! Join a support group for people who take Metformin and have Blood uric acid increased Personalized health information On eHealthMe you can find out what patients like me (same gender, age) reported their drugs and conditions on FDA since 1977. Our tools are simple to use, anonymous and free. Start now >>> * Approximation only. Some reports may have incomplete information. Continue reading >>

Address Correspondence To:
Hyperuricemia has been linked to metabolic syndrome, cardiovascular disease, and chronic kidney disease. Hyperuricemia and type 2 diabetes mellitus were inter-related, type 2 diabetes mellitus was more at risk of having a higher serum uric acid level, and also individuals with higher serum uric acid had higher risk of developing type 2 diabetes in the future. Insulin resistance seems to play an important role in the causal relationship between metabolic syndrome, type 2 diabetes, and hyperuricemia. Oral diabetic drugs that would have additional beneficial effects on reducing serum uric acid levels are of importance. Selective SGLT2 inhibitors were extensively studied in type 2 diabetes mellitus and were found to have improvement of glycemic control, in addition to their proven metabolic effects on weight and blood pressure. Additional beneficial effect of SGLT2 inhibitors on serum uric acid level reduction is investigated. Recently, data have been accumulating showing that they have additional beneficial effects on serum uric acid reduction. As for the postulated mechanism, serum uric acid decreased in SGLT2 inhibitor users as a result of the increase in the urinary excretion rate of uric acid, due to the inhibition of uric acid reabsorption mediated by the effect of the drug on the GLUT9 isoform 2, located at the collecting duct of the renal tubule. Continue reading >>

About This Factmed Analysis Covering Adverse Side Effect Reports Of Metformin Hydrochloride Patients Who Developed Gout.
FactMed provides MD-approved analysis to help both patients, researchers, and physicians accurately assess the risk profile for more than 20,000 different pharmaceutical products. The below report offers compiled information from Food & Drug Administration and FactMed user submissions. Between January 2004 and October 2012, 23 individuals taking METFORMIN HYDROCHLORIDE reported GOUT to the FDA. A total of 8028 METFORMIN HYDROCHLORIDE drug adverse event reaction reports were made with the FDA during this time period. Often the FDA only receives reports of the most critical and severe cases; these numbers may therefore underrepresent the complication rate of the medication. Toxic Arthritis Food List Limit these foods to decrease arthritis pain and inflammation. naturalhealthreports.net Introduction This page is designed to help you determine the relationship, if any, between METFORMIN HYDROCHLORIDE and GOUT. In doing so, we compare METFORMIN HYDROCHLORIDE with other drugs that cause GOUT, to help you evaluate whether or not METFORMIN HYDROCHLORIDE causes GOUT. Likewise, this page shows the most highly-reported side effects of METFORMIN HYDROCHLORIDE, so you can see if GOUT ranks among METFORMIN HYDROCHLORIDE's most well-known side effects. Summary Statistics Reports of METFORMIN HYDROCHLORIDE causing GOUT: 23 Reports of any side effect of METFORMIN HYDROCHLORIDE : 8028 Percentage of METFORMIN HYDROCHLORIDE patients where GOUT is a reported side effect: 0.2865% FDA reports of any drug causing GOUT : 4844 Average percentage for all medicated patients where GOUT is reported as a complication: 0.0304% Overall opinion for all reports of this drug: In addition to reviewing our up-to-date FDA research, users may interact with the FactMed community - currently one million members Continue reading >>