Gout caused by alcohol: The request could not be satisfied
Does Alcohol Cause Gout? | The Recovery Village Drug and Alcohol Rehab
Article at a Glance:
It is essential to know about the relationship between alcohol and gout if you or a loved one struggle with recurring bouts of gout. Knowing how alcohol and gout relate to one another can help you take steps to avoid having a flare-up of the painful condition in the future.
Important points to remember about alcohol and gout include:
- Alcohol makes you create more of the chemical that causes gout
- Alcohol stops your body from getting rid of the chemical that causes gout
- Alcohol makes you dehydrated, which can also lead to a gout flare-up
- All types of alcohol (beer, wine, and liquor included) can cause gout flares
- It is best to avoid alcohol if you have a history of gout
The Relationship Between Alcohol & Gout
Gout is a type of arthritis. Gout does not flare up and cause pain all the time but will occur only occasionally, and months or years can pass between attacks. It usually affects one joint at a time, most often the big toe. A gout attack can happen quickly, and it’s incredibly painful for most people.
The pain of gout leads most people to want to avoid gout in any possible way. One of the best ways to prevent gout starts with diet, especially monitoring alcohol use. Drinking alcohol can cause gout flare-ups.
Why Does Alcohol Cause Gout?
Gout develops from a buildup of a chemical in the bloodstream called uric acid. The body makes uric acid as it breaks down chemicals called purines, which are in foods like seafood and meat. Usually, uric acid is dissolved into the blood and then removed from the body through urine. If there is too much uric acid in the body, it can turn into crystals in your joints and cause a painful gout flare.
Alcohol has been shown to cause gout flare-ups in several ways, including:
The combination of all three of these factors makes a person more likely to have a gout flare if you drink alcohol. Dehydration, specifically, can cause gout flare-ups because, without enough water in the body, the kidneys can’t get rid of the extra uric acid that causes gout. Alcohol only worsens this process. When a person drinks alcohol, it shuts off a chemical in their brain called the antidiuretic hormone, or ADH. Without enough ADH, someone can become extremely dehydrated very quickly because they will urinate a lot in a short time. Dehydration raises a person’s chances of having a gout flare.
Alcohol and Gout Symptoms
If a person drinks alcohol, it is possible that they may suffer a gout attack within a few days, due to increased uric acid and dehydration in their body. The attacks tend to develop suddenly and without warning, and the symptoms of a gout flare are hard to miss. When gout occurs, the symptoms can last days or even weeks, and alcohol use only worsens the gout symptoms.
Common symptoms of alcohol use and gout include:
- Intense pain in one joint (usually the big toe)
- Swelling in one joint
- Redness in one joint
- The feeling that the joint is hot to the touch
- Impaired coordination (if drunk)
- Impaired judgment (if drinking)
- Increased risk of alcohol addiction
What Kinds of Alcohol Cause Gout?
Studies have shown that all kinds of alcohol cause gout flares. Doctors used to think that beer and liquor were more likely than wine to cause gout flare-ups, but recent research shows that all alcohol forms can cause gout.
Also, the amount of alcohol doesn’t matter; gout can flare up even if a person is not drinking heavily or often. Medical professionals usually tell people to avoid all alcohol if they have gout.
Lifestyle Changes to Prevent Gout Flare-Ups
Fortunately, there are ways to prevent gout, even if a person had gout in the past. Certain medicines can help the body remove uric acid more effectively, but lifestyle changes are integral to preventing gout. To avoid gout, be sure to:
- Drink plenty of water
- Maintain a healthy weight and diet
- Limit intake of red meat, organ meat, and fish
- Avoid alcohol, including beer, liquor, and wine
- Talk with a medical professional about medications for gout
If you or a loved one are struggling with alcohol use and finding it hard to stop drinking, The Recovery Village can help. Contact us today to talk to our trained professionals. The Recovery Village offers many different addiction treatment options to help you lead a healthier life without alcohol.
Wine and Gout Flares
Beer and hard liquor have long been known to increase the risk of gout, the most common form of inflammatory arthritis, but according to a 2014 study in The American Journal of Medicine, wine also can contribute to recurrent gout attacks.
Gout occurs when excess uric acid builds up around joints – often in the big toe, but also in the feet, ankles, knees, wrists and elbows – leading to episodes of intense pain, redness and swelling. It affects more than 8 million adults in the United States, and the numbers are rising sharply, due mainly to obesity and other lifestyle factors.
In the 2014 study, 724 gout patients completed questionnaires every few months as well as after gout attacks about their diet, medications, exercise and number of alcoholic drinks consumed. The researchers compared what a participant consumed on an average day to what that participant had consumed in the 24 hours before a gout attack. Researchers looked at the overall effect of alcohol on gout attacks as well as the individual effects of wine, beer and liquor, while taking diet and other factors into account.
Results showed that a single serving of wine, beer or liquor (either straight or in a mixed drink) in a 24-hour period didn’t significantly increase the chance of repeat gout attacks. But consuming more than one to two drinks a day did – by 36%. With two to four drinks, the risk rose 50%, and it continued to rise with the amount of alcohol consumed.
When the three types of alcohol were compared, wine was actually a significant trigger. Drinking between one to two glasses of wine in the 24 hours before the attack raised the risk of recurrent attacks by 138%; in other words, it more than doubled the risk of a gout attack, compared to drinking no wine. By contrast, drinking two to four beers in the 24 hours before an attack increased the risk by 75%.
The researchers point out that these results apply to men; findings for women are less clear, mainly because so few women were in the study. Study author Tuhina Neogi, MD, a professor at Boston University School of Medicine, says, “But the patterns of alcohol’s effects on risk of gout attacks were generally similar to [those] seen in men.”
Dr. Neogi says, “Based on this study, I would counsel gout patients that any type of alcohol may trigger an attack; it’s not just beer or liquor but also wine. Each patient is different, so a ‘safe’ limit can’t be uniformly set, but obviously abstaining from alcohol would avoid any risk of attack due to [its use].”
Gout myths and facts – American Kidney Fund (AKF)
Gout pain is not so bad.
Gout pain can be extremely severe, and some people have gout pain all the time. The pain is caused by tiny, sharp crystals building up under the skin. Gout is one of the most painful types of arthritis.
Gout only happens in people that drink too much alcohol or eat too much unhealthy food.
Although drinking alcohol or eating a diet high in purines can contribute to gout, most people do not get gout for these reasons alone. Instead, when someone has gout, their body does not use uric acid in the right way. Their body either creates too much uric acid, or cannot get rid of uric acid well enough.
Gout attacks only happen in the big toe.
The big toe is the most common place for gout attacks to happen, and many people have their first gout attack in their big toe. But gout can happen in all joints in the body including the hands, elbows, knees, and ankles. When people have chronic gout, often several of their joints are affected.
Gout is the same as arthritis.
Gout is a type of arthritis, but is a specific condition with unique treatments. There are many other types of arthritis that are treated differently. Gout is one of the most painful types of arthritis.
There is not much you can do to prevent gout attacks.
There are medicines that can prevent the buildup of uric acid in the blood, which can lead to fewer gout attacks in people who have chronic gout. There are also lifestyle changes people can make that can prevent future attacks.
You only have gout during an attack.
A gout attack is pain from urate crystals building up under the skin. You may have high levels of uric acid in your body in between attacks, but do not feel symptoms. This can lead to more gout attacks and other complications when left untreated.
Chronic gout is when someone has gout attacks all the time.
Chronic gout is considered having 2 or more gout attacks per year. Having chronic gout can lead to permanent joint stiffness, damage, and deformity, and attacks can increase in frequency over time. There are medicines used for chronic gout that can prevent gout attacks.
Gout only happens in men.
Anyone can get gout, including women. It is more common in men, but once women reach menopause, the rate of gout in men and women evens out. Most women who develop gout show signs and symptoms after menopause.
It is impossible to have gout all the time.
Living with pain and gout symptoms can be almost constant for some people with chronic gout. Attacks happen more regularly, and in more joints, with only short breaks in between attacks. Some people feel symptoms of gout most of the time.
Gout diet: What’s allowed, what’s not
Gout diet: What’s allowed, what’s not
Starting a gout diet? Understand which foods are OK and which to avoid.
By Mayo Clinic Staff
Gout is a painful form of arthritis that occurs when high levels of uric acid in the blood cause crystals to form and accumulate in and around a joint.
Uric acid is produced when the body breaks down a chemical called purine. Purine occurs naturally in your body, but it’s also found in certain foods. Uric acid is eliminated from the body in urine.
A gout diet may help decrease uric acid levels in the blood. A gout diet isn’t a cure. But it may lower the risk of recurring gout attacks and slow the progression of joint damage.
People with gout who follow a gout diet generally still need medication to manage pain and to lower levels of uric acid.
Gout diet goals
A gout diet is designed to help you:
- Achieve a healthy weight and good eating habits
- Avoid some, but not all, foods with purines
- Include some foods that can control uric acid levels
A good rule of thumb is to eat moderate portions of healthy foods.
The general principles of a gout diet follow typical healthy-diet recommendations:
- Weight loss. Being overweight increases the risk of developing gout, and losing weight lowers the risk of gout. Research suggests that reducing the number of calories and losing weight — even without a purine-restricted diet — lower uric acid levels and reduce the number of gout attacks. Losing weight also lessens the overall stress on joints.
- Complex carbs. Eat more fruits, vegetables and whole grains, which provide complex carbohydrates. Avoid foods and beverages with high-fructose corn syrup, and limit consumption of naturally sweet fruit juices.
- Water. Stay well-hydrated by drinking water.
- Fats. Cut back on saturated fats from red meat, fatty poultry and high-fat dairy products.
- Proteins. Focus on lean meat and poultry, low-fat dairy and lentils as sources of protein.
Recommendations for specific foods or supplements include:
- Organ and glandular meats. Avoid meats such as liver, kidney and sweetbreads, which have high purine levels and contribute to high blood levels of uric acid.
- Red meat. Limit serving sizes of beef, lamb and pork.
- Seafood. Some types of seafood — such as anchovies, shellfish, sardines and tuna — are higher in purines than are other types. But the overall health benefits of eating fish may outweigh the risks for people with gout. Moderate portions of fish can be part of a gout diet.
- High-purine vegetables. Studies have shown that vegetables high in purines, such as asparagus and spinach, don’t increase the risk of gout or recurring gout attacks.
- Alcohol. Beer and distilled liquors are associated with an increased risk of gout and recurring attacks. Moderate consumption of wine doesn’t appear to increase the risk of gout attacks. Avoid alcohol during gout attacks, and limit alcohol, especially beer, between attacks.
- Sugary foods and beverages. Limit or avoid sugar-sweetened foods such as sweetened cereals, bakery goods and candies. Limit consumption of naturally sweet fruit juices.
- Vitamin C. Vitamin C may help lower uric acid levels. Talk to your doctor about whether a 500-milligram vitamin C supplement fits into your diet and medication plan.
- Coffee. Some research suggests that drinking coffee in moderation, especially regular caffeinated coffee, may be associated with a reduced risk of gout. Drinking coffee may not be appropriate if you have other medical conditions. Talk to your doctor about how much coffee is right for you.
- Cherries. There is some evidence that eating cherries is associated with a reduced risk of gout attacks.
Here’s what you might eat during a typical day on a gout diet.
- Whole-grain, unsweetened cereal with skim or low-fat milk
- 1 cup fresh strawberries
- Roasted chicken breast slices (2 ounces) on a whole-grain roll with mustard
- Mixed green salad with vegetables, 1 tablespoon nuts, and balsamic vinegar and olive oil dressing
- Skim or low-fat milk or water
- 1 cup fresh cherries
- Roasted salmon (3 to 4 ounces)
- Roasted or steamed green beans
- 1/2 to 1 cup whole-grain pasta with olive oil and lemon pepper
- Low-fat yogurt
- 1 cup fresh melon
- Caffeine-free beverage, such as herbal tea
Following a gout diet can help limit uric acid production and increase its elimination. A gout diet isn’t likely to lower the uric acid concentration in your blood enough to treat your gout without medication. But it may help decrease the number of attacks and limit their severity.
Following a gout diet, along with limiting calories and getting regular exercise, can also improve your overall health by helping you achieve and maintain a healthy weight.
July 02, 2020
- Firestein GS, et al., eds. Etiology and pathogenesis of hyperuricemia and gout. In: Kelley and Firestein’s Textbook of Rheumatology. 10th ed. Philadelphia, Pa.: Elsevier; 2017. https://www.clinicalkey.com. Accessed May 1, 2018.
- Becker MA. Lifestyle modification and other strategies to reduce the risk of gout flares and progression of gout. https://www.uptodate.com/contents/search. Accessed May 1, 2018.
- AskMayoExpert. Gout. Rochester, Minn.: Mayo Foundation for Medical Education and Research; 2018.
- Beyl RN, et al. Update on importance of diet in gout. The American Journal of Medicine. 2016;129:1153.
- Zeratsky KA (expert opinion). Mayo Clinic, Rochester, Minn. May 9, 2018.
See more In-depth
Gout Diet – What to Eat and Understanding the Impact of Alcohol on Gout
Gout & Alcohol: Why It Matters
You won’t necessarily have to give up alcoholic beverages if you’re diagnosed with gout. Why does alcohol intake matter at all? Some people who drink a lot of alcohol never get gout. Alcohol can increase levels of uric acid in your body. So it can be a strong cause of hyperuricemia and gout. Alcohol works to raise urate levels by decreasing how much urate your kidneys excrete. Beer has earned a reputation as being especially bad for gout, since it has this effect on your kidneys, but also because beer has its own proteins that are broken down to urate in the body. So drinking beer raises urate in two different ways.
Beer and liquor are especially linked to higher uric acid levels, and wine is linked to this as well. Moderate intake of alcohol is generally defined as two drinks per day for men and one drink per day for women. However, even moderate drinking on a regular basis (which is common for many adults) is associated with a higher risk of recurring gout attacks.
You may be able to drink occasionally and not experience a gout flare, but regular drinking of any type of alcohol (especially beer and liquor, and mixed drinks with sugary sodas or juices) puts you at risk. Also, heavy or even regular moderate drinking adds calories to your daily intake. It can contribute to weight gain in some people (the “beer belly” or “wine gut”).
Also, when making any changes in your diet or alcohol intake related to gout, remember that timing is important. During the first 6 months of taking a urate lowering medication such as allopurinol to lower your urate, you are at especially at risk for gout attacks. This is a great time to be strict with your diet, and to limit your alcohol intake as much as possible. 6 or 12 months down the line as you continue your medication, often your gout attacks are rare or absent, and a lot of the urate has been removed from your joints. At that point, your risk of gout is less and you may well be able to a little less strict with your diet without as much risk of setting off a gout flare.
While only you can decide how much, what or when to drink alcohol, your doctor and nurses can advise you on how to make these changes in a healthy way. Keep these thoughts in mind when you talk about drinking with your healthcare professionals:
Be honest with your doctor and nurses about your regular alcohol intake. Don’t downplay how much or how often you drink. You are not a “bad person” if you drink. Clear information on your alcohol intake can help your healthcare professionals advise you on your risk.
If you’re not sure how much you drink on a regular night out or don’t keep track, write down what you drink in a diary or notepad for a few weeks. Share it with your healthcare professionals.
If you’re not sure how much alcohol is in a normal serving, ask. In general, 12 ounces of beer, four fluid ounces of wine and one ounce (a jigger) of liquor is a serving. Mixers add liquid and, if they contain sugar, calories to a “drink.” A great idea if you are making a drink at home is to use a liquid measuring cup, then pour the proper amount into your glass.
If you would like to cut back on your drinking—either the amount or frequency—but find that it’s hard, ask for help. Talk with your doctor and nurses about ways you can reduce your intake. Ask about resources like counseling that may help you make these changes.
Tips to Cut Back on Alcohol
Order non-alcoholic drinks when you’re out with friends or family. Iced tea, coffee, flavored seltzers or club soda with a lime wedge may be good alternatives to beer or booze.
Set goals. Pick days when you will drink and days when you won’t drink. Keep track of it on your calendar. Set a limit for how much you will drink that night and stick to it. Don’t “save it up” for one night per week and overdo it.
Don’t keep alcoholic beverages in the house. If they’re on hand, it’s easy to reach for them when you want to unwind or if you feel stressed.
Sip, don’t guzzle. Don’t rush through your drinks so they last longer. Sip or “nurse” a drink while you enjoy talking to your friends or watching the game on TV. Don’t let anyone else push you to drink faster or more than you want.
Avoid tempting scenarios. If you typically drink a lot of alcohol in certain settings or during certain activities, such as when you meet your friends to watch sports or after work for happy hour, it’s OK to skip those outings or cut way back on how many you attend.
Are people who encourage you to drink when you’re trying to cut back on or avoid alcohol really your friends? If you decide to quit drinking, drink non-alcoholic beverages instead or simply cut way back on the nights when you drink, your friends and family members should support your decision. They should understand that you’re doing this for your health. If they tease you or try to encourage you to drink “just this one time because it’s a special occasion,” try to stick with your plan not to drink. It’s your body and your life. You don’t need to drink any alcohol to celebrate an occasion or to have fun. While you can’t change your family, you can stop hanging out with friends who don’t support your decision not to drink.
Don’t get discouraged. If you have been a moderate or even heavy drinker for years, it’s not easy to suddenly quit or cut way back. Many men and women socialize or relax with drinking. Many people associate alcohol with celebrating, such as champagne at weddings or New Year’s Eve, or beer when watching football games. You can make changes to how much and how often you drink, and still be a fun person who enjoys life. Don’t give up! You may have setbacks at times. Ask for support if you need it.
Some drinks may affect gout
Patients who experience gout pain symptoms may benefit from taking a closer look at what they drink.
A group of rheumatologists recently spoke to AOL Health about purines, which can increase the risk of gout. Purines are compounds that can be found in high-protein foods and also in some drinks.
The first drinks mentioned were alcoholic beverages, specifically beer. Rheumatologist Jennifer Sloane, M.D., told the news source that a recent study estimated that people who drink 12 ounces of beer daily are 1.5 times more likely to develop gout than people who do not. Beer was named the drink most likely to cause gout, but other alcoholic beverages also pose a risk.
“Alcohol causes the kidneys to excrete alcohol instead of excreting uric acid. That increases the amount of uric acid in the blood, which could provoke a gout attack in about one or two days,” David Freeman, MD, told AOL Health.
Sloane also recommended against consuming soft drinks. Studies have shown that drinking just one sugary soft drink a day nearly doubles the risk of developing gout for women. Diet soda was not found to increase the chance of getting the disorder, suggesting a connection between the levels of sugar in a beverage and its likelihood of contributing to gout.
In the past, artificially sweetened drinks have been connected to the disease, along with some naturally sweetened beverages. Freeman suggested to AOL Health that fructose levels in sodas and juices could be to blame for their role in increasing a person’s risk of developing gout. While fructose is added to most artificially sweetened beverages, it occurs naturally in orange juice, making it just as likely to affect a person’s risk.
The news source also reported that caffeine has been shown to be somewhat of a contradiction when it comes to gout. While some studies have shown that consuming caffeine can protect against the disease, since it has similar properties to medications used to treat it, others have found that dramatically increasing caffeine intake can raise the risk of gout symptoms by as much as 80 percent.
Until more research can be conducted, the rheumatologists recommended avoiding energy drinks due to their high levels of caffeine and fructose.
According to the National Center for Biotechnology Information, the exact cause of gout is unknown. The groups at a higher risk for the disease are males, postmenopausal women and people who drink alcohol. The organization also states that gout can develop in people who already have another chronic condition. People with kidney disease, diabetes, sickle cell anemia, leukemia and those who are obese may also become afflicted with the disorder.
The Mayo Clinic describes a gout attack as coming on with little warning, and causing extreme pain. The clinic uses the example of feeling like the inflicted joint is on fire, to the point where even the weight of a bed sheet can prove unbearable. It recommends making lifestyle changes to combat the disorder, such as avoiding alcohol and other drinks previously mentioned.
Gout and alcohol | Rheumatology
The title of this editorial is focused on alcohol. However, at least in the venal West, food and drink are inseparable. There has recently been a surge of interest in gout, diet and alcohol. Around Christmas 2003, several pieces appeared in the print and broadcast media. These appeared to be precipitated in part by the various public murmurings about binge-drinking and its threats to law and order. A common question from journalists was: ‘Since young women are increasingly indulging in binge-drinking, is there an epidemic of gout in young women?’. I could personally answer this with neither anecdote nor evidence. I would be interested to know if other rheumatologists are seeing any such trend. Yet it seemed a perfectly reasonable question, predicated upon the hallowed belief in there being a strong relationship between how much alcohol one drinks and one’s risk of developing gout. A second question commonly expressed by journalists around the same time concerned the Atkins diet. Here we are on firmer ground. The relationships between weight loss, urate metabolism and gout are complex. The matter has been the subject of considerable clinical research, much of it predating the electronic databases. For instance, long before Dr Atkins popularized his diet it was known that crash-dieting could provoke acute gout. Provided one does not become ketotic, plasma and urinary urate fall with decreasing body weight [1, 2]. The ‘Atkins breath’ reflects the ketosis induced by this protein-rich, carbohydrate-poor diet. The metabolic explanation is that the increased levels of circulating lactate and hydroxybutyrate compete with urate for renal tubular excretion. This results in reduced urinary urate, increased plasma urate and an increased risk of precipitating gout in the previously hyperuricaemic.
However, things are never simple. Alcoholic gouty patients appear to develop acute episodes at lower blood urate levels than non-alcoholic gouty patients. To put it another way, during attacks of gout alcoholics have lower plasma urate levels than non-alcoholics . Acutely intoxicated alcoholic patients have higher plasma urate levels than after they have sobered up. They are, not surprisingly, very likely not to have been eating whilst drinking heavily. Experimentally high levels (over 200 mg per 100 ml) of plasma ethanol in non-gouty, non-alcoholic normal subjects were associated with reduced urinary urate excretion  and increased plasma levels of urate .
Authors from Hippocrates to Sydenham, and many in between, asserted that gout affected more rich men than poor. Hence ‘aldermanic’ gout of the 18th and 19th centuries [4, 6], and quotations from such as Lord Chesterfield: ‘gout is the distemper of a gentleman—whereas the rheumatism is the distemper of a hackney coachman’ [6, p. 50]. In more recent times, either the profile of sufferers from the disease has changed or its observers have altered their opinions. Talbott  maintained in his excellent monograph of 1967 that ‘the indigent and the well-to-do suffer alike from gout’. The author of ‘Gout in primary care’ in a recent Drugs and Therapeutics Bulletin  was perhaps a little perfectionist in tone, but did have a point when indicating that there is a relative paucity of recent evidence to guide treatment or prophylaxis for gout. However, the US Health Professionals Follow-up Study has provided useful data that illuminate, equally for the present-day consumer and doctor, the topics of gout, diet and alcohol. Fifty-one thousand male dentists, optometrists, osteopaths, pharmacists, podiatrists and veterinarians were followed up over 12 yr. Forty-seven thousand, one hundred and fifty participants, who had not had gout at the outset and who provided complete dietary information, were available for study. The New England Journal of Medicine report by Choi et al. , with its attendant publicity, confirmed the conventional wisdom that seafood and meat carry more risk than dairy products. The Lancet paper by the same authors, soon afterwards, went some way to correct the alcohol stereotype [10, 11]. Beer was more likely to be associated with gout than spirits, and spirits in turn more than wine. The large size of the study naturally makes it likely that there were many exceptions obscured by the numbers. However, it was probably useful for the public to be informed that beer is at least as likely to cause gout as the stereotyped port wine. Whether this will form any influential plank of the Downing Street platform on a public health strategy to reduce harm from alcohol is a different matter.
There are a number of ways in which gout, alcohol and plasma and urinary urate may be inter-related. In the days of lead-lined chambers for moonshine whisk(e)y, tubular nephropathy may have underlined saturnine gout . In addition to the influence of lactate discussed above, there is the question of the contribution to plasma urate of purines, such as guanosine, in alcoholic drinks [13, 14]. The effects of other constituents may be less straightforward. For example, isohumulones derived from hops and responsible for the bitter taste of beer, have been found to reduce the development of body fat in mice . Chronic alcohol intake is a bad idea for gouty patients in at least two ways. The production of oxypurinol, the active metabolite of allopurinol, may be impaired by high alcohol intake; and urate production is stimulated by it [16, 17].
I am not aware of any epidemiological studies on the frequency of gout in vegetarian, teetotal non-obese individuals, or on the prevalence in populations where alcohol intake is minimal. However, for Western populations of gout-prone people, I suppose our medical advice must include the following: Don’t drink to excess, especially if your father had gout. If you must drink to excess, don’t stop eating. If you do eat, rethink your diet [18, 19]. If you are on allopurinol or benzbromarone, watch your urate level if you drink .
The author has declared no conflicts of interest.
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Rheumatology Vol. 43 No. 10 © British Society for Rheumatology 2004; all rights reserved
90,000 Alcohol and gout. Modern look
In the modern world in which we now live, it is no secret to anyone how harmful alcohol consumption has on human life and health. Relationships in the family and in the workplace suffer, and both the psycho-emotional aspects of health and the physical are affected.
One of the manifestations of damage to the body when drinking alcohol is the articular syndrome. This is a symptom complex of lesions of the musculoskeletal system of the human body: the spine, joints, tendons.In which pain occurs, swelling and redness of the joints. The defeat of the musculoskeletal system significantly affects the activity of a person in his professional and non-professional activities.
The most common disease that can be triggered by excessive alcohol consumption is a group of crystalline arthropathies. The most famous representative – gout – will be discussed in this article.
Gout is a systemic tofus disease characterized by metabolic disorders in the body.First of all, we are talking about the accumulation of uric acid in the blood and tissues, as well as its deposition in the form of sodium monourate crystals in the tissues. Gout, like fermentopathy, is one of the manifestations of hereditary metabolic syndrome, which includes diabetes mellitus, hyperlipidemia, and hypertension.
Gout has been known since ancient times, when it was called the “disease of kings”, since it was already noticed that this pathology is most often manifested in obese people who do not follow a diet and abuse alcohol.
Gout is considered a multifactorial disease. The main condition for the development of gout is hyperuricemia (increased uric acid), the main causes of which are hereditary predisposition, increased intake of purines with food (which are found in large quantities in protein foods and alcohol), inhibition of uric acid excretion by the kidneys (with kidney damage)
Gout occurs in stages. It begins with a premorbid stage, characterized by weakness, itching, sweating, then an intermittent stage occurs, which is characterized by an alternation of exacerbations and remission.During an exacerbation, severe pain, swelling, fever, hyperemia of the joints, most often the joint of 1 toe, are usually observed, but other joints may also be involved. Pain during an exacerbation is excruciating, unbearable, and cannot be stopped by taking painkillers. The most common provoking factor in the onset of exacerbations is a violation of the diet, including alcohol consumption. At the final stage of the course of gout, tophuses are formed with uric acid crystals in the tissues of the body.Most often, the kidneys are affected with the development of severe urolithiasis.
Gout is a disabling disease that has a negative impact on a person’s professional and non-professional activities. But it is worth noting that in the treatment of such a well-studied, long-known disease, one of the leading positions is given to diet. And any of the most modern and highly effective drugs will be useless if the patient does not fulfill the doctor’s requirements for adherence to the diet. The diet includes a restriction in protein foods, as well as a complete rejection of alcohol of any strength.
To date, a huge number of various clinical studies have been carried out, in which there is a clear connection between the severity of gout and alcohol intake. So, non-observance of this doctor’s recommendation leads to a faster progression of the disease, the lack of effect from treatment, the appearance of many concomitant diseases, the early development of complications and, as a result, early disability and mortality.
Each patient is given the right to choose, the right to choose a medical institution, the right to choose a doctor, but gout therapy will remain unchanged! And everyone is free to choose what kind of life he will eventually live: to exclude alcohol from his life and find a place for family, rest and work, or choose a short-term joy instead of a long happy life.
Golubeva Maria Georgievna doctor-rheumatologist of the rheumatology department of the State Budgetary Healthcare Institution “TOKB named after V.D. Babenko “
Gout is a joint disease caused by the deposition of uric acid salts in them. The patient has bouts of intense pain in the joints, while the joints swell, the skin over them turns red, most often it is the big toe.
Symptoms of gout appear suddenly, more often at night.
- Severe joint pain. As a rule, first in the big toes, but sometimes in the feet, ankles, knees, hands, wrists. The most intense pain persists during the first 12-24 hours after the onset of the attack.
- Prolonged aching joint pain. After severe pain passes, some discomfort remains in the joints – from several days to several weeks. Over time, pain attacks become more intense and last longer, as more and more joints are affected.
- Inflammation and redness of the joints. The affected joints swell, turn red, and become very sensitive.
- Bumps under the skin (tophus). With a prolonged course of gout, bumps can form under the skin, most often in the area of the fingers and toes, on the elbows, knees, and the skin of the auricles.
Gout occurs when the level of uric acid in the blood rises. Uric acid salts begin to deposit in the joints and surrounding tissues, causing inflammation and severe pain.The concentration of uric acid in the blood can increase as a result of a violation of its excretion from the body, as well as increased formation, which is associated with excessive consumption of purines.
Purines are substances from which uric acid is formed. Some foods contain purines and, accordingly, increase the amount of uric acid in the body:
- alcohol (especially beer, wine),
- honey, coffee, strong tea, chocolate, cocoa,
- broths (meat, chicken, fish),
- uncooked smoked products,
- offal from internal organs (heart, kidneys, liver, brain, tongue),
- fish, canned meat,
- legumes (peas, beans, eggplant, beans, nuts, seeds, soybeans),
- sorrel, spinach,
- mushrooms, mushroom broths,
- raspberries, figs.
Since uric acid is excreted in the urine through the kidneys, in case of kidney disease, the process of its excretion may be disrupted, which predisposes to gout.
In some people, gout flares up frequently, while in others only a few times a year. Medication can help prevent recurrence of gout attacks.
In case of gout under the skin on the fingers, hands, legs, elbows, nodules (tophuses) sometimes appear, consisting of deposits of uric acid salts.They usually do not cause pain, but during gout attacks they become very tender and swollen.
Crystals of uric acid salts can be deposited in the urinary tract of patients with gout, forming stones. In such cases, medications help reduce the risk of kidney stones.
Who is at risk?
The risk group includes people with a high content of uric acid in the body.
The uric acid level is increased:
- regular consumption of alcohol (especially beer),
- chronic diseases (diabetes, hyperlipidemia, atherosclerosis),
- high blood pressure,
- taking certain drugs, such as those used to treat hypertension, heart failure, or prescribed after organ transplants,
- hereditary predisposition,
90,043 age and gender – gout is more common in men, since their normal uric acid levels are higher than in women (however, after menopause, the uric acid level in women rises; in both women and men, gout most often develops at the age of 40 -50 years.
The diagnosis of “gout” is most often made taking into account the characteristic symptoms and history of the development of the disease.
- Serum uric acid. Elevated uric acid levels are an argument in favor of the diagnosis of gout. However, not all people who have elevated uric acid levels suffer from gout. At the same time, in a small number of patients with severe manifestations of this disease, the level of uric acid in the blood may be within normal limits.
- During the acute period of the disease, the serum uric acid level is not so important, since uric acid is released into the tissues and its concentration in the blood may decrease.
- Complete blood count (without leukocyte count and ESR) (CBC). During an acute attack of gout, the level of leukocytes may rise moderately, and the erythrocyte sedimentation rate (ESR) may increase significantly.
- Study of synovial (articular) fluid.The detection of uric acid crystals in it is specific to gout.
- X-ray of joints and bones in gout is of secondary importance. In the later stages of the disease, large bumps can be seen on radiographs of the bones – signs of deposition of uric acid salts in them.
Treatment for gout is usually medication.
Depending on the characteristics of the patient’s organism, the doctor determines the most suitable medicines for him.There are drugs to treat acute attacks, to prevent recurrent attacks, to reduce the risk of complications from gout.
In addition to taking medication, you can relieve a gout attack with:
- drinking a lot of water during an attack (2-4 liters per day),
- complete rest (it is recommended to place the affected limb higher, for example, put a pillow under the foot),
- diet, mainly consisting of liquid food (milk, dairy soups, lactic acid products, jelly, compote, vegetable and fruit juices, liquid cereals).
It is obligatory during an attack to abstain from alcohol and products that increase the level of uric acid in the blood.
- Drinking enough liquid (2-4 liters per day).
- Refusal from alcohol. Alcoholic beverages, especially beer, increase the level of uric acid in the blood.
- Healthy food. Eat more fruits, vegetables, whole grains, and low-fat or low-fat dairy products.You should limit the consumption of meat, poultry, fish.
- Maintaining a normal weight. If you are overweight, it is recommended to gradually, smoothly reduce it with the help of exercise and a healthy diet.
90,000 Gout. Symptoms, treatment – Clinic Health 365, Yekaterinburg
What is gout?
Gout is a form of arthritis that often presents with sudden, severe attacks of pain, soreness, redness, swelling (inflammation) in some joints that may be hot to the touch.A rheumatologist is responsible for the diagnosis and treatment of gout. With gout, the joint of the big toe is more often affected, but other joints of the legs (knee, ankle) can also be affected by gout. Less commonly, gout develops in the joints of the hands (wrist and elbow), and almost never in the joints of the spine.
Symptoms of gout.
- Sudden intense joint pain that often first occurs in the morning;
- Swelling of the joint, hyperemia of the skin in the area of the joint.
What Causes Gout?
Previously, gout was considered a disease of the rich and famous people who could afford too much fatty foods and wine. It is now known that fatty foods and excessive alcohol consumption can contribute to the development of gout, but they are not the determining causes of the disease.
It is now known that gout develops as a result of abnormal deposition of crystals (sodium urate) around the articular cartilage, and in later stages in the articular fluid.This process leads to painful inflammation. Urate crystals can also be deposited in the kidneys, resulting in the formation of “urate” stones in the kidneys. Scientists believe that this is due to excess production of uric acid in the body, or as a result of a decrease in the body’s ability to remove uric acid from the blood through the kidneys. Normally, uric acid dissolved in the blood easily passes through the kidneys and is excreted in the urine. The cause of the so-called primary gout is probably the presence of an abnormal inherited X chromosome.
The consumption of certain foods containing large amounts of uric acid also contributes in some cases to the development of gout. These foods especially include red meat and internal organs (such as liver and kidneys), as well as shellfish and anchovies.
The content of uric acid in the blood may vary depending on:
- How efficiently your kidneys eliminate uric acid;
- What do you eat;
- your general health;
- How much alcohol do you drink;
- What medications are you taking;
- What concomitant diseases do you suffer from.
It is not yet clear to science why every person with high uric acid does not develop gout. It is only known that the ability of the kidneys to excrete uric acid from the body is partially determined by heredity. However, this does not mean that if someone in the family suffers from gout, then all family members will develop gout. Heredity, along with the risk factors mentioned above (which affect the level of uric acid in the blood), as well as male gender and age, increase the risk of developing gout.
How often do gout flare-ups occur?
Gout attacks may recur from time to time in the same or different joints. The first “attack” can last from several days to two weeks if treatment is not started.
Over time, gout attacks may occur more frequently, other joints may be involved, symptoms may become more intense, and the attacks may last longer. Repeated attacks can damage the joint.In some patients, gout manifests itself only once, but this is rather an exception. According to statistics, about 90 percent of patients who have had one gout attack will at least suffer a second attack, although this may occur within a few years after the first attack. In some patients, gout flares may occur every two, three, or more weeks.
Who suffers from gout?
The following groups of people are more likely to suffer from gout:
- Men (generally over 40) and menopausal women;
- People who are overweight;
- People who abuse alcohol;
- People who frequently use diuretics to lower blood pressure or treat chronic heart failure.
Gout can also occur in young patients, provided they take certain medications for a long period of time, abuse alcoholic beverages, or have certain genetic disorders.
How is gout diagnosed?
Gout cannot be diagnosed by blood tests (uric acid levels) alone, as many people have elevated blood uric acid levels but never develop gout.In addition to medical examination and study of the medical history, one of the methods for diagnosing gout is the puncture of the inflamed joint with the intake of intra-articular fluid for research. The resulting liquid is examined under a microscope in order to detect crystals of sodium urate.
In addition to diagnostics, puncture with the removal of fluid from the inflamed joint, in some cases, has a therapeutic, albeit palliative effect. This happens due to a decrease in fluid pressure in the joint capsule, which leads to a decrease in the intensity of pain.The above diagnostic method is simple, but, unfortunately, not always objective. The fact is that with gout, crystals may be absent in the intra-articular fluid. Sometimes crystals are not detected the first time, but can be detected during diagnostic punctures of the joint during subsequent exacerbations.
Since gout can cause chronic joint pain and involve other joints, it is extremely important to get an accurate diagnosis and start specific treatment as soon as possible.
How is gout treated?
Gout belongs to the group of chronic diseases, it is impossible to get rid of it, but at the same time, you can choose a treatment aimed at preventing relapses (exacerbations). With the right treatment, gout symptoms can often be resolved within 24 hours of starting therapy.
The goal of treatment for gout is:
- reduction of intensity or elimination of pain and inflammation;
- Prevention of future flare-ups of gout that can lead to joint damage.
The therapy prescribed by a doctor will depend on several factors, including the age of the patient, the medications being taken (for other medical conditions), general health, medical history, and the severity of the gout attacks.
The following groups of drugs are used in the treatment of gout:
1. Anti-inflammatory drugs. Anti-inflammatory drugs reduce pain and swelling of the joint during an exacerbation. As a rule, they are prescribed until the symptoms of gout have completely stopped.Given that anti-inflammatory drugs have side effects, your doctor will discuss them with you and if they occur, you may be prescribed another drug. Anti-inflammatory drugs used for gout include:
- Non-steroidal anti-inflammatory drugs (NSAIDs) are usually prescribed to treat sudden and severe gout attacks. NSAIDs usually reduce inflammation and pain within a few hours;
- Corticosteroids may be prescribed for patients who cannot take NSAIDs.Corticosteroids, like NSAIDs, reduce inflammation and reduce pain. Corticosteroids can be given as a tablet or injected into the affected joint;
- Colchicine. It is sometimes used in small doses over a long period of time to reduce the risk of gout recurrence. The drug has anti-inflammatory and anti-gout effects.
2. Medicines affecting the level of uric acid in the blood. Some patients may need to be prescribed this group of drugs.Unlike anti-inflammatory drugs, they do not reduce inflammation and pain, but they can lower the level of uric acid in the blood. Such drugs include, for example: allopurinol; probenecid and Febuxostat, also called Uloric. These drugs are recommended for patients with high uric acid levels, repeated recurrence of gout, and patients with uric acid kidney stones. The goal of treatment is to lower blood uric acid levels to less than 6 mg / dL.
As mentioned above, drugs in this group do not relieve symptoms during an exacerbation, but lowering the level of uric acid over time prevents the development of relapses.A sudden drop in uric acid levels can cause an acute attack of gout. For acute gout attacks in patients taking allopurinol or similar drugs, colchicine or NSAIDs are additionally prescribed until symptoms disappear.
Side effects of drugs.
Not everyone develops side effects of drugs, and their manifestation varies from patient to patient. The occurrence of side effects depends on the dose, type of drug, concomitant diseases, or combination with other drugs that the patient is taking.
If a rash or itching develops while taking allopurinol, you must stop taking the drug and notify your doctor.
Can gout be treated with a specific diet?
The elimination of certain foods from the diet, for most patients, does not play a decisive role in maintaining the required level of uric acid. However, limiting the above foods that cause increased uric acid synthesis and reduced alcohol consumption are often beneficial.
Uric acid removes excess nitrogen from the human body. Uric acid is synthesized in the liver and is found in the blood plasma as sodium salt.
The kidneys are responsible for the elimination of uric acid from human blood. In case of impaired renal function, there is a violation of the metabolism of uric acid. As a result, the accumulation of sodium salts in the blood, the level of uric acid increases, causing a variety of damage to organs and tissues.
Increased uric acid or hyperuricemia is the main symptom of primary and secondary gout.
In the diagnosis of gout, the analysis of uric acid is essential. Since primary gout can be asymptomatic, it manifests itself only in an increase in the level of uric acid. Secondary gout can be caused by kidney problems, malignancy, tissue damage, or starvation. Primary gout develops against the background of a slowdown in the excretion of uric acid from the body or with excessive synthesis of uric acid.Crystals of uric acid can be deposited in joints, subcutaneous tissue, kidneys. As a result, gout and chronic arthritis develop.
Hyperuricemia due to secondary gout is observed in diseases such as:
• leukemia, lymphoma
• anemia caused by vitamin B12 deficiency
• some acute infections (pneumonia, scarlet fever, tuberculosis)
• diseases of the liver and biliary tract
• diabetes mellitus
• chronic eczema
• kidney disease
• toxicosis in pregnant women
• secondary “alcoholic gout” (acute alcohol poisoning).
The level of uric acid in the blood rises after exercise, alcohol consumption and prolonged fasting. An increase in uric acid content can occur in people whose food is rich in fats and carbohydrates.
A decrease in the level of uric acid (hypouricemia) is observed at:
• Wilson-Konovalov’s disease
• Fanconi syndrome
• diet poor in nucleic acids
A decrease or increase in uric acid may be affected by taking certain medications (diuretics, etc.)).
Foot in the royal trap | Articles
If in the middle of the night you woke up from unbearable pain in the big toe, it means that you have been visited by the disease of kings and geniuses. Gout is translated from Greek and means “foot in a trap”. Perhaps this is the oldest disease known to medicine. But despite its age, it is still mysterious.
Five questions about gout
1. Why was gout called either the “royal disease” or the “disease of the aristocrats”?
Both in ancient times and in our time, gout chooses victims among people with a high standard of living and especially with good nutrition.The development of the disease provokes an excess of meat dishes, smoked meats, various delicacies, alcohol (especially red wine and beer), as well as frequent stress. Before, of course, these were wealthy and noble people. The portrait of a typical modern “gout” is associated not so much with “nobility” as with the way of life. This is, as a rule, an active, pleasure-loving middle-aged man with high income, often in a leadership position, temperamental. The incidence of the disease is 3-5 cases per thousand people.Women get gout about 10 times less often than men.
2. How and why does gout occur?
The mechanism of the disease is as follows: an excess of animal proteins and alcohol against a background of stress increases the level of uric acid and its salts – urates in the blood. Normally, uric acid, which is the end product of the vital activity of cells, must be excreted by the kidneys. But if its concentration is too high, the kidneys fail.
Excess urates can crystallize and be deposited in the joints, which causes inflammation and severe pain in the fingers and toes, elbows, and knees.But most often, the attack begins with the first joint of the big toe. The pain is so intense that even touching the sheet feels unbearable. Sometimes an abscess occurs on the affected joint, and when it opens, small crystals can be seen in it.
If gout is left untreated and the diet recommended by your doctor is neglected, attacks become more frequent and intense. The disease affects increasingly large joints, kidneys and urinary tract.
3. How is gout treated?
The first thing a rheumatologist or arthrologist will recommend is a strict diet.Meat dishes, liver, fatty fish, smoked meats, caviar, beans, peas, sweets, alcohol are excluded from the diet. Drink plenty of fluids. Medications are prescribed that affect the metabolism, reducing the concentration of uric acid, as well as diuretics, anti-inflammatory and pain relievers. During an attack, complete immobilization (immobilization) of the affected joint is recommended.
4. Why is the procedure of hemocorrection recommended for patients with gout?
In recent years, methods of hemocorrection have been widely used, that is, “correction” of the blood composition outside the patient’s body.One of the forms of hemocorrection – cryoprecipitation – allows you to remove excess uric acid and other harmful substances from the blood. It looks like this: the patient is seated in a chair, a catheter is inserted into a vein and connected to a device through which his blood is “driven”. During the procedure, which can last from 1.5 to 3 hours, the patient is allowed to read, watch TV, make phone calls, talk to medical staff, or just sleep. After such “cleaning” of the blood, the healing of the inflamed joint proceeds faster, the likelihood of a relapse of the disease decreases.
5. Is it true that animals do not have gout?
True. In most mammals, a special enzyme, uricase, is produced in the body, which is capable of breaking down uric acid into simpler compounds. Unfortunately, humans do not have this enzyme, so uric acid seems to be accumulating in the body. However, normally it is filtered by the kidneys and up to 85% (about 1-2 g daily) is removed in the urine. Approximately the same amount re-enters the blood as a result of the breakdown of dietary proteins.As a result, the concentration of uric acid in the human body remains approximately constant. But sometimes, due to errors in nutrition and lifestyle, its concentration jumps 10-20, or even 30 times.
Lame companion of geniuses
Since ancient times it has been noticed that not only kings and emperors, but also famous generals, admirals and philosophers often suffered from gout. In the Middle Ages, historians have noticed a connection between the degree of development and prosperity of cities and states and the spread of gout among the population.
For the first time, the English researcher E. Orvan pointed out a possible direct connection of gout with increased mental activity in his article “The Origin of Man”, published in the journal Nature in 1955. He noted that uric acid is structurally similar to caffeine and theobromine, substances found in coffee and tea that can stimulate mental activity.
Among Russian researchers, an outstanding contribution to the development of the “gouty” theory of genius was made by the Soviet geneticist Vladimir Efroimson.At the end of his eventful life, he wrote Biosocial Factors of Mental Enhancement. At that time – the 80s of the last century – the book was not published. It was released only in 1997 under the title “Prerequisites of Genius”.
Efroimson did not limit himself to listing examples, but took up statistics. And he proved that among talents, the prevalence of gout is 5-10%, which is 10 times higher than the average, and among geniuses it soars to 30-50%. In other words, every second genius was a gout! And for the rest, genius turned out to be linked to other rare genetic abnormalities – the Marfan and Morris syndromes, as well as mental illness – manic-depressive psychosis.Then the development of gout is inevitable n
How to get rid of the trap?
During a gout attack, doctors advise:
1. Observe complete rest. The sore joint should be kept in an elevated state with a pillow under the foot.
2. Drink plenty of water. 5-6 glasses of fluid a day will speed up the elimination of uric acid from the body. It is best to make herbal tea, rosehip decoction or lingonberry juice. Do not add sugar.
3. Avoid aspirin.Aspirin and other non-steroidal anti-inflammatory drugs (voltaren, diclofenac, etc.) can aggravate the condition by slowing down the excretion of uric acid.
4. Use cold. If the affected joint allows itself to be touched, you can attach a bag of ice crushed into a gruel for ten minutes. The cold will have an analgesic effect.
5. Avoid animal food. High-protein animal products – meat, fish, liver, smoked meats, etc. – are harmful to gout. During the period of exacerbation, you can arrange fasting days every other day (vegetable, fruit, juice, dairy).Alcohol is completely excluded.
6. Remove excess uric acid from the body as soon as possible. Acid and its salts (urates) damage not only joints, but also kidneys, blood vessels, and other organs. To quickly remove them from the body, urgently consult a rheumatologist or arthrologist.
Famous gouty were:
– Alexander the Great, Julius Caesar, Charlemagne, Charles XII, Louis XI, Frederick III, Henry VII and Henry VIII, Elizabeth I, Frederick II, Louis XIV, John , Boris Godunov, Peter I, Oliver Cromwell, Admiral Nelson;
– Michelangelo, Dante, Beethoven, Rubens, Auguste Renoir, Guy de Maupassant, Charles Dickens, Ivan Turgenev;
– Martin Luther, Jean Calvin;
– Carl Linnaeus, Charles Darwin, Galileo Galilei;
– Thomas More, Erasmus of Rotterdam, Montaigne, Voltaire, Christopher Columbus, Chaplin, Churchill.
Not to be confused with a “bone”
Quite often, gout is called another, even more common disease – a “bone” or “bump” on the first joint of the big toe, caused by transverse flat feet. Scientifically, it is called “hallux valgus” (curved finger) and occurs among women 4 times more often than among men.
The cause of joint deformation is the weakness of the musculoskeletal system, but uncomfortable, narrow shoes, wearing high heels, and standing work also provoke the development of the “bone”.At first, on the first joint of the thumb, the cartilage tissue simply increases, but then the cartilage ossifies, the finger deviates more and more from the straight line, the foot is deformed, the joint becomes inflamed and hurts mercilessly, and in severe cases does not allow walking at all.
In the early stages, special gymnastics for the feet, wearing orthopedic insoles and special devices – braces – help. In later and severe cases, doctors recommend surgical reconstruction of the entire foot. More than 300 types of various operations have been developed for such indications, which in itself speaks of the complexity of the task.Unfortunately, the results of the operation are not always satisfactory. But there is no other way to fix the foot.
The concept of autoinflammation in the genesis of gout and hyperuricemia. Clinical pharmacology and therapy
Gout, manifested by attacks of acute arthritis, is a vivid example of an inflammatory disease characterized by a pronounced exudative phase, in the development of which neutrophils, macrophages, and other cells of innate nonspecific immunity are of great importance.
Inflammation is a complex reaction to various pathogens that develops not only in the damaged area, but is also accompanied by a pronounced systemic response in order to maximize the restoration of damaged tissues .The simplified formula of the inflammatory response includes 5 known signs, each of which is a manifestation of a vascular reaction in the area of inflammation – hyperemia, swelling, pain, local temperature increase, dysfunction. At the same time, it should be recognized that inflammation cannot be equated with a vascular reaction. This was already noticed by the classics of the theory of inflammation – I.I. Mechnikov and P. Er lich
Since the vascular inflammatory response was formed in animals in parallel with the development of warm bloodedness, I.I. Mechnikov in his publications asks the reader a rhetorical question: does not inflammation exist in fish and lower animals that do not have warm-bloodedness?  Further I.I. Mechnikov proves that the fundamental and most ancient (already in protozoa) process, on the basis of which inflammation develops, is phagocytosis. Mechnikov’s theory of phagocytosis P. Ehrlich, who developed the method of cytological staining, contrasted the hypothesis of degranulation of inflammatory cells, which he observed in cells of the myeloid series.The synthesis of both theories subsequently made it possible to substantiate the concept of innate immunity, which is carried by various phagocytes (neutrophils, macrophages, dendritic cells, etc.).
The cells of innate immunity are able to respond to group ligands specific for related microbes and damaged cells of the body. The innate immune system does not respond to its own antigens as part of a physiological response. Lack of innate immunity is manifested in the absence of immunological memory and a limited set of genetically fixed reactions.
Simultaneously with the works of I.I. Mechnikov and P. Ehrlich published the famous publications of L. Pasteur, who demonstrated the effectiveness of the system of specific immunity based on the reactions of B- and T-lymphocytes. The demonstration of the high efficiency of vaccination against various infections made a deep impression on contemporaries, after which all the attention of specialists dealing with inflammatory diseases was switched to the system of specific immunity.N.F. Gamaley, impressed by the works of L. Pasteur, wrote that “… the days of the theory of phagocytosis by II. Mechnikov are numbered … ”.
is a fairly late evolutionary acquisition and arose only in mammals. The main innovation of this system was the appearance in lymphocytes under the influence of antigenic stimulation of the ability to rearrange genes, and the resulting unlimited number of genetic variations made it possible to synthesize individual antibodies to any antigen.
These discoveries have turned doctors’ views on the mechanisms of inflammation. As a result, for many years, authoritative guidelines on pathology have named only three causes of inflammation – infections, intoxication, and autoimmune processes . The latter was understood as the development of reactions against self antigens, realized mainly by autoreactive T-lymphocytes and / or by the synthesis of autoantibodies by B-lymphocytes. The reactions of innate immunity were given auxiliary importance, considering them necessary only at the stage of inflammation initiation and antigen presentation, while specific immunity was attributed to the main role in the development of effector reactions.
In the last two decades, there has been an increase in interest in the innate immunity system within the framework of the new theory of autoinflammation, which is understood as the independent development of full-fledged inflammatory reactions without the participation of T and / or B-lymphocytes, only due to the activation of the phagocyte system . Most often, such diseases develop due to genetic mutations. Thus, the pathogenesis of a number of rare monogenic familial periodic fevers was explained: periodic illness (pyrine mutations), hyperimmunoglobulinemia D (mevalonate kinase deficiency), cryopyrinopathies (cryopyrin mutations in patients with familial cold urticaria, Macle-Wells syndrome (NOMID-CINPSA) receptor to tumor necrosis factor alpha).Currently, a lot of such monogenic autoinflammatory diseases have been described. Despite the rarity of these conditions, their study made it possible to discover the most important mechanism of autoinflammation, realized by phagocytes, primarily by neutrophils – hypersecretion of interleukin-1 due to the formation of an intracellular macromolecular platform – cryopyrin inflammasome. The assembly of the inflammasome occurs as a result of the activation of cryopyrin with subsequent combination with the proteins ASC, CARDINAL, and caspase-1.The main functional task of cryopyrin inflammasome is the activation of caspase-1, which, in turn, leads to the activation of interleukin-1 .
Cryopyrinopathies are characterized by spontaneous activation of mutant cryopyrin. In case of periodic illness, mutations of pyrine disrupt its ability to control the assembly of the inflammasome, a deficiency of mevalonate kinase leads to insufficient production of isoprenoids necessary for fixing the inflammasome, and, as a result, its untimely activation.Despite the fact that there are other mechanisms of autoinflammation, cryopyrin inflammation is one of the most common mechanisms .
Later it became clear that in many rheumatological and, in general, inflammatory diseases of internal organs, a combination of various heterozygous mutations involving autoinflammatory mechanisms is possible. Such diseases belong to the group of polygenic autoinflammatory diseases. This situation turned out to be quite frequent in the practice of doctors, which makes it really relevant to isolate autoinflammation as an independent variant of inflammatory diseases.Such diseases include, first of all, seronegative spondyloarthropathies (ankylosing spondyloarthritis, psoriatic arthropathy, Crohn’s disease, chronic ulcerative colitis, Still’s syndrome), interstitial lung diseases (sarcoidosis, pneumoconiosis, etc.) and many others .
It turned out that autoinflammation does not always develop due to a genetic predisposition; there are models of an exclusively acquired mechanism of an autoinflammatory disease.An example of such acquired inflammasomopathy is gout. Hyperuricemia itself, as a prerequisite for gout, can be genetically determined , however, an autoinflammatory gouty attack develops as a genetically normal reaction to hyperuricemia, not associated with mutations. In this case, the activation of the inflammasome is associated with the fact that cryopyrin is an intracellular receptor that reacts to various pathogens, including crystal structures (crystals of uric acid, cholesterol) trapped in the bloodstream or interstitium .Since the solubility of uric acid at physiological pH is 6.8 mg / dl, the solubility limit of uric acid can be reached even at normal concentration and an increase in body temperature. In this case, the transformation of dissolved uric acid into a crystalline form is possible, which triggers the activation of inflammasome in neutrophils and provokes an attack of gout . An important factor restraining the uncontrolled crystallization of uric acid is that plasma, having the properties of a colloidal solution, increases the solubility of uric acid, and some of its components inhibit the formation of crystals.For this reason, even with elevated blood uric acid levels, many patients do not develop gout. Nevertheless, this does not exclude the possibility of activation of the inflammasome of phagocytes in persons with hyperuricemia even outside of a gouty attack, which creates preconditions for the persistence of subclinical autoinflammation, which is an important factor in the development of complications.
Over the past decade, it has been proven that hyperuricemia is an independent risk factor for arterial hypertension, atrial fibrillation and cardiovascular diseases, associated with diabetes mellitus, obesity and chronic kidney disease [7-12].This justifies the eligibility of including hyperuricemia in the metabolic syndrome and, consequently, in the group of factors of increased risk of dangerous cardiovascular complications .
Among the mechanisms of arterial hypertension in patients with hyperuricemia, first of all, the blockade of nitric oxide production is discussed [14-24], as a result of which its systemic vasodilating effect decreases, the control of the proliferative activity of smooth myocytes of the arterial walls and the antithrombogenic effect decreases.The resulting increase in total peripheral vascular resistance is a powerful factor in the activation of the renin-angiotensin system with the development of arterial hypertension. The blockade of nitric oxide synthesis in patients with hyperuricemia is associated with overproduction of free peroxide radicals, which, in turn, is due to persistent subclinical activation of autoinflammatory mechanisms [14-24]. H. Zheng et al. in experiments on rabbits showed that hyperuricemia correlated with high reliability with the level of renin and angiotensin II, and the administration of losartan led not only to normalization of renin and angiotensin II activity, but also to suppression of proliferation of smooth myocytes .An important factor in the suppression of the proliferative activity of vascular smooth myocytes is also a decrease in the concentration of adiponectin, which correlates with hyperuricemia [25,26].
Uric acid crystals can directly damage the vascular endothelium, which leads to subendothelial lipid deposition and the development of atherosclerosis. In a case-control study (n = 4884), the level of uric acid correlated with calcification of the coronary arteries, the index of which made it possible to clearly identify patients at high risk of death .According to Chinese researchers who analyzed 6347 patients with coronary heart disease, the presence of hyperuricemia increases the risk of coronary heart disease by 2.76 times . This effect is realized through the inflammatory induction of oxidative stress and endothelial damage by uric acid crystals . With hyperproduction of inflammatory cytokines, oxidative stress M. Kuwabara et al. also associate an increased risk of atrial fibrillation in patients with hyperuricemia [29,30].
The association of hyperuricemia with insulin resistance and disorders of carbohydrate metabolism can also be explained by the action of free peroxide radicals, oxidative stress products of activated neutrophils, blockade of nitric oxide production, activation of cryopyrin inflammasome in the beta cells of the islets of Langerhans with their subsequent apoptosis.Similar processes are also observed in hepatocytes, which leads to fatty degeneration of the liver [31,32].
Thus, at present, the concomitant hyperuricemia conditions are well substantiated. There are sufficient reasons to suggest that they are largely due to chronic subclinical inflammatory activity, the pathogenesis of which is explained by autoinflammatory inflammasomopathy, accompanied by hyperproduction of interleukin-1. In this regard, one of the main ways to prevent arterial hypertension and atherosclerosis in patients with hyperuricemia and gout is long-term anti-inflammatory therapy with the obligatory suppression of interleukin-1 activity.
In the treatment of inflammasomopathies, including polygenic ones, such as Still’s syndrome, inhibitors of interleukin-1, in particular canakinumab, which have a prolonged effect, are highly effective. For gout, there is also experience with this drug. Among patients with contraindications, intolerance or resistance to traditional nonsteroidal anti-inflammatory drugs or colchicine, two multicenter, controlled, randomized trials have been conducted, which have shown the high efficacy of canakinumab in preventing gout attacks [32-34].
The recommended dose of the drug in adults is 150 mg, the drug is administered once subcutaneously during an attack of gouty arthritis. For maximum effect, canakinumab should be administered as early as possible after the onset of an attack of gouty arthritis. In patients with a positive response to drug therapy, if it is necessary to continue treatment, re-administration of canakinumab is possible no earlier than 12 weeks after the previous injection.Optimization of hyperuricemia control should be carried out with appropriate anti-gout drugs.
In rare cases, in patients capable of synthesizing an amyloidogenic variant of the SAA acute phase of inflammation protein, gout can be complicated by secondary AA amyloidosis. Such a complication may indicate that the patient, even outside a gout attack, retains a high acute phase subclinical activity. However, it can be expected that the course of gout in these patients will be characterized by severe polyarticular lesions with the development of deformities and numerous tophi.The only way to stop the progression of amyloidosis in such patients is long-term treatment with an interleukin-1 inhibitor. Here is an observation from our own practice.
Patient T., 66 years old, has been suffering from grade 3 arterial hypertension for many years, does not take antihypertensive drugs on a regular basis. Six years ago, acute arthritis of the left ankle joint first developed, and gout was diagnosed. In the future, he did not go to doctors, periodically repeated acute attacks of arthritis, mainly the large joints of the legs were affected, but the joints of the hands, including small ones, were repeatedly involved, oligoarthritis often developed.He took diclofenac on his own. A year ago, seizures increased up to 2-3 times a month, he noted the limitation of the mobility of the hands. X-ray of the hands and ultrasound examination revealed signs of chronic tofus gout. A high level of uric acid in the blood (650-700 μmol / l) remained in the blood. Colchicine 1 mg / day was prescribed.
In connection with the revealed proteinuria 8-12 g / day and a decrease in the filtration function of the kidneys (serum creatinine 129.4 μmol / l, glomerular filtration rate 47.4 ml / min), a kidney biopsy was performed.Against the background of diffuse global glomerulosclerosis, congophilic masses were revealed predominantly along the course of the kidney vessels, which have the property of birefringence in polarized light. Amyloidosis was diagnosed. The absence of monoclonal gamma pathia according to the results of an immunochemical study using highly sensitive methods excluded the AL type of amyloidosis. The nephropathic variant of amyloidosis, high levels of C-reactive protein (35 mg / L) and the presence of chronic gouty polyarthritis made it possible to diagnose AA amyloidosis.A thorough examination was carried out to exclude the paraneoplastic nature of amyloidosis – esophagogastroduodenoscopy, colonoscopy, multislice computed tomography of the chest and abdominal organs.
Canakinumab 150 mg was added to the treatment with colchicine 1 mg / day, treatment with allopurinol 100 mg / day was resumed. One year after the start of canakinumab treatment, nephrotic syndrome was arrested, proteinuria decreased to 0.67-1.4 g / l, and renal function did not deteriorate.Gout attacks did not recur, the level of C-reactive protein normalized, mobility in the joints of the hands improved, and the tofus in the left wrist area noticeably decreased in size.
The presented observation demonstrates the current possibilities of effective treatment of AA amyloidosis. The use of canakinumab made it possible not only to arrest nephrotic syndrome, but also to delay the progressive deterioration of renal function, which would require the appointment of renal replacement therapy.Perhaps, colchicine 1-2 mg / day should be recognized as the most acceptable regimen for long-term therapy; if it is ineffective, the necessity of prescribing canakinumab should be discussed.
The presented observation also shows the need for complex therapy in patients with gout. Only anti-inflammatory treatment effectively reduces the risk of recurrent gouty attacks, however, it does not make it possible to stop the progression – in patients, erosive arthropathy may worsen, the growth of tophi may continue, which, as a result, contributes to the deterioration of joint function.Therefore, the treatment of a patient with gout and hyperuricemia must necessarily include measures to reduce the level of uric acid in the blood and tissues .
The traditional way to lower the level of uric acid in the blood is to follow a hypopuric diet, since uric acid is a product of the metabolism of purine bases. However, adherence to a low-purine diet in most cases is not sufficient to achieve the target level of uric acid, therefore, adequate drug therapy is the basis for the success of treatment of the disease .Difficulty adhering to a diet is associated with a significant change in lifestyle – refusal from alcohol, a sharp restriction of basic food products (meat), which is unacceptable for people with a hedonistic personality. An equally important reason for the insufficient effectiveness of the diet is also the fact that the balance of intake and excretion of uric acid is primarily due to restrictions in the excretion of uric acid by the kidneys (two thirds of the excreted uric acid is excreted by the kidneys and one third by the gastrointestinal tract).It is known that hyperuricemia develops after a long period of increased excretion of uric acid in the urine and is the result of decompensation of the mechanisms of its excretion, which is considered by many researchers as a manifestation of renal failure. In any case, any detection of hyperuricemia should be considered as a possible sign of chronic urate interstitial nephritis.
Normal uricosuria is 620 ± 75 mg / day (normal clearance 8.7 ± 2.5 ml / min, normal excreted uric acid fraction 7.25 ± 2.98%, or 6-8%), 91-95% of filtered urinary acid undergoes reabsorption in exchange for intracellular anions, there is also a small tubular secretion of uric acid.As a result, the final urine contains only 3-10% of the initially filtered amount of uric acid. Hyperuricosuria is considered to be urinary excretion of more than 800 mg / day in men and more than 750 mg / day in women and is mainly associated with impaired reabsorption of uric acid .
Among the transporters that ensure the reabsorption of uric acid (URAT1, GLUT9, OAT4, OAT10), the main importance is attached to the URAT1 protein. Mutations that cause a complete inactivity of this protein lead to an almost complete cessation of uric acid reabsorption.In this case, the excreted fraction of uric acid is 40-100%, and the concentration in the blood, on average, decreases to a critical level of 0.93 mg / dL. Uric acid concentrations less than 1 mg / dL are considered unsafe and associated with a risk of nephrolithiasis and acute renal injury, probably due to exercise-induced obstruction of the renal tubules by uric acid precipitates. Among the causes of acute renal injury, acute renal ischemia due to renal artery spasm caused by the production of free peroxide radicals is also discussed.Finally, kidney damage may be associated with an excess of toxic anions accumulated in the cytoplasm of the tubular epithelium.
The activity of URAT1 depends on the sodium gradient created by the Na + K + ATPase, since this gradient determines the amount of anions that must be exchanged for uric acid. The activity of the transporter is also directly related to the level of testosterone in the blood and inversely to the concentration of estrogen.This mechanism appears to mediate the higher risk of hyperuricemia in postmenopausal men and women. This protein is considered as the main target for the development of uricosuric therapy .
GLUT9 is a less important transporter of uric acid; however, it is also, along with URAT1, associated with the risk of hyperuricosuria and urate nephrolithiasis and renal failure due to physical overload . It is important to note that hyperuricosuria caused by dysfunction of this transporter is often combined with glucosuria and occurs with significant consumption of fructose (this may be one of the explanations for urate nephrolithiasis in the abuse of products containing fructose).
In patients with gout, the excreted fraction of uric acid decreases to 3-5%, which allows us to consider a decrease in renal excretion as the main factor in the development of hyperuricemia. A decrease in uric acid excretion may be the result of damage to the tubular epithelium due to prolonged hyperuricosuria, or it may be caused by an initial decrease in uric acid secretion. The main transporter providing tubular secretion of uric acid is ABCG2.Mutations in the gene for this protein are clearly associated with hyperuricemia and the risk of gout .
Traditional drug treatment of gout and hyperuricemia is based on the use of xanthine oxidase inhibitors, which stop the degradation of purines at the xanthine stage and thus block the formation of uric acid. These drugs include allopurinol and febuxostat. The main indications for the use of these drugs are gout, urate nephrolithiasis, as well as conditions accompanied by hyperproduction of uric acid – Lesch-Nyhan syndrome, chronic myeloproliferative diseases (tumor lysis syndrome).The most widely used is allopurinol. It is recommended to start treatment with a dose of 100 mg / day, followed by its increase every 2-4 weeks up to 800 mg / day, until the target level of uric acid is less than 6 mg / day. It should be remembered to avoid high doses of allopurinol in patients with renal insufficiency.
Another xanthine oxidase inhibitor is febuxostat, which is used to treat gout (but not asymptomatic hyperuricemia) at doses of 40-80120 mg / day when allopurinol is ineffective or intolerant.Excretion of the drug mainly by the liver allows it to be used in patients with renal insufficiency. Febuxostat interacts poorly with other medications. The drug is especially effective in patients with ABCG2-transporter dysfunction. In the CARES study, the incidence of cardiovascular events with febuxostat was slightly higher than with allopurinol, although many authors point to a number of limitations of this study [36–39].
As a second line of therapy with the ineffectiveness of xanthine oxidase inhibitors, uricosuric drugs are used – lezinurad, probenecid and benzbromarone, which block the reabsorption of uric acid, suppressing the activity of URAT1.By increasing uricosuria, both drugs can provoke the formation of stones in the urinary system, which requires effective alkalization of urine.
Other drugs that lower uric acid levels are currently being evaluated, in particular uricase drugs, etc.
A significant problem in the treatment of patients with gout is the low adherence of patients to long-term therapy, both anti-inflammatory and aimed at lowering the level of uric acid in the blood.Many patients continue to break the hypopurine diet. The correct organization of work with the patient and the implementation of effective educational trainings can almost 5 times increase the chances of achieving the target level of uric acid . This is also facilitated by anti-inflammatory therapy, including the use of colchicine and IL-1 inhibitors .
Is it possible to drink alcohol with gout: when and how much to drink
The cause of gout is a violation of metabolic processes in the body.The consequences are the deposition of salts, which lead to problems with the joints and kidneys. The excretory system works worse, and the concentration of uric acid in the blood increases. Over time, it crystallizes around the joints and causes pain and inflammation. Arthritis most commonly affects the feet and toes, and the attacks of the disease are very painful. Patients are forced to follow a strict diet, so it is very important to know if it is okay to drink alcohol for gout, and if so, which one.
Alcohol as a risk factor
The disease has been known since ancient times, mentions of gout are found in ancient Egyptian papyri, and Hippocrates described in detail the symptoms of the disease in his work Aphorisms.An increased amount of urate in the blood is observed in about 12% of residents of Russia, and in the United States, 8 million people suffer from arthritis caused by uric acid crystals. A number of doctors believe that the causes of metabolic disorders should be sought in genetics, however, the development of gout is facilitated by a whole range of factors, which include:
- increased blood lipids;
- diet rich in fatty foods;
- consumption of sweet and alcoholic beverages.
Both during an exacerbation and during a period of remission, the patient is recommended a diet low in purines, which, when broken down, form uric acid. For gout, avoid high-protein, fatty, and spicy foods, and cut back on alcohol and fructose carbonated drinks. Patients need to drink as much liquid as possible – mineral or spring water.
Alcohol is not only a source of purines, but also a catalyst for the metabolism of nucleotides – substances that promote the synthesis of uric acid.Ethanol has a detrimental effect on the pituitary gland and disrupts the mechanism of production of the hormone vasopressin, which is responsible for the water balance in the body. At first, alcohol acts as a diuretic, forcing the kidneys to work with increased stress. But then the synthesis of the hormone slows down, which increases the level of urate in the blood.
In the United States, the assessment of the relationship between gout and diet was conducted during the Comprehensive Health Worker Survey (HPFS). More than 50 thousand people took part in the survey. In the course of the analysis, doctors concluded that alcohol abuse doubles the risk of developing gout.
What kind of alcohol is possible with gout
Doctors are unanimous in the opinion that those suffering from gout should strictly limit the intake of alcoholic beverages. This is especially important in the first months after diagnosis and treatment initiation. A low-purine diet will take a lifetime to slow down the progression of the disease and avoid painful attacks.
Doctors believe that a small amount of alcohol during remission is usually tolerated by the body normally. It is important to remember that the purine content of spirits varies.Research in this area was carried out by American scientists in 1995. Two groups of patients with gout were given beer or vodka with orange juice and then monitored for urate levels. As a result of the experiment, it turned out that beer rich in purines, unlike vodka, significantly increases the concentration of uric acid in the body.
Liqueurs, balms and sweet liqueurs should be avoided, since fructose is often used in the manufacture of these drinks, which is strictly not recommended for gout.Vodka does not contain purines, but it causes dehydration due to the fact that ethanol interferes with the excretory function of the kidneys. Doctors consider white wine to be the preferred drink for gout, although recent research suggests that it can provoke an attack.
Permissible daily dose:
- beer – 200 ml;
- wine – 150 ml;
- vodka, whiskey, cognac – 30 ml.
Carefully read the information on the composition of the beer before purchasing.Ingredients should be natural, free of the syrups and flavors often found in craft varieties.
Snack wine with fresh herbs that neutralize acid. Spirits should be consumed very carefully and in small quantities to stay hydrated. If the doctor categorically recommends refraining from alcohol, give up the bad habit in order to avoid exacerbation of the disease.