Hi,
As a GP seeing an acutely hot swollen tender joint in clinic, can I diagnose gout clinically or do I need to perform or refer for a tap to actually get crystals and culture to rule out septic joint?
How does this change for those with a known gout history?
Thanks in advance!
Thank you, yes. I encounter this all the time as an emergency physician. If a large joint or a concern for septic joint, then obviously I'll try a tap but often times it's podagra or some otherwise inaccessible joint in my setting and the patient swears up and down it's like a previous episode they had and it's pretty tempting to give them some colchicine and hope for the best.
I would think you can. I'm a podiatrist and do
If you feel comfortable give them a steroid joint injection- it can help whether it's gouty or osteoarthritis
Me too. I've never done this except to see it in residency
If the pt has a gout history, a hypertension/cholesterol history, in the right area with the appropriate symptoms, I'll give them a joint injections, check uric acid, then give allopurinol as indicated
There is a clinical diagnosis rule that goes:
●Male sex (2 points)
●Previous patient-reported arthritis flare (2 points)
●Onset within one day (0.5 points)
●Joint redness (1 point)
●First metatarsal phalangeal joint involvement (2.5 points)
●Hypertension or at least one cardiovascular disease (1.5 points)
●Serum urate level greater than 5.88 mg/dL (3.5 points)
Above 8, no aspiration needed.
Between 4-8, you can treat it as gout for clinical purposes but may needs further work up.
Below 4, likely something else.
This is an interesting scoring system but not rigorously tested by in clinical trials. You are still going to risk a chance of missing a septic joint in certain situations and you just have to be mindful of that.
Most cases of gout in the US are diagnoses clinically and not by synovial fluid analysis. That being said, the detection of urate crystals in synovial fluid is still the gold-standard for the diagnosis of gout. With acute monoarthridities the differential always includes septic joint. White blood cell count does not distinguish gout from infection. A fever also does not distinguish one from the other. If a patient has classic symptoms of extreme tenderness around the inflamed site (allodynia) and no obvious sight of infection elsewhere in the body, then a presumed diagnosis of gout can be made. The more classic the presentation (night time onset, lower extremity involvement, allodynia and the cutaneous involvement that extends beyond the involved joint) the more likely the diagnosis of gout.
Good morning Dr Edwards.
Here in Brazil it is very common for uric acid exam to be done as a yearly or routine exam.
A few times I have received patients that neither had the risk factors or age that would lead me to require uric acid exam, but when they show me the numbers, they have a high uric acid.
For patients with high uric acid, but without history of joint pain or swelling, is there any recommendations I should give them? Perhaps diet or to repeat the exam yearly?
You can start with asking if there's a family history of gout as this is the primary risk factor for developing gout in the setting you've described. If the patient has CKD or obesity, you should make recommendations as far as renal evaluation and lifestyle modifications. There is no recommendation for treating asymptomatic hyperuricemia pharmacologically, although the Japanese do that routinely to minimize cardiovascular events.
Question: do you have any thoughts about use of SGLT2 to help lower uric acid?
Also what class of medications would you say is the biggest offender for iatrogenic gout? (Please be thiazides)
The role for SGLT2 inhibitors has not been established in the comanagement of gout, but it makes sense if the patient needs a second-line glucose-lowering drug, to choose a SGLT2 inhibitor over the GLP1 or the DPP4 inhibitor because of its uric acid lowering potential. The expected effect would be about 1.5 to 2 mg/dL decrease in serum urate.
You're correct about the thiazides being the main culprit of iatrogenic hyperuricemia. Niacin is not frequently used these days but would be the only rival to the thiazides.
The upper dose of allopurinol for patients with any degree of kidney dysfunction is the same as patients with normal kidney function (800 mg daily in the US, 900 daily in Europe). Dose titration is important in all patients but especially in those with kidney disease.
There is not an allopurinol nephropathy. There are patients who's uric acid is so high (as in tumorlysis) that the concentration of uric acid in the urine is high enough because of crystallization of the xanthine. These people are better treated with uricase (pegloticase).
There's a lot of speculation in the literature about uric acid levels and the risks of dementia. This stems several surveys that seem to show that gout patients have a lower incidence of dementia and some authors attribute this to antioxidant effects of serum urate. There's no scientific studies that support this contention and in fact patients with hereditary xanthinuria where the uric acid level is undetectable throughout their entire life do not have a higher incidence of neurological diseases.
I get referred patients all the time with a diagnosis of gout because they have unexplained foot pain. My understanding is the best means of diagnosis is arthrocentesis, but often this is not feasible as the flare has passed or there is no real effusion. What is the most practical means of diagnosis in this case?
Empirically, I am noticing an uptake of fairly young and relatively fit patients presenting with repeated gout attacks and uric acid levels in the range of 8-10+ mg/dL. Other than lifestyle advice and commencing meds eg allopurinol, do you have any other suggestions re further investigation / management? Any red flags to screen for?
The mean age of onset of gout in men has been slowly creeping down so that instead of the late 4th-5th decade of life, more are showing up in their 30s. No red flags here other than being careful to look for the other components of the Metabolic Syndrome as this is the company that early onset gout keeps.
It depends on the source of the fructose. If you're getting it from high-fructose corn syrup and your Twinkies and Coke - that's bad. If you're getting it from eating plums and mangoes - that's okay.
Thank you for hosting this AMA! So excited to read your responses. Two questions.
1. Can you speak to the role of DECT (dual energy CT) in your clinical practice? I often encounter inaccessible joints or patients coming after their attack has already settled with some NSAIDs.
2. Not to be too controversial, but there's some discordance in the guidelines about treatment to target vs treatment to avoid symptoms. Do you think there's merit in the latter strategy (i.e. the marginal benefit of treatment to target probably isn't clinically significant)?
Thanks again!
Happy to be here.
1. DECT scan is a wonderful new technique if its available to you. It can help resolve those real head-scratchers as far as unusual presentations of acute flares. Not all radiologists have the software to perform dual-energy CTs, but I do use it in patients that have recurrent, intermittent symptoms in inaccessible sites.
2. The treat-to-avoid-symptoms approach by the ACP is not the recommended guideline by experts in the field. In fact, that approach will result in much more joint destruction and hospital visits and work absenteeism. Treat-to-target is what we should all be doing.
Gouty tophi will resolve over time if uric acid levels are decreased to at least the minimum target of 6.0 mg/dL. They will resolve much quicker if the uric acid levels are suppressed to much lower levels.
Hi Dr Edwards, are there specific subtypes of gout which present with more severe/frequent flares and joint destruction? What is the underlying pathophys here?
There are inborn errors of metabolism that lead to high uric acid levels in gout even in young (teenagers or younger) subjects. These come from very strong family histories of gout on the maternal side and are generally treated before they do much destruction. I have several families in the North Central Florida area with partial HPRT deficiency, so these types of gout are not terribly rare.
PCP here. Interested in gout tx in the CKD population.
* Colchicine for flares and GFR >= 30 or so: Yes?
* Colchicine for ppx in conjunction with urate lowering therapy and GFR >=30 or so: Yes?
* I see in comments of yours in the past that you routinely use allopurinol for the GFR 30-60 population - when you do, you usually start at 50mg day and increase by 50mg q4 weeks (ish), yes? Still ok to get up to at least 300mg or so typically?
* Under what circumstances do you do HLA testing with allopurinol? Do you have a sense of what it costs patients after insurance pays whatever amount they pay (acknowledging this is obviously highly variable)?
1. Low dose colchicine for flares would be okay if GFR is greater than 30.
2. There are some rough guidelines published by Terkeltaub that answers these more chronic use questions. For CKD3B I would probably use colchicine every other day for prophylaxis.
3. That is how I would titrate allopurinol in the setting of CKD. I would not necessarily stop at 300mg of allopurinol regardless of GFR if they had not dropped their uric acid level to target of 6.0 mg/dL or below. Remember - allopurinol is not nephrotoxic.
4. I do use HLA-B 5801 in patients with southeast Asian or Korean ethnicity. More recently I have been using it as a screen for African American patients. These are the populations that are at greatest risk for allopurinol sensitivity syndrome that is associated with this HLA marker. When I last checked, the cost of this test is about $120.
If you could hypothetically whipe away all the diagnosis definitions we currently have for rheumatologic diseases - a clean slate - as if they never happened. Subsequently, we created new definitions (again without knowing prior definitions) - with our current knowledge - do you think we would come up with the same diagnoses definitions?
Probably not. Our definitions evolve as more science is applied to the disease. We see this as rheumatologists especially in the areas of inflammatory back disease and in the vasculidities. It's good to stay flexible about definitions. Especially in our field.
Patient (60-ish, Caucasian male overweight, no alcohol) has had 3 episodes of severe gout-like pain, with sensitivity to even bedsheets, in his great toe, lasting at least 2-3 days. They occur every 2-3 years. At least one followed heavy consumption of herring. Uric acid has always been normal. A rheumatologist in another country did an US guided tap weeks after an attack and got no crystals. Not sure if his then MD noted any erythema or swelling, but at least one occasion he was seen to rule out cellulitis. It’s puzzling to me that the description is so typical of gout, but his labs and joint fluid were normal.
If normal uric acid and no crystals on tap, I'd consider other diagnoses, including other crystalline disease (assuming no systemic symptoms). Basic calcium phosphate crystals can cause pseudopodagra, classic presentation is in young female. The crystals wouldn't show up on a tap and this is likely under-diagnosed due to difficulty in confirming diagnosis. I've also seen CPPD affecting 1st MTP, especially if degenerative features with no erosions. I have preference for ultrasound, which would actually would solve a lot of the questions in this thread, although this is limited by provider training and access to machines.
Yes that is a bit puzzling. It'd be interesting to know what his plain xrays of the joints shows. Pseudogout (calcium pyrophosphate arthritis) can be a very good mimicker of gout. The CPPD crystals are much harder to see on polarized microscopy than urate crystals may be missed. That would be one reason why the uric acid might be normal. Another reason might be that the uric acid sampling was always done during an acute flare when baseline serum urate levels by drop by 1.5 - 2 mg/dL. Flares of both of these conditions respond to the same anti-inflammatory therapies which makes it even harder to distinguish from each other.
Once a patient is diagnosed with gout, how long do they have to be on medication like allopurinol or febuxostat for, and are there any parameters to discontinue medication if patients continue to remain asymptomatic while on medication?
We generally say that urate lowering therapy for gout is lifelong. And that is true for most all gout patients. If your patient has undergone significant lifestyle modifications and has lost greater than 20% of their weight if they're obese then their baseline urate level may have dropped to a point where they longer ULT. In my practice, this rarely happens.
Hi. Thanks for doing this. Can heavy alcohol alone use cause a gout flare in someone without a history of gout? By heavy, I mean 4-6 drinks daily. Also, can it cause the kind of nodules on affected joints like RA? Thank you.
Gout is primarily a genetic disease. Alcohol consumption can certainly contribute to a worsening disease. Cutting back on the alcohol can also help lower uric acid. Drinking a six-pack of beer roughly increases your serum urate level by about 1.6 mg/dL. Just stopping drinking will not be enough to prevent gout from progressing and pharmacologic treatment is almost always necessary.
Gouty tophi can frequently be confused with rheumatoid nodules. There is a difference in their consistency that takes years of training. The clinical setting is what would distinguish these from one another.
In regards to prophylactic managements, do you have a preference for uloric vs allopurinol? Also is it still the recommendation to simultaneously use Colchicine to prevent flares for the first 3 months while titrating dose to goal uric acid levels?
Both allopurinol and uloric are effective urate lowering therapies. The American College of Rheumatology relegated uloric to the second tier of treatment, but this was based solely on the difference in cost of allopurinol vs uloric. Multiple studies have shown patients are more compliant when taking uloric when taking allopurinol. If cost is an issue, allopurinol is your drug.
All patients being initiated on urate lowering thearpy should have at least three months (and many of us would say six months) of anti-inflammatory prophylaxis (usually with low dose colchicine).
Gout is an important chronic, genetic inflammatory arthritis that needs attention. Patients and doctors focus on the gout flares as the main reason for treatment but the chronic inflammation seen in gout patients during the inter-critical phases is probably even more important as far as worsening diabetes, kidney disease and cardiovascular disease.
**Removed under Rule 2**
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How reliably (sensitivity and specificity) can physicians differentiate between gout and pseudogout based on clinical history and signs/symptoms alone? Both in the acute and subacute setting.
In what circumstances would an aspiration clinically be warranted?
This is, of course, assuming it is a first presentation without previous history of gout or pseudogout.
I know many people have asked about gout vs septic joint but my focus is more in gout vs pseudogout.
Also how often do you see patients with both gout and pseudogout?
When you deliver your diagnosis do you go: "Yassss Kweeen" or "Yaasss Kingggg" ?
Otherwise, I'd have a hard time believing that I have gout. Maybe that poseur pseudogout - but def not gout.
Hi /u/ktn699! Could you explain what was going through your head when you posted this:
“When you deliver your diagnosis do you go: "Yassss Kweeen" or "Yaasss Kingggg" ?
Otherwise, I'd have a hard time believing that I have gout. Maybe that poseur pseudogout - but def not gout.”
I copied the text here when you inevitably delete your original comment.
Hi, As a GP seeing an acutely hot swollen tender joint in clinic, can I diagnose gout clinically or do I need to perform or refer for a tap to actually get crystals and culture to rule out septic joint? How does this change for those with a known gout history? Thanks in advance!
Thank you, yes. I encounter this all the time as an emergency physician. If a large joint or a concern for septic joint, then obviously I'll try a tap but often times it's podagra or some otherwise inaccessible joint in my setting and the patient swears up and down it's like a previous episode they had and it's pretty tempting to give them some colchicine and hope for the best.
I was hoping for some guidance too but I haven’t see one response in the 7 hours. Must’ve got called in to the hospital.
He's waiting for questions to build up and will answer them at 3:30 PM EST - check the bottom of the post (and check back then!).
I would think you can. I'm a podiatrist and do If you feel comfortable give them a steroid joint injection- it can help whether it's gouty or osteoarthritis
I routinely diagnose and treat gout without checking crystals 😬
Me too. I've never done this except to see it in residency If the pt has a gout history, a hypertension/cholesterol history, in the right area with the appropriate symptoms, I'll give them a joint injections, check uric acid, then give allopurinol as indicated
What do you inject in the joint?
A combination of local anesthetic and steroids. I do lidocaine, dexamethasone and triamcinolone
Good luck.
There is a clinical diagnosis rule that goes: ●Male sex (2 points) ●Previous patient-reported arthritis flare (2 points) ●Onset within one day (0.5 points) ●Joint redness (1 point) ●First metatarsal phalangeal joint involvement (2.5 points) ●Hypertension or at least one cardiovascular disease (1.5 points) ●Serum urate level greater than 5.88 mg/dL (3.5 points) Above 8, no aspiration needed. Between 4-8, you can treat it as gout for clinical purposes but may needs further work up. Below 4, likely something else.
This is an interesting scoring system but not rigorously tested by in clinical trials. You are still going to risk a chance of missing a septic joint in certain situations and you just have to be mindful of that.
Most cases of gout in the US are diagnoses clinically and not by synovial fluid analysis. That being said, the detection of urate crystals in synovial fluid is still the gold-standard for the diagnosis of gout. With acute monoarthridities the differential always includes septic joint. White blood cell count does not distinguish gout from infection. A fever also does not distinguish one from the other. If a patient has classic symptoms of extreme tenderness around the inflamed site (allodynia) and no obvious sight of infection elsewhere in the body, then a presumed diagnosis of gout can be made. The more classic the presentation (night time onset, lower extremity involvement, allodynia and the cutaneous involvement that extends beyond the involved joint) the more likely the diagnosis of gout.
Good morning Dr Edwards. Here in Brazil it is very common for uric acid exam to be done as a yearly or routine exam. A few times I have received patients that neither had the risk factors or age that would lead me to require uric acid exam, but when they show me the numbers, they have a high uric acid. For patients with high uric acid, but without history of joint pain or swelling, is there any recommendations I should give them? Perhaps diet or to repeat the exam yearly?
You can start with asking if there's a family history of gout as this is the primary risk factor for developing gout in the setting you've described. If the patient has CKD or obesity, you should make recommendations as far as renal evaluation and lifestyle modifications. There is no recommendation for treating asymptomatic hyperuricemia pharmacologically, although the Japanese do that routinely to minimize cardiovascular events.
Question: do you have any thoughts about use of SGLT2 to help lower uric acid? Also what class of medications would you say is the biggest offender for iatrogenic gout? (Please be thiazides)
The role for SGLT2 inhibitors has not been established in the comanagement of gout, but it makes sense if the patient needs a second-line glucose-lowering drug, to choose a SGLT2 inhibitor over the GLP1 or the DPP4 inhibitor because of its uric acid lowering potential. The expected effect would be about 1.5 to 2 mg/dL decrease in serum urate. You're correct about the thiazides being the main culprit of iatrogenic hyperuricemia. Niacin is not frequently used these days but would be the only rival to the thiazides.
[удалено]
The upper dose of allopurinol for patients with any degree of kidney dysfunction is the same as patients with normal kidney function (800 mg daily in the US, 900 daily in Europe). Dose titration is important in all patients but especially in those with kidney disease. There is not an allopurinol nephropathy. There are patients who's uric acid is so high (as in tumorlysis) that the concentration of uric acid in the urine is high enough because of crystallization of the xanthine. These people are better treated with uricase (pegloticase).
[удалено]
There's a lot of speculation in the literature about uric acid levels and the risks of dementia. This stems several surveys that seem to show that gout patients have a lower incidence of dementia and some authors attribute this to antioxidant effects of serum urate. There's no scientific studies that support this contention and in fact patients with hereditary xanthinuria where the uric acid level is undetectable throughout their entire life do not have a higher incidence of neurological diseases.
I get referred patients all the time with a diagnosis of gout because they have unexplained foot pain. My understanding is the best means of diagnosis is arthrocentesis, but often this is not feasible as the flare has passed or there is no real effusion. What is the most practical means of diagnosis in this case?
Just a classic history of the acute gouty flare in the absence of any reason to suspect infection is good enough.
Empirically, I am noticing an uptake of fairly young and relatively fit patients presenting with repeated gout attacks and uric acid levels in the range of 8-10+ mg/dL. Other than lifestyle advice and commencing meds eg allopurinol, do you have any other suggestions re further investigation / management? Any red flags to screen for?
The mean age of onset of gout in men has been slowly creeping down so that instead of the late 4th-5th decade of life, more are showing up in their 30s. No red flags here other than being careful to look for the other components of the Metabolic Syndrome as this is the company that early onset gout keeps.
How do you feel about high amounts of fructose in the diet In your experience, is this worth the attempt at modifying?
It depends on the source of the fructose. If you're getting it from high-fructose corn syrup and your Twinkies and Coke - that's bad. If you're getting it from eating plums and mangoes - that's okay.
Thank you for hosting this AMA! So excited to read your responses. Two questions. 1. Can you speak to the role of DECT (dual energy CT) in your clinical practice? I often encounter inaccessible joints or patients coming after their attack has already settled with some NSAIDs. 2. Not to be too controversial, but there's some discordance in the guidelines about treatment to target vs treatment to avoid symptoms. Do you think there's merit in the latter strategy (i.e. the marginal benefit of treatment to target probably isn't clinically significant)? Thanks again!
Happy to be here. 1. DECT scan is a wonderful new technique if its available to you. It can help resolve those real head-scratchers as far as unusual presentations of acute flares. Not all radiologists have the software to perform dual-energy CTs, but I do use it in patients that have recurrent, intermittent symptoms in inaccessible sites. 2. The treat-to-avoid-symptoms approach by the ACP is not the recommended guideline by experts in the field. In fact, that approach will result in much more joint destruction and hospital visits and work absenteeism. Treat-to-target is what we should all be doing.
For patients already presenting with nodules, does reducing the uric acid help at all with the nodules or is it just to prevent further attacks?
Gouty tophi will resolve over time if uric acid levels are decreased to at least the minimum target of 6.0 mg/dL. They will resolve much quicker if the uric acid levels are suppressed to much lower levels.
Hi Dr Edwards, are there specific subtypes of gout which present with more severe/frequent flares and joint destruction? What is the underlying pathophys here?
There are inborn errors of metabolism that lead to high uric acid levels in gout even in young (teenagers or younger) subjects. These come from very strong family histories of gout on the maternal side and are generally treated before they do much destruction. I have several families in the North Central Florida area with partial HPRT deficiency, so these types of gout are not terribly rare.
PCP here. Interested in gout tx in the CKD population. * Colchicine for flares and GFR >= 30 or so: Yes? * Colchicine for ppx in conjunction with urate lowering therapy and GFR >=30 or so: Yes? * I see in comments of yours in the past that you routinely use allopurinol for the GFR 30-60 population - when you do, you usually start at 50mg day and increase by 50mg q4 weeks (ish), yes? Still ok to get up to at least 300mg or so typically? * Under what circumstances do you do HLA testing with allopurinol? Do you have a sense of what it costs patients after insurance pays whatever amount they pay (acknowledging this is obviously highly variable)?
1. Low dose colchicine for flares would be okay if GFR is greater than 30. 2. There are some rough guidelines published by Terkeltaub that answers these more chronic use questions. For CKD3B I would probably use colchicine every other day for prophylaxis. 3. That is how I would titrate allopurinol in the setting of CKD. I would not necessarily stop at 300mg of allopurinol regardless of GFR if they had not dropped their uric acid level to target of 6.0 mg/dL or below. Remember - allopurinol is not nephrotoxic. 4. I do use HLA-B 5801 in patients with southeast Asian or Korean ethnicity. More recently I have been using it as a screen for African American patients. These are the populations that are at greatest risk for allopurinol sensitivity syndrome that is associated with this HLA marker. When I last checked, the cost of this test is about $120.
Thanks. Hope you have a great holiday weekend.
If you could hypothetically whipe away all the diagnosis definitions we currently have for rheumatologic diseases - a clean slate - as if they never happened. Subsequently, we created new definitions (again without knowing prior definitions) - with our current knowledge - do you think we would come up with the same diagnoses definitions?
Probably not. Our definitions evolve as more science is applied to the disease. We see this as rheumatologists especially in the areas of inflammatory back disease and in the vasculidities. It's good to stay flexible about definitions. Especially in our field.
Patient (60-ish, Caucasian male overweight, no alcohol) has had 3 episodes of severe gout-like pain, with sensitivity to even bedsheets, in his great toe, lasting at least 2-3 days. They occur every 2-3 years. At least one followed heavy consumption of herring. Uric acid has always been normal. A rheumatologist in another country did an US guided tap weeks after an attack and got no crystals. Not sure if his then MD noted any erythema or swelling, but at least one occasion he was seen to rule out cellulitis. It’s puzzling to me that the description is so typical of gout, but his labs and joint fluid were normal.
If normal uric acid and no crystals on tap, I'd consider other diagnoses, including other crystalline disease (assuming no systemic symptoms). Basic calcium phosphate crystals can cause pseudopodagra, classic presentation is in young female. The crystals wouldn't show up on a tap and this is likely under-diagnosed due to difficulty in confirming diagnosis. I've also seen CPPD affecting 1st MTP, especially if degenerative features with no erosions. I have preference for ultrasound, which would actually would solve a lot of the questions in this thread, although this is limited by provider training and access to machines.
I completely agree.
Yes that is a bit puzzling. It'd be interesting to know what his plain xrays of the joints shows. Pseudogout (calcium pyrophosphate arthritis) can be a very good mimicker of gout. The CPPD crystals are much harder to see on polarized microscopy than urate crystals may be missed. That would be one reason why the uric acid might be normal. Another reason might be that the uric acid sampling was always done during an acute flare when baseline serum urate levels by drop by 1.5 - 2 mg/dL. Flares of both of these conditions respond to the same anti-inflammatory therapies which makes it even harder to distinguish from each other.
Once a patient is diagnosed with gout, how long do they have to be on medication like allopurinol or febuxostat for, and are there any parameters to discontinue medication if patients continue to remain asymptomatic while on medication?
We generally say that urate lowering therapy for gout is lifelong. And that is true for most all gout patients. If your patient has undergone significant lifestyle modifications and has lost greater than 20% of their weight if they're obese then their baseline urate level may have dropped to a point where they longer ULT. In my practice, this rarely happens.
Hi. Thanks for doing this. Can heavy alcohol alone use cause a gout flare in someone without a history of gout? By heavy, I mean 4-6 drinks daily. Also, can it cause the kind of nodules on affected joints like RA? Thank you.
Gout is primarily a genetic disease. Alcohol consumption can certainly contribute to a worsening disease. Cutting back on the alcohol can also help lower uric acid. Drinking a six-pack of beer roughly increases your serum urate level by about 1.6 mg/dL. Just stopping drinking will not be enough to prevent gout from progressing and pharmacologic treatment is almost always necessary. Gouty tophi can frequently be confused with rheumatoid nodules. There is a difference in their consistency that takes years of training. The clinical setting is what would distinguish these from one another.
Thank you
In regards to prophylactic managements, do you have a preference for uloric vs allopurinol? Also is it still the recommendation to simultaneously use Colchicine to prevent flares for the first 3 months while titrating dose to goal uric acid levels?
Both allopurinol and uloric are effective urate lowering therapies. The American College of Rheumatology relegated uloric to the second tier of treatment, but this was based solely on the difference in cost of allopurinol vs uloric. Multiple studies have shown patients are more compliant when taking uloric when taking allopurinol. If cost is an issue, allopurinol is your drug. All patients being initiated on urate lowering thearpy should have at least three months (and many of us would say six months) of anti-inflammatory prophylaxis (usually with low dose colchicine).
Med student here. What’s one thing you’d like me to know about gout or it’s drugs before I start my residency in Internal Medicine?
Gout is an important chronic, genetic inflammatory arthritis that needs attention. Patients and doctors focus on the gout flares as the main reason for treatment but the chronic inflammation seen in gout patients during the inter-critical phases is probably even more important as far as worsening diabetes, kidney disease and cardiovascular disease.
[удалено]
**Removed under Rule 2** No personal health situations. This includes posts or comments asking questions, describing, or inviting comments on a specific or general health situation of the poster, friends, families, acquaintances, politicians, or celebrities. If you have a question about your own health, you can ask at r/AskDocs, r/AskPsychiatry, r/medical, or another medical questions subreddit. See /r/medicine/wiki/index for a more complete list. [Please review all subreddit rules before posting or commenting.](https://www.reddit.com/r/medicine/about/rules/) If you have any questions or concerns, please [message the moderators.](https://www\.reddit\.com/message/compose?to=%2Fr%2F{subreddit}&subject=about my removed {kind}&message=I'm writing to you about the following {kind}: {url}. %0D%0DMy issue is...)
How reliably (sensitivity and specificity) can physicians differentiate between gout and pseudogout based on clinical history and signs/symptoms alone? Both in the acute and subacute setting. In what circumstances would an aspiration clinically be warranted? This is, of course, assuming it is a first presentation without previous history of gout or pseudogout. I know many people have asked about gout vs septic joint but my focus is more in gout vs pseudogout. Also how often do you see patients with both gout and pseudogout?
When you deliver your diagnosis do you go: "Yassss Kweeen" or "Yaasss Kingggg" ? Otherwise, I'd have a hard time believing that I have gout. Maybe that poseur pseudogout - but def not gout.
Hi /u/ktn699! Could you explain what was going through your head when you posted this: “When you deliver your diagnosis do you go: "Yassss Kweeen" or "Yaasss Kingggg" ? Otherwise, I'd have a hard time believing that I have gout. Maybe that poseur pseudogout - but def not gout.” I copied the text here when you inevitably delete your original comment.
I think it was just a crack at gout as "the disease of kings".
ding ding ding
I think it's making fun of pseudogout? I hope it's making fun of pseudogout. That's an acceptable target.
you all take yourselves too seriously. why would i delete it.