Gout is an in-born metabolic error and what’s going on is 1 of 2 things. The body is overproducing urates (such as uric acid) and/or under-excreting urates through the kidneys. In that latter scenario, it’s not that there’s too much uric acid, but the body is not getting rid of it so in either scenario, the blood levels of uric acid are increasing. The most predominant joint where it crystallizes is in the joint of the big toe. A person having a gout attack is having severe pain. Our body’s immune system sees this crystal that forms in the joint as a foreign agent and tries to destroy the crystal. What chance does a WBC have to destroy a crystal? Zero. As it’s trying to gobble up the crystal, it starts to destroy the surrounding joint. As it causes damage to the surrounding joint area, the environment of the joint changes and it becomes slightly more acidic, causing the crystal to get even larger and it turns into a vicious cycle. The more attacks a person has in their lifetime, the more damage to their toe, until eventually the big toe needs to be amputated.
There’s also secondary gout. The person doesn’t have true gout but has another disease where they can have the primary symptoms.
Sickle Cell Anemia: When someone with sickle cell anemia is having a sickle cell crisis, it leads to the extra presence of uric acid.
Thiazide and Loop Diuretics: There are certain diuretics that could increase uric acid levels and potentially lead to a gout attack.
We have two kinds of therapy: acute and prophylactic. Acute means they are in pain right at this moment and something needs to happen about this pain. The drug that has historically worked the best is Colchicine. This blocks the migration of granulocytes to the inflamed area, causing less urate deposits.
The side effect of this is severe diarrhea. Once they experience diarrhea, that means they are getting toxic on this drug and need to stop. They need to take this drug every hour until the gout attack is over. The problem with this is it’s one of those grandfathered drugs from the 1960’s. When the drug company did the study, all the generics had to be pulled off because they now owned the patent. Instead of the drug costing $8-9/month it’s now costing $400/month.
This is when we want to prevent a gout attack from occurring.
Prevention includes a diet low in purines (they get converted to acid) and high in carbohydrates.
- Avoid beans, peas, spinach and mushrooms.
- Restrict amounts of meat, fish, seafood and alcohol
- Increase intake of water.
We have a couple of drug choices, but before we choose one, we have to figure out what’s the patients cause of gout. They could either be an overproducer or an underexcretor and we need to figure that out to know what they could use prophylactically.
- If their urine is loaded with uric acid, the body is producing too much uric acid.
- If their urine levels are low in uric acid, their kidneys are not excreting enough.
Allopurinol (Zyloprim) causes a decrease in metabolic formation. This would be used in an over-producer.
Probenecid (Benemid) or Sulfinpyrazone: These are uricosuric agents which push uric acid into urine. We talked about this when we talked about high dose salicylates. This is good for under-excretors.