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Gout

Gout is a different disease for both male and female. Men tend to present at a younger age because of the association with uric acid and antigen levels in the blood with gout, gowt. Some are between the ages of 35 and 55, is the average onset of gout in a male patient. Usually it presents as an acute podagra, which is the great toe or possibly a knee or an ankle depending upon the saturation of the soft tissue.

In female patients who donít have problems with renal insufficiency or donít have an enzyme defect, these patients will present about 20 years after menopause. So that is 45 give or take 20, that is the amount of time it is required to saturate soft tissue with uric acid. Female patients will present in their 60s. They tend to present with a more subtile illness and more chronic. It is not uncommon to see a patient present in her 60s with tophaceous gout with never an attack of acute podagra.

These women tend to have history of hypertension, mild renal insufficiency and not infrequently osteoarthritis because crystals like to deposit in damaged joints. If you have osteoarthritis of the knuckles it is not uncommon to get superimposed crystal, which of course raises difficulty when you see the patient. It is a little bit different in terms of onset, male and female.

Cyclosporin. As we move on, drugs like CellCept and Prograf are replacing cyclosporin, but cyclosporin can take a normal person and give him tophaceous gout in about 24 months. Because it is a causer of renal insufficiency it also inhibits the secretion of uric acid by the kidney and resorption from uric acids, so it is a three-fold toxin in terms of developing gout in patients. It can develop raging tophaceous gout, and one of the problems was is that most patients with renal and heart transplant were on drugs such as Imuran and Cyclosporin, and Allopurinol interact with one another. You have a real difficult time of using Allopurinol.

Important items, uric acid levels can be normal enough to half of patients with their first gout attack. Getting a serum uric acid level on a 35 or 38 year old may or may not tell you much. Because it is not uncommon for it to be normal. The most important test to know is the serum creatinine. Because creatinine is important in terms of treatment with anti-inflammatories.

Another clinical pearl, gout can be triggered by infections. Septic joint and gout can co-exist. Anything that causes inflammation of the joint can shake loose crystals so you always have to be absolutely certain your not treating a cellulitis/septic joint. I, not infrequently treat the patients for both until I am absolutely certain over a time course. Meaning they will get antibiotics.

How do we treat this? That is the background. We wonít really talk about hydroxy appetite crystals. Today, we are going to talk about gout and pseudogout. These are the nice crystals. Again, we talked about polarizing. This is just from tophaceous, no white cells. Gout crystals are easy to see, you can even see them without the use of a polarizing scope because of their size.

Pseudogout crystals are small enough and dull enough that theyíre relatively difficult to see. Well, how do you see them? You take a pallet spin it down or take fluids spin it down to a pallet resuspend it, your chances of seeing pyrophosphate crystals go up about 70% or if you use a pallet. This is clinically an acute podagra. The inflammation is so intense that you actually peel off the skin like a blister. How come this is not cellulitis, sometimes it is difficult to sort out, as I say, the two can co-exist.

Whatís the workup? I keep mentioning creatinine because of the toxicities of these medications because they are renally excreted. You must know your serum kidney functions. Allopurinol has to be rationed down depending upon the creatinine and clearance. For example if the creatinine clearance is 50cc, the uric acid that will be lowered by Allopurinol dose of 50 mg every other day, as opposed to the standard 300 mg, so you must know that.

We get a 24-hour urine creatinine clearance in uric acid. Most patients are under excreters, they donít secrete enough uric acid in the urine, and they need to secrete more. Only 20% are overproducers with uric acid of more than 1000 mg a day. Those are your stone formers. Why is it important? Patients technically that are under excreters will be treated quite nicely by either Benemid or sulfinpyrazone, they are very good as long as the kidney function is normal. If the kidney function is not normal they donít work well. We use Allopurinol. By increasing uric acid obviously secretion, if youíre a stone former I give you sulfinpyrazone or Benemid, I will give you kidney stones and you wont be happy. So you must know your urine and uric acid secretion.

Usually you wait about a month after a gout attack to let the equilibrium stabilize and get your numbers and decide where the patient is at. Most patients again are under excreters, so theriatrically they would benefit from either sulfinpyrazone or Probenecid. Most patients end up on uric acid lowering Allopurinol because by the time they are picked up they have other problems. They have renal insufficiency related to hypertension, there on Cyclosporin, they have tophaceous gout, etc.

Acute gout in younger individuals is usually not a problem, any of the anti-inflammatories in full dose can be used including the new Cox II inhibitors. In older patients you must know the serum creatinine, indomethacin is very potent at decreasing renal blood flow by inhibiting prostaglandins so that is not a good drug in an elderly patient, I donít use it. The old Colchicine p.o. causes diarrhea by the time it treats the illness, we donít use that much anymore. In recent years, IV Colchicine 1 mg every 12 hours, usually two doses is enough. Colchicine is also metabolized by the kidney.