In this gout case study, a 66-year-old female has a past medical history of diabetes, neuropathy, depression, migraines, insomnia, gout, and hypertension. She has numerous complaints. Her gout has not been in good control as she is requiring significant indomethacin use for flare management. She says that capsaicin doesn’t help her knee pain. In addition, her blood sugars have been elevated. Her current medication list includes:
- Aspirin 81 mg daily
- Capsaicin cream prn
- Diphenhydramine 25 mg at night
- Metformin 500 mg BID
- hydrochlorothiazide 50 mg daily
- Glipizide 5 mg daily
- Allopurinol 200 mg daily
- Indomethacin 50 mg TID PRN
- Duloxetine 30 mg daily
- Topiramate 50 mg BID
Before I bring up anything else, I always try to address the patient’s issues first; so let’s do that.
First, let’s address the gout flares as we would like to minimize NSAID use. I would be inclined to obtain a uric acid level to see where that is at. From there, we will likely have to consider an increase in allopurinol (I’d also like renal function labs). There are two other considerations that I would think about here as well. Hydrochlorothiazide could increase uric acid and directly oppose uric acid lowering therapy. If it is being used simply for hypertension it would be a good opportunity to select another agent. What agent would make sense? An ACE/ARB would be beneficial in a patient with diabetes but more specifically, losartan may be purported to have some activity that may reduce uric acid levels. Lots of potential wins with a transition off hydrochlorothiazide to an antihypertensive like losartan.
Capsaicin needs to be scheduled to have analgesic relief. Patient education and inquiring about how she was using this medication would be my first step in this situation. If she had tried a scheduled course of at least a few weeks, a topical NSAID would be a consideration. You’d think the knee pain would be improved if she was using indomethacin frequently, but obviously, we’d like to avoid this long-term.
Let’s talk about blood sugars. It is unclear why metformin is at a lower dose. Titration of that medication would be most appropriate. An investigation into whether an SGLT-2 or GLP-1 would be an option would be another consideration with the potential of getting rid of the sulfonylurea. Also, remember that thiazide diuretics may have modest effects on hyperglycemia so maybe changing the hydrochlorothiazide would help for one more reason.
Lastly, I’m never a big fan of diphenhydramine. It is often a cause of the prescribing cascade which I talk about extensively in my latest book Perils of Polypharmacy. I’d seek to inquire about why this medication is being used. This in combination with topiramate could potentially lead to some cognitive issues so I would definitely like to review this with the patient and ensure that these drugs are both safe and effective for what they are being used for.
What else would you look at here in this gout case study?
- 30 medication mistakes PDF
- 18+ Page Drug Interaction PDF
- 10 Commandments of Polypharmacy Webinar based on my experiences in clinical practice
I’d also like to take a look at her lifestyle- specifically diet and exercise- for a person who has also had a fair share of gout attacks I have been able to reduce the frequency on diet modifications….
I would like to offer the following comments.
One consideration is whether she has gout. Without a definitive diagnosis (seeing crystals in synovial fluid) this could be something else. Having monoarticular knee pain would make me think more about an incorrect diagnosis of gout. When I had someone like this it was unusual for them to say that anyone had “stuck a needle” into any joint. What can occur is finding crystals in the synovial fluid of the knee even if the presentation is “classic” podagra. Doing arthrocentesis on joints in the toe is harder than the knee. If the history was very clear she had podagra, I would be more likely to believe that gout was a correct diagnosis.
Having drug-induced hyperuricemia is not a disease and does not need to be treated. Since she is prescribed HCTZ, that needs to be sorted. As noted, her glucose might be slightly lower without taking HCTZ.
As noted, It is critical to know her renal function and serum uric acid. I would want to know the serum uric acid after the resolution of an acute painful episode. The serum uric acid can be low, normal, or elevated during acute gouty arthritis. I would also want to know the serum uric acid after stopping HCTZ.
If this is gout, the target for the serum uric acid is <6.5 mg/dl. There is no “dose” of allopurinol in the absence of knowing the serum uric acid. I would also assess the persistence and adherence of refilling allopurinol (and meds in general). Someone who thinks they are doing great and stops taking allopurinol might develop a flare. The dose of allopurinol should not be “increased”. It must be increased to reach the target serum concentration. Rarely, doses up to 900 mg/d are needed.
Losartan is not purported to lower uric acid, it lowers uric acid (unique among ARBs). It is unknown if there are fewer flares of gout if losartan is used. Realistically, hypouricemic therapy will be used rather than just losartan.
I disagree about using NSAIDs for a week. If someone has acute gouty arthritis, I would have no issue treating the patient with high doses of any NSAID (e.g., naproxen 500 mg BID x 5-7 days) except aspirin. Unless the dose of aspirin is in the range of 3.5 g/d, it blocks urate excretion. Every NSAIDs studied reduces pain in acute gout (naproxen, ibuprofen, sulindac, etc.). If someone had another reason to avoid an NSAID (e.g., heart failure and using ACEI and loop diuretics), I would use prednisone 35 mg/d for 7 days (no tapering needed). I would not be concerned about the glucose effect of prednisone for one week. If the pain is more chronic and then flares, I would not use colchicine since it is less likely to be effective if the acute event is longer than 24 hours.
The patient’s weight is not listed. Since T2DM is most often seen in obese patients, I would try to change the diet before adding more drugs. The diet effect on gout is insignificant. The use of SGLT-2 and GLP-1 needs to be considered with the cost of these drugs, especially for Medicare patients who will reach the donut hole. These drugs compared to placebo had less than a 2% absolute benefit over the 2-5 years of the clinical trials. The NNT for these drugs is about 60 to 130 to prevent ONE composite event. The cost of the drug alone to prevent ONE composite event ranges from $1 million to $3 million. The effect of marketing and the ADA has made these drugs sound remarkable. I would change metformin to extended-release for convenience and give 1500 mg/d. The only information I was ever able to find is the labeling to show a small difference between 1500 mg and 2000 mg of metformin. Glipizide can also be increased to 10 mg/d. Knowing the control of diabetes is important before any changes are made.