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Disease Flares
Left arm claudication
Reductions in prednisone likely vary from one physician to another – some literature recommend guidelines for taper. One indicated a 50% increase upon flare indication, followed by gradual decreases back to a controlling level. Another advised 2.5 mg reductions every two weeks between 20 and 10 mg/day, then 1 mg decrease per month below 10 mg. It would seem prudent to make small changes once evidence of active inflammation is present, such as leg arteries stenosis and ischemia, and finding a significant increase in sed rate. Pearl’s doctor reduced prednisone from 15 to 10 – a 33% decrease – a month after an elevated sed rate of 50.
The subclavian artery, located in the shoulder, is a focal point for GCA inflammation according to literature. Pain and arm numbness developed in this area in Pearl after the sed rate had increased to 50. Like the leg arteries, this also went unrecognized as a GCA symptom. A few years later poor circulation to her left shoulder would result in rotator cuff tendonitis and bursitis (both symptoms of PMR) and necrosis and fracture of her shoulder blade. Necrosis is bone death due to lack of adequate blood supply.
A Berkeley Heart Panel Test was done by the Cardiologist. A blood specimen was sent to the U of California at Berkeley where it was subjected to a profile of tests. Pearl’s indicated low risk of heart disease, no hypertension and no atherosclerosis – confirming the Cardiologist’s view that Pearl’s leg problems were arteritis rather than atherosclerosis. But that was his opinion – others retained their original judgment despite this new information.
The left shoulder/neck pain was followed about two weeks later by flu-like symptoms which likely were manifestations of smoldering GCA – coughing, earache, runny nose, pain throughout her body and a slight fever. Two courses of antibiotics didn’t help. Sed rate was found to have increased once again - this time to 34. Prednisone was at 10 mg/day. Dr increased it by 2.5 mg. A few weeks later her right eye socket became inflamed and bulged out about 2 mm. An MRI showed nothing. The next sed rate measurement was still elevated at 24 but Dr wouldn’t increase the prednisone. His rationale was he wants to wean Pearl off of prednisone as soon as possible – long-term effects are bad so the sooner we can reduce or stop the better. However, all through her treatment this prevailing attitude meant that she continued to have "smoldering GCA" which continued to take its toll. He wasn’t treating the disease he was continually focussed on fear of secondary effects of prednisone.
I found literature recommending the use of C-rP in managing GCA. I asked the Rheumatologist why C-rP isn’t being measured. He advised that it isn’t necessary to monitor both sed rate and C-rP; since he’s been tracking sed rate he’ll continue with that. This attitude and lack of recognition of GCA symptoms when they occurred led me to seek a second opinion – this will be described later.