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Disease Flares
Rotator cuff tendonitis and bursitis, both shoulders and momentary loss of all vision
The obsession with prednisone reduction continued over the years of treatment. The Clinic Rheumatologist who was seen twice up to this point for a second opinion about several issues caused two significant changes in treatment. C-rP was recommended along with sed rate and clinical symptoms in managing GCA. Pearl’s rheumatologist accepted this advice. A year later in the second visit the Clinic Rheumatologist advised GCA should have run its course because Pearl had GCA for over three years at that time. His advice in October, 2002, was to taper off of prednisone without monitoring sed rate and C-rP any longer. This advice clearly contradicted all literature I’d read about managing GCA. Her rheumatologist agreed with this approach. Pearl and I agreed also but insisted on measuring sed rate and C-rP just for information.
Pearl experienced a sharp pain in her right upper arm as she reclined on the couch on 7/21/03. Her prednisone was at 4 mg, being decreased at 1 mg/wk. The Rheumatologist advised that she not increase prednisone for this trauma. An Orthopedist suggested that X-rays indicated rotator cuff tendonitis or bursitis – these are symptoms of PMR but he didn’t think that PMR was the cause. Sed rate increased to 56 and CrP was elevated at 2.4 mg/dl on 8/4/03. I sent an Email to the Clinic Rheumatologist for advice and received no response. Two weeks later the Rheumatologist advised Pearl to increase prednisone to 4 mg (it was 3 mg by that time, on a reducing schedule). He was alarmed at the sudden increase of sed rate from 6 on 5/21/03. Oddly he still wasn’t attuned to the value of C-rP in managing GCA – it was .6 mg/dl (normal) on 5/1/03 but was significantly elevated at 2.32 mg/dl on 5/21/03. Only sed rate continued to be important to him. Finally on 8/20/03 when sed rate and C-rP remained elevated he increased prednisone to 10 mg. This attempt at tapering off of prednisone was to be the last.
Pearl made an emergency visit to the Ophthalmologist after losing sight momentarily in her left (good) eye while shopping on 12/12/03. He increased Prednisone to 60 mg/day of prednisone for 3 days, then tapered. C-rP was 2.1 mg/dl and sed rate was 26 – both indicating flare. MRI showed no problem in the left eye but the right optic nerve was inflamed which became a curiosity item without conclusion. Both eyes appeared to be healthy based on photos with dye taken of the retinas.
Two weeks later a large welt appeared on Pearl’s upper right arm a couple of hours after rolling out pumpkin pie shells on Christmas Eve. This led to stopping use of Plavix which promotes circulation by making platelets "slippery". A month later the Orthopedist prescribed light physical therapy for Pearl’s upper arms which had been painful to move for much of the past year. Sed rate and C-rP continued to be elevated much of the time with prednisone cycling continuing. After 9 sessions of therapy didn’t make a difference he prescribed more intense therapy for another round of 10 sessions. MRIs taken after showed both rotator cuffs were completely torn. An Orthopedic Surgeon advised that both were not repairable surgically. Pearl could only raise arms to shoulder height. Bones in both shoulders were badly degenerated and dislocated. The left shoulder blade was necrotic and fractured. She received several injections of corticosteroids by various doctors for pain relief. Injections are limited to three per year to avoid bone disintegration.
The shoulder problems were not attributed to GCA or PMR by the specialists involved. Since they have characteristic symptoms associated with PMR in literature, along with vision loss, while sed rate and CrP were elevated convinces me that they are a result of the on-going partially controlled GCA/PMR condition. I began to suspect at this point that even 10 mg/day was not enough to maintain control of Pearl’s GCA.