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Disease Flares
Legs claudication
The Rheumatologist continued to decrease prednisone even as sed rate was increasing though still in the normal range. After start of prednisone in December, 1998, sed rate reduced to 10 mm/hr or less and remained there through May, ’99. Sed rate rose to 23 in June. It decreased to 10 once again in July after the hospital administered a stress dose of > 100 mg of a corticosteroid to perform an arteriogram to evaluate her leg arteries. We learned over the years following that having a sed rate of 20 was an indicator for Pearl that GCA/PMR wasn’t being managed with enough prednisone. In retrospect sed rate values over 10 for Pearl should have been the level for increase in prednisone. The Rheumatologist said at one point early in her treatment that anything below 15 was normal. Had prednisone been increased when sed rate increased to 15 in March, 1999, Pearl’s leg arteries likely would have remained open. Sed rate eventually reached 50 a few months later, finally triggering an increase in prednisone by the Rheumatologist.
Decreased circulation in the feet became apparent in June, 1999, so Pearl was referred to a Vascular Surgeon to evaluate the legs. Within four days after the Vascular Surgeon did a doppler scan on the legs, circulation diminished to a point of being an emergency, prompting her to go the hospital for care. The hospital repeated the doppler scan and followed up with an arteriogram. Significant blockages and restrictions were found in most large arteries of both legs. Also, the blockages and restrictions were spasmodic, that is, opening and closing in a periodic manner – about an hour per cycle. A large dose of prednisone was administered for the arteriogram. That broke the spasms and restored circulation.
Despite the evidence of arteritis in the large leg arteries all doctors involved at this time regarded Pearl’s problem as atherosclerosis, not related to GCA. They assumed that all of Pearl’s arteries were atherosclerotic because of a probable genetic condition – this was erroneous. There was no history of atherosclerosis in Pearl or her siblings. She never smoked, had very low risk in lipids tests – high HDL, low LDL and total cholesterol. Her rheumatologist had never heard or read of GCA affecting a patient’s leg arteries. Because of this erroneous speculation the Rheumatologist continued to decrease Pearl’s prednisone dosage resulting in ulceration of the right heel.
A Cardiologist will be called upon who will make the correct diagnosis that the leg artery problems were due to GCA/PMR and not atherosclerosis. This will be discussed later.
Allegra-D (the D component is pseudoephedrine – a vasoconstrictor) was started by Pearl in April, 1999. It was prescribed by her allergist to eliminate coughing. It was considered benign but I speculate it would have been better for her if it had not been started. Over the years I attempted to get Pearl off of it but she found it too helpful for the cough to give it up. I had no support from any of her physicians to help stop its use. They supported the belief that it had no effect on her leg arteries.
Pain behind Pearl’s left eye was reported on 4/23/99 but ignored – it felt similar to the pain behind her right eye at the beginning of her illness. This and headaches reported a month later were symptoms of GCA the Ophthalmologist and Rheumatologist failed to act upon. Both the headaches and the sed rate of 15 in March should have caused prednisone to be increased by the Rheumatologist but didn’t.