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Treatment began immediately. Visits were made in quick succession to several specialists in an attempt to confirm the diagnosis and ensure there wasn’t something else occurring. After the additional screening was completed and GCA was proven via biopsy there was routine type follow-up with some of the specialists.
GCA/PMR must be managed with the judicious use of prednisone – enough to control inflammation but no more than necessary because of damaging side effects of long-term use of prednisone. So, how much is enough? That was a point of controversy we had with her rheumatologists throughout her illness. Her rheumatologist initially used only sed rate to determine if GCA/PMR were being controlled. He established less than (<) 15 mm/hr as a normal range limit, yet when values higher than that were measured he didn’t always increase prednisone as would be expected. That inconsistency likely caused more arteritic damage to Pearl over the years.
C-reactive Protein (C-rP) measurement is another tool for GCA management – some think it is more important than the sed rate measurement. The medical consensus at that time according to published literature was that both should be used to manage the illness, along with symptoms. However, her rheumatologist used only sed rate (inconsistently) during the first year which was unfortunate for Pearl. We weren’t aware of C-rP or of its importance at the time.
Methotrexate is another prescription medication used sometimes in treating GCA/PMR. It was used on three different occasions by Pearl. Its purpose is steroid-sparing. The intent is to try to reduce the daily amount of prednisone needed by getting help from methotrexate to reduce inflammation.
The first use of methotrexate was for a year-long period starting in October, 2000. It was stopped at the recommendation of a Clinic Rheumatologist who considered it to be ineffective for GCA. Pearl sought the advice of the Clinic Rheumatologist when a second opinion was desired in 2001.
Methotrexate was started again for a four-month period in November, 2004. At that time an attempt was made to reduce prednisone from the normal management level on alternate days. Flare resulted so the methotrexate was stopped.
It was restarted in August, 2007, six weeks before her death. The reason it was tried once more was it had been demonstrated to be helpful after all. A medical journal article studied its past use on GCA patients and concluded methotrexate was beneficial but it took six months to a year to become effective. Review of Pearl’s use of it in 2000 and 2001 indicated a benefit did show up in the two years following its use. Prednisone requirements seemed to have been several milligrams per day lower during that period.
The FPP insisted on a CT scan and liver biopsy to determine the cause of elevated alkaline phosphatase in the blood test a month before diagnosis. Several specialists did not want these done because management of Pearl’s illness was much more important at the time. These tests would involve an allergic dye, significant stress dose of prednisone and would be non-contributory - but the FPP had his way. The Gastroenterologist performed the tests in January, 1999, and results showed proper liver function as expected. Elevated alk phos could indicate GCA inflammation. Had that been recognized by the FPP in November Pearl wouldn’t have lost vision. Once prednisone treatment started the alk phos returned to normal. The alk phos would become elevated once again nine years later and would again be unrecognized by medical professionals as a potential indicator of GCA inflammation. At that time the oversight may have been vitally detrimental for Pearl.