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Letters to the Editor

Staff  |  Issue: January 2008  |  January 1, 2008

In “Know Your Unknown Unknowns,” (October 2007 TR, p. 6), we asked for your thoughts on whether or not to administer steroids post-surgery for a woman with giant cell arteritis (GCA) of the aorta. (See patient description below). We’ve published a selection of those responses here, and we want to thank everyone who wrote in. Keep those letters coming!—The Editors

Mixed Views on Steroid Use

No doubt that steroids were needed in this case. The key question: Were the margins of the graft involved or free of giant cell inflammation? If the inflammatory process was extensive at the graft-tissue interface, I would be concerned about healing at the interface. If the interface was clear and the patient would be followed closely for amaurosis or other ominous symptoms, then I would be more likely to be patient on starting steroids. Do no harm.

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The Patient

  • Woman in her 70s with age-related medical conditions and ill-defined chest pain;
  • Aneurysm of the ascending thoracic aorta treated surgically with a graft; and
  • Pathologically diagnosed GCA of the aorta.

Now the question is how long does it take normally for an aortic graft-tissue interface to heal in a 70-year-old patient? We now know that atherosclerosis is an inflammatory process and that many of these grafts will go into an area of inflammatory atheromatous aorta—at times flagrantly inflamed. Yet from what I gather they usually heal. This patient may have had both giant cell aortitis and inflammatory atherosclerosis.

My guess is that steroids were held, the graft healed, and steroids were started later with no end point to follow. A PET scan can show active inflammation in giant cell aortitis and smaller arteries and may provide some additional information about extent and activity.

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Robert Thoburn, MD,
adjunct clinical assistant professor of rheumatology,
University of Florida College of Medicine,
Gainesville

 

I hate to say that the surgeon is probably right and the rheumatologist wrong in this case. Why? The vasculitis (of the aorta) was found by accident (vague abdominal pains). No other stigmata of vasculitis whatsoever were found on physical or imaging examination. This was probably an isolated vasculitis of the aorta.

Therefore—although this sounds a bit weird—surgery could have cured her vasculitis, and steroids can be withheld.

On the other hand, if there were other symptoms, such as headache or blurred vision, or stigmata like elevated erythrocyte sedimentation rate (ESR) (which she did not have, we were told), then we’d have cause to seriously consider systemic therapy.

George Bruyn, MD, PhD,
honorary consultant rheumatologist,
Medisch Centrum,
Leeuwarden, The Netherlands

 

I would treat this woman’s GCA with 1 gm of solumedrol qd for three days. She has a significant segmental vasculitic process that is not suppressed. Older patients frequently don’t complain. Perhaps an ESR or C-reactive protein elevated significantly would make everyone feel better about steroid use. There is a good likelihood that the surgeon’s fancy surgery will fall apart because of active vasculitis in the suture line if left untreated.

Andrew Daugavietis, MD,
Arthritis Clinic,
Grand Rapids, Mich.

 

I may have at least a partial answer for you. Please check our article, “Occult active giant cell aortitis necessitating surgical repair” (J Thorac Cardiovasc Surg. 2000;120:813-815).

In essence, we looked at all surgical specimens at Mt. Sinai requiring surgery for aortic aneurysms. Pathological studies showed that about 2% had giant cell arteritis. This had not been acted upon by the physicians taking care of the patients and—to our knowledge—none were treated with corticosteroids. From perusal of the charts there were no symptoms suggestive of GCA. Dr. Kerr followed five of the 12 patients, and only one apparently developed polymyalgia rheumatica. None had any vision loss.

When we diagnose GCA we are seeing only the tip of the iceberg. In a study done many years ago in Malmo (where every person who died has had an autopsy), when sections of the aorta and temporal arteries were studied about 2% had histological evidence of arteritis (not necessarily GCA). Interestingly, that matches the 2% incidence of aortitis that we found, in “Temporal arteritis in a large necropsy series” (Ann Rheum Dis. 1971:30 224-235). I suspect that the frequency of vision loss in GCA is less than is commonly believed. Obviously, we need better data as to the natural history of GCA.

Harry Spiera, MD,
clinical professor of medicine/rheumatology,
Mt. Sinai Medical Center,
New York

Dilemmas test our ability to understand principles. The principle being tested in your clinical scenario is that reality trumps probability. Steroids should not be given to this patient in the post-operative period and every effort should be made to help the patient—first and foremost—recover from surgery.

A compromise might be to start imuran, but a significant unknown already identified is whether the aortic GCA may have been remedied by surgical excision. Therefore, observation would be the best approach, especially because none of the telltale signs and symptoms of GCA were present before the surgery. The reality of needing to heal from surgery trumps the probability of all the other scenarios for which steroids are being recommended.

Craig D. Scoville, MD, PhD,
rheumatologist,
Idaho Falls, Idaho

 

NEED TO KNOW

Send us your clinical case!

Want to hear how your colleagues would treat a challenging medical case from your practice? Send us details at [email protected] and we may publish your case in an upcoming issue of The Rheumatologist.

Health Professionals Offer “Crisis” Control

I would like to suggest that, along with the funding to increase rheumatology’s presence in academia (suggested in “Avert Rheum’s Coming Crisis,” September 2007 TR, p. 6), consideration should be given to nurse practitioners (NPs) and physician assistants. I’m suggesting that a focused training program for rheumatology mid-level providers (akin to a fellowship) would benefit the physician, provider, and public. The level of education required of mid-level providers, especially NPs, prepares them for both academic and clinical pursuits. Thoughtful inclusion of a select group of mid-level providers in your endowment plan could support and enhance physician-led efforts to meet the growing needs in rheumatology while protecting and preserving overall funding.

Fortunately I am in a position to personally support my suggestion. I am in the last year of an NP program and am working with a group of research-oriented rheumatologists. There is an active fellowship program for physicians at the University of Arizona. Though there is currently no parallel track for mid-level providers, I hope my continued association with the University of Arizona may allow for the creation of such a pathway.

Steve Edelman, RN, BSHCS, CCRP,
research nurse,
University of Arizona Arthritis Center,
Tucson

 

Evidence-based Medicine Has Limits

I read with much interest your article, “Make Peace with Complexity” (May 2007 TR, p. 6), where you stated that, “While, as professionals, we may pride ourselves for being evidence based, often the evidence simply does not exist.” In the past few years (and this will probably continue in the near future), the craziness to discuss evidence-based medicine in almost every discipline of medicine worldwide has seemingly (and unfortunately) made evidence-based medicine the only reason to learn and practice medicine. In reality, evidence-based medicine studies only clinical cases with many exclusions and inclusions. Based on my clinical practice for more than 20 years (excluding those five years in United States), evidence-based medicine quite often does not fit well with the complexity of real-life, daily patient conditions that need a lot of decision-making.

As for your case of acute gouty attack with moderate renal insufficiency, obvious heart failure, previous pulmonary embolism, and chest X-ray infiltration of unknown cause, I would like to use colchicine 0.5 mg qd (the uniform tablet dosage available in Taiwan) together with a short-term, small dose of oral prednisolone (for example, 0.2–l0.3 mg/day/kg for two days with monitoring of clinical improvement or aggravation). Of course, a lung infiltrate study has to be worked up aggressively at the same time. By the way, do you think the above-mentioned small prednisolone dose for two days will affect the immunologic function significantly?

Lambert, Lieh-bang Liou, MD, PhD,
rheumatologist,
Chang Gung Memorial Hospital,
Lin-kou Medical Center,
Tao-yuan, Taiwan

Correction

“Disappearing Dollars,” (October 2007 TR, p. 14), stated: “The ACR supports a proposal to triple NIH funding for FY 2008 and provide annual increases to the NIAMS budget, and opposes the use of budgetary mechanisms that arbitrarily limit research funding.”

To clarify, the ACR supported tripling the percentage requested of NIH funding—not the entire NIH budget.

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Filed under:Conditions Tagged with:aortaatherosclerosisgiant cell arteritis (GCA)inflammationLettersSteroids

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