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Infectious complications complications of cyclophosphamide treatment for vasculitis.

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with symptoms consistent with transient ischemic attacks
and hemiplegia, have been reported as presentations and
features associated with ICA dissection (1-7). The variety of
possible presentations make this diagnosis understandably
While magnetic resonance imaging has recently been
shown to correctly diagnose arterial dissection through
demonstration of an intramural hematoma and narrowed
lumen (8), the diagnosis has classically required artenography, coupled with a compatible clinical picture (2). The
most common angiographic findings include irregular arterial
narrowing (due to subintimal hemorrhage), which if severe
and extensive, results in the “string sign.” The dissection
usually begins just distal to the internal carotid origin, where
an intimal flap may be seen. A tapered occlusion is not
uncommon. Arterial dilation (pseudoaneurysm) may also be
seen, likely following subadventitial bleeding (2).
Neurologic sequelae of ICA dissections are now
believed to be predominantly due to thromboembolic events,
rather than flow limitation alone. Patients with documented
ICA dissection should probably be given anticoagulation
therapy to prevent cerebral embolization (2). Whether this
therapy can help facilitate recanalization remains unclear.
Patients who continue to have symptoms despite anticoagulation therapy will undoubtedly need surgical intervention,
which may include resection with insertion of a graft.
Resolution of the angiographic findings has been noted from
3 weeks to 12 months later, but this is not universal (9-12).
A good prognosis with a complete recovery has been
reported to occur in 85% of patients with spontaneous ICA
dissection. Bogousslavsky et a1 reported a good prognosis in
those who had evidence of early recanalization of the carotid
artery, and only transient neurologic symptoms or a small
cerebral infarct (3). A poor outcome was associated with
persisting ICA occlusion, larger cerebral infarcts, decreased
consciousness on admission, and evidence of distal cerebral
Rosalia M. Lomeo, MD
Richard M. Silver, MD
Medical University of South Carolina
Charleston, SC
Michael Brothers, MD
Duke University Medical Center
Durham, NC
1. Mokri B, Sundt TM Jr, Houser OW, Piepgras DG: Spontaneous
dissection of cervical internal carotid artery. Ann Neurol 19:
126-138, 1986
2. Hart RG, Easton JD: Dissections of cervical and cerebral
arteries. Neurol Clin 1:155-182, 1983
3. Bogousslavsky J, Despland P-A, Regli F: Spontaneous carotid
dissection with acute stroke. Arch Neurol 44:137-140, 1987
4. Francis KR, Williams DP, Troost BT: Facial numbness and
dysesthesia: new features of carotid artery dissection. Arch
Neurol44:345-346, 1987
5. Davies L: A case of vagal palsy due to dissecting aneurysm of
the carotid artery. Med J Aust 147:352-353, 1987
6. Lieschke GJ, Davis S, Tress BM, Ebeling P: Spontaneous
internal carotid artery dissection presenting as hypoglossal
nerve palsy. Stroke 19:1151-1155, 1988
Maitland CG, Black JL, Smith WA: Abducens nerve palsy due
to spontaneous dissection of the internal carotid artery. Arch
Neurol40:448-449, 1983
Norman D: Vascular disease: hemorrhage, Magnetic Resonance
Imaging of the Central Nervous System. First edition. Edited by
M Brant-Zawadzki, D Norman. New York, Raven Press, 1987
Sellier N , Chiras J , Benhamou M, Bones J: Spontaneous
dissection of the internal carotid artery. J Neuroradiol 1 0
243-259, 1983
Mas JL, Goeau C, Bousser MG, Chiras J, Verret JM, Touboul
PJ: Spontaneous dissecting aneurysms of the internal carotid
and vertebral arteries: two case reports. Stroke 16:125-129,
Bradac GB, Kaernbach A, Bolk-Weischedel D, Finck GA:
Spontaneous dissecting aneurysm of cervical cerebral arteries:
report of six cases and review of the literature. Neuroradiology
21:149-154, 1981
Alpert JN, Gerson LP, Hall RJ, Hallman GL: Reversible
angiopathy. Stroke 13:lOO-105, 1982
Infectious complications of cyclophosphamide
treatment for vasculitis
To the Editor:
Bradley et a1 recently reported their findings of
infectious complications of cyclophosphamide and glucocorticosteroid therapy for systemic necrotizing vasculitis and
isolated angiitis of the central nervous system (1). Ten of 15
patients treated experienced 17 episodes of infection. The
authors state that they have adhered to the guidelines that
we have previously recommended (2,3) for the treatment of
these disorders, but note a higher rate of infectious complications than has been our experience. As stated in the title of
this letter (the same as their report), they have attributed
most infectious complications to cyclophosphamide.
We are concerned that the authors have not adhered
to our guidelines for glucocorticosteroid therapy and, therefore, their conclusions may be inaccurate. None of their
glucocorticosteroid-treated patients received <3 months of
daily therapy, and their goal of every-other-day treatment
was eventually achieved in only 3 patients. In these 3
patients, every-other-day glucocorticosteroid treatment was
achieved after 3-7 months. The authors acknowledge that
this represents a longer period of daily glucocorticosteroid
treatment than we have recommended. In 8 of their 10
patients, the first episode of infection occurred after a mean
of 15 weeks of daily prednisone, at which time the mean
daily dosage was 43.1 mg. The findings in Table 3 of their
report reveal that of 17 episodes of infection, 12 occurred in
patients receiving at least 15 mg of prednisone/day, and in 9
instances, the daily dosage was at least 30 mg. Among the 3
patients receiving glucocorticosteroid therapy every other
day, only 1 infection occurred, compared with 15 infections
in the 11 patients receiving glucocorticosteroid therapy
each day.
Among the complications of this medical therapy, the
authors include 5 episodes of infection associated with open
lung biopsy, leptomeningeal biopsy, bowel resection necessitated by mesenteric infarction, and antibiotic therapy-related
Clostridium dificile enterocolitis. It is not possible to determine in such complex cases whether these infections might
also have occurred in the absence of any immunosuppressive
We remain concerned about any infectious complications of cyclophosphamide and glucocorticosteroid therapy. However, we believe that Bradley et al have observed
an unusually high incidence of such problems because they
did not adhere to our guidelines for reduction of glucocorticosteroid therapy, and they included 5 sequential complications of intestinal infarction and surgery in 1 patient. The
title of their report implicates cyclophosphamide as the
principal cause of infection. It would appear from their data
that a much stronger case could be made for the role of
glucocorticosteroid therapy.
Gary S. Hoffman, MD
Randi Y. Leavitt, MD, PhD
Anthony S. Fauci, MD
National Institute of Allergy
and Infectious Diseases
National Institutes of Health
Bethesda. MD
Bradley JD, Brandt KD, Katz BP: Infectious complications of
cyclophosphamide treatment for vasculitis. Arthritis Rheum 32:
45-53, 1989
Fauci AS, Haynes BF, Katz P: The spectrum of vasculitis:
clinical, pathological, immunological and therapeutic considerations. Ann Intern Med 89:660-676, 1978
Fauci AS, Haynes BF, Katz P, Wolff SM: Wegener’s granulomatosis: prospective clinical and therapeutic experience with 85
patients for 21 years. Ann Intern Med 98:76-85, 1983
To the Editor:
Hoffman et a1 correctly identified several important
features of our series of patients: 1) many infections occurred as complications of the underlying vasculitis (e.g.,
bowel infarction) or of procedures performed (e.g., placement of an indwelling catheter, thoracotomy); 2) the mode of
corticosteroid therapy (every other day versus daily) appeared to be related to the incidence of infection; and 3) the
duration of corticosteroid therapy, and particularly, daily
corticosteriod therapy, was longer than that previously
recommended (Cupps TR, Fauci AS: The Vasculitides.
Philadelphia, WB Saunders, 1981).
While we could not determine a causal relationship
with infection for either corticosteroid or cyclophosphamide
therapy, in 6 of 10 patients in our series who became
infected, infection occurred within 4 weeks of the initiation
of cyclophosphamide therapy. Only 2 of 10 developed an
infection within the first month of corticosteroid therapy.
While the average daily corticosteroid dosage at the onset of
the first infection was >40 mg, it was consistent with the
guidelines promulgated by Cupps and Fauci for the administration of concomitant corticosteroids during the first
month of cyclophosphamide therapy. As stated in our report, infection did not correlate with the dosage or duration
of corticosteroid therapy, but seemed more closely associated with the initiation of cyclophosphamide therapy.
We agree with Hoffman et al that in the complicated
cases we reported, it is difficult to determine the cause(s) of
the infections observed. Our report explored a number of
probable factors in addition to those mentioned herein. It
would be as much an oversimplification to attribute these
infections entirely to the corticosteroid component as it
would be to single out the cyclophosphamide component of
the therapeutic regimen.
John D. Bradley, MD
Kenneth D. Brandt, MD
Barry P. Katz, MD
Indiana University School of Medicine
Indianapolis, IN
Effect of temperature and humidity on daily pain
score in a patient with rheumatoid arthritis
To the Editor:
In studying the possible effects of weather on pain in
rheumatoid arthritis (RA), the problem arises that pain
cannot be measured. It can only be scored subjectively by
the RA patients themselves, as has been done in several
studies (1-3). Since January 1983, I have been quantifying
the RA pain of myself, a 42-year-old man, with classic,
seropositive RA, defined according to the criteria of the
American Rheumatism Association (4), who underwent joint
surgery in 1985, 1986, and 1988 (Figure 1). In order to
increase the reliability of my pain score, the scoring method
was standardized in 3 specific ways. First, scoring was done
in the morning, immediately after arising. Second, because
joint pain depends strongly upon the positioning and movements of the joints, the pain score was determined during the
execution of a standardized exercise program. Third, pain
was scored for each separate joint or group of joints (e.g.,
right hand) on a scale of &9, where 0 = no pain and 9 = very
severe pain. From January 1983 through June 1988, 21 RA
pain scores were collected daily for the hands, wrists,
elbows, shoulders, jaw, hips, knees, ankles, feet, and the
neck, back, and costosternal joints.
During scoring, I was not aware of the weather
parameters. The 24-hour means of temperature and vapor
pressure were taken from the monthly reports (5) of a local
weather station (Groningen Airport, Groningen, The Netherlands) located 3 km from my home. For time spent abroad,
data from the local weather station were substituted.
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treatment, vasculitis, complications, infectious, cyclophosphamide
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