Infectious complications complications of cyclophosphamide treatment for vasculitis.код для вставкиСкачать
LETTERS 1626 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 difficult. 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 emboli. 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 7. 8. 9. 10. 11. 12. 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, 1985 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. LETTERS 1627 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 medications. 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 Reply 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.