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Nitroprusside in systemic lupus erythematosus vasospasm.

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Nitroprusside in systemic lupus erythematosus
Raynaud’s phenomenon was described in 1862 as
“local asphyxia and symmetrical gangrene of the extremities,” and has been postulated to be due to increased serum
viscosity or vasospasm. The vasospasm has been proposed
to be secondary to either humoral mediation by catecholamine or to neurogenic a-adrenergic medication. I report a case of Raynaud’s phenomenon associated with
systemic lupus erythematosus (SLE) that was refractory to
conventional therapy.
The patient, a 33-year-old black woman with a 5-year
history of SLE, complicated by cerebritis, myositis, and
Raynaud’s phenomenon, presented with a 2-week history of
numbness, tingling, and swelling in both hands. She denied
having fever, chills, rash, headache, or exposure to cold, or
noncompliance with her medication regimen (ibuprofen and
prednisone 5 mg/day). She had similar symptoms with previous exacerbations of Raynaud’s phenomenon, however.
On admission, the patient was normotensive and
afebrile. Head, eyes, ears, nose, throat, and pulmonary
examination findings were normal, and cardiac examination
revealed a soft IINI systolic murmur. Upper extremity
examination was notable for acrocyanotic, cold fingers and
early gangrenous changes on the right third finger. The
remainder of her physical and neurologic examination findings were within normal limits. Admission laboratory data
were normal.
Her erythrocyte sedimentation rate was 28 mdhour,
antinuclear antibody was positive at 1:5,120 in a speckled
pattern, anti-double-stranded DNA was negative, as were
cryoglobulins and anticardiolipin antibodies. Total hemolytic complement and C4 showed normal values; however,
C3 was decreased (61 mg/dl, normal 83-177). Creatinine
clearance was 86 mllminute, with 2.1 gm of protein in 24
The patient was given parenteral steroids, and was
subsequently tried on courses of diltiazem, nifedipine, prazosin, and pentoxifylline, without relief. A vascular surgery
consultant recommended, and unsuccessfully performed, a
right stellate ganglion block. A Bier block was considered;
however, parenteral reserpine is not available in the United
States. Arteriography of the right upper extremity demonstrated a vasospastic component, with increased distal flow
after tolazoline HCI (Priscoline; Ciba, Edison, NJ), a vasodilating agent.
Despite these measures, the patient had developed
necrosis of the right third distal phalanx, and the other
fingers were increasingly cyanotic. The patient was transferred to the medical intensive care unit and given parenteral
sodium nitroprusside (1 p&g/minute) for approximately 48
hours; there was no hypotension or other complication.
Followup Doppler studies demonstrated increased distal
flow, and the patient improved clinically. One month after
discharge from the hospital, followup revealed total resolution of all changes except a small region of cyanosis on the
right third distal phalanx, which by 4 months, had resolved.
Raynaud’s phenomenon has been reported to occur
in at least 25% of patients with SLE. In addition to therapy
directed at other manifestations of SLE, therapy for digital
vasospasm includes avoidance of triggering behaviors, such
as cold exposure and smoking, as well as certain medications, including beta blockers, ergot preparations, estrogens,
and sympathomimetic preparations (1). Treatment includes
sympatholytic agents, a-adrenergic blockers, beta-2 stimulants, and serotonin H,-receptor blockers. Vasodilators,
including calcium channel blockers (2), griseofulvin, nicotinic acid, angiotensin-converting enzyme inhibitors, and
topical nitrates (3), have been used. F’rostacyclin analogs and
anabolic steroids have been used to decrease serum viscosity (43). Other less successful therapies include pentoxifylline and triiodothyronine. Surgical intervention with sympathectomy or ganglion block is considered a less desirable
alternative (6).
Sodium nitroprusside (7-9) is an arteriolar and venous smooth-muscle vasodilator most commonly used in
hypertensive emergencies. There are no reported cases of its
use clinically for peripheral vasospasm. Low-dosage intraarterial nitroprusside has been effective in experimentally
induced humoral vasoconstriction and relatively ineffective
in neurogenic a-mediated vasoconstriction (2). These results
are similar to those found with calcium channel blocking
agents in humoral vasoconstriction.
Although intravenous nitroprusside is not a first-line
drug for the treatment of vasospastic disease, given its
proven experimental and clinical effectiveness, it should be
considered an alternative agent for refractory disease.
Lawrence I. Kaplan, MD
Cooper Hospital-Robert Wood Johnson
Medical School
Camden, NJ
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ment of finger ischemia with Bier block reserpine. Surg Gynecol
Obstet 154:39-43, 1982
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nitroprusside treatment of ergotarnine induced peripheral ischemia. JAMA 227:308-309, 1974
8. Coffman J, Cohen R: Intra-arterial vasodilator agents to reverse
human finger vasoconstriction. Clin Pharmacol Ther 41 574-578,
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Pharmacological Basis of Therapeutics. Sixth edition. New
York, Macmillan, 1980
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lupus, nitroprusside, systemic, erythematosus, vasospasm
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