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Rapid-onset colchicine myoneuropathy.

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1535
CONCISE COMMUNICATIONS
Rapid-onset colchicine myoneuropathy
Several recent reports have demonstrated that some
patients taking colchicine over a prolonged period of time
will develop a subacute, often severe, myopathy in conjunction with a relatively mild polyneuropathy (1-3). Chronic
renal failure is the only known risk factor for this syndrome,
which typically becomes manifest several months or years
after colchicine treatment has been started and resolves
within several weeks of its discontinuation (3,4). We describe a patient in whom the clinical syndrome developed
within 1-2 weeks of beginning colchicine. Our patient displayed weakness of cranial musculature, a feature not previously reported in colchicine myoneuropathy.
The patient, a 71-year-old woman with a history of
gout, adult-onset diabetes, mild chronic renal insufficiency
(creatinine 1.2-2.1 mgldl), hypertension, and coronary artery disease, was admitted to the hospital because of the
subacute onset of diarrhea and generalized weakness. She
had taken colchicine intermittently in the past for flares of
gout, but none had been taken during the preceding year.
Two weeks before admission, she sought medical care for
knee and ankle pain and was started on colchicine at a
dosage of 0.6 mg 3 times a day. One week later she noted
diarrhea, and generalized muscle weakness caused difficulty
walking.
She denied alcohol use, prior weakness, diplopia,
dysarthria, dysphagia, sensory abnormalities, neck or back
pain, muscle pain or tenderness, or change in the color of her
urine. In addition to colchicine, she regularly took furosemide, potassium chloride, enteric-coated aspirin, isosorbide dinitrate, cimetidine, NPH insulin, verapamil, and
diltiazem.
On examination, she had no orthostatic hypotension
or rash. She had bilateral ptosis and symmetric bifacial
weakness, with weak eye closure and a transverse smile.
Power in her neck flexors was 4+/5. She had symmetric,
proximal greater than distal, weakness in all extremities,
with power in the proximal arms 415, distal arms 4+/5,
proximal legs 315, and distal legs 4 4 + / 5 . She was too weak
to stand up. There were no fasciculations or muscle atrophy,
and muscle stretch reflexes were absent. Vibratory sensation
was decreased to the ankles and cold sensation to the knees.
Laboratory results included normal findings on complete blood count and serum electrolyte studies, blood urea
nitrogen 25 mgldl, creatinine 2.0 mgldl, erythrocyte sedimentation rate 79 mdhour, alanine aminotransferase 28 IU/liter,
aspartate aminotransferase 74 IUAiter, serum alkaline phosphatase 137 IUAiter, and total bilirubin 0.4 mgldl. Results of
thyroid function tests and serum protein electrophoresis
were normal, and tests for rheumatoid factor, antinuclear
antibodies, and Lyme titer were negative. The creatine
phosphokinase (CPK) level was 1,121 IUAiter, with 0% MB
fraction. A total eosinophil count was 280 IUAiter, and stool
examination for ova and parasites was unrevealing.
Spinal fluid was acellular, with a protein value of 58
Arthritis and Rheumatism, Vol. 35, No. 12 (December 1992)
mgldl. Electrophysiologic testing demonstrated normal median, peroneal, and tibial nerve conduction velocities and
F-wave latencies, with mildly diminished sensory and compound muscle action potential amplitudes. Needle examination of the quadriceps showed increased insertional activity,
with very frequent fibrillations and complex repetitive discharges. She did not tolerate the needle examination, and
motor unit action potentials and interference pattern could
not be assessed. The results were interpreted as consistent
with myopathy and mild axonal neuropathy.
Colchicine was discontinued, and the patient’s weakness markedly improved over the next several days, and she
was able to stand and take a few steps. Her biceps reflex
became elicitable, and her CPK level decreased to normal
over 1 week. Within a few weeks, her muscle power was full,
and she has had no recurrence over the past year.
The diagnosis of colchicine myopathy can be made
clinically, although in difficult cases, the finding of distinctive lysosomal, vacuolar changes without prominent necrosis on muscle biopsy is useful in differentiating the effects of
colchicine from inflammatory myopathies such as polymyositis (3). In this patient with preexisting renal insufficiency,
the typical clinical picture and the response to stopping
colchicine strongly support the diagnosis of ‘‘colchicine
myoneuropathy.” The normal nerve conduction velocities,
the CPK elevation, and the absence of spinal fluid protein
elevation are evidence against acute inflammatory demyelinating polyneuropathy. Ptosis and bifacial palsy have not
been previously reported in colchicine myoneuropathy , and
this finding may help distinguish this entity from polymyositis, in which facial weakness is rarely seen (5).
Another distinctly unusual feature of our patient was
the onset of symptoms within 1-2 weeks of starting colchicine. In our review of previous reports, only one other
case began within 6 months of starting colchicine (6). That
woman, who had autoimmune thrombocytopenic purpura
and chronic alcohol-related liver disease, had received vinca
alkaloids until 6 months earlier and prednisone until 3 weeks
earlier; myoneuropathy developed 16 days after starting
colchicine. The authors hypothesized that her chronic liver
disease and an inhibition of the microsomal enzyme system
by tolbutamide predisposed the patient to colchicine myoneuropathy despite normal renal function. Like colchicine,
vincristine is a microtubule inhibitor that produces myoneuropathy and, along with prednisone, may also have been a
contributing factor (7).
In our patient, inhibition of the cytochrome P450
system by cimetidine and calcium-channel blockers may
have contributed to the unusually rapid onset of her syndrome. In patients with chronic renal failure, particularly
those who are taking other hepatically transformed drugs,
colchicine should be used with great caution if at all.
David Schiff, MD
Frank W. Drislane, MD
Beth Israel Hospital and
Harvard Medical School
Boston, M A
1536
1 . Kontos HA: Myopathy associated with chronic colchicine toxicity. N Engl J Med 266:38-39, 1962
2. Riggs JE, Schochet SS, Gutmann L, Crosby TW, DiBartolomeo
AG: Chronic human colchicine neuropathy and myopathy. Arch
Neurol43521-523, 1986
3. Kuncl RW, Duncan GJ, Watson D, Alderson K, Rogawski MA,
Peper M: Colchicine myopathy and neuropathy. N Engl J Med
3 16:1562-1 568, 1987
4. Wallace SL, Singer JZ, Duncan GJ, Wigley FM, Kuncl RW:
Renal function predicts colchicine toxicity: guidelines for the
prophylactic use of colchicine in gout. J Rheumatol 18:264-269,
1991
5. Brooke MH: A Clinician’s View of Neuromuscular Diseases.
Second edition. Baltimore, Williams and Wilkins, 1986
6. Besana C, Comi G , Baldini V, Ciboddo G , Bianchi R: Colchicine
myoneuropathy. Lancet 11: 1271-1272, 1987
7. Bradley WG, Lassman LP, Pearce GW, Walton JN: The neuromyopathy of vincristine in man: clinical, electrophysiological,
and pathological studies. J Neurol Sci 10:107-131, 1970
Nitroprusside in systemic lupus erythematosus
vasospasm
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
hours.
The patient was given parenteral steroids, and was
CONCISE COMMUNICATIONS
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
1. Rodnan G, Schumacher HR, editors: Primer on the Rheumatic
Diseases. Ninth edition. Atlanta, Arthritis Foundation, 1983
2. Lapper RW, Barron KW, Faber JE, Brody MJ: Selective antag-
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