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Drug-induced peripheral neuropathy in a patient with psoriatic arthritis.

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22 1
BRIEF REPORT
DRUG-INDUCED PERIPHERAL NEUROPATHY IN A PATIENT WITH
PSORIATIC ARTHRITIS
RALPH J. ROTHENBERG and ROBERT L. SUFIT
A patient with psoriatic arthritis developed a
peripheral neuropathy while taking hydroxychloroquine
and naproxen. Although it was initially suspected that
hydroxychloroquine was responsible for the neuropathy, subsequent rechallenge with naproxen demonstrated that clinical and electrophysiologic findings were
related to routine pharmacologic doses of naproxen.
Peripheral neuropathy has been noted to occur
in patients with rheumatoid arthritis (RA) or systemic
lupus erythematosus (SLE) (1,2). It can sometimes be
difficult to distinguish whether a peripheral neuropathy
in this setting is due to vasculitis or to a drug side
effect. In particular, antimalarial agents have been
reported to induce neuromyopathies (3-7). Because
these drugs, as well as nonsteroidal antiinflammatory
agents (NSAIDs), are commonly used in RA or SLE,
the ability to distinguish a drug-induced peripheral
neuropathy from that due to the underlying disease
can be very difficult. This is especially true when
fluctuations in neurologic findings are due to changes
in disease activity. In contrast, psoriatic arthritis might
be associated with entrapment neuropathies (8), but
From the Rheumatology Section and the Neurology Section, William S. Middleton Memorial Veterans Hospital and the
University of Wisconsin Clinical Science Center, Madison.
Supported by the Medical Research Service of the William
S. Middleton Memorial Veterans Hospital and by the Department of
Medicine and the Department of Neurology, University of Wisconsin, Madison.
Ralph J. Rothenberg, MD: Rheumatology Section; Robert
L. Sufit, MD: Neurology Section.
Address reprint requests to Ralph J. Rothenberg, MD,
Medical Service Room B5112C, William S. Middleton Memorial
Veterans Hospital, 2500 Overlook Terrace, Madison, WI 53705.
Submitted for publication April 14, 1986; accepted in revised form August 5 , 1986.
Arthritis and Rheumatism, Vol. 30, No. 2 (February 1987)
we are not aware of any generally accepted reports of
peripheral neuropathies associated directly with psoriatic arthritis. We describe a patient with psoriatic
arthritis, who developed a peripheral neuropathy
while taking hydroxychloroquine and naproxen. We
identified naproxen, rather than hydroxychloroquine,
as the cause of her neuropathy because of an exacerbation of her findings upon rechallenge with this drug.
CASE REPORT
In August 1982, the patient, a 43-year-old white
woman with psoriasis, a family history of psoriasis,
and a protracted history of foot, heel, and ankle pain,
presented with low back pain, 4 hours of morning
stiffness, and swelling of multiple small joints of the
hand. Tenderness was noted in 6 distal interphalangeal
joints, the left third proximal interphalangeal (PIP)
joint, both second metacarpophalangeal (MCP) joints,
and the right first MCP joint. The right sacroiliac joint
and the metatarsophalangeal (MTP) joints were also
tender. Diffuse nail pitting and onycholysis were
present. Multiple patches of psoriasis (1-2 cm) were
present on the scalp, especially in the area of the
occiput and on the forehead near the hairline. The
rheumatoid factor test was negative and the Wintrobe
erythrocyte sedimentation rate (ESR) was 40 mmhour.
A diagnosis of psoriatic arthritis was made.
Hydrocortisone (1% cream) controlled, but did not
eradicate, the psoriatic lesions. Previous therapeutic
trials with enteric-coated aspirin (325 mg, 12
tabletdday) and later, ibuprofen (1,600 mg/day) did not
relieve her symptoms. Naproxen (250 mg, 2-3 times a
day) relieved some arthritic symptoms. Treatment
BRIEF REPORTS
222
Table 1. Nerve conduction studies during hydroxychloroquine and naproxen therapy (I) and 5
months after its discontinuation (II)*
Velocity (ms)
Nerve tested
Right
Median sensory
Ulnar sensory
Median motor
Ulnar motor
Below elbow
Across elbow
Transcarpal
Sural
Left
Median sensory
Ulnar sensory
Median motor
Ulnar motor
Below elbow
Across elbow
Transcarpal
Sural
I
I1
59
62.5
52
61.8
63.5
54.5
60
61
58
-
Distal latency
(ms)
Amplitude (mV)
I
I1
1
I1
3.3
2.6
4.0
3.2
2.5
3.8
0.030
0.035
414
0.030
0.030
717
2.9
2.35t
3.4
2.7
2.1
3.3
10110
10
0.060
0.005t
616
0.040
0.020
-
-
62
61
51.5
59.5
59.9
53.4
3.1
2.4
3.2
2.9
2.5
2.9
0.030
0.030
717
0.040
0.030
919
62
42t
59.4
55.2
2.2
-
-
-
-
2.0
3.3
2.3
2.0
3.4
919
9
0.075
0.007t
6
717
0.040
0.020
-
* Skin temperature was above 30°C for all extremities evaluated
t Abnormal result
with hydroxychloroquine (200 mg twice daily: 5.2
mg/kg)l was begun. After 2 months, most of her symptoms of arthritis resolved. The morning stiffness had
disappeared, and minimal synovitis that involved
small joints of her hands or feet was only occasionally
detected.
In September 1984, the patient reported a mild
exacerbation of her symptoms. Psoriatic plaques had
enlarged, and the patient again experienced stiffness
for 1-:! hours in the morning. Joint examination revealed minimal synovitis in 1 PIP joint of the finger and
some IMTP joints. There was mild tenderness at the
insertion of the left Achilles tendon. The patient
complained of bilateral carpal tunnel symptoms. No
wrist synovitis was noted. Tinel’s sign was absent, but
Phalen’s sign was present bilaterally.
By March 1984, the patient noted chronic
numbness in her hands, especially when driving a car
and after sleep. She began to drop objects and complainedl that her hands were cold and had a bluish
tinge. Despite subjective complaints of decreased sensation below the mid-forearm and mid-thigh, a detailed
neurologic examination revealed normal responses for
light touch, vibration, 2-point discrimination, and position sense. Deep tendon reflexes and muscle strength
were nlormal. Only minimal synovitis was present;
however, both Tinel’s sign and Phalen’s sign were
present bilaterally. A nerve conduction study was
performed (Table 1). Results of electromyographic
studies were normal. The prolonged right median
transcarpal conduction velocity was either consistent
with a carpal tunnel syndrome or reflected the sensory
neuropathy. Similarly, slowing of the left ulnar nerve
across the elbow reflected entrapment of the nerve or
constituted part of the generalized toxic neuropathy .
Tests were performed to determine the cause of
the peripheral neuropathy ; the hematocrit was 40
ml/dl, the mean cell volume was 87 fl/red blood cell,
and ESR was 17 mm/hour. Results of tests for oral
glucose tolerance, thyroid function, and complement
levels, and of a VDRL test were normal. The antinuclear antibody titer was 1:40 (clinically not significant)
and the rheumatoid factor test was negative. Results of
visual field testing while the patient was taking hydroxychloroquine were normal. With the strong suspicion that hydroxychloroquine was responsible for
causing these neurologic symptoms, hydroxychloroquine and naproxen were discontinued in March 1985.
After 2 weeks, the patient reported that symptoms of
numbness in her hands had improved by 50%, and her
hands no longer became numb when driving.
Symptoms continued to improve over the following 4 months. Nerve conduction studies were
repeated in October 1985 (Table 1). Sural nerve amplitudes had improved threefold, and right transcarpal
distal latency was reduced. The left ulnar cubital
223
BRIEF REPORTS
Table 2. Selected nerve conduction studies upon rechallenge with naproxen (I) and 5 weeks after
rechallenge (II)*
Velocity (ms)
Nerve tested
Right
Transcarpal
Sural
Left
Transcarpal
Ulnar sensory
Ulnar motor
Below elbow
Across elbow
Sural
I
I1
-
-
65.5
65
61.3
433
65.7
50.0
Distal latency
(ms)
Amplitude (mV)
I
I1
I
I1
2.1
3.4
2.0
3.612.8
0.084
0.013’i
0.076
0.015
1.9
2.4
2.0
2.4
0.080
0.037
0.114
0.046
2.4
5.5
3.4
2.4
5.9
3.512.7
9110.2
9.619
0.010t
9.319.3
9.219.3
0.016
* Skin temperature was above 30°C for all extremities evaluated.
t Abnormal results.
tunnel velocity had returned to normal. Temporally
related to the discontinuation of hydroxycbloroquine
and naproxen, this patient’s psoriatic arthritis recurred. Three hours of morning stiffness were present.
Small effusions were detected in both knees. Mild-tomoderate swelling and tenderness of the right thumb
interphalangeal joint, first MCP joint, and the left
subtalar joint were noted, as was tenderness of the
right sacroiliac joint. Arthralgias were present in multiple other small joints of both hands, but the wrists
and elbows were spared. Tolmetin sodium (400 mg, 4
times daily) failed to relieve her symptoms.
Because it was suspected that the antimalarial
drug was the cause of the peripheral neuropathy,
naproxen (250 mg, twice daily) was resumed in December 1985. Within 2-3 weeks, the patient again
noted increased numbness in the distal portion of her
legs and in her hands. A nerve conduction study was
repeated in January 1986 (Table 2). Once again, abnormalities in sural nerve function, as well as changes in
the left ulnar nerve function across the elbow, were
noted. Within 2 days of withdrawal of naproxen, her
symptoms began to resolve. Meclofenamate (100 mg, 3
times daily) partially controlled the synovitis and did
not cause symptoms of neuropathy. A nerve conduction study was again performed 5 weeks later and
again showed normalization of the previous changes.
Methotrexate was given to control this patient’s arthritis, but oral ulcers occurred on doses as low as 2.5 mg,
12 hours apart, for 2 doses each week.
Hydroxychloroquine (200 mg daily) was resumed, and no exacerbation of neuropathic symptoms
has occurred during the 3-month observation period.
Unfortunately, relief of the patient’s joint symptoms
while taking this dose of hydroxychloroquine has been
modest at best. She continues to note 3 hours of
morning stiffness and diffuse arthralgias. On examination, mild-to-moderate tenderness and swelling of several joints has been noted.
DISCUSSION
This study demonstrates that naproxen can
cause a reversible neuropathy in a susceptible patient.
In this case, the patient’s clinical history was confirmed by reversible decreases in sural nerve amplitudes, which are diagnostic of a peripheral neuropathy. Only 1 other report has noted this type of
complication from taking NSAIDs. In that report, 4
patients were taking indomethacin for various arthritic
conditions (9). In each case, a neuropathy which
regressed upon discontinuation of this drug was noted.
Like the current case, 2 of 4 patients first complained
of hand paresthesias. This is unusual for peripheral
neuropathies, in which lower extremity findings typically predominate; thus, the onset of upper extremity
paresthesias may be a clue suggesting a NSAIDinduced peripheral neuropathy. In view of the ability
of our patient to tolerate tolmetin sodium and
meclofenamate, it appears that the induction of a
peripheral neuropathy is not a generalized reaction to
all NSAIDs in a susceptible patient, but rather is due
to a specific drug in a sensitive patient. It may be
pertinent to note that naproxen is a proprionic acid
derivative, while tolmetin sodium and sodium
meclofenamate belong to different classes of NSAIDs.
In order to attribute all of our patient’s neurologic findings to the single diagnosis of a drug-induced
224
peripheral neuropathy , we propose that the evanescent nature of our patient’s entrapment symptoms and
electrodiagnostic findings can be attributed to the
“double crush” phenomenon. It is clear that an individual nerve is more susceptible to entrapment if a
generalized neuropathy exists (10). In our patient, the
electrophysiologic evidence of slowing across the elbow and across the wrist indicates an entrapment
neuropathy ; however, synovitis was never detected in
the right wrist or left elbow. Also, the patient’s symptoms and findings improved with discontinuation of
naproxen, even while synovitis worsened in her hands
and riight ankle because of the discontinuation of
hydroxychloroquine. We postulate that a subclinical
entrapment neuropathy existed in the wrist and elbow,
which was not in itself sufficient to cause even
electrophysiologic abnormalities. These findings became evident because of the generalized peripheral
neuropathy that was caused by naproxen.
We cannot exclude the possibility that fluid
retention, secondary to the use of naproxen, caused
the entrapment syndromes in the wrist or elbow, but
the palient did not experience a reversible weight gain
while on naproxen and did not complain of reversible
swelling or tightness in the affected areas. Even in the
very unlikely event that fluid retention did cause the
entrapment syndromes, this does not negate the clear
electrophysiologic evidence of a reversible peripheral
neuropathy based upon the sural nerve conduction
studies. The course of the sural nerve, where tested,
runs solely in the subcutaneous adipose tissue, so that
this nerve could not be affected by an entrapment
syndrome.
Hydroxychloroquine may also be responsible
for a peripheral neuropathy (3-7), although that did not
seem to be the case in our patient. The presence of a
peripheral neuropathy is uncommon with antimalarial
drugs, and apparently is extremely uncommon with
NSAIIIs; however, NSAIDs are used extensively in
RA and SLE, and peripheral neuropathies are ob-
BRIEF REPORTS
served in these groups of patients (1,2). While
neuropathies can be attributed to the underlying disease processes, one should suspect that peripheral
neuropathies, and especially those which have an
atypical distribution (upper extremities before lower
extremities) or those which appear to fluctuate over
time (such as when a patient is noncompliant with
medications), are secondary to changes in NSAID
usage by patients.
Acknowledgment. We thank Dr. Walter R. Sundstrom for critical review of our manuscript.
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