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needed to clarify if an association exists. Patients taking
natalizumab should be warned regarding the potential risk of
melanoma, and physicians should remain vigilant in screening
for melanoma, especially in patients with a history of atypical
moles.
Ocrelizumab
Ocrelizumab (Ocrevus®, Genentech, Inc, San Francisco, CA,
USA) is a humanized monoclonal antibody targeting CD20
antigen on B cells that is FDA approved for the treatment of
relapsing and primary progressive MS.
127,128
There has been
one report of biopsy-proven psoriasiform dermatitis in an
elderly woman 3.5 months after starting ocrelizumab. This
was determined to be a “probable” drug reaction by the
authors.
129
Rituximab
Rituximab (Rituxan®, Biogen-IDEC/Genentech, San
Francisco, CA, USA) is a chimeric mouse/human anti-CD20
antibody that results in selective reduction of mature B
lymphocytes and has been shown to be effective in MS
treatment.
130
In a nonrandomized, single-arm study of
rituximab for the treatment of primary cutaneous B cell
lymphoma, 356 patients (37%) developed infusion-associated
reactions, including itching, rash, and urticaria.
131
Mucocutaneous reactions, including fatal cases of StevensJohnson syndrome or toxic epidermal necrolysis, are less
commonly reported complications after treatment with
rituximab. Other reactions include paraneoplastic pemphigus,
lichenoid dermatitis, and vesiculobullous dermatitis.
131
The
onset of these reactions varies but can be seen as soon as the
first infusion. In one case, toxic epidermal necrolysis
developed 12 hours post rituximab infusion and demonstrated
a successful response to etanercept.
132
In another case, a 36-
year-old man developed mucositis and fevers after the first
two infusions and maculopapular rash with severe urogenital
ulceration after the third.
133
However, this case was later
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reported to be more likely due to a paraneoplastic pemphigus
and not consistent with Stevens-Johnson syndrome given the
chronic nature of the disease.
134
Another report described a
fatal case of Stevens-Johnson syndrome/toxic epidermal
necrolysis overlap in a patient receiving his first cycle of
allopurinol, rituximab, and bendamustine treatment for nonHodgkin B cell lymphoma.
135
The combination of rituximab
and bendamustine in contributing to fatal toxic epidermal
necrolysis has been previously reported.
136
In addition, seven
cases of iatrogenic Kaposi sarcoma in human
immunodeficiency virus–negative patients have been reported
with the use of rituximab.
137-140
The authors suggest screening
for human herpesvirus-8 in high-risk patients before initiating
rituximab. Similarly, a few cases of cutaneous vasculitis as
well as serum sickness reactions have been reported.
141-144
Oral Therapies
Teriflunomide
Teriflunomide (Aubagio®, Genzyme Corporation) is a oncedaily oral immunomodulator for the treatment of relapsing
remitting MS. Teriflunomide inhibits dihydro-orotate
dehydrogenase, a key enzyme in de novo pyrimidine synthesis
required for lymphocyte proliferation.
145
Teriflunomide is the
active metabolite of leflunomide, which was approved for the
treatment of rheumatoid arthritis in 1998.
146
The primary
dermatologic side effect associated with teriflunomide is hair
thinning. Pooled safety and tolerability data from four
placebo-controlled studies and extension studies with
treatment duration exceeding 12 years and a cumulative
exposure to teriflunomide exceeding 6800 patient-years
reported dose-dependent hair thinning.
147
Hair thinning,
defined as decreased hair density or hair loss, occurred more
frequently in the 14-mg cohort (13.9%) compared with the 7mg (10.0%) and placebo (5.1%) groups. Sixteen patients
discontinued treatment because of hair thinning. Onset was
during the first 6 months, and most cases improved during
treatment continuation.
147
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Fingolimod
Fingolimod (Gilenya, Novartis Pharma AG, Basel,
Switzerland) is an immunomodulatory medication approved
by the FDA in 2010 for the treatment of MS.
148
Fingolimod is
a sphingosine-1-phosphate receptor modulator that causes
internalization of the receptor. As a result, immune cells are
unable to receive signals to leave the lymphoid tissue and
enter the central nervous system.
149,150
Clinical trials support an increased incidence of cutaneous
malignancy in patients taking fingolimod compared with
placebo.
151,152
A phase 3 clinical trial of fingolimod reported
an increased risk of basal cell carcinoma in 14 (4%) patients
compared with 9 (2%) patients in the placebo cohort.
Squamous cell carcinoma occurred in 6 (2%) compared with 1
(<1%) in the placebo group, whereas melanoma occurred in 1
(<1%) versus 0 in the placebo group.
151
Another phase 3
clinical trial reported basal cell carcinoma in 6 (2%) patients in
the 1.25-mg cohort and 10 (3%) in the 0.5-mg cohort
compared with 2 (1%) in the placebo group.
152
In addition,
there have been multiple reports of Merkel cell carcinoma, a
rare neuroendocrine skin cancer, with fingolimod therapy.
153-
156
Melanoma was reported in some of the safety and efficacy
trials for fingolimod, with the majority of cases determined to
be melanoma in situ.
157-159
In a phase 3 trial, three cases of
melanoma in situ occurred in 429 patients treated with 0.5 mg
daily, whereas none occurred in 420 patients treated with
1.25 mg daily.
157
It has since been postulated that the
increased incidence of melanoma in situ is possibly due to the
increased monitoring for adverse events during study periods.
160
In another 24-month placebo-controlled clinical trial, one
melanoma occurred in 429 patients treated with 1.25 mg daily,
no melanomas in 425 patients treated with 0.5 mg daily, and 1
melanoma in 418 patients in the placebo cohort.
158
Furthermore, a 3-year phase 2 study showed no difference in
melanoma incidence between the fingolimod and placebo
cohorts.
159
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A recent case series reported five cases of superficial
spreading melanoma (Breslow depth 0.5-2.3 mm) in 1000
patients taking fingolimod after 12 to 32 months of treatment
in the Netherlands.
160
The authors hypothesized that the
decreased number of circulating lymphocytes leads to a
decrease in immune surveillance of melanoma. Additional
reports include melanoma arising in a preexisting nevus in a
middle-aged Caucasian woman (Breslow depth 0.9 mm)
57 months after starting fingolimod 1.25 mg daily as well as
another middle-aged Caucasian woman (Breslow depth
1.125 mm) after taking fingolimod 0.5 mg for 61 months.
161,162
Another case of melanoma arising in a long-standing nevus
was reported after 2 months of fingolimod 0.5 mg daily.
Histopathology confirmed superficial spreading melanoma
(Breslow depth 1.5 mm).
163
In contrast, there are in vitro studies suggesting a protective
role for fingolimod in the development of melanoma.
164,165
In
general, patients should be informed regarding a potentially
higher risk for skin cancers with fingolimod. Patients should
have routine full-body skin examinations with a dermatologist
to monitor for skin cancers, especially if the duration of
therapy is greater than 6 months.
162
Drug Interactions and Contraindications
in Patients With MS: What to Know When
Treating Skin Conditions
Psoriasis
A Canadian population-based study in 2008 reported a 54%
higher risk of incident psoriasis in the population with MS.
166
More recent Danish and United States–based studies also
support a significant association between psoriasis and MS.
167,168
Although the exact mechanism has not been elucidated,
there appears to be similar pathophysiology as well as
overlapping genetic risk variants between MS and psoriasis.
167
This argument is challenged by other studies that do not
support such an association.
169-172
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In managing patients with MS and concomitant psoriasis, it is
important to be aware of specific drug interactions and
contraindications. It is well known that IFN-β can exacerbate
or induce de novo psoriasis.
13,71,74,173,174
As discussed
previously, worsening of psoriasis has also been reported in
patients taking natalizumab.
114-116
In addition, there are reports
of patients developing psoriatic arthritis while on IFN-β
therapy.
73,117
TNF-α inhibitors can worsen demyelination and
are therefore contraindicated in demyelinating disorders,
including MS and Guillain-Barré syndrome. Demyelinating
disorders such as optic neuritis and MS have been reported
with the use of etanercept, infliximab, adalimumab, and
golimumab, with an incidence of 0.02% to 0.2%.
175-182
For any
patient taking a TNF-α inhibitor, regular neurological
examinations are recommended.
183
Traditional agents used to treat psoriasis, including
methotrexate and cyclosporine, have shown benefit in MS.
184-
188
Newer biologic agents have been evaluated for the
treatment of MS. In a phase 2 clinical trial of ustekinumab, a
neutralizing monoclonal antibody against the IL-12/23 p40
chains, there was no demonstrated benefit or harm in the
treatment of relapsing remitting MS.
189
Although there is no
clear benefit for MS, ustekinumab has been safely used to treat
psoriasis in patients with MS.
190
Secukinumab, a monoclonal
antibody that inhibits IL-17A, has been shown to significantly
reduce the cumulative number of new enhancing T1 magnetic
resonance imaging lesions compared with placebo.
Secukinumab was well tolerated in patients with MS with no
reports of worsening disease.
191
Data are limited for
apremilast and IL-23 inhibitors; however, there are no reports
of MS worsening with these drugs.
183
Skin Cancer
Screening for skin cancer in patients with MS requires an
evolving partnership between neurologists and dermatologists.
Before the era of disease-modifying therapies, patients with
MS had a lower risk of developing both melanoma and
nonmelanoma skin cancer.
192,193
However, with the use of
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immunosuppressive medications, the risk of cutaneous
malignancy has been shown to be increased.
193
More
specifically, alemtuzumab and fingolimod require a routine
skin examination by a dermatologist at the start of treatment
and yearly thereafter to monitor for skin cancer.
107,156
Although the association between melanoma and natalizumab
is controversial, yearly skin cancer screening is recommended.
Cosmetic Procedures
Although there are no specific MS-associated medical
contraindications to most cosmetic procedures, caution should
be exercised and individual medical history should be
reviewed for each patient. For example, when injecting dermal
fillers in patients with MS, physicians should ensure that
patients have normal vascular supply to ensure appropriate
wound healing in the area of desired treatment.
194
In patients
with MS taking immunosuppressive medications, infection
awareness and prevention is important for cosmetic
procedures, as well as manicures, pedicures, and tattoos.
Furthermore, patients with MS may require screening for loss
of sensation to the affected areas before undergoing laser
treatments.
195
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