r e v ie w

Treatment of Refractory Psoriasis with Ustekinumab

in an HIV-Positive Patient: A Case Presentation and
Review of the Biologic Literature
Shira Wieder, B.A.,1 Ethan Routt, B.A.,2 Jacob Levitt, M.D.,3 Mark Lebwohl, M.D.3

ABSTRACT:

Here we describe a case of a 39-year-old male with HIV and a 20-year history of generalized plaque psoriasis and psoriatic arthritis.
The patient had been refractory to all treatments until initiating ustekinumab, the monoclonal antibody against IL-12/23. While using
ustekinumab, the patients CD4 T-cell count and HIV viral load have remained stable. Due to the questions surrounding the use of
biologics in HIV-positive patients, we review the successful use of anti-TNF agents in patients with chronic HIV infection as well as
the single other reported case of ustekinumabs use in an HIV-positive patient. We therefore begin to build the case for ustekinumab
as an alternative biologic therapy for the HIV-infected psoriasis patient.

INTRODUCTION

soriasis is a chronic inflammatory immunemediated skin condition characterized

by well demarcated, erythematous, scaly
plaques that is seen in 2-3% of the worlds population.1
Patients with human immunodeficiency virus (HIV)
infection and psoriasis represent 1.3%-5% of HIV
patients.2 A patients psoriasis may worsen with HIV
or can be detected as a cutaneous manifestation
of HIV.1 HIV-associated psoriasis has been shown
to have a severe and prolonged course with more
frequent exacerbations.1 Widespread psoriasis
is a therapeutic challenge in HIV patients due to
possible complications of immune suppression with
biologic therapies.1 While tumor necrosis factor
(TNF)- targeted therapies have been found to
be relatively well-tolerated in HIV patients with
psoriasis, causing minimal change to CD4 counts

1
3

and viral load, 3 there are only limited data on

the treatment of HIV-associated psoriasis with
ustekinumab.4 Therefore, we report both a case of
successful treatment of psoriasis in an HIV-positive
patient with ustekinumab and present a review of
the literature.

CASE REPORT
The patient is a 39-year-old heterosexual Chinese
male with a medical history significant for HIV
diagnosed in 1996 and a 20-year history of generalized
plaque psoriasis and psoriatic arthritis. His psoriasis
has been refractory to treatment with topical
steroids, calcipotriene, psoralen plus ultraviolet
A (PUVA), methotrexate, acitretin, hydroxyurea,
etanercept, adalimumab, and golimumab. His
current medications include ustekinumab, tenofovir,
lopinavir/ritonavir, and raltegravir. Prior to starting

Albert Einstein College of Medicine, Bronx, New York; 2University of Hawaii, John A. Burns School of Medicine, Honolulu, Hawaii;
Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, New York

Corresponding author
Mark Lebwohl, M.D.
5 East 98th Street Floor 5
New York, New York 10029
Tel: 212.241.7568
Fax: 212.987.1197

Financial Disclosure and Conflicts of Interest

Dr. Lebwohl is a consultant or investigator for Janssen Biotech, Inc.,
Celgene, Pfizer, Amgen, Novartis, GSK Stiefel, and AbbVie. Dr. Levitt has
been on advisory boards for Amgen, Roche/Genentech, Janssen, and
Medac, for which he received honoraria.

Key words: ustekinumab, TNF inhibitors, infliximab, adalimumab, etanercept, HIV, psoriasis, psoriatic arthritis
96

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Fall 2014

ustekinumab, his body surface area (BSA) was 90%,

his Psoriasis Area and Severity Index (PASI) was
48, and his CD4 count was 847 per mm3 with an
undetectable viral load. On presentation, he had
generalized plaque psoriasis affecting his forehead,
scalp, trunk, and upper and lower extremities.

load has remained undetectable, and his weight

has been stable at 65 kg throughout his treatment
with ustekinumab. He has suffered only persistent
condyloma acuminata of the genitals and verruca
vulgaris of the trunk and neck, both of which were
present prior to starting ustekinumab and have
not worsened. Otherwise, he has been free of any
significant opportunistic infections or side effects.

The patient began ustekinumab therapy in August

of 2012 and received induction doses at weeks 0 and
4, but was lost to follow up for four months. Therapy
was reinitiated on a 3-month schedule with the
patient demonstrating modest results. Currently,
he is scheduled to receive ustekinumab every eight
weeks, though he continues to be poorly compliant.
He has received six 45-mg doses of ustekinumab
and most recently one 90-mg dose to try to improve
his responsiveness in the past 17 months. His BSA
has dropped to 35% and his PASI is 19. He was free
of joint pain at his most recent visit in January 2014.

DISCUSSION
HIV infection establishes a state of chronic generalized
immune activation. It is typically characterized
by many immune cell types such as CD4+ T cells,
CD8+ T cells, B cells, NK cells, and monocytes,
among others. 5 These immune cells express
markers of activation, proliferation, and apoptosis5
that result in a disequilibrium of cytokines. It has
been demonstrated that HIV infection is associated
with decreased production of interleukin (IL)-2 and
interferon (IFN)-g and increased production of IL-1,
IL-4, IL-6, IL-8, and TNF-.6 These dysregulated
cytokines have varying effects on HIV-1 replication.
IFN-, IFN-, IFN-, granulocyte macrophage-colony

Additionally, the patient feels that his psoriasis has

notably improved. His CD4 count has remained
stable between 847 and 960 mm3 (Figure 1), his viral

Figure 1 - CD4+ count and HIV RNA Viral Load in Patient During Ustekinumab Treatments

Doses of Ustekinumab

CD4+ Count

HIV RNA (copies/ml)

12

9.48

8.56

9.6

8.47

6
1/7
/14

/13

/13

11

/13

8/9

6/1

4/1

5/1

1/1

/12
9/1 12
1/

8/1

CD4+ Count (/mm3)

10

2
0

Fall 2014

Apr-12

Jul-12

Oct-12

Jan-13

May-13 Aug-13 Nov-13

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Mar-14
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Table 1: Case Reports Describing the Use of TNF- Antagonists on HIV-Positive Psoriasis Patients and Their Outcomes

98

Author

Drug

Disease and
Comorbidities

Baseline
CD4+ Cell
Count

Baseline HIVRNA Viral Load

Duration of
Therapy

Outcome

Aboulafia,
200018

Etanercept

Psoriasis, psoriatic
arthritis, HIV on HAART

0.05x10 9/L

4200 copies/mL

6 months

The patients CD4 cell count

and HIV viral load all remained
stable. His psoriasis and
joint deformities improved
substantially. Therapy was
discontinued due to recurrent
polymicrobial infections.

Linardaki,
200719

Etanercept

Psoriasis, psoriatic
arthritis, HIV on
HAART, HCV,
hemophilia A

380/mm3

2 years
(ongoing)

Patient had complete remission

of his polyarthritis with
occasional psoriatic plaques.
His HIV RNA was undetectable
and his CD4 cell count was
>450/mm.3

Kaur,
200720

Etanercept

RA, HIV on HAART,

HBV, HCV, asthma

299/mm3

203 copies/mL

3 months
(ongoing)

The patients HIV viral load

fluctuated to 115 copies/mL at 1
month which then decreased to
<50 copies/mL. Absolute CD4
cell counts increased ranging
from 236 to 530/mm.3

Mikhail,
2008 3

Etanercept

Pustular psoriasis,
psoriatic arthritis, HIV
on HAART

435/L

<75/L

20 weeks
(ongoing)

The patient remained free of

his pustular lesions and his
psoriatic arthritis but has had
some recurrence of the plaque
psoriasis. His CD4 cell count
had increased to 633/L with
an undetectable HIV viral load.

Barco,
201015

Etanercept

Psoriasis, psoriatic
arthritis, AIDS on
HAART, history of
hepatitis A, epilepsy

36/mm3

2040 copies/mL

13 months
(ongoing)

The patient had complete

clearance of his skin lesions.
His lymphocyte counts and HIV
RNA viral load became stable
after restarting HAART.

Lee,
2012 21

Etanercept

Psoriasis, HIV on
HAART

1370/mm3

6 years
(ongoing)

The patient was treated with

etanercept continuously for
6 years. Throughout, he had
stable CD4 counts (consistently
>1000/ mm3) and undetectable
HIV viral loads and experienced
no opportunistic infections.

Di Lernia,
201322

Etanercept

Psoriasis, HIV on
HAART, HCV

132 weeks

The patient remains partially

free of his psoriasis. His CD4
count remained stable while
his HIV viral load gradually
declined and was undetectable
by 18 months.

Bartke,
200423

Infliximab

Psoriasis, psoriatic
arthritis, AIDS on
HAART

193/mm3

6 weeks
(ongoing)

The patients skin lesions and

joint inflammation improved.
There was an increase in CD4
cell count to 107/mm,3 with
undetectable HIV viral load.

Beltran,
200624

Infliximab

Crohns disease, HIV on

HAART

410 cells/mL

14 weeks
(ongoing)

The patient experienced a

complete remission. Her CD4
count remained stable and viral
load <200 copies.

7930 copies/mL

<200 copies

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Fall 2014

Table 1: Case Reports Describing the Use of TNF- Antagonists on HIV-Positive Psoriasis Patients and Their Outcomes, continued
Author

Drug

Disease and
Comorbidities

Baseline
CD4+ Cell
Count

Baseline HIVRNA Viral Load

Duration of
Therapy

Outcome

Sellam,
200725

Infliximab

Psoriasis, psoriatic
arthritis, HIV on HAART

425/mm3

<50 copies/mL

22 months
(ongoing)

Patient experienced complete

remission of joint disease. His
CD4 cell count remained stable
at 435/mm3 but viral load
increased to 2818 copies/mL
possibly from poor compliance
to HAART regimen.

Psoriasis, psoriatic
arthritis, AIDS on
HAART

16/mm3

300,000 copies/
mL

45 months
(ongoing)

The patients skin and joint

manifestations improved. The
patients HIV remained stable.
Most recent HIV viral load was
5900 copies/mL and CD4 count
of 233/mm.3

6 weeks

The patient had clinical and

endoscopic response. His
CD4 counts after the first and
second doses of infliximab
were 990 and 830 million/L,
respectively, and he was lost to
follow up after 6 weeks.

Habib,
200926

Infliximab

Crohns disease, HIV

not on HAART

290 million/L

Alecsandru,
201027

Infliximab

Hidradenitis
suppurativa, HIV
not on HAART, acne
conglobata

546 cells/L

24,840 copies/
mL-1

1 year
(ongoing)

The patient had good clinical

response. After his CD4 count
and viral load increased, he
was initiated on HAART and
then restarted on infliximab.
His CD4 counts increased and
have remained stable around
644 cells/L. His HIV viral
load became and remains
undetectable.

Gaylis, 2012 28

Infliximab

Reactive arthritis, HIV

on HAART

770 cells/
mm3

<500Qn:US
copies/mL

10 years
(ongoing)

The patients symptoms

improved. His viral load was
undetectable and his CD4 count
was within reference range.

Almoallim,
201329

Adalimumab

Chronic inflammatory
arthritis, HIV on HAART

871/mm3

undetectable

2 months
(ongoing)

The patient had greater than

70% improvement in her
symptoms, a stable CD4 count,
and undetectable HIV viral load.

Inflammatory arthritis,
HIV on HAART, HBV,
type II DM

256/mm3

451 copies/mL

12 months
(ongoing)

Patient demonstrated
improvement in his
inflammatory arthritis. His
CD4 counts and HIV viral loads
remained stable.

Reactive arthritis, AIDS

on HAART, HBV, HCV,
ESRD

130/mm3

358 copies/mL

5 months

The patients reactive arthritis

symptoms improved. His HIV
viral load, CD4 count, and
transaminases remained stable.

ESRD - End Stage Renal Disease, DM - Diabetes, HAART Highly Active Antiretroviral Therapy, HAV - Hepatitis A, HBV - Hepatitis B, HCV
- Hepatitis C, RA - Rheumatoid Arthritis

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stimulating factor (GM-CSF), IL-10, IL-13, IL-16, and

chemokines have been shown to have inhibitory
effects while macrophage-colony stimulating factor
(M-CSF), TNF-, TNF-, IL-1, and IL-6 have shown to
be stimulatory.7 IL-4 has been shown to have dual
functions as it is both stimulatory and inhibitory.7
Activation of T cells by these cytokines upregulates
several transcription factors, including NF-kB,
thereby activating the transcription of HIV proviral
DNA.8 In particular, an over-expression of serum
TNF has been seen in all stages of HIV infection. HIV
infection has been shown to induce TNF expression
in cell culture and exogenous TNF- is known to
stimulate HIV transcription in vitro.9 Elevated
levels of TNF have been linked to greater viral load,
reduction of CD4+ T-cell count, and clinical signs
and symptoms of worsening HIV infection, such
as fatigue, fever, cachexia, aphthous ulcers, and
dementia.9 Thus, inhibition of TNF- in the setting of
HIV infection has been appealing, at least in theory.
As opposed to HIVs broad effects on the immune
system, the mechanisms of the biologic therapies are
limited and specific. Etanercept binds to solubilized
TNF-a and blocks its interaction with cell surface
receptors.10 Inf liximab and adalimumab bind
solubilized and receptor-bound TNF-, blocking
its activity.11,12 Ustekinumab prevents IL-12 and IL-23
from binding to their respective receptors.13 Due to
the known risks of infection associated with HIV,
it is understandable why use of biologic therapies
would be considered potentially dangerous due to
their immunosuppressive effects. These agents have
not been studied systematically for the treatment of
psoriasis in HIV. However, due to their specificity,
the biologics mentioned above have no theoretical
contraindications for use in HIV-infected patients.
A number of case reports describe the successful use
of specific biologics, most commonly etanercept and
infliximab, in patients with chronic HIV infection and
psoriasis (Table 1). The important role TNF- plays in
promoting protective granulomatous inflammation
coupled with predisposition to infection in HIV
raises concern that TNF- antagonism could further
predispose an HIV patient to infection.14 Fortunately,
TNF- plays a significant role in promoting both
psoriasis and the progression of HIV infection. Data
are available to support both the efficacy and safety
of TNF- antagonists in the treatment of cutaneous
psoriasis and psoriatic arthritis in HIV-infected

100

patients.15 In addition to case reports, a number of

studies have shown that anti-TNF- agents increase
CD4 counts in HIV negative16 and HIV-positive
patients17 or have no effect at all on the patients
HIV infection (Table 2).
As ustekinumabs mechanism of action is to inhibit
IL-12 and 23 from binding to its receptors, there might
be concern as to its use in HIV-positive individuals
due to possible compounded immunosuppression.
However, this seems unlikely as inherited deficiencies
in this branch of the immune system have shown
to have little effect on the ability to fight infection.
In patients with genetic IL-12 or IL-12 receptor
deficiencies, IL-12 was found to be redundant in
defense against intracellular microorganisms with
the exception of Mycobacteria and Salmonella.33
In a study by Fieschi et al., the only opportunistic
infections in 41 patients with complete IL-12 receptor
1 chain (IL-12R1) deficiency were of childhood
onset and caused by weakly virulent Mycobacteria
or Salmonella. In addition, these patients overall
prognosis was good due to broad resistance to
infection as well as the low penetrance and favorable
outcome from the infections.34
Due to this redundant protective immunity against
most microorganisms, ustekinumab should be a good
option for patients with HIV infection. However, thus
far, only one case report in the literature describes
the use of ustekinumab in an HIV patient. Paparizos
et al. reports a case of a 61-year-old male with HIV
and a 35-year history of plaque psoriasis. The patient
was refractory to treatment that included HAART,
acitretin, PUVA, methotrexate, cyclosporine, and
etanercept. Before initiating ustekinumab, he had a
CD4 count of 429 cells/ml and a viral load of 50 copies/
ml. He received ustekinumab 45 mg subcutaneously
at weeks 0, 4, and 16. By week 12, he had demonstrated
good response. He continues to receive ustekinumab
every 12 weeks. Throughout treatment, the patients
CD4 count had increased to 530 cells/ml, and his
viral load remained undetectable.4
Our patients ustekinumab therapy led to
modest objective improvements in his BSA and
PASI score, no change in his CD4 count or viral
load, and no opportunistic infections. Given the
growing literature evidence supporting the use
of TNF- blockade for psoriasis in HIV patients, it
would appear that TNF- inhibitors are a viable

Wieder et al. | psoriasis forum , Vol . 2 0, No. 3

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option for psoriasis patients with HIV who have

no concomitant acute infections, cancers, latent
tuberculosis, or chronic hepatitis B. Our report of
the safe use of ustekinumab in an uncomplicated
HIV patient with psoriasis begins to build the case
for this agent as an alternative biologic therapy
for HIV-infected psoriasis patients. Initiating an
HIV-positive patient on a biologic must be done
in close association with the patients infectious
disease physician, and the patient should be closely
monitored for any adverse changes in CD4 count,

viral load, and general health, with special attention

paid to the increased risk of infections.

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Table 2: Studies that Describe the Effects of TNF- Antagonists on CD4+ T Cell Counts and HIV-RNA Viral Load
Author

Drug

Number of
Patients

Disease and
Comorbidities

Baseline CD4+ Baseline HIV-RNA

Cell Count
Viral Load

Duration of Outcome
Therapy

Walker,
1996 30

Infliximab

HIV-1 on HAART

58/mm3
(range:
36-140)

256,000 copies/mL
(range: 20,0003.6X10 6)

42 days

This study showed no

consistent changes in
CD4 counts or plasma
HIV-RNA levels.

Sha,
2002 31

Etanercept

11

HIV-1 on HAART

50-350 cells/
mm3

<5000 copies/mL

28 weeks

To study effects on
cytokines induced
by IL-2 therapy in
patients prescribed
HAART. Single dose
resulted in decreased
IL-6 and CRP; no
change in IL-4, IL-10,
IL-12, IFN-gamma
or HIV-1 RNA levels;
no serious adverse
events attributed to
etanercept.

Wallis,
200417

Etanercept

16

HIV-1, sputum smear

positive tuberculosis

394+/-128
cells/L

5.00+/-0/7/mL

4 weeks

Phase 1 study that

showed superior
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Ferkolj,
200616

Infliximab

25

Crohns disease

1 infusion

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significant increase in
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activated T cells while
the percentage of NK
cells was reduced.

Cepeda,
2008 32

Etanercept
and
Infliximab

2 with RA, 3 with

psoriatic arthritis, 1
with undifferentiated
spondyloarthritis,
1 with ankylosing
spondylitis, all had HIV
(5 patients were on
HAART, 3 were not)

28.1 (SD
20.9)
months
(range
2.555)

This study showed

no adverse events.
CD4 cell count
and HIV viral load
remained stable.
Three of the patients
on etanercept and
two on infliximab
showed clinical
improvement.

Fall 2014

268-974 cells/
mm3

<50-22,148 copies/
mm3

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