Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts 763


 
 Table of Contents  
CASE REPORT
Year : 2014  |  Volume : 5  |  Issue : 1  |  Page : 70-73

A case of subacute thyroiditis in a patient on adalimumab for treatment of refractory palmo-plantar psoriasis


1 Department of Dermatology, Nicolina Medical Center, Iasi, Romania
2 Department of Dermatology, University of Medicine Gr T Popa Iasi, Iasi, Romania
3 Department of Dermatology, University of Medicine V Babes Timisoara, Timisoara, Romania
4 6th Military Support Unit, Ustka, Poland

Date of Web Publication15-Mar-2014

Correspondence Address:
Piotr Brzezinski
Department of Dermatology, 6th Military Support Unit, os. Ledowo 1N, 76-270 Ustka
Poland
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-9727.128955

Rights and Permissions
  Abstract 

Recent reports indicate different side-effects of the new medication for psoriasis. Adalimumab. Adalimumab is a biologic agent acting as tumor necrosis factor alpha inhibitor. It is wildly used in treating psoriasis, following a national guide treatment. We report a clinical case of subacute thyroiditis induced by adalimumab in a psoriatic patient. A 54-year-old Caucasian female addressed to our dermatology clinic in 2008 with a 3 years history of moderate to severe psoriasis. The patient had been experiencing non-disabling joint pain in both knees and wrists for several years. Her medical history was remarkable for pulmonary sarcoidosis (at the age of 32), arterial hypertension and angina pectoris. The patient was started on adalimumab 40 mg twice monthly with good clinical evolution, but she was diagnosed, a few months after starting the therapy, with subacute thyroiditis with severe evolution, with transitory hyperthyroidism (thyroid stimulating hormone 0.1 uIU/ml). The treatment with adalimumab was discontinued, the symptoms cleared in 3 weeks with non-steroidal anti-inflammatory drugs and a fully recovered thyroid status was obtained in 1 month. The patient continued the psoriatic medication (adalimumab) with no influence on thyroid status. We describe a case of subacute thyroiditis in a psoriatic patient treated with adalimumab, with a very good clinical evolution with non-steroidal anti-inflammatory medication. Liaison between dermatologists and in this case, endocrinologists and rheumatologists, will help to determine the prevalence of these reactions and to provide insights into the very complex mechanisms of both diseases.

Keywords: Adalimumab, psoriasis, thyroiditis, tumor necrosis factor alpha


How to cite this article:
Chiriac A, Foia L, Chiriac AE, Gorduza VE, Solovan C, Brzezinski P. A case of subacute thyroiditis in a patient on adalimumab for treatment of refractory palmo-plantar psoriasis. Muller J Med Sci Res 2014;5:70-3

How to cite this URL:
Chiriac A, Foia L, Chiriac AE, Gorduza VE, Solovan C, Brzezinski P. A case of subacute thyroiditis in a patient on adalimumab for treatment of refractory palmo-plantar psoriasis. Muller J Med Sci Res [serial online] 2014 [cited 2019 Oct 16];5:70-3. Available from: http://www.mjmsr.net/text.asp?2014/5/1/70/128955


  Introduction Top


Psoriasis is a chronic inflammatory disorder seen in approximately 2-3% of the world's population, affecting the skin and often joints. [1] The formation of psoriatic plaques involves the interplay of T cells, cytokines and keratinocytes. The presence of activated T cells within psoriatic plaques and the response to T cell-directed therapy suggest an immunologic nature of the disease. [2] Various cytokines, such as tumor necrosis factor alpha (TNF-α), are also present in psoriatic lesions and may be a target for drug therapy. [3],[4] Both cytokines and activated T cells promote the dysregulated growth of keratinocytes, leading to patches of erythematous, scaly skin. The course of chronic inflammatory diseases, such as psoriasis and rheumatoid arthritis (RA), has been greatly modified by the relatively recent introduction of biologic drugs. [5] Numerous other systemic biologic agents are available and are categorized into three classes: Anti-T cell agents (efalizumab, which was removed from the United States market in 2009 and alefacept), anti-TNF agents (adalimumab, infliximab, golimumab (monoclonal antibodies) and etanercept (dimeric fusion protein) and anti-interleukin-12/23 agents (ustekinumab and an investigational agent briakinumab). [2],[6]

TNF-α inhibitors represent efficacious therapeutic agents in many chronic inflammatory diseases such as psoriasis and RA. [3],[7]

We describe a case of subacute thyroiditis in a psoriatic patient treated with adalimumab, with a very good clinical evolution with non-steroidal anti-inflammatory medication.


  Case Report Top


This was a case report of a 54-year-old Caucasian female addressed to our dermatology clinic in 2008 with a 3 years history of moderate to severe psoriasis. The lesions were first noticed on the hands and feet [Figure 1], with some involvement of the scalp and trunk. The patient had been experiencing non-disabling joint pain in both knees and wrists for several years. Her medical history was remarkable for pulmonary sarcoidosis (at the age of 32), arterial hypertension and angina pectoris.
Figure 1: Psoriasis on the feet at the beginning of the treatment

Click here to view


The patient's initial psoriatic lesions were managed with a variety of topical regimens including steroids class II, calcipotriene, tacrolimus, with only minimal clearing of her skin lesions. The patient had also been treated with methotrexat and phototherapy ultraviolet B (UVB) (short wave narrowband UVB wavelength shall be 311) in the past, but with no results.

The patient was started on adalimumab 40 mg twice monthly, the plaques on her trunk demonstrated marked improvement, but the psoriatic lesions on the palms and feet were only mildly improved.

After several months of treatment, with good response to adalimumab, the patient was diagnosed with subacute thyroiditis at the endocrinology department, for sudden onset of pain in the region of the thyroid gland, fever, cervical lymphadenopathy. The pain was aggravated by turning the head and radiated to the ear and jaw. She was nervous, tired and complained for palpitation. On palpation, the gland was moderately enlarged, tender, the right lobe being more affected then left one.

A complete laboratory and imaging evaluation was performed in order to investigate possible associated systemic disorders, infectious, or inflammatory conditions. Routine laboratory tests were normal, except for an elevated white blood cell count (11.2 × 10΃/μL) with neutrophilia (67%); a C reactive protein of 48 mg/dL; and an erythrocyte sedimentation rate of 78 mm/h. In addition, renal function tests, serum protein electrophoresis and immunoelectrophoresis were within normal values. Findings were also normal or negative for immunological tests (rheumatoid factor, anti-nuclear antibodies, anti-double stranded deoxyribonucleic acid antibodies, anti-extractable nuclear antigen antibodies and complement). Circulating antibodies to thyroid peroxidase were also present in normal titers, thyroid stimulating hormone (TSH) was within normal values: 0.2 (normal ranges between 0.39 and 6.16 uIU/ml).

The thyroid ultrasound-scan showed:

On the first examination: Right thyroid lobule: 1.5 cm × 2 cm × 5 cm (7.5 cm), slight non-homogenous aspect, with no nodules;

Left thyroid lobule: 2 cm × 2.5 cm × 5 cm (12.5 cm) slight hipoechogenous, thyroid volume 20 ml.

On second examination (2 weeks later): Right thyroid lobule: 2.5 cm × 2 cm × 6 cm (15 cm) non-homogenous aspect;

Left thyroid lobule: 1.5 cm × 2 cm × 6 cm (9 cm) non-homogenous aspect.

Basal serum TSH was now suppressed (0.1 uIU/ml), the patient being in transitory hyperthyroidism phase.

The treatment was started with non-steroidal anti-inflammatory drugs and the symptoms cleared in about 3 weeks. Corticotherapy was not allowed due to biological treatment for psoriasis.

A reevaluation of the patient 2 weeks after the initiation of the anti-inflammatory therapy revealed no hyperthyroidism manifestations, tender or pain. Mild increase of TSH (4.5 IU/ml) reflected the transitory hypothyroidism phase for which no treatment was necessary.

A full thyroid function was recovered in 1 month.

Adalimumab was continued 1 year after the episode of thyroiditis. It was discontinued 13 months later for peritonitis and hepatic hidatic cyst (ruptured).


  Discussions Top


TNF-α inhibitors represent efficacious and relatively safe therapeutic agents in many chronic inflammatory diseases. An association between their use and an increased risk of complications has received much attention in the past.

Adalimumab is a fully human monoclonal antibody that binds specifically to TNF-α but not TNF-β. It lyses cells that express TNF-α on their surface in vitro. [8],[9] Adalimumab is widely used in the treatment of RA, juvenile idiopathic arthritis, ankylosing spondylitis, psoriatic arthritis, psoriasis and Crohn's disease. [8],[10],[11] Adalimumab is approved as a SC injection for the treatment of moderate-to-severe psoriasis. The Food and Drug Administration-approved standard dosing regimen for adalimumab is an initial dose of 80 mg at week 0 that is followed by 40 mg every other week (EOW) starting at week 1. [8],[9]

Although the biologic agents have demonstrated efficacy in patients with psoriasis and are generally considered safe and well tolerated, rare but serious safety issues (i.e., demyelination, infection, tuberculosis, malignancy, lymphoma, cardiovascular outcomes, hepatitis, pregnancy, surgery and vaccination) have been observed. [3],[7],[8]

Safety data from the adalimumab were recorded. [12],[13],[14]

After dose escalation to 40 mg QW adalimumab therapy, Gordon et al. reported one case (1/50) of recent-onset latent TB infection and one death (1/50) due to cerebrovascular accident in the 40 mg QW group and one case of coccidioidomycosis (1/97) in the 40 mg EOW group. With regard to malignancies, there were three malignancies (3/50) in the 40 mg QW group compared with two malignancies (2/97) in the 40 mg EOW group. [12]

Menter et al. in their study have reported aggregate safety data for the 52 week study period and did not attribute adverse events (AEs) specifically to the withdrawal-retreatment phases. [13] During the 16 week retreatment period with 285 patients, Papp et al. reported one malignant melanoma in situ, two serious infections (pneumonia and hepatitis C) and seven serious AEs. [14] Specifically, the serious AEs were coronary artery disease, abdominal adhesions, umbilical hernia, chest discomfort, nephrolithiasis and fracture of humerus. [14]

Adalimubab used because of other diseases (including RA) may also induce psoriasis. [15]

Armstrong et al. studies whether systemic treatments for psoriasis or psoriatic arthritis affect cardiovascular comorbidities. [16] Objective of the study was to examine the effects of biologic agents and other disease-modifying antirheumatic drugs used to treat psoriasis and psoriatic arthritis on cardiovascular risk factors and adverse cardiovascular outcomes. The preliminary epidemiologic studies found that the use of TNF inhibitors may be associated with reduced risk of adverse cardiovascular events.

Hemmati and Kur reported of case antiphospholipid syndrome in a 67-year-old woman which was treatment by adalimumab. [17]

Sauder and Glassman described that subcorneal pustular dermatosis, in addition to psoriasis vulgaris and pustular psoriasis may occur in patients treated with TNF-α inhibitors like adalimumab. [18] Clinical and histopathological features of a pustular skin condition which occurred in a 48-year-old woman with RA who had started adalimumab 4 months prior.

In a study by Park et al. described a patient who developed lymphomatoid papulosis after being treated with adalimumab, whereby a clear causality could be established [19] and Imafuku et al. described a cutaneous pseudolymphoma in other patient with arthropathic psoriasis treatment with adalimubab. [20]

New Zealand authors presented a 67-year-old man with chronic plaque psoriasis previously treated with psoralen plus ultraviolet A, ciclosporin, methotrexate and acitretin developed eruptive squamous cell carcinoma after seven doses of adalimumab. [21]

Described by one case alopecia areata in patient treatment with adalimubab. [22] A 43-year-old man with psoriasis and psoriatic arthritis who developed AA during his treatment with adalimumab and leflunomide.

One of varieties of psoriasis is palmoplantar pustulosis (PP). More authors presented good effect treatment of adalimubab of PP. [23],[24] We described a case of subacute thyroiditis in a psoriatic patient treated with adalimumab.

Among the side effects of the drug (adalimubab), into the available publications, we did not find description subacute thyroiditis after treatment of adalimubab.

Authors from Italy described that yours results demonstrate a significantly higher prevalence of thyroid autoimmunity (positive anti-thyroid peroxidase antibodies [AbTPO], hypoechoic thyroid) findings in men and women with prostate-specific antigen (PsA) and of subclinical hypothyroidism in women with PsA than in the general population. [25] However patients were not treated with biological agents. AbTPO, a hypoechoic thyroid and subclinical hypothyroidism were significantly more frequent in women with PsA than in control women and their frequency was similar to that in patients with RA (positive AbTPO titer 28%, 12% and 31%; hypoechoic thyroid 31%, 16% and 36%; subclinical hypothyroidism 25%, 8% and 12%, respectively). Among men, positive AbTPO titers and a hypoechoic thyroid were found more frequently in patients with PsA and RA than in controls (positive AbTPO titer 14%, 5% and 2%; hypoechoic thyroid 16%, 10% and 3%, respectively). All patients with PsA with subclinical hypothyroidism had polyarticular involvement (P ≤ 0.05) and a longer disease duration (years 19 ± 15 vs. 11 ± 8, P = 0.03) than patients with euthyroid PsA. The prevalence of subclinical hyperthyroidism, thyroid nodules and thyroid enlargement was not significantly different among the three groups.


  Conclusion Top


As the use of biologic drugs becomes more widespread over years (adalimumab is effective treatments for psoriasis patients who are not well controlled by conventional therapy), clinicians from a variety of disciplines are increasingly likely to encounter different side effects of this treatment. Liaison between dermatologists and in this case, endocrinologists and rheumatologists, will help to determine the prevalence of these reactions and to provide insights into the very complex mechanisms of both diseases.

Patient was diagnosed with thyroiditis during treatment with adalimumab for the 1 st time. We present a case of subacute thyroiditis in a psoriatic patient treated with adalimumab considering it not a coincidence but rather a side-effect of treatment.

 
  References Top

1.Puri N, Mahajan BB, Sandhu SK. Clinical evaluation of different therapeutic modalities in psoriasis by pasi score. Our Dermatol Online 2013;4:16-22.  Back to cited text no. 1
    
2.Vergou T, Moustou AE, Sfikakis PP, Antoniou C, Stratigos AJ. Pharmacodynamics of TNF-α inhibitors in psoriasis. Expert Rev Clin Pharmacol 2011;4:515-23.  Back to cited text no. 2
    
3.Baker EL, Coleman CI, Reinhart KM, Phung OJ, Kugelman L, Chen W, et al. Effect of biologic agents on Non-PASI outcomes in moderate-to-severe plaque psoriasis: Systematic review and meta-analyses. Dermatol Ther (Heidelb) 2012;2:9.  Back to cited text no. 3
    
4.Abreu Velez AM, Howard WR, Howard MS. Upregulation of anti-human ribosomal protein S6-p240, topoisomerase II ?, Cyclin D1, BCL-2 and anti-corneal antibodies in acute psoriasis. N Dermatol Online 2011;2:113-7.  Back to cited text no. 4
    
5.Rana S, Zeeba JS, Sujata J, Madhur K. A comparative study of psoriasis and psoriasiform lesion on basis of CD4 and CD8 cell infiltration. Our Dermatol Online 2012;3:292-7.  Back to cited text no. 5
    
6.Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med 2009;361:496-509.  Back to cited text no. 6
    
7.Papp KA, Dekoven J, Parsons L, Pirzada S, Robern M, Robertson L, et al. Biologic therapy in psoriasis: Perspectives on associated risks and patient management. J Cutan Med Surg 2012;16:153-68.  Back to cited text no. 7
    
8.Brezinski EA, Armstrong AW. Off-label biologic regimens in psoriasis: A systematic review of efficacy and safety of dose escalation, reduction, and interrupted biologic therapy. PLoS One 2012;7:e33486.  Back to cited text no. 8
    
9.Aubin F, Barthelemy H. Adalimumab. Ann Dermatol Venereol 2011;138:842-4.  Back to cited text no. 9
    
10.Hassan I, Yaseen U, Ahmad M, Masood Q. Manubriosternal joint involvement in psoriatic arthritis. N Dermatol Online 2011;2:68-9.  Back to cited text no. 10
    
11.Puri N. Infantile psoriasis treated successfully with topical calcipotriene. Our Dermatol Online 2013;4:205-7.  Back to cited text no. 11
    
12.Gordon KB, Langley RG, Leonardi C, Toth D, Menter MA, Kang S, et al. Clinical response to adalimumab treatment in patients with moderate to severe psoriasis: Double-blind, randomized controlled trial and open-label extension study. J Am Acad Dermatol 2006;55:598-606.  Back to cited text no. 12
    
13.Menter A, Tyring SK, Gordon K, Kimball AB, Leonardi CL, Langley RG, et al. Adalimumab therapy for moderate to severe psoriasis: A randomized, controlled phase III trial. J Am Acad Dermatol 2008;58:106-15.  Back to cited text no. 13
    
14.Papp K, Crowley J, Ortonne JP, Leu J, Okun M, Gupta SR, et al. Adalimumab for moderate to severe chronic plaque psoriasis: Efficacy and safety of retreatment and disease recurrence following withdrawal from therapy. Br J Dermatol 2011;164:434-41.  Back to cited text no. 14
    
15.Al-Mutairi A, Elkashlan M, Al-Fayed HM, Swayed M. TNF-α inhibitor (adalimumab) induced psoriasis: A case report. Australas J Dermatol 2012;53:157.  Back to cited text no. 15
[PUBMED]    
16.Armstrong AW, Brezinski EA, Follansbee MR, Armstrong EJ. Effects of biologic agents and other disease-modifying antirheumatic drugs on cardiovascular outcomes in psoriasis and psoriatic arthritis: A systematic review. Curr Pharm Des 2014;20:500-12.  Back to cited text no. 16
    
17.Hemmati I, Kur J. Adalimumab-associated antiphospholipid syndrome: A case report and review of the literature. Clin Rheumatol 2013;32:1095-8.  Back to cited text no. 17
    
18.Sauder MB, Glassman SJ. Palmoplantar subcorneal pustular dermatosis following adalimumab therapy for rheumatoid arthritis. Int J Dermatol 2013;52:624-8.  Back to cited text no. 18
    
19.Park JH, Lee J, Lee JH, Lee DY, Koh EM. Lymphomatoid papulosis in a patient treated with adalimumab for juvenile rheumatoid arthritis. Dermatology 2012;225:259-63.  Back to cited text no. 19
    
20.Imafuku S, Ito K, Nakayama J. Cutaneous pseudolymphoma induced by adalimumab and reproduced by infliximab in a patient with arthropathic psoriasis. Br J Dermatol 2012;166:675-8.  Back to cited text no. 20
[PUBMED]    
21.Simpkin S, Oakley A. Multiple eruptive squamous cell carcinoma in a patient with chronic plaque psoriasis on adalimumab. Australas J Dermatol 2013;54:55-8.  Back to cited text no. 21
    
22.Navarro R, Daudén E, Gallo E, Santiago Sánchez-Mateos D, García-Diez A. Alopecia areata during treatment of psoriasis with adalimumab and leflunomide: A case and review of the literature. Skin Pharmacol Physiol 2012;25:107-10.  Back to cited text no. 22
    
23.Mishra V, Daniel RC, Elmets CA, Levin A, Elewski BE. Palmoplantar pustulosis with fulminant dystrophic 20-nail psoriasis in a patient receiving adalimumab therapy. J Drugs Dermatol 2013;12:16-7.  Back to cited text no. 23
[PUBMED]    
24.Vijayashankar M, Raghunath N. Pustular psoriasis responding to probiotics - A new insight. Our Dermatol Online 2012;3:326-9.  Back to cited text no. 24
    
25.Antonelli A, Delle Sedie A, Fallahi P, Ferrari SM, Maccheroni M, Ferrannini E, et al. High prevalence of thyroid autoimmunity and hypothyroidism in patients with psoriatic arthritis. J Rheumatol 2006;33:2026-8.  Back to cited text no. 25
    


    Figures

  [Figure 1]


This article has been cited by
1 Subacute thyroiditis in a patient with psoriasis treated with a tumor necrosis factor-a inhibitor
Yu-An Wei,Wan-Chi Chuang,Chien-Hui Hong
International Journal of Dermatology. 2018;
[Pubmed] | [DOI]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Case Report
Discussions
Conclusion
References
Article Figures

 Article Access Statistics
    Viewed3451    
    Printed79    
    Emailed0    
    PDF Downloaded260    
    Comments [Add]    
    Cited by others 1    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]