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  Table of Contents  
BRIEF REPORT
Year : 2020  |  Volume : 11  |  Issue : 5  |  Page : 771-776  

The association of thyroid dysfunction with chronic plaque psoriasis: A hospital-based retrospective descriptive observational study


1 Department of Dermatology, Venereology and Leprosy, Dr. R. P. Govt. Medical College, Kangra (Tanda), Himachal Pradesh, India
2 Department of Biochemistry, Dr. R. P. Govt. Medical College, Kangra (Tanda), Himachal Pradesh, India

Date of Submission26-Aug-2019
Date of Decision11-Oct-2019
Date of Acceptance26-Nov-2019
Date of Web Publication19-Sep-2020

Correspondence Address:
Vikram K Mahajan
Department of Dermatology, Venereology and Leprosy, Dr. R. P. Govt. Medical College, Kangra (Tanda) - 176 001, Himachal Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/idoj.IDOJ_432_19

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   Abstract 


Background: Associations among thyroid dysfunction, thyroid autoimmunity, and clinical features including age, gender, disease duration, and severity of psoriasis is less studied. Objectives: To study frequency of thyroid dysfunction and thyroid autoimmunity and examine association among thyroid dysfunction, thyroid autoimmunity, and clinical features including gender, age, duration, and severity of psoriasis. Material and Methods: The medical records of 290 (m:f 2.15:1) patients aged 13–75 years with plaque psoriasis were analyzed for thyroid dysfunction and thyroid autoimmunity. Thyroid dysfunction was defined as 10% variation in any thyroid hormone levels. Thyroid autoimmunity was diagnosed from presence of antithyroid peroxide (anti-TPO) antibodies. Results: The majority, 57.9% patients, was aged ≥41 years (Type-2 psoriasis) and duration of disease was <5 years in 58.6% patients. Mild and moderate to severe psoriasis was present in 58.3% and 41.7% patients, respectively. Deranged thyroid functions were present in 29 (10%) patients. Hypothyroidism and hyperthyroidism occurred in 5.4% and 2.7% patients, respectively. Anti-TPO antibodies were observed in 13.5% patients; 11had hypothyroidism. There was no statistically significant difference in gender, age, duration, and severity of psoriasis when compared with patients having normal thyroid function tests. Conclusion: The study suggests possible thyroid dysregulation and thyroid autoimmunity in psoriasis but results need careful interpretation and clinical application. Their significance as standalone risk factor for the chronicity, severity, and relapses in psoriasis or whether thyroid hormone replacement or antithyroid drugs become a useful therapeutic option remains tenuous at best for need of more robust evidence. Retrospective, observational, cross-sectional study design, small number of patients, and lack of controls remain major limitations.

Keywords: Hyperthyroidism, hypothyroidism, plaque psoriasis, thyroid autoimmunity, thyroid dysfunction


How to cite this article:
Rana A, Mahajan VK, Chauhan PS, Mehta KS, Sharma SB, Sharma A, Sharma R. The association of thyroid dysfunction with chronic plaque psoriasis: A hospital-based retrospective descriptive observational study. Indian Dermatol Online J 2020;11:771-6

How to cite this URL:
Rana A, Mahajan VK, Chauhan PS, Mehta KS, Sharma SB, Sharma A, Sharma R. The association of thyroid dysfunction with chronic plaque psoriasis: A hospital-based retrospective descriptive observational study. Indian Dermatol Online J [serial online] 2020 [cited 2020 Oct 22];11:771-6. Available from: https://www.idoj.in/text.asp?2020/11/5/771/295573




   Introduction Top


Genetic, immunologic and metabolic mechanisms have been implicated in etiopathogenesis of psoriasis that remains largely elusive. Currently, psoriasis is considered a multiorgan systemic disease due to chronic inflammation. Epidermal hyperproliferation is considered secondary to Th1 type of immune reaction and inflammatory milieu in the dermal microenvironment induced by inflammatory cells, elevated TNF-α and other cytokines, chemokines and growth factors.[1] This inflammation is also implicated for enhanced risk of metabolic syndrome or its individual components (obesity, dyslipidemia, atherosclerosis, type-2 diabetes mellitus), cardiovascular disease (hypertension, myocardial infarction, stroke), chronic kidney disease, cancer, Crohn's disease, and depression that significantly impair quality of life in psoriatics.[2],[3],[4],[5] The role of various hormones such as thyroid hormones, thyroid stimulating hormone, cortisol, and prolactin in the pathogenesis of psoriasis has been studied previously.[6],[7],[8] Thyroid hormone levels have been reported to change during the active phase of psoriasis and psoriasis showed improvement in patients with hyperthyroidism, suggesting a possible role of thyroid hormones in the pathogenesis of psoriasis.[8] The T3 receptors on the skin have been identified and suggested to play a role in keratin synthesis, cell growth, and differentiation and proliferation of keratinocytes.[9],[10],[11] T3 and T4 have hyperproliferative effect on the skin via epidermal growth factor which is increased by thyroid hormones.[8],[12] Reported resolution of psoriasis following surgical thyroidectomy and usefulness of antithyroid drug propyl thiouracil in topical and systemic treatment of psoriasis by some workers further support this hypothesis.[9],[13],[14],[15],[16] However, how exactly pathophysiology of thyroid abnormalities and psoriasis is interlinked remains less understood and several inflammatory or non-inflammatory pathways have been proposed. Interleukin (IL)-17, one of the important cytokines in the pathophysiology of epidermal barrier disruption, keratinocyte hyperproliferation, and sustained inflammation in psoriasis, also plays an important role in Graves' disease and Hashimoto thyroiditis.[17],[18],[19] Similarly, various other chemokines such as CCL2 (monocyte chemo attractant protein-1; MCP1), CCL22 (macrophage-derived chemokine; MDC), CXCL9 (monokine induced by IFN-γ; Mi-g), and CXCL10 [interferon (IFN)-inducible protein-10; IP-10] are expressed both in autoimmune thyroiditis and psoriasis.[20],[21],[22],[23],[24],[25] Furthermore, a prolonged clinical course of both psoriatic arthritis and Graves' disease has been attributed to CCL2- and CCL22-meditated shift from a Th1- to Th2-type immune response.[22],[24],[25] Besides, both psoriasis and autoimmune thyroid disease along with several other autoimmune diseases have been associated with disruption in the nuclear factor-κB (NF-κB) signaling pathway.[26] However, any association between thyroid dysfunction and psoriasis remains unclear and the exact role of thyroid hormones in etiopathogenesis of psoriasis needs elucidation by experimental studies for their antiproliferative effect or that of antithyroid drugs on keratinocytes. Nevertheless, it may be useful to assess thyroid functions in patients with uncontrolled and relapsing psoriasis for a holistic management. We studied the frequency of thyroid dysfunction and thyroid autoimmunity in patients with psoriasis and also examined the associations among thyroid dysfunction, thyroid autoimmunity, and clinical features including age, gender, disease duration, and severity of psoriasis for paucity of relevant data in Indian context.


   Material and Methods Top


The medical records of patients with chronic plaque psoriasispresenting in dermatology clinicbetween Jan 2014 and Dec 2018 were analyzed retrospectively for this hospital-based descriptive observational study. The study was approved by Institutional Ethics Committee (regn no. ECR/490/Inst/HP/2013/RR-16). The demographic profile, duration and evolution of skin disease, detailed medical history and clinical details of psoriasis were recorded. Children aged <12 years, pregnant and lactating women, and patients on antipsoriatic or immunomodulator medications (methotrexate, folic acid, ciclosporin, acitretin, biologicals), or other drugs effecting thyroid metabolism (corticosteroids, anticonvulsants, NSAIDs, furosemide, lithium, amiodarone), or with psoriatic arthritis, palmoplantar psoriasis, pre-existing thyroid disorders on treatment, hypertension, diabetes mellitus, morbid obesity (BMI >30kg/m2), hepatorenal disease, collagen vascular disorders, or malignancy were excluded. The diagnosis of psoriasis was clinical and the severity of psoriasis was assessed by body surface area (BSA) measured by Wallace rule of nine and psoriasis area severity index (PASI) score as described by Fredriksson and Pettersson.[27] The severity of psoriasis was defined as mild (PASI <6 or BSA 10%), moderate (PASI 6–12 or BSA 11–20%), or severe (PASI >12 or BSA >20), giving precedence to PASI score in case of ambiguity.[28]

After overnight fasting, blood sample (5 ml) was collected between 8am and 10am by antecubital venepuncture for relevant tests performed in institutional central research laboratory. Complete blood counts and serum biochemistry including blood sugar, lipid profile, and hepatorenal function tests were carried out by standard protocols. Thyroid function tests and antithyroid peroxide antibody (Anti-TPO Ab) were measured using chemiluminescent immunoassay (CLIA). Thyroid dysfunction was defined as 10% variation in any thyroid hormone levels (triiodothyronine [T3, normal 6-202 ng/dl], thyroxine [T4, normal 4.4-11.6 ng/dl] and thyroid-stimulating hormone [TSH, normal 0.5–5.4 μIU/ml]). Subclinical hypothyroidism was defined as high TSH and normal T3 and T4 levels and subclinical hyperthyroidism was defined for low TSH and normal T3 and T4 levels along with absence of thyroid-related clinical features. A diagnosis of probable thyroid disease was considered in case of discordant results. The presence of anti-TPO Abs indicated thyroid autoimmunity.

Data analysis

The medical records of six patients were incomplete and were excluded from final analysis. MS Word Excel software was used to tabulate and analyze the data. The continuous data are presented as mean and categorical variables are presented as frequencies and percentages. The Chi-square test and student t-test were used for the statistical analysis of the categorical and parametric data, respectively. A P < 0.05 calculated at 5% level (95% confidence limit) was considered statistically significant.


   Results Top


[Table 1] depicts baseline clinicodemographic features and thyroid function abnormalities of 290 patients comprising 190 (68.3%) men and 92 (31.7%) women (m:f 2.15:1) aged between 13 and 75 years (mean 41.9 years) at presentation. The majority, 168 (57.9%) patients were aged between 41 and 75 years (type-2 psoriasis). The duration of psoriasis varied between1 month and 30 years (mean 5.1 years) and the majority, 170 (58.6%) patients had presented within 5 years. The disease was mild in 169 (58.3%) patients, while 121 (41.7%) patients had moderate to severe psoriasis. Deranged thyroid functions were present in 29 (10%) patients consistent with subclinical hypothyroidism in 21 (5.4%) and subclinical hyperthyroidism in one (2.7%) patient, respectively. A diagnosis of probable thyroid disease; hypothyroidism in five and hyperthyroidism in two patients was considered because of discordant results. Thirty-nine (13.5%) patients demonstrated elevated anti-TPO Ab levels indicating autoimmune thyroiditis and 11 (28.2%) of them showed serodiagnosis of hypothyroidism.
Table 1: Baseline characteristics of psoriasis patients

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Comparative clinicoepidemiologic features of patients with normal thyroid function tests and thyroid dysfunction are shown in [Table 2]. Greater number of males than females (58.6% vs. 41.4%), and patients aged above 41 years than younger ones (55.2% vs. 44.8%), having psoriasis for more than 5 years than 5 years or less (51.7% vs. 48.3%), or moderate to severe psoriasis (both by PASI score and BSA involvement) than mild disease (51.7% vs. 48.3%) showed thyroid dysfunction. However, there was no statistically significant difference in gender, age, duration, and severity of psoriasis when compared with patients having normal thyroid function tests.
Table 2: Characteristics of psoriasis patients with abnormal thyroid functions

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[Table 3] depicts comparative clinicoepidemiologic features of normal patients and those having thyroid autoimmunity with no statistically significant difference in gender, age, duration, and severity of psoriasis. Men and patients aged above 41 years outnumbered women and younger patients to have autoimmunity (58.6% vs. 41.4%) and (55.2% vs. 44.8%), respectively. However, greater number of patients with thyroid autoimmunity showed mild disease both in terms of PASI score (66.7% vs. 57%) and BSA involved (74.4% vs. 54.2%).
Table 3: Characteristics of psoriasis patients with abnormal Anti TPO Ab

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   Discussion Top


The overall clinico-epidemiologic features in our study subjects, majority comprising males, aged above 41 years and having type-2 psoriasis of more than 5-year duration with remissions and relapses corroborates previous reports.[29],[30],[31],[32] However, it is possible that exclusion of females, as in most studies, accounts for their number being less in this study. Although no significant association between psoriasis and thyroid disease has been observed in U.S. based National Health and Nutrition Examination Survey data analysis, thyroid abnormalities in psoriasis patients are not uncommon and presence of anti-TPOAb, hypothyroidism and hyperthyroidism were associated with prevalent psoriatic disease, particularly in patients with psoriatic arthritis, in a recent meta-analysis.[33],[34],[35] Arican et al.[36] observed elevated levels of at least one thyroid hormone and high PASI score in 22% patients in a case-control study. They imputed high PASI score to excessive thyroid hormones because of direct or indirect role played byT3 receptors in keratin synthesis and resultant psoriasis severity. Hyperthyroidism in 4%, hypothyroidism in 3%, and anti-TPO Ab in 9% patients, respectively, were also reported in another study.[37] Recently, Manvi et al.[30] reported prevalence of hypothyroidism with elevated anti-TPO Ab, suggestive of autoimmune thyroid dysfunction in their 8.6% patients. However, the prevalence of thyroid autoimmunity has been not found different between psoriatic patients and normal population.[37],[38] We also observed deranged thyroid status in 10% patients and majority, 72.4% of them had subclinical hypothyroidism while 28.2% of 39 patients with autoimmunity also had hypothyroidism. Comparatively, hyperthyroidism was noted in fewer patients only. However, the interpretation of these observations remains complex in the absence of any statistically significant difference between various clinicoepidemiologic parameters between psoriatic patients with normal and abnormal thyroid function tests or autoimmunity as was also noted by Borges et al.[39] It remains distinctly possible that the pattern of biochemistry indicative of mild hypothyroidism in our majority patients reflects a general trend of its prevalence of 4–10% in general population which is still higher in the elderly particularly affecting up to 20% women aged 60 years and above.[40] We also cannot rule out with impunity a possibility of non-thyroid illness (sick euthyroid syndrome) defined as abnormal thyroids function tests usually in patients with acute or chronic systemic illnesses including organic and psychiatric diseases.[41] This seems logical in view of the emerging evidence that favors psoriasis being more of an autoimmune systemic disease of chronic inflammation and multiorgan complications causing significant psychosocial distress. However, whether thyroid hormone replacement, surgical thyroidectomy, or propyl thiouracil becomes a useful therapeutic option in these patients, or these serological changes reflect associated pathology or is just an adaptive response to stress to lower the metabolic rate to the benefit of patient needs further elucidation. The presence of thyroid autoimmunity and normal thyroid function tests in this study observed as elevated serum anti-TPO Ab concentration in 13.5% patients and 71.8% of them with euthyroid status indicating possible subclinical autoimmune thyroiditis also needs careful interpretation. This is important as assay interference by cross-reacting heterophilic (intrinsic) antibodies such as human anti-animal antibodies, auto antibodies to TSH, T4 or T3, or nonspecific antibodies can cause unpredictable results in 0.03–3% of all samples tested for thyroid autoimmunity.[42],[43]

Limitations

The hospital-based retrospective, observational, cross-sectional study design, small number of patients especially with psoriatic arthritis, lack of controls, no screening for concurrent autoimmune or other systemic disorders, anti-thyroid antibodies other than anti-TPO Ab, and no follow-up for thyroid status or therapeutic outcome remain major limitations.


   Conclusion Top


Deranged thyroid status in 10% patients and thyroid autoimmunity in 13.5% patients with subclinical hypothyroidism in majority suggests thyroid dysfunction and autoimmunity in psoriasis patients in this study. However, the significance of thyroid dysfunction as a risk factor for the chronicity, severity, and relapses in psoriasis appears tenuous at best for want of robust evidence. Whether thyroid dysfunction/autoimmunity is a culprit or bystander in the etiopathogenesis and overall systemic inflammatory process in psoriasis or treatment with antithyroid drugs can be an option in psoriasis needs confirmation with well-designed experimental and prospective clinical studies.

Statement of ethics

All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, as revised in 2013. All patients were provided treatment and care as per standard guidelines. The authors also certify that they have obtained all appropriate patient consent forms. In the form, the patients or their parents/guardians have given their consent for the patient's images and other clinical information to be reported in the journal. The patient/parents/guardians understand that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Joshi R. Immunopathogenesis of psoriasis. Indian J Dermatol Venereol Leprol 2004;70:10-2.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Lin HW, Wang KH, Lin HC, Lin HC. Increased risk of acute myocardial infarction in patients with psoriasis: A 5-year population based study in Taiwan. J Am Acad Dermatol 2011;64:1-7.  Back to cited text no. 2
    
3.
Ghiasi M, Nouri M, Abbasi A, Hatami P, Abbasi MA, Nourijelyani K. Psoriasis and increased prevalence of hypertension and diabetes mellitus. Indian J Dermatol 2011;56:533-6.  Back to cited text no. 3
[PUBMED]  [Full text]  
4.
Bhosle MJ, Kulkarni A, Feldman SR, Balkrishan R. Quality of life in patients with psoriasis. Health Qual Life Outcomes 2006;4:35.  Back to cited text no. 4
    
5.
Oliveira Mde F, Rocha Bde O, Durate GV. Psoriasis: Classical and emerging comorbidities. An Bras Dermatol 2015;90:9-20.  Back to cited text no. 5
    
6.
Khatri G, Mahajan VK, Mehta KS, Sharma KK, Bhushan S, Chauhan PS. Serum prolactin levels in Indian patients with psoriasis: Results of a pilot study. Indian J Med Res 2017;145:250-2.  Back to cited text no. 6
[PUBMED]  [Full text]  
7.
Arican O, Bilgic K, Koc K. The effect of thyroid hormones in psoriasis vulgaris. Indian J Dermatol Venereol Leprol 2004;70:354-6.  Back to cited text no. 7
    
8.
Robati RM, Toossi P, Rahmati-Roodsari M, Khalilazar S, Abolhasani E, Namazi N, et al. Association of psoriasis severity with serum prolactin, thyroid hormones, and cortisol before and after treatment. Scientific World Journal 2013;2013:921819.  Back to cited text no. 8
    
9.
Elias AR, Barr RJ. Low dose oral propyl thiouracil in the treatment of plaque psoriasis. Int J Dermatol 1995;34:519-20.  Back to cited text no. 9
    
10.
Ribeiro RC, Apriletti JW, West BL, Wagner RL, Fletterick RJ, Schaufele F, et al. The molecular biology of thyroid hormone action. Ann N Y Acad Sci 1995;758:366-89.  Back to cited text no. 10
    
11.
Wagner RL, Apriletti JW, McGrath ME, West BL, Baxter JD, Fletterick RJ. A structural role for hormone in the thyroid hormone receptor. Nature 1995;378:690-7.  Back to cited text no. 11
    
12.
Hoath SB, Lakshmanan J, Scott SM, Fisher DA. Effect of thyroid hormones on epidermal growth factor concentration in neonatal mouse skin. Endocrinology 1983;112:308-14.  Back to cited text no. 12
    
13.
Elias AN, Goodman MM, Liem WH, Barr J. Propyl thiouracil in psoriasis: Result of an open trial. J Am Acad Dermatol 1993;29:78-81.  Back to cited text no. 13
    
14.
Chowdhury MM, Marks R. Oral propyl thiouracil for the treatment of resistant plaque psoriasis. J Dermatol Treat 2001;12:81-5.  Back to cited text no. 14
    
15.
Elias AN, Dangaran K, Barr J, Rohan K, Goodman MM. A controlled trial of topical propyl thiouracil in the treatment of patients with psoriasis. J Am Acad Dermatol 1994;31:455-8.  Back to cited text no. 15
    
16.
Kuchel J, Barakate M, Delbridge L, Agarwal G, Beattie J, Barnetson R. Short-term resolution of psoriasis after total thyroidectomy for euthyroid multinodular goitre. Australas J Dermatol 2002;43:214-7.  Back to cited text no. 16
    
17.
Lynde CW, Poulin Y, Vender R, Bourcier M, Khalil S. Interleukin 17A: Toward a new understanding of psoriasis pathogenesis. JAm Acad Dermatol 2014;71:141-50.  Back to cited text no. 17
    
18.
Li JR, Hong FY, Zeng JY, Huang GL. Functional interleukin-17 receptor A are present in the thyroid gland in intractable Graves disease. Cell Immunol 2013;281:85-90.  Back to cited text no. 18
    
19.
Li D, Cai W, Gu R, Zhang Y, Zhang H, Tang K, et al. Th17 cell plays a role in the pathogenesis of Hashimoto's thyroiditis in patients. Clin Immunol 2013;149:411-20.  Back to cited text no. 19
    
20.
Garcia-Lopez MA, Sancho D, Sanchez-Madrid F, Marazuela M. Thyrocytes from autoimmune thyroid disorders produce the chemokines IP-10 and Mig and attract CXCR3+ lymphocytes. JClin Endocrinol Metabolism 2001;86:5008-16.  Back to cited text no. 20
    
21.
Antonelli A, Ferrari SM, Giuggioli D, Ferrannini E, Ferri C, Fallahi P. Chemokine (C-X-C motif) ligand (CXCL) 10 in autoimmune diseases. Autoimmunity Rev 2014;13:272-80.  Back to cited text no. 21
    
22.
Romagnani P, Rotondi M, Lazzeri E, Lasagni L, Francalanci M, Buonamano A, et al. Expression of IP-10/CXCL10 and MIG/CXCL9 in the thyroid and increased levels of IP-10/CXCL10 in the serum of patients with recent-onset Graves' disease. Am J Pathol 2002;161:195-206.  Back to cited text no. 22
    
23.
Goebeler M, Toksoy A, Spandau U, Engelhardt E, Brocker EB, Gillitzer R. The C-X-C chemokine Mig is highly expressed in the papillae of psoriatic lesions. J Pathol 1998;184:89-95.  Back to cited text no. 23
    
24.
Antonelli A, Fallahi P, Delle Sedie A, Ferrari SM, Maccheroni M, Bombardieri S, et al. High values of Th1 (CXCL10) and Th2 (CCL2) chemokines in patients with psoriatic arthtritis. Clin Exp Rheumatol 2009;27: 22-7.  Back to cited text no. 24
    
25.
Liu C, Papewalis C, Domberg J, Scherbaum WA, Schott M. Chemokines and autoimmune thyroid diseases. Hormone Metabolic Res 2008;40:361-8.  Back to cited text no. 25
    
26.
Kurylowicz A, Nauman J. The role of nuclear factor-kappaB in the development of autoimmune diseases: A link between genes and environment. Acta Biochimica Polonica 2008;55:629-47.  Back to cited text no. 26
    
27.
Fredriksson T, Pettersson U. Severe psoriasis-oral therapy with a new retinoid. Dermatologica 1978;157:238-44.  Back to cited text no. 27
    
28.
Feldman SR. A quantitative definition of severe psoriasis for use in clinical trials. J Dermatolog Treat 2004;15:27-9.  Back to cited text no. 28
    
29.
Wadhwa D, Mahajan VK, Mehta KS, Chauhan PS, Sharma V, Sharma A, et al. Malondialdehyde, lipoprotein-a, lipoprotein ratios, comprehensive lipid tetrad index and atherogenic index as surrogate markers for cardiovascular disease in patients with psoriasis: A case- control study. Arch Dermatol Res 2019;311:287-97.  Back to cited text no. 29
    
30.
Manvi S, MahajanVK, Mehta KS, Yadav RS, Bhushan S, Chauhan PS. Psoriasis and co-morbidities: Is hyperhomocystenemia the common link? J Assoc Physic India 2019;67:29-32.  Back to cited text no. 30
    
31.
Henseler T, Christophers E. Psoriasis of early and late onset: Characterization of two types of psoriasis vulgaris. JAm Acad Dermatol 1985;13:450-6.  Back to cited text no. 31
    
32.
Singh S, Kalb RE, deJong EMGJ, Shear NH, Lebwohl M, Langholff W, et al. Effect of age of onset of psoriasis on clinical outcomes with systemic treatment in the Psoriasis Longitudinal Assessment and Registry (PSOLAR). Am J Clin Dermatol 2018;19:879-86.  Back to cited text no. 32
    
33.
Lai YC, Yew YW. Psoriasis and thyroid profile: Analysis of U.S. based National Health and Nutrition Examination Survey database. Indian J Dermatol Venereol Leprol 2016;82:310-2.  Back to cited text no. 33
    
34.
Khan SR, Bano A, Wakkee M, Korevaar TIM, Franco OH, Nijsten TEC, et al. The association of autoimmune thyroid disease (AITD) with psoriatic disease: A prospective cohort study, systematic review and meta-analysis. Eur J Endocrinol 2017;177:347-59.  Back to cited text no. 34
    
35.
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. 35
    
36.
Arican O, Bilgic K, Koc K. The effect of thyroid hormones in psoriasis vulgaris. Indian J Dermatol Venerol Leprol 2004;70:354-6.  Back to cited text no. 36
    
37.
Gul U, Gonul M, Kaya I, Aslan E. Autoimmune thyroid disorders in patients with psoriasis. Eur J Dermatol 2009;19:221-3.  Back to cited text no. 37
    
38.
Vassilatou E, Papadavid E, Papastamtakis P, Alexakos D, Koumaki D, Katsimbri P, et al. No association of psoriasis with autoimmune thyroiditis. J Eur Acad Dermatol Venereol 2017;31:96-101.  Back to cited text no. 38
    
39.
Borges AS, Moura M, Coelho V, Brasileiro AB. A possible association between psoriasis and thyroid dysfunction. Eur J Dermatol 2016;28:715-6.  Back to cited text no. 39
    
40.
Gharib H, Tuttle RM, Baskin HJ, Fish LH, Singer PA, McDermott MT. Sub clinical thyroid dysfunction: A joint statement on management from the American association of clinical endocrinologists, the American thyroid association, and the endocrine society. J Clin Endocrinol Metab 2005;90:581-7.  Back to cited text no. 40
    
41.
Warner MH, Beckett GJ. Mechanisms behind the non-thyroidal illness syndrome: An update. J Endocrinol 2010;205:1-13.  Back to cited text no. 41
    
42.
Preissner CM, O'Kane DJ, Singh RJ, Morris JC, Grebe SK. Phantoms in the assay tube: Heterophile antibody interferences in serum thyroglobulin assays. J Clin Endocrinol Metab 2003;88:3069-74.  Back to cited text no. 42
    
43.
Kricka LJ. Human anti-animal antibody interferences in immunological assays. Clin Chem 1999;45:942-56.  Back to cited text no. 43
    



 
 
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