Silvia Martina Ferrari

Università degli Studi di Modena e Reggio Emilia, Modène, Emilia-Romagna, Italy

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Publications (150)453.79 Total impact

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    ABSTRACT: Objectives: Patients with SSc have an increased risk of malignancy compared with the general population. Before now, no study has evaluated the risk of thyroid cancer (TC) in SSc patients. The aim of the study was to evaluate the prevalence of TC in SSc patients. Methods: We studied the prevalence of TC in 327 unselected SSc patients in comparison with two population-based, gender- and age-matched control groups (654 subjects from an iodine-deficient area and 654 subjects from an iodine-sufficient area). Thyroid status was assessed by measurement of circulating thyroid hormones and autoantibodies, thyroid ultrasonography and fine-needle aspiration cytology (when necessary). Results: Circulating thyroid-stimulating hormone, anti-thyroglobulin and anti-thyroperoxidase antibody levels, and the prevalence of hypothyroidism were significantly higher in SSc patients (P < 0.01, for all). Six patients with papillary TC (PTC) were detected among SSc patients, whereas only one case was observed in each of controls 1 and 2 (P = 0.007, for both). In SSc all patients with TC had evidence of thyroid autoimmunity vs 40% of the other SSc patients (P = 0.001). Conclusion: These data suggest a high prevalence of papillary TC in SSc patients, in particular in the presence of thyroid autoimmunity; careful thyroid monitoring would be opportune during the follow-up of these patients.
    Rheumatology (Oxford, England) 10/2015; DOI:10.1093/rheumatology/kev358 · 4.48 Impact Factor
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    ABSTRACT: We have studied the antitumor activity of two new "pyrazolo[3,4-d]pyrimidine" compounds (CLM29 and CLM24) that inhibit several targets (including the RET tyrosine kinase, epidermal growth factor receptor, vascular endothelial growth factor receptor, with an antiangiogenic effect) in primary anaplastic thyroid cancer (ATC) cell cultures and in the human cell line 8305C (undifferentiated thyroid cancer). The antitumor effect of CLM29 and CLM24 was tested in: nine primary ATC cultures obtained from patients at the time of surgery at the concentrations of 1, 5, 10, 30, 50 µM; in 8305C cells at 1, 5, 10, 30, 50 µM for CLM29, and 0.001, 0.01, 0.1, 1, 10, 100 µM for CLM24. CLM29, and CLM24 significantly inhibited the proliferation of 8305C cells. A significant reduction of proliferation with CLM29 and CLM24 in ATC cells (P < 0.01, for both, ANOVA) was shown. CLM29 and CLM24 increased the percentage of apoptotic ATC cells dose-dependently (P < 0.001, ANOVA). The (V600E) BRAF mutation was observed in three ATCs; the results about the inhibition of proliferation by CLM29 and CLM24, obtained in ATC from tumors with (V600E) BRAF mutation were similar to those from tumors without BRAF mutation. CLM29 inhibited migration and invasion (P < 0.01) of primary ATC cells, while CLM24 had no significant effect. The antitumor activity of two new "pyrazolo[3,4-d]pyrimidine" compounds (CLM24, CLM29) in vitro in ATC, independent from BRAF mutation, has been shown, allowing a future clinical evaluation.
    Endocrine 08/2015; DOI:10.1007/s12020-015-0717-4 · 3.88 Impact Factor
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    ABSTRACT: Chemokine (C-X-C motif) ligand (CXCL)10 is involved in the pathogenesis of psoriasis. It has been demonstrated that chemokine (C-X-C motif) receptors (CXCR)3 and CXCL10 were detected in keratinocytes and the dermal infiltrate obtained from active psoriatic plaques and that successful treatment of active plaques decreased the expression of CXCL10. Elevated CXCL10 serum levels have been shown in patients with psoriasis, with a type 1 T helper cells immune predominance at the beginning of the disease, while a decline of this chemokine has been evidenced later, in long lasting psoriasis. Circulating CXCL10 is significantly higher in patients with psoriasis in the presence of autoimmune thyroiditis. It has been hypothesized that CXCL10 could be a good marker to monitor the activity or progression of psoriasis. Efforts have been made to modulate or inhibit the CXCR3/CXCL10 axis in psoriasis to modify the course of the disease. Copyright © 2015. Published by Elsevier Urban & Partner Sp. z o.o.
    Advances in Medical Sciences 08/2015; 60(2):349-354. DOI:10.1016/j.advms.2015.07.011 · 1.11 Impact Factor
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    ABSTRACT: More than half a century after their discovery, benzodiazepines (BDZs) still represent one of the largest and most widely prescribed groups of psychotropic compounds, not only in clinical psychiatry but also in the entire medical field. Over the last two decades, however, there has been an increased focus on the development of antidepressants and antipsychotics on the part of the pharmaceutical industry, clinicians, and researchers, with a reduced interest in BDZs, in spite of their widespread clinical use. As a consequence, many psychiatric residents, medical students, nurses, and other mental health professionals might receive poor academic teaching and training regarding these agents, and have the false impression that BDZs represent an outdated chapter in clinical psychopharmacology. However, recent advances in the field, including findings concerning epidemiology, addiction risk, and drug interactions, as well as the introduction of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition with related diagnostic changes, strongly encourage an updated appraisal of the use of BDZs in clinical practice. During a recent thematic event convened with the aim of approaching this topic in a critical manner, a group of young Italian psychiatrists attempted to highlight possible flaws in current teaching pathways, identify the main clinical pros and cons regarding current use of BDZs in clinical practice, and provide an updated overview of their use across specific clinical areas and patient populations. The main results are presented and discussed in this review.
    Neuropsychiatric Disease and Treatment 08/2015; 11:1885-909. DOI:10.2147/NDT.S83130 · 1.74 Impact Factor
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    ABSTRACT: Cytokines and chemokines, hepatitis C virus (HCV) infection-induced, participate in viral control and liver damage. The complex cytokine network, operating during initial infection allows a coordinated and effective development of innate and adaptive immune responses. "HCV interferes with cytokines at various levels and escapes immune response by inducing a T helper (Th)2/T cytotoxic 2 cytokine profile". A predominance of the Th1 immune response (and related cytokines) has been evidenced in chronic hepatitis C infection and in extrahepatic manifestations. Interferon (IFN)- and IFN--inducible chemokine (C-X-C motif) ligand (CXCL)9, -10 and -11 recruit inflammatory infiltrates into the liver parenchyma due to the incapability to control the infection process, resulting in extensive liver damage and liver cirrhosis. "The most important systemic HCV-related extrahepatic diseases - mixed cryoglobulinemia, lymphoproliferative disorders, diabetes and autoimmune thyroid disorders - are associated with a complex dysregulation of the cytokine/chemokine network and involve pro-inflammatory and Th1 chemokines. The therapeutical administration of cytokines such as IFN- may result in viral clearance during persistent infection and reverts this process" reducing circulating CXCL10 levels. "Several studies have reported interleukin (IL)-28B polymorphisms, and circulating CXCL10, may be prognostic markers for HCV treatment efficacy in HCV infection". Other studies have also shown that HCV clearance by directly acting antiviral agents therapy decreases circulating CXCL10 levels. "Theoretically agents that selectively neutralize CXCL10 could increase patient responsiveness to traditional IFN-based HCV therapy", simultaneously reducing inflammatory immune cell activation.
    Current drug targets 08/2015; · 3.02 Impact Factor
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    ABSTRACT: Cabozantinib is an oral once-daily multitarget tyrosine kinase inhibitor of MET, VEGFR2, RET, acting against KIT, AXL, FLT3 and Tie-2. Cabozantinib has shown anti-cancer effects in preclinical and clinical models of cancers derived from both epithelial and mesenchymal origins [prostate cancer, non small lung cancer, medullary thyroid cancer (MTC) and differentiated thyroid cancer (DTC), renal cell carcinoma, etc.]. In a phase III clinical study, cabozantinib improved PFS (11.2 months versus 4.0 months in the placebo group) of patients with MTC (independently of age, bone metastases, RET status and prior treatment). Cabozantinib was approved in 2012 by FDA for metastatic MTC and in 2013 by EMA. Cabozantinib has been also evaluated in metastatic DTC patients, because they have activation on tyrosine kinases, including MET, VEGFR2 and RET, suggesting the possible use of cabozantinib in metastatic DTC. Actually, two phase II trials of cabozantinib in DTC patients resistant to RAI are ongoing. To increase the antineoplastic effect of cabozantinib, and to overcome the occurrence of drug resistance, combination studies with other anticancer agents are ongoing. In conclusion cabozantinib has shown to exert an important therapeutic effect in patients with MTC improving PFS. In DTC patients, cabozantinib has shown promising results.
    07/2015; 10(3). DOI:10.2174/1574892810666150708110816
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    ABSTRACT: Sorafenib has been evaluated in several Phase II and III studies in patients with locally advanced/metastatic radioactive iodine–refractory differentiated thyroid carcinomas (DTCs), reporting partial responses, stabilization of the disease and improvement of progression-free survival. Best responses were observed in lung metastases and minimal responses in bone lesions. On the basis of these studies, sorafenib was approved for the treatment of metastatic DTC in November 2013. Few studies suggested that reduction of thyroglobulin levels, or of average standardized uptake value at the fluorodeoxyglucose-PET, could be helpful for the identification of responding patients; but further studies are needed to confirm these results. Tumor genetic marker levels did not have any prognostic or predictive role in DTC patients.The most common adverse events observed included skin toxicity and gastrointestinal and constitutional symptoms. Encouraging results have also been observed in patients with medullary thyroid cancer. Many studies are ongoing to evaluate the long-term efficacy and tolerability of sorafenib in DTC patients.
    Expert Review of Anti-infective Therapy 07/2015; 15(8). DOI:10.1586/14737140.2015.1064770 · 3.46 Impact Factor
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    ABSTRACT: Vandetanib is a once-daily orally available tyrosine kinase inhibitor that works by blocking RET (REarranged during Transfection), vascular endothelial growth factor receptor (VEGFR-2, VEGFR-3), and epidermal growth factor receptor and to a lesser extent VEGFR-1, which are important targets in thyroid cancer (TC). It is emerging as a potentially effective option in the treatment of advanced medullary thyroid cancer (MTC) and in dedifferentiated papillary thyroid cancer not responsive to radioiodine. The most important effect of vandetanib in aggressive MTC is a prolongation of progression-free survival and a stabilization of the disease. Significant side effects have been observed with the vandetanib therapy (as fatigue, hypertension, QTc prolongation, cutaneous rash, hand-and-foot syndrome, diarrhea, etc), and severe side effects can require the suspension of the drug. Several studies are currently under way to evaluate the long-term efficacy and tolerability of vandetanib in MTC and in dedifferentiated papillary TC. The efficacy of vandetanib in patients with MTC in long-term treatments could be overcome by the resistance to the drug. However, the effectiveness of the treatment could be ameliorated by the molecular characterization of the tumor and by the possibility to test the sensitivity of primary TC cells from each subject to different tyrosine kinase inhibitor. Association studies are evaluating the effect of the association of vandetanib with other antineoplastic agents (such as irinotecan, bortezomib, etc). Further research is needed to determine the ideal therapy to obtain the best response in terms of survival and quality of life.
    Drug Design, Development and Therapy 07/2015; 9:3459-70. DOI:10.2147/DDDT.S72495 · 3.03 Impact Factor
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    ABSTRACT: Sorafenib (Nexavar), is a multikinase inhibitor, which has demonstrated both anti proliferative and anti-angiogenic properties in vitro and in vivo, inhibiting the activity of targets present in the tumoral cells [c-RAF (proto-oncogene serine/threonine-protein kinase), BRAF, (V600E)BRAF, c-KIT, and FMS-like tyrosine kinase 3] and in tumor vessels [c-RAF, vascular endothelial growth factor receptor (VEGFR)-2, VEGFR-3, and platelet-derived growth factor receptor β]. Sorafenib was initially approved for the treatment of hepatocellular carcinoma and advanced renal cell carcinoma. Experimental studies have demonstrated that sorafenib has both anti-proliferative and anti-angiogenic properties in vitro and in vivo, against thyroid cancer cells. Furthermore, several completed (or ongoing) studies have evaluated the long-term efficacy and tolerability of sorafenib in patients with papillary, follicular and medullary aggressive thyroid cancer. The results of the different studies showed good clinical responses and stabilization of the disease and suggested that sorafenib is a promising therapeutic option in patients with advanced thyroid cancer that is not responsive to traditional therapeutic strategies (such as radioiodine). Currently, USA Food and Drug Administration has approved the use of sorafenib for metastatic differentiated thyroid cancer.
    Minerva endocrinologica 06/2015; · 1.46 Impact Factor
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    ABSTRACT: Background: The Burnout Syndrome (BS) is a common condition among health care professionals, yet data concerning its prevalence and associated factors among psychiatric residents are lacking. Objectives: To report the results of the Italian contribution to “BOSS”, an international multicentre research project aiming at estimating the burden of BS among residents in psychiatry, and at identifying factors contributing to its development and prevention. Methods: Cross-sectional study. The BOSS online questionnaire, which collected socio-demographic data and five psychometric tools (MBI-GS, AWLS, PHQ-9, SIBQ, BFI), was administered electronically to 180 Italian residents in psychiatry. Simple and multiple linear regressions were performed to analyse data. Results: 108 questionnaires provided data for the study (response rate: 60%). Mean age: 30.5±3.7 years. Eighty percent of the sample were female. A moderate level of BS emerged, related to work conditions, absence of major depression, satisfaction with pay or less academic activity. Only 0.9% (N=1) of the sample showed PHQ-9 scores suggestive of major depression, while lifetime suicidal ideation was admitted by 16% of residents. For the three dimensions of the MBIGS, Italian sample scores were consistent with previously published results concerning pooled data in a French- Croatian sample, reporting moderate levels of BS. Higher workload, symptoms of depression and lower satisfaction predicted higher levels of Emotional Exhaustion and Cynicism. Conclusions: Italian residents in psychiatry showed overall moderate levels of BS, related to workload and work organization. Other alerts of psychic distress were found among participants, namely symptoms of depression, suicidal ideation and use of psychotropic medications.
    La Medicina del lavoro 05/2015; 106(3):172. · 0.55 Impact Factor
  • 05/2015; 2(2):1-8. DOI:10.2217/ije.15.4
  • 05/2015; DOI:10.1530/endoabs.37.EP867
  • Alessandro Antonelli · Silvia Martina Ferrari · Poupak Fallahi
    05/2015; 3(Suppl 1):S16. DOI:10.3978/j.issn.2305-5839.2015.03.02
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    ABSTRACT: In this paper we will describe cultural, social and scientific changes occurred in psychiatry in the last years, identifying the new target for mental health professionals. Groups of young psychiatrists from the Italian Psychiatric Association, the European Psychiatric Association and the World Psychiatric Association have established an international network that launched a debate on the future role of psychiatry. In a rapidly changing world, there is the need to: 1) adapt training in psychiatry to the modern world; 2) identify the new target of mental health professionals; 3) enhance the image of psychiatry in the society; 4) overcome stigma towards people with mental disorders. In recent years, socio-cultural and scientific changes have had a significant impact on the psychiatrists' clinical practice. Mental health professionals should deal with these changes appropriately in order to overcome the current "crisis" of psychiatry, which should be considered as a developmental phase rather than a conceptual one. From time to time psychiatry is criticized both from inside and outside the profession. The current crisis was unavoidable due to the recent socio-cultural changes, but it should be considered an opportunity to adapt the profession to modern times.
    03/2015; 50(1):3-7. DOI:10.1708/1794.19524
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    ABSTRACT: The number of thyroid cancers is increasing. Standard treatment usually includes primary surgery, thyroid-stimulating hormone suppressive therapy, and ablation of the thyroid remnant with radioactive iodine (RAI). Despite the generally good prognosis of thyroid carcinoma, about 5% of patients will develop metastatic disease, which fails to respond to RAI, exhibiting a more aggressive behavior. The lack of specific, effective and well-tolerated drugs, the scarcity of data about the association of multi-targeting drugs, and the limited role of radioiodine for dedifferentiated thyroid cancer, call for further efforts in the field of new drugs development. Rearranged during transfection (RET)/papillary thyroid carcinoma gene rearrangements, BRAF (B-RAF proto-oncogene, serine/threonine kinase) gene mutations, RAS (rat sarcoma) mutations, and vascular endothelial growth factor receptor 2 angiogenesis pathways are some of the known pathways playing a crucial role in the development of thyroid cancer. Targeted novel compounds have been demonstrated to induce clinical responses and stabilization of disease. Sorafenib has been approved for differentiated thyroid cancer refractory to RAI.
    International Journal of Molecular Sciences 03/2015; 16(3):6153-6182. DOI:10.3390/ijms16036153 · 2.86 Impact Factor
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    ABSTRACT: Peroxisome proliferator-activated receptor- (PPAR-) γ expression has been shown in thyroid tissue from patients with thyroiditis or Graves' disease and furthermore in the orbital tissue of patients with Graves' ophthalmopathy (GO), such as in extraocular muscle cells. An increasing body of evidence shows the importance of the (C-X-C motif) receptor 3 (CXCR3) and cognate chemokines (C-X-C motif) ligand (CXCL)9, CXCL10, and CXCL11, in the T helper 1 immune response and in inflammatory diseases such as thyroid autoimmune disorders. PPAR-γ agonists show a strong inhibitory effect on the expression and release of CXCR3 chemokines, in vitro, in various kinds of cells, such as thyrocytes, and in orbital fibroblasts, preadipocytes, and myoblasts from patients with GO. Recently, it has been demonstrated that rosiglitazone is involved in a higher risk of heart failure, stroke, and all-cause mortality in old patients. On the contrary, pioglitazone has not shown these effects until now; this favors pioglitazone for a possible use in patients with thyroid autoimmunity. However, further studies are ongoing to explore the use of new PPAR-γ agonists in the treatment of thyroid autoimmune disorders.
    PPAR Research 02/2015; 2015:232818. DOI:10.1155/2015/232818 · 1.64 Impact Factor
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    ABSTRACT: Interferon (IFN)-γ-induced protein 10 (IP-10/CXCL10) and its receptor, C-X-C motif receptor 3, appear to contribute to the pathogenesis of hepatitis C virus (HCV)-related mixed cryoglobulinaemia (MC) (HCV+MC). The secretion of CXCL10 by cluster of differentiation (CD) CD4+, CD8+, and natural killer-T cells is dependent on IFN-γ, which is itself mediated by the interleukin-12 cytokine family. Under the influence of IFN-γ, CXCL10 is secreted by several cell types including lymphocytes, hepatocytes, endothelial cells, fibroblasts, etc. In tissues, recruited T helper 1 lymphocytes may be responsible for enhanced IFN-γ and tumour necrosis factor-α production, which in turn stimulates CXCL10 secretion from the cells, therefore creating an amplification feedback loop, and perpetuating the autoimmune process. High levels of CXCL10 in circulation have been found in HCV+MC, especially in patients with clinically active vasculitis. Furthermore, HCV+MC patients with autoimmune thyroiditis (AT) have higher levels than those without AT. Further studies are needed to investigate interactions between chemokines and cytokines in the pathogenesis, and to evaluate whether CXCL10 is a novel therapeutic target in HCV-related MC.
    Clinical and experimental rheumatology 01/2015; 33(3). · 2.72 Impact Factor
  • Alessandro Antonelli · Silvia Martina Ferrari · Ilaria Ruffilli · Poupak Fallahi
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    ABSTRACT: Cytokines are intercellular mediators involved in viral control and liver damage being induced by infection with hepatitis C virus (HCV). The complex cytokine network operating during initial infection allows a coordinated, effective development of both innate and adaptive immune responses. However, HCV interferes with cytokines at various levels and escapes immune response by inducing a T-helper (Th)2/T cytotoxic 2 cytokine profile. Inability to control infection leads to the recruitment of inflammatory infiltrates into the liver parenchyma by interferon (IFN)-γ-inducible CXC chemokine ligand (CXCL)9, -10, and -11 chemokines, which results in sustained liver damage and eventually in liver cirrhosis. The most important systemic HCV-related extrahepatic diseases-mixed cryoglobulinemia, lymphoproliferative disorders, thyroid autoimmune disorders, and type 2 diabetes-are associated with a complex dysregulation of the cytokine/chemokine network, involving proinflammatory and Th1 chemokines. The therapeutical administration of cytokines such as IFN-α may result in viral clearance during persistent infection and revert this process. Theoretically agents that selectively neutralize CXCL10 could increase patient responsiveness to traditional IFN-based HCV therapy. Several studies have reported IL-28B polymorphisms and circulating CXCL10 may be a prognostic markers for HCV treatment efficacy in HCV genotype 1 infection.
    Immunologic Research 11/2014; 60(2-3). DOI:10.1007/s12026-014-8569-1 · 3.10 Impact Factor
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    ABSTRACT: To our knowledge, no study has evaluated the involvement of T helper (Th)1- and Th2-chemokines in extra-ocular muscle (EOM) myopathy in “patients with thyroid-associated ophthalmopathy” (TAO-p). We tested the effects of interferon (IFN)γ and tumor necrosis factor (TNF)α stimulation, and of increasing concentrations of peroxisome proliferator-activated receptor (PPAR)γ agonists (pioglitazone or rosiglitazone; 0.1 μM–20 μM), on Th1-chemokine [C-X-C motif ligand (CXCL)10] and Th2-chemokine [C-C motif ligand (CCL)2] secretion in primary EOM cultures from TAO-p vs. control myoblasts. Moreover, we evaluated serum CXCL10 and CCL2 in active TAO-p with prevalent EOM involvement (EOM-p) vs. those with prevalent orbital fat expansion (OF-p). Serum CXCL10 was higher in OF-p and EOM-p vs. controls, while serum CCL2 was not significantly different in controls, or in OF-p and EOM-p. We showed the expression of PPARγ in EOM cells. In primary EOM cultures from TAO-p: a) CXCL10 was undetectable in the supernatant, IFNγ dose-dependently induced it, whereas TNFα did not; b) EOM produced basally low amounts of CCL2, TNFα dose-dependently induced it, whereas IFNγ did not; c) the combination of TNFα and IFNγ had a significant synergistic effect on CXCL10 and CCL2 secretion; and d) PPARγ agonists have an inhibitory role on the modulation of CXCL10, while they stimulate CCL2 secretion. EOM participates in the self-perpetuation of inflammation by releasing both Th1 (CXCL10) and Th2 (CCL2) chemokines under the influence of cytokines, in TAO. PPARγ agonist activation plays an inhibitory role on CXCL10, but stimulates the release of CCL2.
    Autoimmunity Reviews 11/2014; 13(11). DOI:10.1016/j.autrev.2014.08.025 · 7.93 Impact Factor
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    ABSTRACT: Autoimmune thyroid diseases (AITD) result from a dysregulation of the immune system leading to an immune attack on the thyroid. AITD are T cell-mediated organ-specific autoimmune disorders. The prevalence of AITD is estimated to be 5%; however, the prevalence of antithyroid antibodies may be even higher. The AITD comprise two main clinical presentations: Graves' disease (GD) and Hashimoto's thyroiditis (HT), both characterized by lymphocytic infiltration of the thyroid parenchyma. The clinical hallmarks of GD and HT are thyrotoxicosis and hypothyroidism, respectively. The mechanisms that trigger the autoimmune attack to the thyroid are still under investigation. Epidemiological data suggest an interaction among genetic susceptibility and environmental triggers as the key factor leading to the breakdown of tolerance and the development of disease. Recent studies have shown the importance of cytokines and chemokines in the pathogenesis of AT and GD. In thyroid tissue, recruited T helper 1 (Th1) lymphocytes may be responsible for enhanced IFN-γ and TNF-α production, which in turn stimulates CXCL10 (the prototype of the IFN-γ-inducible Th1 chemokines) secretion from the thyroid cells, therefore creating an amplification feedback loop, initiating and perpetuating the autoimmune process. Associations exist between AITD and other organ specific (polyglandular autoimmune syndromes), or systemic autoimmune disorders (Sjögren's syndrome, rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, cryoglobulinemia, sarcoidosis, psoriatic arthritis). Moreover, several studies have shown an association of AITD and papillary thyroid cancer. These data suggest that AITD patients should be accurately monitored for thyroid dysfunctions, the appearance of thyroid nodules, and other autoimmune disorders.
    Autoimmunity Reviews 10/2014; 14(2). DOI:10.1016/j.autrev.2014.10.016 · 7.93 Impact Factor

Publication Stats

2k Citations
453.79 Total Impact Points


  • 2008–2015
    • Università degli Studi di Modena e Reggio Emilia
      • • Department of Diagnostic Medicine, Clinical and Public Health
      • • Department of Biomedical, Metabolical and Neurosciences
      Modène, Emilia-Romagna, Italy
  • 2004–2015
    • Università di Pisa
      • Department of Clinical and Experimental Medicine
      Pisa, Tuscany, Italy
  • 2004–2007
    • University of Florence
      Florens, Tuscany, Italy
  • 2005
    • National Research Council
      • Institute of Clinical Physiology IFC
      Roma, Latium, Italy