**5. Future directions and therapeutic implications**

Future and near-future directions in the area of autoimmune diseases will be influenced by the general role and directions in medicine. Thus, more and more immune biology modulators and therapies directed against specific molecular pathways will become available. This may alter the need for HSCT as the only curative modality or further subject it to those who would fail all the biological treatments.

Individualize or personalized treatment will become the main stream in therapy. This is extremely true for autoimmune diseases where variety of sub-classes and genom-based mapping will give the opportunity to treat each patient in a different, more specific way. On the other hand, it is expected that HSCT would become safer with less treatment-related morbidity and mortality, making transplants more accessible to wider range of patient populations. Thus, we will see more and more allogeneic transplants done for large-scale indications.

#### **6. References**


either exacerbate or ameliorate disease severity. For example, in experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis (MS), growth factors such as Flt-3 ligand, stem cell factor (SCF), and G-CSF exacerbate disease, while thrombopoietin (TPO) mobilizes stem cells without affecting disease severity. G-CSF may also cause an exacerbation of MS, sometimes with significant neurological deterioration [60, 62]. In both EAE and MS, simultaneous use of daily corticosteroids or infusion of cyclophosphamide prior to starting G-CSF prevents disease flares [62]. The same may be for RA where G-CSF may cause an increase in joint swelling, tenderness and pain that responds to corticosteroids. On the other hand, G-CSF has not been reported to exacerbate scleroderma. Based on the above, growth factors selected for mobilizing HSCs from patients with autoimmune diseases need to be considered on a disease-specific basis. Hematopoietic growth factors that stimulate production of proinflammatory cytokines or alter trafficking of neutrophils, lymphocytes or dendritic cells may exacerbate some autoimmune diseases. This effect may be prevented by either administration of corticosteroids or mobilization with combined cyclophosphamide and G-CSF. Mobilization with chemotherapy alone or in combination with G-CSF may cause neutropenic fevers and infection-related mortality if prophylactic antibacterial and antifungal antibiotics are not utilized. This can be prevented if only G-CSF will be used. Nevertheless, combined cyclophosphamide with G-CSF for mobilization will sum in higher stem cell yields, an in vivo purge effect by selectively killing

Future and near-future directions in the area of autoimmune diseases will be influenced by the general role and directions in medicine. Thus, more and more immune biology modulators and therapies directed against specific molecular pathways will become available. This may alter the need for HSCT as the only curative modality or further subject

Individualize or personalized treatment will become the main stream in therapy. This is extremely true for autoimmune diseases where variety of sub-classes and genom-based mapping will give the opportunity to treat each patient in a different, more specific way. On the other hand, it is expected that HSCT would become safer with less treatment-related morbidity and mortality, making transplants more accessible to wider range of patient populations. Thus, we will see more and more allogeneic transplants done for large-scale

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**20** 

*Italy* 

**Thionamides-Related Vasculitis in** 

Giuseppa Perdichizzi1 and Domenico Cucinotta1

**Current Literature and Case Reports** 

*1Department of Internal Medicine, University of Messina, Messina,* 

**Autoimmune Thyroid Disorders: Review of** 

Elisabetta L. Romeo1, Giuseppina T. Russo1, Annalisa Giandalia1, Provvidenza Villari1, Angela A. Mirto1, Mariapaola Cucinotta2,

*2Section of Nuclear Medicine, Department of Radiology, University of Messina, Messina,* 

Hyperthyroidism is the consequence of excessive thyroid hormone action (AACE Thyroid Guidelines, 2002). In many cases, it results from excessive activity of the thyroid gland, with a pathologically increased production of thyroid hormones. The causes of hyperthyroidism

**1. Introduction** 

• Toxic adenoma

include several conditions, that are listed in Table 1.

• Toxic multinodular goiter (Plummer's disease)

• Excessive pituitary TSH or trophoblastic disease

• Excessive ingestion of thyroid hormone

as ophthalmopathy and pretibial myxedema.

• Silent thyroiditis, including lymphocytic and postpartum variations

Table 1. Causes of hyperthyroidism (AACE Thyroid Guidelines,2002*)*

• Iodine-induced hyperthyroidism (for example, related to amiodarone therapy)

Graves' disease is the most common cause of hyperthyroidism. It is an autoimmune disorder, caused by the presence of autoantibodies directed against the thyroid-stimulating hormone (TSH) receptor (TRAb), chronically stimulating thyroid hormone synthesis and secretion, and resulting in an excessive amount of triiodothyronine (T3) and thyroxine (T4) and gland growth. In iodine sufficient areas, this prototypical autoimmune disease is the most common cause of thyrotoxicosis in young women as well as in children and adolescents, and it is characterized by thyrotoxicosis, goitre and typical manifestations such

According to the American Association of Clinical Endocrinologists guidelines (AACE, 2002), the diagnosis of hyperthyroidism relates on TSH values. Thus, with the exception of the excess of TSH secretion, hyperthyroidism of any cases results in a lower-than-normal or

• Toxic diffuse goiter (Graves' disease)

• Painful subacute thyroiditis

