Such heterogeneous manifestations are explained at two level

Such heterogeneous manifestations are explained at two levels: glandular and systemic extraglandular levels. Hitherto, the analyses of gene expression profiles of salivary gland tissues, obtained from patients with SS, confirmed the presence of T cells, B cells, dendritic KY02111 and macrophages. Systemically, chronic inflammation in several organs, mostly immunologically-induced, is responsible for the extraglanular manifestations [7]. Pursuing the dysfunctional pathways, genetic background was identified in SS patients. More often, the inflammatory fire is attributed to abnormal regulation of ApoE, BAFF, CCR5, Fas, FasL, GSTM1, HA-1, IgKM, IkBα, IkBβ, IL-1, IL-6, IL-10, IL-4Rα, IRF5, MBL, PTPN22, STAT4, TcRBV, TGF-β, TNF-α, and 52 kDa Ro/SS-A [3]. The question of ameliorating or exacerbating the severity of SS during pregnancy is rarely negotiated in the medical literature. However, hormonal contribution to the pathogenesis of SS was suggested especially after demonstrating higher ratios of prolactin/progesterone and estrogen/progesterone in a number of SS patients [8]. Furthermore, microchimeristical involvement of cells transfer between fetus and mother during pregnancy, which can persist in both decades later, has been suggested to cause autoimmune disease including SS [9]. Moreover, acinar cells of minor salivary glands were demonstrated to fail maintaining cysteine-rich secretory protein-3 and dihydrotestosterone in SS and so is the case in female-dominant autoimmune exocrinopathy. This was attributed to androgen depletion and defective dehydroepiandrosterone (DHEA) in SS salivary glands [10]. However, restoration of systemic androgen levels by DHEA treatment did not correct local androgen depletion [11]. This can be simply attributed to secondary role dendritic cells play in chronic inflammation of SS minor salivary glands. Given the impairing influence of elevated levels of DHEA on dendritic cells but not on lymphocytes [12], failure of treating SS by restoring DHEA can be comprehended. In a trial to explain the initial dramatic improvement and relapse, intercalated duct cells are postulated to carry a heavier weight than acinar cells in restoring the normal function of salivary glands. Given the overexpression REG Iα in salivary ductal cells is induced by IL-6 but not by IL-8 at the transcriptional level. IL-6/JAK-STAT3 is expected to play the major pathogentic role in maintain the chronic inflammatory status of SS salivary glands [13]. Estrogen, which is decreased after menopause and after delivery, may be of therapeutic effect on SS via regulating immune tolerance (growth, differentiation and proliferation of lymphocyte; antigen presentation; cytokine production; antibody production; as well as cell survival and apoptosis). In early pregnancy, low molecular mass polypeptide (LMP) 2 and LMP7, which underlie the downregulation of human leukocyte antigen class I antigen, may be responsible for promoting SS. TAP-LMP genetic abnormality is known to be responsible for several autoimmune conditions [14]. Prophylactic measures are mandatory in order not to aggravate the severity of SS. Dietary and beverage must be caffeine-free and non-cariogenic. Exposure to ionized radiation must be avoided unless very necessary. Radiological Follow up should be confined to sonography and MRI. Scrupulous oral hygiene is mandatory [2]. Treating Sjögren\'s syndrome is also problematic and banks heavily on alleviating the severity of symptomatic signs and symptoms as well as on educating patients about their medical condition. Applying topical fluoride and remineralizing solutions, using artificial saliva and oral lubricants, sipping water, washing eyes, wetting skin, and artificial tears are useful. Therapeutic effect of corticosteroid in SS patients is controversial [2,15]. Our patient was initially treated with low-doses of corticoids which were suspended during pregnancy and on.
Conclusions
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