It can thus be hypothesized that there would be a decreased effect of cevimeline in patients with greater salivary gland tissue damage. In addition, autoantibodies that bind to muscarinic type 3 receptors (M3R) were detected in the sera obtained from Sjögren’s syndrome patients [16], and IgG in patients with primary Sjögren’s syndrome was observed to reduce the carbachol-evoked increase in Ca2+ in both mouse and human acinar cells, showing that IgG from patients with primary Sjögren’s syndrome contains autoantibodies capable of damaging saliva production [17]. These Volasertib datasheet studies suggest the involvement of autoantibodies to the receptors in the response to cevimeline in patients with Sjögren’s syndrome. Therefore,

the clinical effect of cevimeline

on the enhancement of salivary secretion thus appears to be influenced multifactorially. If the efficacy of cevimeline could be predicted from the findings Selleck GSK1120212 of diagnostic clinical examinations before treatment, it would be useful for determining the prognosis of patients with Sjögren’s syndrome, and for determining whether another therapy should be selected. Therefore, we previously conducted a study to elucidate the relationship between the effect of cevimeline and the findings of diagnostic clinical examinations in patients with Sjögren’s syndrome [18]. The relationship between the pre-treatment sialometry (saliva flow rate) and clinical examination was the first to be studied. Patients with positive sialography findings (Stages I–IV) had significantly lower pre-treatment whole stimulated sialometry (WSS) findings compared to those with negative findings (Stage 0) (p = 0.003) ( Fig. 1A, open column). In contrast, findings of labial minor salivary gland biopsy were not related to pre-treatment WSS in patients with Sjögren’s syndrome (p = 0.806) ( Fig. 1B, open column). As WSS is principally

secreted from the parotid gland [19], this discrepancy might be due to the differences in the evaluation site (parotid gland versus minor salivary gland). These results are congruent with those reported by Saito et al. [20]. Fig. 1A shows the pre- and post-treatment WSS in groups classified according to the sialography findings. In both the Stage 0 and the Stages I–IV groups, the post-treatment WSS demonstrated a significant increase compared with the pre-treatment values (p = 0.008 only and p = 0.015, respectively). The magnitude of the increase in WSS after cevimeline treatment in the Stage 0 group was significantly higher than that in the Stages I–IV group (p < 0.001). The increment rate of WSS after cevimeline treatment in the Stage 0 group was significantly higher than that in the Stages I–IV group (p = 0.042). Fig. 1B shows the pre- and post-treatment WSS in groups classified according to the findings of the labial minor salivary gland biopsy. In both the Grades 0–2 and the Grades 3 and 4 groups, post-treatment WSS demonstrated a significant increase compared to the pre-treatment values (p = 0.018 and p = 0.