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Fibromyalgia syndrome (FM) is a musculoskeletal disease characterized by chronic diffuse pain and increased pain sensitivity. 1 Although the etiopathogenesis of FM is not yet clear, genetic, environmental and immunological factors, and peripheral and central mechanisms are thought to play a role. 2 In clinical studies, central sensitization has been thought to be responsible for the pathogenesis of FM and it has been claimed that abnormalities in the perception and/or processing of pain in the central nervous system may play a role. 3,4

Background:Mast cells (MCs) can stimulate angiogenesis, releasing several proangiogenic cytokines stored in their cytoplasm. In particular, MCs can release tryptase, a potent in vivo and in vitro proangiogenic factor via protease-activated receptor-2 (PAR-2) activation and mitogen-activated protein kinase (MAPK) phosphorylation. Nevertheless, no data are available concerning the relationship among tryptase MC density (TMCD), endothelial cells (ECs) positive to PAR-2 microvascular density (PAR-2-MVD) and classical MVD (C-MVD) in gastric cancer (GC) angiogenesis.Methods:In this study, we analyzed the correlation of TMCD, PAR-2-MVD, C-MVD with each other and with the main clinicopathological features in GC patients who underwent surgery. A series of 77 GC patients with stage T2-3N2-3M0 (classified by the American Joint Committee on Cancer for Gastric Cancer, 7th edition) were selected and then underwent surgery.Results:Tumour tissue samples were evaluated by mean of immunohistochemistry and image analysis methods in terms of numbers of TMCD, PAR-2-MVD and C-MVD. A significant correlation between the TMCD, PAR-2-MVD and C-MVD groups with each other was found by Pearson t-test analysis (r ranged from 0.64 to 0.76; p value ranged from 0.02 to 0.03). There was no other significant correlation between the above parameters and clinicopathological features.Conclusions:Our in vivo preliminary data suggest that TMCD and PAR-2-MVD may play a role in GC angiogenesis and they could be further evaluated as a target of antiangiogenic therapy.

Dermatomyositis (DM), a subtype of idiopathic inflammatory myopathies (IIMs), is characterized by skin rash, proximal muscle weakness, and inflammatory infiltrates in the muscle tissue. The peak incidence of the disease is at the age of 50–60 years, and only 14% of the patients with IIMs are estimated to present during reproductive years. Because of the limited pregnancy experience in patients with IIMs, little is known regarding the effects of DM on pregnancy or vice versa. We herein report a 40-year-old woman who developed DM in the second trimester of her pregnancy and did not respond to treatment with methylprednisolone. Her pregnancy was terminated at the 32nd week of gestation, due to preeclampsia and fetal distress. She delivered a healthy baby and improved rapidly after delivery. We have searched PubMed for relevant articles and reviewed previously published cases.

The purpose of the study was to assess the efficacy and safety of transition from ranibizumab to aflibercept intravitreal injections in treatment-resistant retinal pigment epithelial detachment (PED). The data of intravitreal ranibizumab treatment-resistant patients who have been switched to aflibercept treatment were reviewed retrospectively. After three monthly injections, bimonthly regimen was performed. The changes of PED height and radius, and the best-corrected visual acuity (BCVA) were analyzed retrospectively. Mean baseline PED height decreased from 297 ± 151 to 122 ± 42 µm at month 12 (P = 0.0007). Mean baseline PED radius decreased from 2371 ± 882 to 1859 ± 779 µm at month 12 (P = 0.0007). No complete PED resolution occurred in any of the patients at the end of the 12 months. Baseline BCVA improved from 0.63 ± 0.21 to 0.43 ± 0.17 logMar at month 12 (P = 0.0049). Mean BCVA gain was 1.4 decimal chart lines (7 letters) at month 12. Switching to aflibercept seems to have promising functional and anatomical outcomes with a reasonable complication rate in treatment-resistant PED.