No abstract

The incidence of perinatal complications in 219 sets of MD twins managed from early gestational age to the neonatal period in one perinatal center was demonstrated. The incidence of TTTS was 8%; the survival rate was 89% at 28 days of age.

Objective Biological disease-modifying anti-rheumatic drugs (bDMARDs) represent an important advance in alleviating rheumatoid arthritis (RA), but their effect on rheumatic airway disease (AD) and interstitial lung disease (ILD) is still unclear. This study was performed to evaluate the association of the use of different bDMARDs with new-onset or worsening of RA-AD/ILD. Methods We performed a retrospective cohort study of RA patients who received bDMARDs and assessed their AD/ILD before and after drug initiation in our hospital over the past 10 years. We evaluated the serial changes in computed tomography (CT), classified patients according to AD/ILD progression, and analyzed associations between clinical characteristics and outcomes. Results We enrolled 49 patients. Thirty patients received tumor necrosis factor inhibitors (TNFis), 12 received abatacept (ABT), and the remaining 7 received tocilizumab (TCZ). Seventeen patients had ILD, 10 had AD, and 6 had both AD and ILD before the initiation of bDMARDs. New emergence or exacerbation of AD/ILD was observed in 18 patients after drug initiation, while the remaining 31 remained stable or improved. Multiple logistic regression analyses revealed that pre-existing AD was an independent risk factor against the emergence or exacerbation of RA-AD/ILD, and ABT use was a protective factor against it. Conclusion Our study showed that pre-existing RA-AD is associated with future worsening of RA-AD/ILD, and ABT over other bDMARDs was associated with a better prognosis. Future studies to confirm our results are needed.

Perinatal outcomes in our study were relatively good irrespective of high frequency of cord entanglement. Close fetal monitoring may allow MM twin pregnancies to extend gestational age, which may contribute to reduce both fetal death and neonatal morbidity by immaturity, although the best delivery weeks remained undetermined.

Low CRP and high hemoglobin can predict a positive response to corticosteroid monotherapy while high serum ferritin and low leukocyte count can predict a positive response to CsA in patients with ALHS and therefore, when corticosteroid monotherapy is not effective in such cases, CsA could be the first choice of an additional immunosuppressive agent.

BackgroundAlthough patients with systemic lupus erythematosus (SLE) may experience various gastrointestinal disorders, SLE and Crohn’s disease (CD) rarely coexist. The diseases may have gastrointestinal (GI) manifestations, laboratory results, and radiographic findings that appear similar and consequently differentiating between GI involvement in CD and in SLE may be difficult. We present the case of a patient with SLE and CD who developed continuous GI bleeding and diarrhea that was initially treated as SLE-related colitis to little effect.Case presentationA 55-year-old Japanese woman with systemic lupus erythematosus (SLE) developed continuous gastrointestinal bleeding and diarrhea since the patient was aged 30 years that was initially treated as SLE-related colitis. Although a longitudinal ulcer and aphthous ulcers in the colon were observed every examination, biopsy showed only mild inflammation and revealed neither granuloma nor crypt abscess. The patient underwent surgery for anal fistulas twice at 50 and 54 years of age and her symptoms were atypical of lupus enteritis. Colonoscopy was performed again when the patient was 55 years of age because we suspected she had some type of inflammatory bowel disease (IBD). Cobblestone-like inflammatory polyps and many longitudinal ulcers were detected between the descending colon and the cecum. Macroscopic examination strongly suggested CD. Histopathological examination revealed non-caseating granuloma and no evidence of vasculitis, consistent with CD. Introduction of infliximab dramatically relieved the patient’s melena and abdominal symptoms.ConclusionDiagnostic criteria for CD and SLE overlap, making them difficult to diagnose correctly. It is important to consider CD for patients who have SLE with gastrointestinal manifestations. The pathology of lupus enteritis should be clarified through the accumulation of cases of SLE combined with CD.

No abstract

ObjectiveAn increased proportion of circulating follicular helper T (Tfh) cells was reported in rheumatoid arthritis (RA), but it remains uncertain how Tfh cells affect antibody hyposialylation. We investigated the regulation of autoantibody hyposialylation by Tfh cells in RA using murine model.MethodsBehaviours of Tfh cells and their function on B cell promotion were analysed. Change of arthritogenicity and sialylation of autoantibodies during the course of arthritis was examined by mass spectrometry. Tfh-mediated regulation of hyposialylation was investigated, and the responsible cell surface molecule was specified both in vitro and in vivo. The relation between circulating Tfh cells and hyposialylation was analysed in patients with RA.ResultsAn increase in Tfh, particularly interleukin-17 producing Tfh (Tfh17) cells, at the onset of arthritis and their enhancement of autoantibody production were found. Autoantibodies at the onset phase demonstrated stronger inflammatory properties than those at the resolution phase, and mass spectrometric analysis revealed their difference in sialylation. In vitro coculture showed enhanced hyposialylation by the Tfh cells via OX40, which was highly expressed in the Tfh and Tfh17 cells. Blockade of OX40 prevented the development of arthritis with reduction in Tfh17 cells and recovery of autoantibody sialylation. Analysis of patients with RA showed abundance of OX40-overexpressing Tfh17 cells, and their proportion correlated negatively with the expression of α2,6-sialyltransferase 1, an enzyme responsible for sialylation.ConclusionsOX40 expressed on Tfh cells can regulate autoantibody sialylation and play a crucial role in the development of autoimmune arthritis.