Long-term breastfeeding influences disease activity in a low-income juvenile idiopathic arthritis cohort.

To determine the influence of breastfeeding duration in the clinical activity of low-income juvenile idiopathic arthritis (JIA). Ninety-one JIA patients followed in Fortaleza-CE, Brazil, were cross-sectionally evaluated from May 2015 to April 2016. Breastfeeding duration was obtained by interviewing mothers. Mean age was 14.6 ± 5.2 years with 10.31 ± 3.7 years of disease duration. Polyarticular category predominated, with 39 (42.8%) patients, followed by 23 (25.3%) oligoarticular and 17 (18.7%) enthesitis-related. Forty-seven (61.8%) were receiving methotrexate isolated or combined to leflunomide, which was used by 12 (15.4%); 30 (32.9%) were on biologic DMARD with 16 (53.3%) etanercept, 8 (26.7%) adalimumab, 3 (10%) tocilizumab, and 1 (3.3%) each on infliximab, abatacept, and canakinumab. Mean(SD) CHAQ and JADAS27 were 0.37 ± 0.36 and 5.03 ± 6.1, respectively and 22 (24%) had permanent joint deformities. No family declared monthly income over US$900.00 and 32 (37.2%) earned less than US$300.00. Eighty-three (91%) were ever breastfed; over two-thirds were breastfed for more than 3 months. Those breastfed for more than 6 months had less joint deformities and a tendency to lower JADAS27 and CHAQ scores using minimally adjusted general linear or logistic models, as appropriate. Parental smoking or literacy and family income did not differ regarding breastfeeding time. This is a low-income JIA cohort with the highest breastfeeding prevalence ever reported. Breastfeeding over 6 months was associated with less disease activity.Key Point• Long-term breastfeeding benefits juvenile idiopathic arthritis.

Neutrophils contribute to the pathogenesis of hemorrhagic cystitis induced by ifosfamide.

Ifosfamide (IFO) is an antineoplastic drug that is commonly used to treat gynecological and breast cancers. Hemorrhagic cystitis (HC) is a common side effect associated with IFO injection, which courses with neutrophil accumulation and affects 6-50% of patients depending on dose intensity. Here, we investigated the role of neutrophils in this inflammatory process. Female Swiss mice (n = 8/group) were injected with saline, IFO (400 mg/kg, i.p.), fucoidan (a P- and L-selectins inhibitor, 100 mg/kg, i.v.) or IFO + fucoidan (1-100 mg/kg) alone or combined with mesna (80 mg/kg i.p.). Another group of mice received anti-Ly6G antibody (500 µg/mouse, once daily for 2 days) for neutrophil depletion before IFO injection. In another experimental setting, animals received granulocyte colony-stimulating factor (G-CSF, 400 µg/kg), IFO (200 mg/kg), G-CSF (25-400 µg/kg, for 5 days) + IFO (200 mg/kg, i.p.) or fucoidan + G-CSF + IFO. Bladder injury was evaluated 12 h after IFO injection. IFO 400 mg/kg significantly increased visceral hyperalgesia, bladder edema, hemorrhage, vascular permeability, MPO, IL-1ß and IL-6 tissue levels, and COX-2 immunostaining and expression versus the saline group (P < 0.05). Conversely, fucoidan (100 mg/kg) significantly attenuated these parameters compared to IFO-injected mice (P < 0.05). Additionally, fucoidan potentiated mesna protective effect when compared with IFO + mesna group (P < 0.05). Accordingly, neutrophil depletion with anti-Ly6G reduced inflammatory parameters and bladder injury compared to IFO (P < 0.05). In contrast, G-CSF enhanced IFO (200 mg/kg)-induced HC, which was significantly attenuated by treatment with fucoidan (P < 0.05). Therefore, neutrophils contribute to the pathogenesis of HC.