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Purpose. The purpose of this study was to identify variations in external load measures between sets (3 × 4'/2' rest) of small-sided and conditioned game formats (goalkeeper + 5 vs. 5 + goalkeeper with specific tactical demands). Methods. Overall, 10 male professional soccer players (age: 28.1 ± 3.8 years, experience: 7.9 ± 2.9 years, height: 180.3 ± 5.8 cm, weight: 76.5 ± 6.3 kg) from a team competing in the first Portuguese league and in the UEFA Europa league participated in the study. Distance covered, high intensity running (HIr), maximal velocity (MV), high speed running (HSr), very high intensity running (VHIr), and player load (PL) were monitored by using global positioning system units. Results. Very large decreases in HIr (-62.6, effect size [ES]:-2.04) were found from set 1 to set 3. Large decreases in distance covered (-12.8%, ES:-1.28) and MV (-19.4, ES:-1.95) were observed from the first to the third set. Large decreases in HSr (-80.2%, ES:-1.78), moderate decreases in PL (-7.6%, ES:-0.64), and large decreases in VHIr (-83.0%, ES:-1.88) were reported between the first and the third set. Conclusions. The results of the present study indicate a significant drop in external load performance when comparing the first and the second sets with the third set.

The number of bronchiectasis diagnoses has increased in the last two decades due to several factors. Research carried out over the last years showed that an aetiological diagnosis could change the approach and treatment of a relevant percentage of patients and consequently the prognosis. Currently, systematic investigation into aetiology, particularly of those disorders that can be subject to specific treatment, is recommended. Given the complexity of the aetiological diagnosis, the Pulmonology Portuguese Society Bronchiectasis Study Group assembled a working group which prepared a document to guide and standardize the aetiologic investigation based on available literature and its own expertise. The goal is to facilitate the investigation, rationalize resources and improve the delivery of care, quality of life and prognosis of patients with bronchiectasis.

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Gastric carcinoma (GC) represents the most common cause of death in patients with common variable immunodeficiency (CVID). However, a limited number of cases have been characterised so far. In this study, we analysed the clinical features, bacterial/viral infections, detailed morphology and immune microenvironment of nine CVID patients with GC. The study of the immune microenvironment included automated digital counts of CD20+, CD4+, CD8+, FOXP3+, GATA3+ and CD138+ immune cells, as well as the evaluation of PD-L1 expression. Twenty-one GCs from non-CVID patients were used as a control group. GC in CVID patients was diagnosed mostly at early-stage (n = 6/9; 66.7%) and at younger age (median-age: 43y), when compared to non-CVID patients (p < 0.001). GC pathogenesis was closely related to Helicobacter pylori infection (n = 8/9; 88.9%), but not to Epstein-Barr virus (0.0%) or cytomegalovirus infection (0.0%). Non-neoplastic mucosa (non-NM) in CVID-patients displayed prominent lymphocytic gastritis (100%) and a dysfunctional immune microenvironment, characterised by higher rates of CD4+/CD8+/Foxp3+/GATA3+/PD-L1+ immune cells and the expected paucity of CD20+ B-lymphocytes and CD138+ plasma cells, when compared to non-CVID patients (p < 0.05). Changes in the immune microenvironment between non-NM and GC were not equivalent in CVID and non-CVID patients, reflecting the relevance of immune dysfunction for gastric carcinogenesis and GC progression in the CVID population.

Common Variable Immunodeficiency (CVID), the most prevalent symptomatic primary immunodeficiency, is frequently associated with severe inflammatory complications that determine its morbidity and mortality. We hypothesize that Helicobacter pylori (HP), a very common worldwide infection, may contribute to the clinical and immune phenotype of CVID. We stratified 41 CVID patients into HP+ (n=26) and HPneg (n=15) groups, according to previous urease breath test and/or gastric biopsies, and compared their clinical manifestations and immune profile evaluated by flow cytometry. No genetic variants with known potential impact in HP infection were found upon WES/WGS. Gastric complications were significantly more frequent in HP+ patients. Importantly, the six CVID patients with gastric cancer were infected with HP. In contrast, a significantly higher frequency of cytopenias was observed in the HPneg. Moreover, HP+ did not feature higher prevalence of organ auto-immunity, as well as of lung, liver or intestinal inflammatory manifestations. We observed the same B-cell profiles in HP+ and HPneg groups, accompanied by marked CD4 and CD8 T-cell activation, increased IFNγ production, and contraction of naïve compartments. Notably, HP+ patients featured low CD25 despite preserved Foxp3 levels in CD4 T cells. Overall, HP impact in CVID inflammatory complications was mainly restricted to the gastric mucosa, contributing to increased incidence of early onset gastric cancer. Thus, early HP screening and eradication should be performed in all CVID patients irrespective of symptoms.

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