The grounds for rare involvement of conjunctiva in pemphigus vulgaris is unclear. We hypothesize that inactivation of conjunctival desmoglein 3 may be compensated by other desmosomal proteins. Severe conjunctivitis may be the dominating clinical manifestation in pemphigus vulgaris. This implies a need of establishing distinct severity criteria and therapeutic standards for ocular pemphigus. In our patient rapid clinical response was achieved after introducing combined treatment with prednisone and oral cyclophosphamide.

Aim of the studyThe aim of our study was to evaluate selected inflammatory markers in children with untreated primary hypertension and to establish the relation between inflammatory markers and 24-hour ambulatory blood pressure monitoring (ABPM) and clinical and biochemical parameters.Material and methodsIn 54 children (15.12 ±2.02 years) with untreated primary hypertension, with excluded overt inflammation, we evaluated: neutrophils (NEU; 1000/μl), lymphocytes (LYM; 1000/μl), platelets (PLT; 1000/μl), mean platelet volume (MPV; fl), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), ABPM (OSCAR 2 SUNTECH), and selected clinical and biochemical parameters. The control group consisted of 20 healthy children (15.55 ±2.27 years).ResultsChildren with primary hypertension had (p < 0.01) higher 24-hour systolic, diastolic and mean blood pressure, systolic and diastolic blood pressure loads, and pulse pressure. Hypertensive children did not differ in inflammatory indicators (NEU, LYM, PLT, MPV, NLR, PLR) from the control group. In 54 hypertensive children we found the following correlations: between office systolic and diastolic blood pressure and MPV (r = 0.35, p = 0.011, r = 0.36, p = 0.008), between 24-hour ambulatory mean arterial pressure Z-score and NLR (r = 0.30, p = 0.030), 24-hour systolic blood pressure load and NLR (r = 0.38, p = 0.005), plasma renin activity and neutrophil count, NLR, PLR (r = 0.47, p = 0.016, r = 0.64, p < 0.001, r = 0.42, p = 0.033), urinary albumin loss and neutrophil count, NLR (r = 0.46, p = 0.001 and r = 0.42, p = 0.003). Multivariate analysis revealed that office SBP Z-score was related to MPV (β = 0.35, p = 0.008) and albuminuria to neutrophil count (β = 0.62, p = 0.018).ConclusionsIn children with primary arterial hypertension there may be a relation between blood pressure, urinary albumin loss, and subclinical inflammation.

MSs are specific immune active lymphatic structures on the greater omentum. They play a key role in defense mechanism, especially in peritonitis. Their function is not completely clear in cancer, some authors suggest they might play a significant role in omental metastasis. Further analysing of the morphology and cells interactions of MSs is needed (Tab. 2, Fig. 6, Ref. 20).

Introduction: The 3020insC mutation of NOD2 predisposes to many types of common cancers, e.g. breast cancer. In this report we compare NOD2 3020insC mutation carriers with non-carriers in a similar age range at diagnosis according to clinicopathological factors and survival in breast cancer patients from the Silesia region in Poland. Material and methods: We reviewed the medical records of 72 early breast cancer patients, who were diagnosed and treated in COI in Gliwice. Genetic diagnostics was conducted in all patients. Twenty-eight (39%) patients were NOD2 mutation carriers and 44 (61%) were non-carriers. Results: Triple-negative breast cancer (TNBC) was detected more often in NOD2 mutation carriers than non-carriers (25% vs. 11.4%, p = 0.194). Similarly, lymph nodes without metastases (N0) were reported more frequently in patients with NOD2 mutation (71.4% vs. 43.2%, p = 0.029). HER2 without overexpression was observed insignificantly more often in group with NOD2 mutation (82.1% vs. 63.6%, p = 0.115). Similarly, lower histological grade (G1+G2). There was no difference in tumor size (T1-T2) (89.3% vs. 86.4%, p = 1.00) or steroid receptor status (28.6% vs. 29.5%, p = 1.00) between groups. The median follow-up was 5.1 years (range: 0.6-26.1 years) for NOD2 carriers and 5.3 years (range: 2.0-19.7 years) for non-carriers. There was no difference between mutation carriers and non-carriers according to overall survival (5-year OS: 96% vs. 93%, p = 0.427). Conclusions: There were no differences between NOD2 (3020insC) mutation carriers and non-carriers, according to comorbid condition, drugs, tumor size, steroid receptor status and 5-year overall survival.

Background and Purpose Hypertension is a multifactorial disease, manifested by vascular dysfunction, increased superoxide production, and perivascular inflammation. In this study, we have hypothesized that 1,2,3,4,6‐penta‐O‐galloyl‐β‐d‐glucose (PGG) would inhibit vascular inflammation and protect from vascular dysfunction in an experimental model of hypertension. Experimental Approach PGG was administered to mice every 2 days at a dose of 10 mg·kg−1 i.p during 14 days of Ang II infusion. It was used at a final concentration of 20 μM for in vitro studies in cultured cells. Key Results Ang II administration increased leukocyte and T‐cell content in perivascular adipose tissue (pVAT), and administration of PGG significantly decreased total leukocyte and T‐cell infiltration in pVAT. This effect was observed in relation to all T‐cell subsets. PGG also decreased the content of T‐cells bearing CD25, CCR5, and CD44 receptors and the expression of both monocyte chemoattractant protein 1 (CCL2) in aorta and RANTES (CCL5) in pVAT. PGG administration decreased the content of TNF+ and IFN‐γ+ CD8 T‐cells and IL‐17A+ CD4+ and CD3+CD4−CD8− cells. Importantly, these effects of PGG were associated with improved vascular function and decreased ROS production in the aortas of Ang II‐infused animals independently of the BP increase. Mechanistically, PGG (20 μM) directly inhibited CD25 and CCR5 expression in cultured T‐cells. It also decreased the content of IFN‐γ+ CD8+ and CD3+CD4−CD8− cells and IL‐17A+ CD3+CD4−CD8− cells. Conclusion and Implication PGG may constitute an interesting immunomodulating strategy in the regulation of vascular dysfunction and hypertension. Linked Articles This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc