Paraneoplastic symptoms caused by a malignancy but not directly related to tumour invasion are the result of a wide variety of tumour-derived biologic mediators, such as hormones, peptides, antibodies, cytotoxic lymphocytes, autocrine and paracrine mediators. Recognition of paraneoplastic syndromes is important, as it may lead to an early diagnosis of cancer. On the other hand, the clinical severity of the symptoms can be used as a guide to the extent of response to underlying tumour therapy. The quality of life of the patient is affected, therefore the palliative treatment of paraneoplasia is very important.

The purpose of this study was to evaluate the association between platelet (PLT) count and mean platelet volume (MPV) and venous thromboembolism (VTE). Thus, this study reviewed and performed a quantitative synthesis on data from the literature. This meta-analysis was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. 18 studies were included in this paper. A random-effect meta-analysis was conducted for the assessment of heterogeneity using thrombosis place, type of analyzer, type of anticoagulant and incubation time of samples as covariates. A mixed-effect meta-regression was performed based on the subgroup for the whole samples using thrombosis place and method of measurement as moderators for MPV and PLT, respectively. The cumulative estimates and 95% confidence interval (95%CI) of specificity, sensitivity, area under the receiver operator characteristic curve (AUC) and diagnostic odds ratio (DOR) for MPV were calculated using a random effect model. The quality assessments were evaluated according to the quality assessment and diagnostic accuracy tool-2 (QUADAS-2). The primary outcome was the occurrence of VTE. Secondary outcomes included PLT and MPV. Patient with deep vein thrombosis is likely to have a higher value of MPV than control group (P < 0.001). The presence of pulmonary embolism (PE) had no significant effect on the standardized mean difference of MPV between patients and controls. Patients are likely to have less PLT than the control group regarding all studies. However, subgroup analysis demonstrated that this effect was significant for patients with PE (P < 0.05). The summary receiver operating characteristic (SROC) curve indicated that AUC was 0.745 (95% CI: 0.672-0.834). The DOR for MPV was 4.76 (95%CI: 2.3-9.85), with diagnostic accuracy of 0.66.

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Changes of mean platelet volume (MPV) and platelet count (PC) could be a marker or a predictor of acute stroke (AS). We conducted a systematic review and meta-analysis of the published literature on the reporting of MPV and PC in AS. Studies were included in accordance with Patient Population or Problem, Intervention, Comparison, Outcomes, and Setting framework. The PRISMA strategy was used to report findings. Risk of bias was assessed with the Newcastle-Ottawa Scale. We included 34 eligible articles retrieved from the literature. PC was significantly lower in AS patients [standardized mean difference (SMD) = − 0.30, (95% CI: − 0.49 to − 0.11), N = 2492, P = .002] compared with controls (N = 3615). The MPV was significantly higher [SMD = 0.52 (95% CI: 0.28-0.76), N = 2739, P < .001] compared with controls (N = 3810). Subgroup analyses showed significantly lower PC in both ischemic stroke (Difference SMD = −0.18, 95% CI: −0.35-0.01) and hemorrhagic stroke (−0.94, −1.62 to −0.25), but only samples by citrate anticoagulant showed significantly lower result for patients compared to controls (−0.36, −0.68 to −0.04). Ischemic stroke patients had higher MPV (0.57, 0.31-0.83), and samples by Ethylenediaminetetraacetic acid (EDTA) anticoagulant showed significantly higher result for patients compared to controls (0.86, 0.55--1.17). PC and MPV appeared to be significantly different between patients with AS and control populations. MPV was significantly higher in ischemic stroke and PC was significantly lower in both ischemic and hemorrhagic strokes. These characteristics might be related to AS and associated with it. It is advisable to pay attention to elapsed time between phlebotomy and hematology analysis, anticoagulant and hemocytometer types in AS. Systematic review registration: This meta-analysis is registered on the International Prospective Register of Systematic Reviews (PROSPERO) under registration number CRD42017067864 (https:// www.crd.york.ac.uk/prospero/display_record.php?RecordID=67864).

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Hp infection may be associated with the development and progression of HSP. IgG antibodies to Hp may be present mostly in acute HSP, while IgA antibodies may be involved in sustaining gastrointestinal symptoms underlying the chronic phase of the disease.

IntroductionWe studied the effect of rosuvastatin on endothelial and macrovascular function, cardiovascular risk factors and the complement pathway in patients with systemic sclerosis (SSc).MethodsAltogether 28 patients with SSc underwent laboratory and complex vascular assessments before and after six months of 20 mg rosuvastatin treatment. Flow-mediated dilation (FMD) of the brachial artery, as well as carotid artery intima-media thickness (ccIMT), carotid-femoral and aorto-femoral pulse wave-velocity (PWV) were analyzed by ECG-synchronized ultrasound. Ankle-brachial index (ABI) was determined by Doppler, and forearm skin microcirculation was assessed by Laser Doppler perfusion monitoring.ResultsBrachial artery FMD significantly improved upon rosuvastatin therapy (2.2% ± 3.3% before versus 5.7% ± 3.9% after treatment, P = 0.0002). With regard to patient subsets, FMD significantly improved in the 21 lcSSc patients (from 2.1% to 5.6%, P = 0.001). In the seven dcSSc patients, we observed a tendency of improvement in FMD (from 3% to 6%, P = 0.25). Changes in PWV, ccIMT and ABI were not significant. Mean triglyceride (1.7 ± 0.97 versus 1.3 ± 0.46 mmol/l, P = 0.0004), total cholesterol (5.3 ± 1.6 mmol/l versus 4.2 ± 1.3 mmol/l, P = 0.0003), low density lipoprotein cholesterol (3.0 ± 1.3 versus 2.2 ± 1.0 mmol/l, P = 0.005) and C-reactive protein levels (CRP) (5.1 ± 5.2 versus 3.4 ± 2.7, P = 0.01) levels significantly decreased after rosuvastatin treatment. Mean C3, C4 and IC levels also decreased significantly as compared to pretreatment values.ConclusionsSix-month rosuvastatin therapy improves endothelial function and lowers CRP, C3, C4 and IC levels indicating possible favourable effects of this statin on the cardiovascular and immune system in SSc.

Besides traditional risk factor, it has been proved that genetics and gene-environment interaction have a possible independent role in the development and progression of peripheral arterial disease (PAD). Knowledge about such genetic factors will increases our understanding about pathophysiologic mechanisms of PAD and could facilitate the therapeutic approaches. Human genetics has gone through an advanced improvement and it increases our chance to acquire better diagnostic and therapeutic approaches. In this chapter, we try to provide an update on the genetics of PAD, which is mostly about genome-wide association studies, linkage analyses, heritability, candidate gene studies, and epigenetics. Finally, we discuss challenges and future developments of researches in PAD genetics.