Manifestations Of Chronic Disease Research Articles

Manifestation of Chronic and Non-Communicable Diseases Among Filipino Internationally Educated Nurses in Finland: A Qualitative Study.

Limited research has explored the impact of migration on the manifestation of noncommunicable diseases (NCDs) among internationally educated nurses (IENs) in Finland. This study aimed to describe Filipino IENs' experiences with the manifestation of NCDs among them. Secondary data from 10 IENs working in two hospitals were analyzed using Braun and Clarke's thematic analysis. The study adhered to the consolidated criteria for reporting qualitative research (COREQ) checklist. Three key themes emerged: insufficient knowledge and lack of interest in health promotion, migration as a factor, and occupational health challenges. Migration was found to impact NCD occurrence. Inadequate knowledge and underutilization of occupational health services were identified as a barrier to prevent the risk of getting NCDs. Long waiting periods for appointments and language barriers exacerbated these risks. Limited awareness of available occupational health services and disinterest in health promotion contributed to NCD manifestation among IENs. Lengthy waiting times highlighted the need for educational campaigns on health-promoting activities. Cultural competence training for local healthcare providers can improve culturally sensitive occupational healthcare for IENs. Health promotion education should be provided to IENs before their migration. Upon arrival, nurse managers should inform the nurses about the availability of occupational healthcare services provided by the employer, ensuring easy access. Additionally, efforts should be made to ensure that nurses integrate well into society, including facilitating access to recreational activities.

Reactive oxygen species regulate early development of the intestinal macrophage-microbiome interface.

Controlled development of cellular intestinal immunity in the face of dynamic microbiota emergence constitutes a major challenge in very early life, and a bottleneck for sustained growth and well-being. Early-onset inflammatory bowel disease (IBD) represents an extreme disturbance of intestinal immunity. It is a hallmark, and often the first manifestation of chronic granulomatous disease (CGD), caused by inborn defects in the NADPH oxidase NOX2 and thus the failure to produce reactive oxygen species (ROS) in phagocytes. However, in contrast to the known role of ROS in antimicrobial defense, the mechanisms underlying intestinal immunopathology in CGD remain enigmatic. This is partly due to the incomplete recapitulation of the CGD-IBD phenotype in established mouse models. We found that mice deficient in the NOX2 subunits p47phox or gp91phox showed similar baseline disturbances in lamina-propria macrophage differentiation, but they responded differently to chemically-induced colitis. Although p47phox and gp91phox-deficient mice differed markedly in microbiota composition, cross-fostering failed to equalize discrepant IBD phenotypes and microbiota, pointing at extremely early and functionally important microbiota fixation under specific pathogen-free housing conditions. In contrast, neonatal acquisition of a complex wild-mouse-microbiota triggered spontaneous IBD, granuloma formation and secondary sepsis with intestinal pathogens in both NOX2-deficient mouse lines, which was in part dependent on NOX2 in intestinal macrophages. Thus, in experimental CGD, the aberrant development of tissue immunity and the microbiota are closely intertwined immediately after birth.

Pentoxifylline (Vasonit®) – a pathogenetic approach for the correction of cognitive impairment in cerebrovascular diseases. A review

Cognitive impairment is one of the key manifestations of chronic cerebrovascular diseases. Among the factors contributing to their development are microcirculatory disturbances, changes in blood rheological properties, endothelial dysfunction and oxidative stress. This review is devoted to the analysis of the clinical application potential of the nonspecific phosphodiesterase inhibitor pentoxifylline (Vasonit®) in the therapy of patients with chronic cerebral ischaemia in order to correct haemorheological and haemodynamic factors. Data from experimental and clinical studies indicating the possibility and pathogenetic validity of the use of pentoxifylline (Vasonit®) in the complex therapy of cognitive disorders associated with chronic cerebrovascular diseases are considered. The authors describe their own experience of using Vasonit® in a patient with vascular cognitive impairment.

Characteristics and Endoscopy Findings of Liver Cirrhosis Patients at Waled Hospital, Cirebon, Indonesia (2020-2023)

Background: Hepatic cirrhosis is a terminal manifestation of chronic liver disease. The causes of cirrhosis in the Asia Pacific it was caused by hepatitis B. Older adults are more likely to experience complications, which might be due to abnormalities in the liver. Various complications occurred during the progression from compensated to decompensated, and endoscopic examination showed images of gastroesophageal varices or PHG. Aims: The aim was to determine the characteristics of liver cirrhosis patients and the endoscopy findings at waled hospital from 2020 to 2023. Methods: This research used descriptive observational methods. The sample in this study were patients with liver cirrhosis at Waled hospital from 2020-2023, there were 135 sample who were selected using total sampling techniques. Information was acquired from medical records of 33 patients who met the consideration rules. Results: This study showed that the largest number of patients with liver cirrhosis based on age 45 years old (12.1%), predominantly male (72.7%), with the etiology hepatitis B (69.7%), and all (100%) were in decompensated stage. Endoscopy results revealed that the majority of patients experiences esophageal varices and PHG (54.5%), with grade 3 esophageal varices (81.8%) and mild grade PHG (60.6%) dominating. Conclusion: The majority of patients with liver cirrhosis were 45 years old, predominantly male, with the most common etiology hepatitis B, and all were in the decompensated stage. The most common endoscopy results showed esophageal varices and PHG, with grade 3 esophageal varices and mild grade PHG. Received: 26 September 2024 | Reviewed: 23 October 2024 | Revised: 30 November 2024 | Accepted: 12 December 2024.

Metagenomics and metabolomics to investigate the effect of Amygdalus mongolica oil on intestinal microbiota and serum metabolites in rats.

Renal fibrosis (RF) is an inevitable consequence of multiple manifestations of progressive chronic kidney diseases (CKDs). Mechanism of Amygdalus mongolica (Maxim.) in the treatment of RF needs further investigation. The study further investigated the potential mechanism of A. mongolica in the treatment of RF. A rat model of RF was induced by unilateral ureteral obstruction (UUO), followed by treatment with varying dosages of A. mongolica oil for 4 weeks. Body weight was measured weekly. We detected serum levels of interleukin (IL)-6, IL-1β, type Ⅲ procollagen (Col-Ⅲ), type IV collagen (Col-Ⅳ), laminin (LN), hyaluronidase (HA), and tissue levels of albumin (ALB), blood urea nitrogen (BUN), creatinine (Cre), superoxide dismutase (SOD), malondialdehyde (MDA), and hydroxyproline (HYP). Shotgun metagenomics analyzed the composition of the intestinal microbiota. High-performance liquid chromatography coupled with a quadrupole-exactive mass spectrometer (HPLC-Q-Exactive-MS) monitored changes in metabolite levels in serum and gut. Multiple reaction monitoring-mass spectrometry (MRM-MS) determined the levels of amino acids in serum. A. mongolica oil significantly alleviated indicators related to RF (p < 0.05). A. mongolica oil reduced the ratio of Firmicutes to Bacteroidetes and restored the balance of intestinal microbiota in rats with RF. A. mongolica oil modulated levels of metabolites in gut content and serum. It regulated 11 metabolic pathways including arachidonic acid metabolism. Targeted metabolomics of amino acids showed that 17 amino acids were significantly changed by A. mongolica oil, including L-glycine, L-serine and L-glutamine. A. mongolica oil regulates intestinal microbiota and metabolites, restoring amino acid metabolism to treat RF.

Erdosteine in the treatment of acute and chronic diseases of the respiratory system: resolution of the scientific forum of experts “In the Spotlight”

Airway mucus hypersecretion is a pathophysiologic manifestation of acute and chronic airway inflammatory disease. Mucolytics can reduce mucus viscosity and promote mucus discharge and therefore can be considered pathogenetically based therapy.The purpose of this publication with the resolution of the scientific forum of experts was to discuss pharmacological features, efficacy, and safety of erdosteine.Results. Experts of thescientific forum not only reviewed the results of clinical trials, but also voted on the use of mucoactive drugs according to the principle of Delphi consensus. Comparison of the efficacy and safety of mucoactive drugs (erdosteine, acetylcysteine, carbocysteine, ambroxol) in patients with respiratory diseases by the experts during voting showed that the highest level of agreement among the experts was achieved for the drug Elmucin® (erdosteine) in terms of its mucolytic activity and other pharmacological features, as well as when discussing the safety of the compared drugs in the officially recommended doses. The highest level of agreement was also noted on the erdosteine efficacy in COPD patients in reducing the frequency and duration of disease exacerbations, as well as reducing the risk of hospitalization of COPD patients when used long-term as part of combination therapy. The demonstrated safety profile was the most beneficial among the reviewed mucoactive drugs.Conclusion. Elmucin® is a mucolytic with pleiotropic effects such as complex mucoactive action, potent antioxidant, anti-inflammatory and antibacterial activity with anti-adhesive effect for pathogens that determine its clinical efficacy in the treatment of acute and chronic airway diseases.

Comparative Study between Endovenous Radiofrequency Ablation and Conventional Surgery of Primary Varicose Veins of Lower Limbs

Abstract Background Varicose veins are the main manifestations of chronic venous disease (CVD), and present as dilated and elongated incompetent superficial veins in the lower limbs. The most common method of treatment for this condition is an open surgery proposed by W. Keller 110 years ago. Radio- Frequency ablation (RFA) was proved to be effective in the treatment in many randomized controlled trials. Aim of the Work to throw light and compare Radio-Frequency Ablation to conventional surgery in treating primary varicose veins in lower limbs. Patients and Methods This prospective study included 30 patients, who were treated for symptomatic varicose veins of the lower limbs divided into two groups. In first one, 15 patients underwent open surgery (the surgery group), while in the other, 15 patients received the Radio- Frequency Ablation (the RF group). The patients were invited to follow-up evaluations at first and second weeks then one and six months after the surgery. Results VCSS scores at one month were better in the RFA group (median VCSS scores 1 (0–2) vs. 4 (3 – 5), p &amp;lt; 0.0001). Patients in the RFA group experienced less postoperative pain (p &amp;lt; .00163). In addition, patients in the RFA group managed to return to work and normal activities sooner than those in the surgery group (p &amp;lt; 0.0001). No statistically significant differences were found between groups for overall satisfaction, rate of complications except hematoma which was higher in surgery group. Conclusion Both treatment techniques yielded similar results in terms of efficacy, complications and overall patient satisfaction. However, early postoperative results in the RF group were superior to those of patients in the surgery group.

NEUROPROTECTIVE THERAPY OF CEREBROVASCULAR INSUFFICIENCY

One of the leading manifestations of chronic cerebrovascular diseases is impairment of cognitive and motor functions. Drugs recognized as neuroprotectors are used to correct such impairments. They intervene in and inhibit the pathogenetic cascade that results in the cell death in vascular pathology. The aim of the study is to evaluate the effectiveness of neuroprotective therapy for cerebrovascular insufficiency (CVI). Materials and Methods. The study was conducted at the neurological department of the Ulyanovsk Central Clinical Medical Sanitary Station. The study included data analysis on 60 patients divided into two groups of 30 people each. Patients of the main group received neuroprotective therapy with Cortexin and Neuromexol (Geropharm, Russia) for 10 days along with standard treatment. Patients of the comparison group received only standard treatment. Blood was sampled twice: before and after treatment. The total antioxidant status (TAS) was determined in the blood serum. Such markers as neuron -specific enolase (NSE), antibodies to NR2 peptide were also examined. Statistical processing of the results was performed using Microsoft Excel 2010 and Statistica 13.0. Differences were considered statistically significant at p&lt;0.05. Results. Against the background of neuroprotective therapy, patients of the main group with cerebrovascular insufficiency demonstrated a statistically significant improvement in TAS (by 87.7 %), a decrease in the NSE level (by 2 times) and concentration of antibodies to NR2 peptide (by 47.1 %) compared with the comparison group (p&lt;0.05), which pathogenetically justified use of neuroprotective drugs. Conclusions. According to our study, neuroprotective therapy is effective in the treatment of patients with cerebrovascular insufficiency.

Satisfactory result of great saphenous vein endovenous laser ablation until below the knee on active venous leg ulcer: a case series

Background Active venous leg ulcer (VLU) is the most severe manifestation of chronic venous disease which not only affects patients’ health, but also decreases the quality of life, and delivers economic burdens. Treatment of superficial venous reflux with early endovenous laser ablation (EVLA) has been associated with reducing ulcer recurrence levels and promoting faster VLU healing. We reported three cases of patients with active VLU undergoing EVLA with different approaches. Case illustration Three patients came with complaint of leg ulcer, diagnosed with C6sEpAsdPr, with venous clinical severity scores (VCSS) of 15, 23, and 22 respectively. Severe great saphenous veins (GSV) reflux was found in all patients by duplex ultrasound examination. The second patient had undergone above-the-knee EVLA. All patients underwent EVLA using 1470-nano meter wavelength laser device and ELVeS radial fiber (Biolitec, Bonn, Germany). The laser energy protocol used was 6 W linear endovenous energy density (LEED) 50 J/cm for proximal until media ATK GSV ablation, 5 W LEED 40 J/cm for media ATK until proximal below-the-knee (BTK) GSV, and 2 W LEED 20 J/cm for proximal until distal BTK GSV. The third patient was also treated with EVLA for small saphenous vein severe reflux. Follow-up until 6 months post-EVLA showed significant healing of the ulcer with 14, 16, and 17 VCSS reduction consecutively without any complication. Conclusion We’ve reported three cases of patients with active VLU undergoing EVLA until BTK with significant results. The EVLA of GSV until BTK where there is still significant reflux is safe and provides satisfactory results in patients with VLU.

Advances in the understanding of the role and mechanism of action of PFKFB3‑mediated glycolysis in liver fibrosis (Review).

Liver fibrosis is a pathophysiologic manifestation of chronic liver disease and a precursor to cirrhosis and hepatocellular carcinoma. Glycolysis provides intermediate metabolites as well as energy support for cell proliferation and phenotypic transformation in liver fibers. 6‑Phosphofructo‑2‑kinase/fructose‑2,6‑bisphosphatase 3 (PFKFB3) is a key activator of glycolysis and plays an important role in the process of glycolysis. The role of PFKFB3‑mediated glycolysis in myocardial fibrosis, renal fibrosis and pulmonary fibrosis has been demonstrated, and the role of PFKFB3 in the activation of hepatic stellate cells by aerobic glycolysis has been proven by relevant experiments. The present study reviews the research progress on the role and mechanism of action of PFKFB3‑mediated glycolysis in the progression of hepatic fibrosis to discuss the role of PFKFB3‑mediated glycolysis in hepatic fibrosis and to provide new ideas for research on PFKFB3 as a target for the treatment of hepatic fibrosis.

Key Regulators of Angiogenesis and Inflammation Are Dysregulated in Patients with Varicose Veins.

Varicose veins (VVs) are the most common manifestation of chronic venous disease (CVD) and appear as abnormally enlarged and tortuous superficial veins. VVs result from functional abnormalities in the venous circulation of the lower extremities, such as venous hypertension, venous valve incompetence, and venous reflux. Previous studies indicate that enhanced angiogenesis and inflammation contribute to the progression and onset of VVs; however, dysregulations in signaling pathways associated with these processes in VVs patients are poorly understood. Therefore, in our study, we aimed to identify key regulators of angiogenesis and inflammation that are dysregulated in patients with VVs. Expression levels of 18 genes were analyzed in peripheral blood mononuclear cells (PBMC) using real-time PCR, as well as plasma levels of 6 proteins were investigated using ELISA. Higher levels of CCL5, PDGFA, VEGFC, TGF-alpha, TGF-beta 1, and VEGF-A, as well as lower levels of VEGFB and VEGF-C, were found to be statistically significant in the VV group compared to the control subjects without VVs. None of the analyzed factors was associated with the venous localization of the varicosities. The presented study identified dysregulations in key angiogenesis- and inflammation-related factors in PBMC and plasma from VVs patients, providing new insight into molecular mechanisms that could contribute to the development of VVs and point out promising candidates for circulatory biomarkers of this disease.

Frequency of Anemia among Patients of Rheumatoid Arthritis: Cross Sectional Study

Anemia of inflammation is the common manifestation of chronic inflammatory diseases like rheumatoid arthritis. There is a lack of local data regarding this heath issue so we conducted this study order to assess the frequency of anemia among RA patients. Our results will help clinicians to manage anemia actively with chronic inflammatory disorders in our clinical setups. Objective: To evaluate the frequency of anemia of inflammation in rheumatoid arthritis patients. Methods: Both male and female patients having age 40-70 years with confirmed rheumatoid arthritis were enrolled. Patients with history of any previous blood loss or any co-morbidities like CLD, CRF and thalassemia were ruled out. Blood sample drawn from each patient was sent for laboratory measurement of hemoglobin levels thus indicating the presence or absence of anemia. Results: Mean age was 50.85 ± 9.07 years. Out of the 79 patients, 63 (79.75%) were female and 16 (20.25%) were females. Frequency of anemia in rheumatoid arthritis was found in 64 (81.01%) patients, whereas there was no anemia in 15 (18.99%) patients. Conclusions: It was concluded that anemia is a common disorder and its frequency is very high among patients of rheumatoid arthritis.

Development of novel technology for the visualization and quantitation of microvascular progenitor-driven adaptive angiogenesis during chronic lung disease

Introduction: Adaptive angiogenesis can drive repair or underlie the pathogenesis of tissue remodeling. Pulmonary vascular dysfunction is a major manifestation of chronic lung disease (CLD) but the role of angiogenesis in CLD is not well defined. Microvascular capillaries are the vessels most affected by pruning and remodeling in the lung resulting in reduced capillary length and density. Our lab has previously demonstrated that microvascular progenitors (ABCG2+ MVPCs) drive adaptive angiogenesis or loss of tissue structure downstream of the Wnt or mTOR signaling pathways. Therefore, we hypothesize that visualization of the pulmonary microvasculature and MVPC-driven adaptive angiogenesis in three-dimensions is essential to define the role of MVPC-driven adaptive angiogenesis during repair or the pathogenesis of CLD. Methods: To evaluate the contribution of Wnt activated MVPCs to angiogenesis in three-dimensions during injury repair, we crossed ABCG2-CreERT2 mice to a BOE strain (flΔex3) with stabilized β-catenin expression and a fluorescent membrane eGFP reporter strain to facilitate lineage tracing. The development and resolution of fibrosis were induced in vivo via aspiration of bleomycin sulfate (0.05U). Mice were retro-orbitally perfused with fluorescently conjugated tomato lectin. Lung tissue was inflated with agarose and up to 500μm thickness precision cut lung slices (PCLS) were mounted for imaging. PCLS were imaged on the Zeiss LSM900 and Z-stacks were obtained. Imaris software (Oxford Instruments) was used for three-dimensional reconstruction and FIJI and Wimasis Image Analysis (Onimagin Technologies) were utilized to segment vessels, quantitate vessel density, volume, diameter, and length. Results: Following perfusion, vascular staining of both the lung and kidney was observed, suggesting successful systemic perfusion and labeling. The pulmonary microvasculature was visualized to a diameter of 1-3μm in high fidelity. We observed a significant reduction in vessel density in mice treated with bleomycin compared to mice treated with a vehicle control. In our three-dimensional reconstructions we observed increased density of ABCG2+ MVPC-derived de novo angiogenic structures in areas of fibrosis. Conclusion: De novo angiogenesis driven by ABCG2+ MVPCs likely plays a role in tissue repair following bleomycin induced lung injury. In addition, we have developed a simple and reliable perfusion technique allowing for the visualization and quantitation of the pulmonary microvasculature in three-dimensions. This tool will allow the quantitation of microvessel remodeling underlying pathogenesis and repair in multiple lung injury models. Thus, this methodology will further support the study and understanding of angiogenesis during CLD and repair following injury. This approach may be utilized in various organ systems to visualize microvasculature structure and its role in disease. NIA RAG073317 NHLBI 1R35HL161238. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Differentially co-expressed myofibre transcripts associated with abnormal myofibre proportion in chronic obstructive pulmonary disease.

Skeletal muscle dysfunction is a common extrapulmonary manifestation of chronic obstructive pulmonary disease (COPD). Alterations in skeletal muscle myosin heavy chain expression, with reduced type I and increased type II myosin heavy chain expression, are associated with COPD severity when studied in largely male cohorts. The objectives of this study were (1) to define an abnormal myofibre proportion phenotype in both males and females with COPD and (2) to identify transcripts and transcriptional networks associated with abnormal myofibre proportion in COPD. Forty-six participants with COPD were assessed for body composition, strength, endurance and pulmonary function. Skeletal muscle biopsies from the vastus lateralis were assayed for fibre-type distribution and cross-sectional area via immunofluorescence microscopy and RNA-sequenced to generate transcriptome-wide gene expression data. Sex-stratified k-means clustering of type I and IIx/IIax fibre proportions was used to define abnormal myofibre proportion in participants with COPD and contrasted with previously defined criteria. Single transcripts and weighted co-expression network analysis modules were tested for correlation with the abnormal myofibre proportion phenotype. Abnormal myofibre proportion was defined in males with COPD (n=29) as <18% type I and/or >22% type IIx/IIax fibres and in females with COPD (n=17) as <36% type I and/or >12% type IIx/IIax fibres. Half of the participants with COPD were classified as having an abnormal myofibre proportion. Participants with COPD and an abnormal myofibre proportion had lower median handgrip strength (26.1 vs. 34.0kg, P=0.022), 6-min walk distance (300 vs. 353m, P=0.039) and forced expiratory volume in 1s-to-forced vital capacity ratio (0.42 vs. 0.48, P=0.041) compared with participants with COPD and normal myofibre proportions. Twenty-nine transcripts were associated with abnormal myofibre proportions in participants with COPD, with the upregulated NEB, TPM1 and TPM2 genes having the largest fold differences. Co-expression network analysis revealed that two transcript modules were significantly positively associated with the presence of abnormal myofibre proportions. One of these co-expression modules contained genes classically associated with muscle atrophy, as well as transcripts associated with both type I and type II myofibres, and was enriched for genetic loci associated with bone mineral density. Our findings indicate that there are significant transcriptional alterations associated with abnormal myofibre proportions in participants with COPD. Transcripts canonically associated with both type I and type IIa fibres were enriched in a co-expression network associated with abnormal myofibre proportion, suggesting altered transcriptional regulation across multiple fibre types.

Dual blockade of interleukin-17A and interleukin-17F as a therapeutic strategy for liver fibrosis: Investigating the potential effect and mechanism of brodalumab

Liver fibrosis is a terminal manifestation of various chronic liver diseases. There are no drugs that can reverse the condition. Recently, the importance of interleukin-17 (IL17) in the pathophysiology has been revealed and has attracted attention as a therapeutic target. We aimed to reveal the roles of IL17A and IL17F in liver fibrosis, and to validate the potential of their dual blockade as therapeutic strategy. First, we retrospectively reviewed the longitudinal change of FIB-4 index, a clinical indicator of liver fibrosis, among psoriasis patients treated by brodalumab, which blocks IL17 receptor A (IL17RA). Next, we examined anti-fibrotic efficacy of anti-IL17RA antibody (Ab) in two murine liver fibrosis models by histopathological investigation and real-time reverse transcription polymerase chain reaction (RT-PCR). Finally, we analyzed the effect of IL17A and IL17F upon human hepatic stellate cells with RNA sequencing, real-time RT-PCR, western blotting, chromatin immunoprecipitation, and flow cytometry. Clinical data showed that FIB-4 index significantly decreased among psoriasis patients treated by brodalumab. In vivo studies additionally demonstrated that anti-IL17RA Ab ameliorates liver fibrosis induced by tetrachloride and methionine-choline deficient diet. Furthermore, in vitro experiments revealed that both IL17A and IL17F enhance cell-surface expression of transforming growth factor-β receptor II and promote pro-fibrotic gene expression via the JUN pathway in human hepatic stellate cells. Our insights suggest that IL17A and IL17F share their pro-fibrotic function in the context of liver fibrosis, and moreover, dual blockade of IL17A and IL17F by anti-IL17RA Ab would be a promising strategy for the management of liver fibrosis.

Varicose Eczema: Current State of The Problem

Varicose eczema, being a common dermatological manifestation of chronic venous diseases, nevertheless remains an insufficiently studied problem. Without being a dangerous disease, varicose eczema significantly reduces the quality of life of patients. The term “varicose eczema,” although it has become commonly used, is ambiguous. The problem of varicose eczema is primarily organizational: effective diagnosis and treatment requires interaction between surgeons and dermatologists. To date, there are no uniform approaches to diagnosing skin lesions in chronic venous insufficiency

Differences in risk profile associated with varicose veins and chronic venous insufficiency - results from the Bonn Vein Study 1.

Background: The aim of this publication is to demonstrate similarities and differences in the association of risk factors with the prevalence of different manifestations of chronic venous disease (CVD), like varicose veins (VV), venous oedema (C3) and severe chronic venous insufficiency (CVI) in the population-based cross-sectional Bonn Vein Study 1 (BVS). Patients and methods: In the BVS 1 between 13.11.2000 and 15.3.2002, 3.072 participants, 1350 men and 1722 women, from a simple random sample of the general population of the city of Bonn and two rural townships aged 18-79 years were included. The overall response proportion was 59%. All participants answered a standardized questionnaire including information about socio-economic data, lifestyle, physical activity, medical history, and quality of life. Venous investigations were performed clinically and by a standardized duplex examination by trained investigators. The CEAP classification in the version of 1996 was used to classify the findings. Logistic regression models were performed for the association of possible risk factors with VV, venous edema (C3) and severe CVI (C4-C6). The predictive risk (PR) describes the association of the diseases and the possible influencing factors. Results: VV, venous oedema (C3) and severe CVI (C4-C6) have common risk factors like higher age, number of pregnancies, family history of VV and overweight or obesity. Female gender is significantly associated with VV and C3 but not with severe CVI (C4-C6). High blood pressure and urban living are only associated with C3 and C4-C6 disease whereas prolonged sitting is associated with C3 and lower social class with C4-C6 exclusively. Discussion: In many epidemiological studies risk factors were associated with chronic venous disorders in general. Our data show that VV, venous edema and severe CVI may have different risk profiles. Venous edema is more often associated with arterial hypertension and sedentary lifestyle whereas lower social class seems to be a risk factor for severe CVI including venous ulcers. Conclusions: The differences in the association of risk factors to VV, venous edema and severe CVI should be considered if prevention and treatment of chronic venous diseases are planned. As examples, compression stockings could be proposed in sitting profession to prevent oedema, VV patients with risk factors like obesity might benefit from early treatment for VV and obesity. More longitudinal evaluation of risk factors is necessary to evaluate the true risk profile of CVD.

Respiratory problems associated with liver disease in children.

Respiratory manifestations of chronic liver disease have a profound impact on patient clinical outcomes. Certain conditions within paediatric liver disease have an associated respiratory pathology. This overlap between liver and respiratory manifestations can result in complex challenges when managing patients and requires clinicians to be able to recognise when referral to specialists is required. While liver transplantation is at the centre of treatment, it opens up further potential for respiratory complications. It is established that these complications place patients at risk of longer stays in hospital and reduced survival. Additionally, late post-transplant complications can occur, including post-transplant lymphoproliferative disease and immunosuppression-induced interstitial lung disease. Although rare, it is important for clinicians to recognise these conditions to allow for prompt management. Finally, as liver disease progresses in children, respiratory complications can occur. Hepatopulmonary syndrome can occur in the context of portal hypertension, resulting in increased mortality and poorer quality of life for patients. Another consequence is portopulmonary hypertension, which can be associated with poor survival. Failure to recognise these complications in children may result in poorer outcomes and therefore it is vital that clinicians can establish when referral to a paediatric respiratory medicine specialist is required.

Satisfactory result of great saphenous vein endovenous laser ablation until below the knee on active venous leg ulcer: a case series

Background Active venous leg ulcer (VLU) is the most severe manifestation of chronic venous disease which not only affects patients’ health, but also decreases the quality of life, and delivers economic burdens. Treatment of superficial venous reflux with early endovenous laser ablation (EVLA) has been associated with reducing ulcer recurrence levels and promoting faster VLU healing. We reported three cases of patients with active VLU undergoing EVLA with different approaches. Case illustration Three patients came with complaint of leg ulcer, diagnosed with C6sEpAsdPr, with venous clinical severity scores (VCSS) of 15, 23, and 22 respectively. Severe great saphenous veins (GSV) reflux was found in all patients by duplex ultrasound examination. The second patient had undergone above-the-knee EVLA. All patients underwent EVLA using 1470-nano meter wavelength laser device and ELVeS radial fiber (Biolitec, Bonn, Germany). The laser energy protocol used was 6 W linear endovenous energy density (LEED) 50 J/cm for proximal until media ATK GSV ablation, 5 W LEED 40 J/cm for media ATK until proximal below-the-knee (BTK) GSV, and 2 W LEED 20 J/cm for proximal until distal BTK GSV. The third patient was also treated with EVLA for small saphenous vein severe reflux. Follow-up until 6 months post-EVLA showed significant healing of the ulcer with 14, 16, and 17 VCSS reduction consecutively without any complication. Conclusion We’ve reported three cases of patients with active VLU undergoing EVLA until BTK with significant results. The EVLA of GSV until BTK where there is still significant reflux is safe and provides satisfactory results in patients with VLU.

Isolated massive pleural effusion as a manifestation of chronic graft versus host disease successfully treated with corticosteroid

Isolated pleural effusion is a rare manifestation of chronic graft versus host disease (cGVHD) after hematopoietic stem cell transplantation (HSCT). We herein report a 58-year-old woman presenting with massive pleural effusion approximately 1 year after allogeneic HSCT, who was successfully treated with corticosteroid. She had discontinued tacrolimus approximately 1 month before she presented with pleural effusion, which was attributed to cGVHD after a thorough exclusion process. This case illustrates a unique manifestation of atypical cGVHD and highlights the need for prompt therapy initiation.