Contemporary biochemical analysis of normal pericardial fluid

Heart ◽  
2019 ◽  
Vol 106 (7) ◽  
pp. 541-544 ◽  
Author(s):  
Massimo Imazio ◽  
Andrea Biondo ◽  
Davide Ricci ◽  
Massimo Boffini ◽  
Emanuele Pivetta ◽  
...  

ObjectiveBiochemical analysis of pericardial fluid (PF) is commonly performed for the initial assessment of PF, and the results are usually interpreted according to Light’s traditional criteria for the differential diagnosis of transudates versus exudates. However, Light’s criteria have been formulated for the biochemical analysis of pleural fluid. The aim of the present paper is to evaluate the normal composition of PF in candidates for cardiac surgery.MethodsCohort study with analysis of PF from candidates for cardiac surgery. Exclusion criteria were previous pericardial disease or cardiac surgery, prior myocardial infarction within 3 months, systemic disease (eg, systemic inflammatory diseases, uremia) or drug with potentiality to affect the pericardium.ResultsFifty patients (mean age was 67 years; 95% CI 64 to 71, 29 males, 58.0%) were included in the present analysis. Levels of small molecules were similar in blood and PF. Total proteins in PF was, on average, 0.5 times lower than corresponding plasma levels (p=0.041), while the level of pericardial lactate dehydrogenase was, on average, 1.06 times higher than plasma (p=0.55). Moreover, mononuclear cells were more concentrated in PF than plasma (p=0.17). Traditional Light’s criteria misclassified all PFs as exudates.ConclusionsTraditional Light’s criteria misclassified normal PFs in candidates for cardiac surgery as exudates. This study suggests their futility for the biochemical analysis of PF in clinical practice.

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C S A Chang ◽  
H C W Hyeon ◽  
C J Y Choi ◽  
K E K Kim ◽  
P S J Park ◽  
...  

Abstract Background Pericardial disease is frequently associated with systemic diseases. Diagnosis is often troublesome because pericardial fluid does not always give an answer and limited assessment for the acquisition of tissue in effusive-constrictive or constrictive pericarditis. Even after biopsy of pericardium, diagnostic yield is very low without further information for the underlying case. 18FDG-PET can visualize both the inflammation and malignancy through whole body assessment; therefore, it can visualize both pericardium and other organs to provide further insight to the systemic disease. Purpose To assess the role of 18FDG-PET for differential diagnosis of pericardial disease in real clinical practice. Methods Patients who admitted to our pericardial disease clinic who underwent 18FDG-PET for diagnostic methods were derived from electrical medical system database and reviewed. Exclusion criteria were known the advanced stage of malignancy, or already diagnosed from pericardial effusion analysis (positive for malignancy or bacterial culture) by pericardiocentesis. Results Forty patients were finally analyzed. Most common final diagnosis was Idiopathic (n=13, 33%) and tuberculosis (n=12, 28%). Malignancy was diagnosed in 6 patients (15%). Diagnosis of malignancy in all the patients was not confirmed in pericardial effusion. One patient was diagnosed by pericardial biopsy and one by pericardial effusion. Other four were diagnosed by biopsy of other organs. Post-radiation therapy associated pericarditis in two patients, post-operative pericarditis in 5 patients, and transudate, hematoma associated pericarditis, parasite infection in one patient each. Lymph node uptake was found in 28 cases, and four of them was “suggestive malignancy”, 18 was “suggestive benign” and other 6 was “need further evaluation”. All of the patients categorized as “suggestive malignancy” was helped by 18FDG-PET which indicated the optimal biopsy site and 3 of them finally diagnosed as malignancy and one as parasite infection. All of the patients who were categorized as “suggestive benign” were finally diagnosed as a non-malignant disease. Pericardial biopsy was performed in 19 cases (48%) and only 4 were diagnostic. Other 15 specimen showed “chronic inflammation”. Guiding the optimal biopsy site by 18FDG-PET was achieved in 6 patients. 19 cases had normal SUV in the pericardium and 7 patients had very high pericardial SUV more than 10. 6 patients with benign LV pattern was finally diagnosed as tuberculosis pericarditis and one patient with the malignant pattern was finally diagnosed as angiosarcoma Conclusion 18FDG-PET is helpful in the initial assessment of pericardial disease in the aspects of 1) presumptive diagnosis of malignancy in especially in nondiagnostic pericardial effusion or technically risky for pericardiocentesis, 2) Selection of optimal biopsy site with a higher yield of disease, and 3) possibly non-invasive diagnosis of tuberculosis pericarditis. Acknowledgement/Funding None


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
F Canonico ◽  
R Vinci ◽  
D Pedicino ◽  
E Pisano ◽  
P Ciampi ◽  
...  

Abstract Background Several studies suggest that an alteration of monocyte metabolism might be implicated in inflammatory diseases. Enhanced glycolysis might be a hallmark of pro-inflammatory monocyte subsets. Improved glycolysis enables the immune cells to generate sufficient ATP and biosynthetic intermediates to carry out its particular effector functions. For macrophages this includes phagocytosis and inflammatory cytokine production. Pyruvate Kinase isozyme M2 (PKM-2) catalyzes the final step of glycolysis producing pyruvate and ATP. Latest studies have shown that a member of Jumonji family (JMJD8) acts as a positive regulator in TNF-induced NF-kB signaling leading to pro-inflammatory pathways in macrophages and is involved in angiogenesis and cellular metabolism through interacting with PKM-2 in endothelial cells. Purpose The aims of the study are to assess the expression of the glycolytic key enzyme PKM-2 in CD14+ monocytes obtained from patients with non-ST-elevation myocardial infarction (NSTEMI) or with stable angina (SA). Furthermore, the expression of JMJD8 was evaluated. Methods 30 patients with NSTEMI and 30 patients with SA were enrolled. Peripheral blood mononuclear cells were obtained from whole blood samples. For cytoplasmatic protein identification, cells were fixed and permeabilized and then incubated with fluorochrome-conjugated mAbs anti-CD14, anti-PKM-2 and anti-JMJD8. For analysis we used Two-tailed Mann-Whitney non parametric Comparison test. Results CD14+ monocytes from NSTEMI patients showed reduced expression of the key glycolytic enzyme PKM-2 as compared to CD14+ monocytes from SA patients (p=0.02) (Figure 1). JMJD8 expression in NSTEMI patients is increased compared with SA patients (p=0.02) (Figure 2). Conclusion This study introduces a role for immune-metabolism in the immunity dysregulation described in ACS patients and provides novel insights into the mechanisms responsible for coronary instability. Taking their potential interaction into account, our data suggest that in acute setting glycolysis key enzyme PKM2 expression is downregulated. Besides, JMJD8 protein levels increase in NSTEMI patients acting as potential limiting factor of PKM2 function. Moreover, our data propose the potential roles of immune-metabolism to detect novel therapeutic targets, associated with an accurate patient stratification based on immune-metabolic profiles, for prevention and treatment of atherosclerosis, in the perspective of a personalized medicine approach. Funding Acknowledgement Type of funding source: Private hospital(s). Main funding source(s): Fondazione Policlinico A. Gemelli


1996 ◽  
Vol 37 (3P2) ◽  
pp. 775-778 ◽  
Author(s):  
O. Duvernoy ◽  
A. Magnusson

Purpose: Pericardial effusion in patients who have recently undergone cardiac surgery is often trapped in compartments. CT of the pericardium provides good information about the distribution of pericardial fluid in the postoperative period after cardiac surgery. Contrary to echocardiography, CT imaging is not affected by postoperative mediastinal emphysema and pain from the wound. A method for CT-guided pericardiocentesis was developed. Material and Methods: CT-guided pericardiocentesis was carried out with a stereotactic device in 10 patients. The pericardium was punctured with a 0.9-mm needle and a 0.46-mm guide wire was introduced through the needle. An indwelling catheter was introduced over the guide wire and was left in the pericardium. Both the subxiphoid and parasternal approaches were used. Results: CT guidance facilitated placement of an indwelling catheter into the pericardial space in positions difficult to reach in patients with postoperative pericardial compartments, i.e. near the right atrium and adjacent to the cardiac apex/left ventricle. Conclusion: CT-guided pericardiocentesis offers a new possibility in patients where fluoroscopically or echocardiographically guided pericardiocentesis is difficult.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hikaru Kanemasa ◽  
Masataka Ishimura ◽  
Katsuhide Eguchi ◽  
Tamami Tanaka ◽  
Etsuro Nanishi ◽  
...  

AbstractCD71+ erythroid cells (CECs) are recognized to have an immunoregulatory function via direct cell–cell interaction and soluble mediators. Circulating CECs appear in newborns or patients with hemolytic and cardiopulmonary disorders. To assess the biological role of CECs in systemic inflammation, we studied the gene expression and function in systemic-onset juvenile idiopathic arthritis (SoJIA). Peripheral blood mononuclear cells of SoJIA patients expressed upregulated erythropoiesis-related genes. It represented the largest expansion of CECs during active phase SoJIA among other inflammatory diseases. Despite the opposing roles of erythropoietin and hepcidin in erythropoiesis, both serum levels were in concert with the amounts of SoJIA-driven CECs. Circulating CECs counts in inflammatory diseases were positively correlated with the levels of C-reactive protein, IL-6, IL-18, or soluble TNF receptors. Co-culture with active SoJIA-driven CECs suppressed secretions of IL-1β, IL-6, and IL-8 from healthy donor monocytes. The top upregulated gene in SoJIA-driven CECs was ARG2 compared with CECs from cord blood controls, although cytokine production from monocytes was suppressed by co-culture, even with an arginase inhibitor. CECs are driven to the periphery during the acute phase of SoJIA at higher levels than other inflammatory diseases. Circulating CECs may control excessive inflammation via the immunoregulatory pathways, partly involving arginase-2.


2021 ◽  
pp. 112067212110676
Author(s):  
Ahmad Abdel-Aty ◽  
Ninani Kombo

Chronic inflammatory diseases can cause significant psychosocial stress in affected patients. Few studies have examined the psychological effects of ocular inflammatory disease and no studies have examined the psychological effects of scleritis. In this study we evaluate the prevalence of mental health disorders in scleritis patients and we conduct a comprehensive review of the literature on the mental health effects of ocular inflammatory diseases. 162 patients (195 eyes) presenting to a tertiary care center with scleritis were identified. At least one comorbid mental health disorder was diagnosed in 35 patients (21.6%), most commonly major depression in 11.7%, generalized anxiety disorder in 9.3%, and substance use disorder in 6.2%. There were no significant differences in the length of an episode of scleritis or in the probability of symptom resolution between patients with a mental health disorder and other patients. In a review of the literature, 30 manuscripts met the inclusion criteria. The majority of manuscripts (83.3%) were focused on uveitis patients. Eight of these studies were focused on patients with uveitis in the context of systemic disease. The most commonly reported mental health disorders reported were anxiety and depression. An average of 31.3% of patients with ocular inflammatory disease had depression and 35.0% had anxiety. Similar to other chronic illnesses, ocular inflammatory disease may be a significant psychosocial stressor. Future studies will further elucidate the relationship between these diseases and mental health.


2005 ◽  
Vol 133 (7-8) ◽  
pp. 372-378 ◽  
Author(s):  
Tatjana Todorovic ◽  
Ivan Dozic ◽  
Dusan Pavlica ◽  
Dejan Markovic ◽  
Mirjana Ivanovic ◽  
...  

Saliva is a secretion of the salivary and mucous glands and is of major importance in the maintainance of oral health. Over the last few decades, saliva has been evaluated as a diagnostic fluid in medicine for determining systemic disease markers as well as for monitoring numerous drugs, narcotics, and hormones. The biochemical analysis of saliva is particularly important in dentistry. The estimation of the risk of appearance and diagnosis of disease, monitoring of disease progression, evaluation of therapy efficacy for caries, periodontitis, premalignant and malignant oral lesions, as well as infectious diseases of the oral cavity, can be assessed by analyzing different constituent: of saliva, individuals at risk of caries can be identified using test: that determine saliva flow rate, saliva buffer capacity, and colonization of the oral cavity by cariogenic bacteria. Today, these rapid and simple diagnostic tests are used routinely in caries risk determination. The study and use of saliva-based diagnostics have increased over the last few decades. Clinical testing of saliva shows much promise. However, there is a need for much additional research in this area, before the true clinical value of saliva as a diagnostic fluid in dentistry can be determined.


2003 ◽  
Vol 127 (9) ◽  
pp. 1207-1210 ◽  
Author(s):  
Michael Schoppet ◽  
Sabine Pankuweit ◽  
Bernhard Maisch

Abstract Sarcoidosis is a chronic systemic disease of unknown etiology, which is characterized by noncaseating epitheloid granulomas usually in multiple organs. Here we describe changes in cytokine mRNA expression by peripheral blood mononuclear cells (PBMCs) and changes of cytokine protein levels in plasma over a time course of 12 months in a patient with sarcoidosis confined to the heart as diagnosed by endomyocardial biopsy. Mitogen-stimulated PBMCs exhibited a more TH1 cytokine profile at onset of symptoms before immunosuppressive therapy was initiated, with a change to a TH0 response in the course of the disease as evidenced by multiplex-polymerase chain reaction. In plasma, high levels of interleukin-6 could be detected by an enzyme-linked immunosorbent assay system, with rapid decline correlating with immunosuppression and improving clinical course. These changes may point to a role of TH1 and TH2 cytokines in the pathogenesis and the healing process of cardiac sarcoidosis.


2020 ◽  
pp. 5259-5262
Author(s):  
Chris Hatton

The histiocytoses are disorders derived from the dendritic cell and monocyte/macrophage lineages, with the classification of this group of disorders relating to the underlying cell of origin. Dendritic cell disorders—there has been much debate about the nature of these conditions, and their status as neoplastic or primary inflammatory diseases; for Langerhans’ cell histiocytosis in particular, there is increasing evidence of their clonal nature, as manifest by recurrent BRAF mutations. Clinical features and diagnosis—these are highly variable and dependent on the sites affected by histiocytic infiltration. Symptoms and signs may include rashes, bony pain, lymphadenopathy, hepatomegaly and splenomegaly, cough and dyspnoea, features of marrow failure, and endocrine presentations (classically diabetes insipidus). Diagnosis typically follows imaging and biopsy, with the demonstration of a histiocytic infiltrate confirmed by immunostaining. Treatment and prognosis—the rarity and heterogeneity of these diseases has made it difficult to achieve a consensus on treatment. For localized disease, curettage, steroid injections, or targeted radiotherapy may be helpful. For more systemic disease, combination chemotherapy is typically used. Treatment schedules differ between adults and children. Prognosis is dependent mainly on the site(s) of involvement. Our expanding appreciation of the molecular basis of these conditions also provides some justification for the use of BRAF inhibitors and other targeted small molecule therapies. Macrophage-related disorders—these include haemophagocytic lymphohistiocytosis, a collection of macrophage-activating syndromes which may be either reactive to underlying inflammatory, infective, or neoplastic disease, or consequent upon a primary genetic lesion affecting cytotoxic T-cell killing function. Rosai–Dorfman disease is a separate macrophage proliferation syndrome, thought to be non-neoplastic, which causes massive cervical lymphadenopathy, usually in children.


Blood ◽  
1993 ◽  
Vol 81 (7) ◽  
pp. 1871-1879 ◽  
Author(s):  
WE Kaminski ◽  
E Jendraschak ◽  
R Kiefl ◽  
C von Schacky

Abstract Platelet-derived growth factor (PDGF) is a potent mitogen thought to propagate atherosclerosis and other proliferative or inflammatory diseases. Some of these diseases are ameliorated in humans by ingestion of omega-3 fatty acids. We investigated mRNA expression of both PDGF-A and PDGF-B in quiescent peripheral blood mononuclear cells from healthy male volunteers. For this, a highly sensitive, quantitative polymerase chain reaction strategy (3n-PCR) was developed. In contrast to granulocytes, both PDGF-A and PDGF-B mRNAs are expressed in mononuclear cells. This expression occurs at a remarkably constant rate. Moreover, effects of 7 g/d of a 85% omega-3 fatty acid fish oil concentrate were investigated in a 6-week controlled, randomized, observer-blind study in 14 human volunteers, 7 of whom served as controls. omega-3 Fatty acids increased in mononuclear cell phospholipids. We demonstrate for the first time that diet affects human gene regulation. Dietary omega-3 fatty acids downregulate gene expression of both PDGF-A (-66%), and PDGF-B (-70%). This may represent a novel mechanism for the antifibrotic and antiatherosclerotic action of omega-3 fatty acids.


2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Xiaoyi Shi ◽  
Chunhui Lai ◽  
Lianyu Zhao ◽  
Mingying Zhang ◽  
Xi Liu ◽  
...  

IL-37 is a cytokine that plays critical protective roles in many metabolic inflammatory diseases, and its therapeutic potential has been confirmed by exogenous IL-37 administration. However, its regulatory mechanisms remain unclear. U937 cells were treated with autophagy-modifying reagents (3-MA, chloroquine, and rapamycin) with or without LPS stimulation. Thereafter, IL-37 expression and autophagic markers (Beclin1, P62/SQSTM1, and LC3) were determined. For regulatory signal pathways, phosphorylated proteins of NF-κB (p65 and IκBα), AP-1 (c-Fos/c-Jun), and MAPK signal pathways (Erk1/2 and p38 MAPK) were quantified, and the agonists and antagonists of MAPK and NF-κB pathways were also used. Healthy human peripheral blood mononuclear cells were treated similarly to confirm our results. Four rhesus monkeys were also administered chloroquine to evaluate IL-37 induction in vivo and its bioactivity on CD4 proliferation and activation. IL-37 was upregulated by rapamycin and chloroquine in both U937 cells and human PBMCs in the presence of LPS. IL-37 was preferentially induced in autophagic cells associated with LC3 conversion. AP-1 and p65 binding motifs could be deduced in the sequence of the IL-37 promoter. Inductive IL-37 expression was accompanied with increased phosphorylated Erk1/2 and AP-1 and could be completely abolished by an Erk1/2 inhibitor or augmented by Erk1/2 agonists. In monkeys, chloroquine increased IL-37 expression, which was inversely correlated with CD4 proliferation and phosphorylated STAT3. IL-37 levels were induced by rapamycin and chloroquine through the LC3, Erk1/2, and NF-κB/AP-1 pathways. Functional IL-37 could also be induced in vivo.


Sign in / Sign up

Export Citation Format

Share Document