The usefulness of speckle tracking echocardiography for the prediction of cardiac involvement in patients with biopsy-proven sarcoidosis.

Introduction: Cardiac sarcoidosis (CS) is commonly diagnosed based on clinical criteria and abnormalities in noninvasive imaging reported in patients with biopsy-proven extracardiac sarcoidosis. Electrocardiogram and two-dimensional echocardiography have a low sensitivity for CS detection. Cardiovascular magnetic resonance imaging (CMR) and positron emission tomography (PET) have limitations in terms of cost and availability.

Evaluation of genetic risk, its clinical manifestation and disease management based on 18 susceptibility gene markers among West-Slavonic patients with sarcoidosis.

Sarcoidosis is a heterogenous, multisystemic inflammatory disease that primarily affects lungs. In this study, we multiplex genotyped 18 single-nucleotide polymorphisms (SNPs) to replicate the findings from previous genome-wide association studies (GWAS) and candidate gene studies, and extended analyses to different clinical manifestations (Löfgren's syndrome and chest X-ray [CXR] stages) including treatment response among West-Slavonic subjects (564 sarcoidosis patients and 301 healthy controls). We confirm the replication (with Bonferroni's correction) of ANXA11 rs1049550 as protective variant for sarcoidosis (odds ratio [OR] = 0.

Comparative Analysis of Fcγ and Complement Receptors Presence on Monocytes in Pulmonary Sarcoidosis and Tuberculosis.

Sarcoidosis (SA) is a granulomatous disorder, which mostly affects the lungs. Its clinical characteristics resemble tuberculosis (TB), but its treatment is different. The etiology of SA is unknown; however, mycobacterial antigens were proposed as environmental factors in its development.

Comparative Analysis of Gene Polymorphism in Pulmonary Sarcoidosis and Tuberculosis.

The clinical outcome of sarcoidosis (SA) is very similar to tuberculosis (TB); however, they are treated differently and should not be confused. In search for their biomarkers, we have previously revealed changes in the phagocytic activity of monocytes in sarcoidosis and tuberculosis. On these monocytes we found a higher expression of receptors for the Fc fragment of immunoglobulin G (FcγR) in SA and TB patients vs.

Mycobacterial Heat Shock Proteins in Sarcoidosis and Tuberculosis.

Pathological similarities between sarcoidosis (SA) and tuberculosis (TB) suggest the role of mycobacterial antigens in the etiopathogenesis of SA. The Dubaniewicz group revealed that not whole mycobacteria, but Mtb-HSP70, Mtb-HSP 65, and Mtb-HSP16 were detected in the lymph nodes, sera, and precipitated immune complexes in patients with SA and TB. In SA, the Mtb-HSP16 concentration was higher than that of Mtb-HSP70 and that of Mtb-HSP65, whereas in TB, the Mtb-HSP16 level was increased vs.

Presence and possible impact of Fcγ receptors on resident kidney cells in health and disease.

Fcγ receptors (FcγRs) bind the Fc fragment of immunoglobulin G (IgG), mostly after IgG opsonizes a bacterial or viral antigen or danger/damage-associated molecule. Consequently, classic FcγRs initiate phagocytosis of the IgG-antigen immune complex and stimulate an immune reaction against the threat. Signals from activating FcγRs (FcγRI, FcγRIIa/c, FcγRIIIa/b) are balanced by inhibitory FcγRIIb and likely also by two FcR-like proteins (FCRL4 and FCRL5).

[Cutaneous sarcoidosis - a great imitator].

Skin manifestation occurs in approximately 25% of patients with sarcoidosis and is often the first symptom of the disease. The availability of skin biopsy material is helpful in establishing the early diagnosis. Cutaneous sarcoidosis is characterized by clinical polymorphism and therefore its diagnosis may cause dilemma.

[Neurosarcoidosis - diagnosis, clinical picture and therapy].

Sarcoidosis (SA) is a granulomatous, multisystem disease of unknown etiology. Most often the disease affects lungs and mediastinal lymph nodes, but it may occur in other organs. Neurosarcoidosis (NS) more commonly occurs with other sarcoidosis forms, in 1% of cases it involves only nervous system.

[The diagnostic algorithm of practice in pulmonary and extrapulmonary sarcoidosis].

Sarcoidosis (SA) is a granulomatous multisystem disease of unknown ethiology. Pulmonary, lymphadenopathy, liver, spleen, skin, and bone sarcoidosis are more frequent but also SA of the heart, central nervous system, eye, and hypercalcemia with following kidney failure also occur. Sarcoidosis may co-exist with extrapulmonary forms, which may overtake or precede each other.

["Danger theory"as a common mechanism of sarcoidosis induction by infectious and non- infectious factors - a role of environmental factors and autoimmunity].

In the light of modified the Matzinger's model of immune response, human heat shock proteins (hsp) as main "danger signals" tissue damage-associated molecular patterns (DAMPs) or/and microbial hsp as pathogen-associated molecular patterns (PAMPs) recognized by pattern recognition receptors (PRR), may induce sarcoid granuloma by both infectious and non-infectious factors in genetically different predisposed host. Regarding infectious causes of sarcoid models, low-virulence strains of, e.g.

["Danger theory" as a common mechanism of sarcoidosis induction by infectious and non-infectious factors - a role of genetics factors].

In the light of modified the Matzinger's model of immune response, human heat shock proteins (hsp) as main 'danger signals' (tissue damage-associated molecular patterns-DAMPs) or/and microbial hsp as pathogen-associated molecular patterns (PAMPs) recognized by pattern recognition receptors (PRR), may induce sarcoid granuloma by both infectious and non-infectious factors in genetically different predisposed host.

Phenotypes of organ involvement in sarcoidosis.

Sarcoidosis is a highly variable, systemic granulomatous disease of hitherto unknown aetiology. The GenPhenReSa (Genotype-Phenotype Relationship in Sarcoidosis) project represents a European multicentre study to investigate the influence of genotype on disease phenotypes in sarcoidosis.The baseline phenotype module of GenPhenReSa comprised 2163 Caucasian patients with sarcoidosis who were phenotyped at 31 study centres according to a standardised protocol.

Relationship of emotional distress and physical concerns with fatigue severity in sarcoidosis.

Fatigue is one of the most common and disabling symptoms of sarcoidosis. The cause of fatigue remains unclear and is usually multifactorial. The majority of previous studies evaluated clinical parameters with only few of them including assessment of psychological factors as contributing to the severity of the symptoms.

Microbial Lineages in Sarcoidosis. A Metagenomic Analysis Tailored for Low-Microbial Content Samples.

Rationale: The etiology of sarcoidosis is unknown, but microbial agents are suspected as triggers.

Objectives: We sought to identify bacterial, fungal, or viral lineages in specimens from patients with sarcoidosis enriched relative to control subjects using metagenomic DNA sequencing. Because DNA from environmental contamination contributes disproportionately to samples with low authentic microbial content, we developed improved methods for filtering environmental contamination.

Association of anxiety sensitivity-physical concerns and FVC with dyspnea severity in sarcoidosis.

Objective: The purpose of the study was to evaluate the relationship of an objective functional lung parameter (FVC) and a subjective psychological factor (physical symptom concerns) with dyspnea in sarcoidosis. Dyspnea constitutes one of the most common and burdensome symptoms in sarcoidosis, yet little is known about its mechanisms and, in particular, psychological.

Method: A total of 107 hospitalized sarcoidosis patients (Female=50, M=45.

Copy number variation of FCGR genes in etiopathogenesis of sarcoidosis.

We have previously revealed that, in contrast to polymorphism of FCGR2B and FCGR3B, polymorphism of FCGR2A, FCGR2C and FCGR3A genes, encoding receptors for Fc fragment of immunoglobulin G (Fcγ receptors), play a role in increased level of circulating immune complexes with occurrence of Mycobacterium tuberculosis heat shock proteins in patients with sarcoidosis. However, this immunocomplexemia might also be caused by decreased clearance by immune cells due to a changed copy number of FCGR genes. Thus, the next step of our study was to evaluate copy number variation of FCGR2A, FCGR2B, FCGR2C, FCGR3A and FCGR3B in this disease.

Overview of neurosarcoidosis: recent advances.

Sarcoidosis (SA) is a granulomatous, multisystem disease of unknown etiology. Most often the disease affects lungs and mediastinal lymph nodes, but it may occur in other organs. Neurosarcoidosis (NS) more commonly occurs with other sarcoidosis forms, in 1 % of cases it involves only nervous system.

Polymorphism of FCGR3A gene in sarcoidosis.

We showed increased level of immune complexes (ICs) with mycobacterial heat shock proteins (Mtb-hsp) and increased expression of receptors for Fc fragment of immunoglobulin G (FcγR) I-III on blood monocytes with their increased phagocytic activity, responsible for clearance of these ICs in sarcoidosis (SA). Since FcγRIIIa is the most crucial in this process, we genotyped 77 SA patients and 143 healthy controls with polymerase chain reaction for V158F polymorphism of FCGR3A gene, encoding FcγRIIIa. We revealed significantly higher percentage of 158F and 158FF and lower of 158FV variants in Stage I of SA versus controls.

Microbial and human heat shock proteins as 'danger signals' in sarcoidosis.

In the light of the Matzinger's model of immune response, human heat shock proteins (HSPs) as main 'danger signals' (tissue damage-associated molecular patterns-DAMPs) or/and microbial HSPs as pathogen-associated molecular patterns (PAMPs) recognized by pattern recognition receptors (PRR), may induce sarcoid granuloma by both infectious and non-infectious factors in genetically different predisposed host. Regarding infectious causes of sarcoid models, low-virulence strains of, e.g.

Tuberculosis in the course of sarcoidosis treatment: is genotyping necessary for personalized therapy?

Pathological similarities between sarcoidosis (SA) and tuberculosis (TB) suggest that mycobacterial antigen(s), in genetically different predisposed hosts, may be a cause of SA. The authors' work and other published comparative analyses of HLA and non-HLA alleles in patients with SA or TB from different ethnic groups in the world revealed that some antigens were connected with high risk of SA or TB development, but others were comparable in both patient populations. The authors also showed a possibility of predominant occurrence of HLA alleles characteristic for TB as a cause of TB in patients with SA on corticosteroid therapy.

Is mycobacterial heat shock protein 16 kDa, a marker of the dormant stage of Mycobacterium tuberculosis, a sarcoid antigen?

We demonstrated opposite presence of mycobacterial heat shock proteins (Mtb-hsp) 70 kDa, 65 kDa, 16 kDa in sera and lymph nodes in sarcoidosis (SA). Higher occurrence of serum Mtb-hsp70 than Mtb-hsp 65 and Mtb-hsp 16 could be caused by sequestration of Mtb-hsp 65 and Mtb-hsp 16 in circulating immune complexes (CIs). It is possible that in genetically different predisposed hosts, Mtb-hsp 16 induced by dose-dependent nitrate/nitrite (NOx) may be involved in latent tuberculosis (TB), active TB, or SA development.