73 research outputs found
Levels of tissue factor pathway inhibitor in patients with inflammatory bowel disease
Endothelial dysfunction has been reported to be involved in the pathogenesis of inflammatory bowel disease (IBD) and concomitant thromboembolic complications. Inflammation stimulates the expression of tissue factor and tissue factor pathway inhibitor (TFPI) by endothelial cells. This study assessed the relationship between TFPI levels and disease activity in patients with IBD. A total of 50 consecutive adult patients with ulcerative colitis (UC), 50 patients with Crohn disease (CD), and 50 healthy controls were enrolled to the study. Plasma levels of total TFPI, free TFPI, and von Willebrand factor were measured. Associations among these levels, disease activity, and inflammatory marker levels were assessed. Total TFPI levels were higher in patients with IBD (median, 68.5 [IQR, 60.2-80.1] ng/ml) than in controls (median, 61.1 ng/ml [IQR, 54.3-74.2]; P = 0.01). Free TFPI levels were higher in patients with active UC (median, 12.8 ng/ml [IQR, 11.1-15.4]), inactive UC (median, 9.9 ng/ml [IQR, 7.3-11.5]), active CD (median, 11.7 [IQR, 9.7-14.4] ng/ml), and inactive CD (median,], 9.7 ng/ml [IQR, 8.6-11.6]) than in controls (median, 5.5 ng/ml [IQR, 4.3-7.2]; P <0.001). In the CD and UC groups, free TFPI levels correlated with the levels of inflammatory markers and disease activity. The von Willebrand factor level was higher in patients with UC (median, 143.4 IU/dl [IQR, 115.5–170.4]) and those with CD (median, 151.8 IU/dl [IQR, 112.8-189.4]) than in controls (85.1 IU/dl [IQR, 77.1-101.5]; P <0.001 for both comparisons). The anticoagulant TFPI pathway is activated during remissions and flares in patients with IBD. The free TFPI level correlates with biochemical markers of inflammation and disease activity
The use of selected neutrophil protein plasma concentrations in the diagnosis of Crohn's disease and ulcerative colitis : a preliminary report
Background: Difficulties in diagnosis of inflammatory bowel disease (IBD) motivate the search for new diagnostic tools, including laboratory tests. The aim of this study was to evaluate concentrations of the neutrophil (NEU) proteins leukocyte elastase (HLE-α1AT), lactoferrin and calprotectin as potential biomarkers used in the diagnosis and assessment of clinical activity of Crohn’s disease (CD) and ulcerative colitis (UC).Material/Methods: The study included 27 patients with CD, 33 patients with UC and 20 healthy controls. Plasma concentrations of calprotectin, lactoferrin and HLE-α1AT were measured using ELISA.Results: In patients with CD higher concentrations of HLE-α1AT (64.3±43.1 vs. 30.1±7.7 ng/l, P&amp;lt;0.001), calprotectin (151.6±97.8 vs. 69.9±22.1 ng/l, P&amp;lt;0.001) and lactoferrin (243.2±102.0 vs. 129.7±32.7 ng/l, P&amp;lt;0.001) than in the control group were found. In patients with UC higher plasma concentrations of HLE-α1AT (62.0±30.9 vs. 30.1±7.7 ng/l, P&amp;lt;0.001), calprotectin (149.6±72.3 vs. 69.9±22.1 ng/l, P&amp;lt;0.001) and lactoferrin (242.6±107.5 vs 129.7±32.7 ng/l, P&amp;lt;0.001) than in the control group were found. HLE-α1AT/NEU and lactoferrin/NEU ratios in patients with UC were significantly higher compared with patients with CD. Calprotectin (P=0.010) and lactoferrin (P=0.023) levels were higher in patients with the active compared with inactive phase of CD.Conclusions: The diagnostic characteristics of plasma granulocyte protein concentrations indicate the usefulness of these tests in the diagnosis of IBD. Higher HLE-α1AT and lactoferrin/NEU ratios in patients with UC than with CD may suggest the usefulness of these ratios in differential diagnostics. Plasma calprotectin and lactoferrin levels may be useful in CD activity assessment
Role of interleukins in therapy of inflammatory bowel diseases
Wrzodziejące zapalenie jelita grubego (WZJG) oraz choroba
Leśniowskiego-Crohna (ChLC) określane są mianem nieswoistych zapaleń jelit (NZJ). Na ich rozwój wpływ mają złożone
interakcje między czynnikami środowiskowymi, predysponującymi cechami genetycznymi, zmianami w zakresie flory jelitowej oraz w systemie immunologicznym. Szczególnie istotną
rolę przypisuje się procesom immunologicznym, w które zaangażowane są zarówno mechanizmy komórkowe, jak i humoralne. Terapia biologiczna to leczenie ukierunkowane na różne
etapy przebiegu procesu zapalnego. Podstawowe kierunki leczenia obejmują neutralizację cytokin prozapalnych, wykorzystanie cytokin przeciwzapalnych oraz hamowanie adhezji
neutrofili. W terapii biologicznej wykorzystuje się przeciwciała przeciw receptorowi IL-2, receptorowi IL-6 czy przeciwciała
przeciwko IL-12, IL-17 i IL-23. Podejmuje się również próby podawania interleukin przeciwzapalnych, takich jak rekombinowana IL-10 i IL-11. Obecnie najwięcej uwagi w badaniach klinicznych poświęca się IL-23 i IL-23R, a zahamowanie ich
aktywności może być w przyszłości celem terapeutycznym
w NZJ. Złożoność terapii biologicznej wymaga dalszych badań
klinicznych w celu wykazania, który rodzaj leczenia jest najlepszy w obserwacji długoterminowej.Ulcerative colitis (UC) and Crohn’s disease (CD) are described
as inflammatory bowel diseases (IBD). Their development is
affected by complex interactions between environmental
factors, predisposing genetic factors, changes in intestinal
flora and the immune system. A special role is ascribed to
immunological processes, which involve both cellular and
humoral mechanisms. Biological therapy is focused on
different stages of the inflammatory process. It includes
pro-inflammatory cytokine neutralization, use of antiinflammatory cytokines, and inhibition of neutrophil
adhesion. Antibodies against the IL-2 receptor, IL-6 receptor
and against IL-12, IL-17 and IL-23 are used in biological
therapy. There are also some trials regarding the use of
anti-inflammatory interleukins such as recombinant IL-10 and
IL-11. Nowadays many clinical trials are focused on IL-23 and
IL-23R. In the future the inhibition of its activity may be
a therapeutic goal in IBD. The complexity of biological therapy
requires further clinical trials to show which kind of treatment
is the best in long-term follow-up
Nonerosive reflux disease is more common in patients with chronic thyroid disease : preliminary results
Serum concentration of selected biochemical markers of endothelial dysfunction and inflammation in patients with the varying activity of inflammatory bowel disease
Introduction Endothelial dysfunction leads to an increased expression of cell adhesion molecules, leukocyte diapedesis, vascular smooth‑muscle tone, excessive permeability of vascular walls, and increased procoagulant activity. Objectives We investigated whether serum levels of several endothelial and platelet activation markers correlated with disease activity in patients with inflammatory bowel disease (IBD). Patients and methods This study included 56 patients with ulcerative colitis, 66 with Crohn disease, and 40 healthy controls. We measured the complete blood count and levels of fibrinogen, C‑reactive protein, albumin, interleukin 6, tumor necrosis factor α, E‑selectin, P‑selectin, monocyte chemoattractant protein 1 (MCP‑1), soluble CD40 ligand (sCD40L), and microparticles. Results There were no significant differences in the median levels of E‑selectin, P‑selectin, MCP‑1, sCD40L, and microparticles between patients with active IBD, those with inactive IBD, and healthy controls. The clinical disease activity assessed with the Mayo scale in the ulcerative‑colitis group was weakly, positively correlated with sCD40L (R = 0.32, P = 0.02), P‑selectin (R = 0.32, P = 0.02), and inflammatory marker levels. The clinical disease activity index in the Crohn disease group was positively correlated with the markers of inflammation yet not with the markers of endothelial activity. Conclusions E‑selectin, P‑selectin, sCD40L, MCP‑1, and microparticle levels do not significantly differ between patients with the varying activity of IBD. However, due to the observed correlations, further studies of a larger patient group should be conducted to confirm our observations
Oral ulceration in patient with active Crohn’s disease
Choroba Leśniowskiego-Crohna (ChLC) jest przewlekłym procesem zapalnym, który może umiejscawiać się w każdym odcinku przewodu pokarmowego. Wbrew wcześniejszym opiniom uważa się, że zmiany patologiczne w obrębie jamy ustnej występują dość często, lecz rzadko są rozpoznawane.
Przedstawiono 30-letniego chorego, u którego w czasie zaostrzenia objawów ChLC wystąpiło owrzodzenie jamy ustnej.
Za pomocą badania histologicznego błony śluzowej z otoczenia wrzodu zdiagnozowano zapalenie ziarniniakowe. Zmiany
typowe dla ChLC obejmowały dystalny odcinek jelita cienkiego z przetoką między pętlami jelita cienkiego oraz esicę
i prostnicę, a potwierdzone były badaniem kolonoskopowym
i histologicznym wycinków błony śluzowej oraz badaniem radiologicznym jelita cienkiego. Autorzy zwracają uwagę
na przydatność badania stomatologicznego u chorego z zaostrzeniem ChLC. Umożliwia ono rozpoznanie zmian patologicznych błony śluzowej i potwierdzenie w ocenie histopatologicznej nieswoistego zapalenia ziarniniakowego. U chorych
na ChLC owrzodzenia w jamie ustnej są przewlekłe i trudno
poddają się leczeniu miejscowemu. Podstawowe znaczenie
w tych przypadkach ma standardowe leczenie aktywnej ChLC.Crohn’s disease (CD) is a chronic inflammatory process with
pathological changes which can involve any part of the
gastrointestinal tract. Contrary to previous opinions,
involvement of the oral cavity is frequent, but is rarely
diagnosed. A thirty-years-old patient with deep ulceration of
the oral mucosa which appeared during exacerbation of CD is
presented. Granulomatous inflammation of the oral mucosa
was confirmed by histopathology. Inflammatory changes
typical for CD were present in the distal small bowel with
ileo-ileal fistula and in the distal colon, and were confirmed by
colonoscopy, histopathological examination of mucosal
biopsies and double-contrast radiographic examination of the
small bowel. Dental examination of a patient with active CD
is helpful in the diagnosis of oral manifestations of the
disease and mucosal biopsies can easily be taken for
histopathological confirmation of granulomatous
inflammation. In patients with CD the oral ulcerations are
chronic and difficult to treat. The standard treatment of
active CD plays the main role in the approach to these
patients
Insulin-like growth factor system in remission and flare of inflammatory bowel diseases
Insulin‑like
growth factor 1 (IGF‑1)
is involved in the modulation of immunity and inflammation.
It also plays a role in regulating the migration of endothelial cells and production of vasoactive
agents. This study assessed the concentrations of IGF‑1
and insulin‑like
growth factor-binding protein
3 (IGFBP‑3)
and their relationships to disease activity in patients with inflammatory bowel disease (IBD). A total of 129 adult patients with IBD (69 with Crohn disease [CD] and 60 with
ulcerative colitis [UC]) were involved in the study. The control group consisted of 31 healthy volunteers.
Biochemical serum analyses were performed and the associations of IGF‑1
and IGFBP‑3
with inflammatory
markers and disease activity were assessed. IGF‑1
levels were decreased in patients with active UC compared with those with nonactive
UC (mean [SD], 78.3 [22.7] ng/ml and 96.2 [24.5] ng/ml, respectively; P = 0.02) and controls
(94.5 [26.5] ng/ml; P = 0.03). The IGF‑1
level was lower in patients with active CD compared with
those with nonactive CD (mean [SD], 79.2 [24.9] ng/ml and 110.1 [43.4] ng/ml, respectively; P <0.001).
The IGFBP‑3
level was lower in patients with active UC compared with those with nonactive UC (P = 0.04)
and controls (P = 0.04). IGF‑1
correlated negatively with C‑reactive
protein (CRP) levels (P <0.01),
disease activity (P <0.05), and disease duration (P <0.05). IGFBP‑3
levels correlated negatively with
CRP levels (P <0.05). The IGF system is disrupted in patients with IBD. Systemic levels of the IGF axis components
are related to disease activity and duration
Znaczenie polimorfizmu "IL28B" w odpowiedzi na leczenie interferonem pegylowanym α i rybawiryną przewlekłego zapalenia wątroby wywołanego genotypem 1b HCV
Wstęp: Leczenie przewlekłego zapalenia wątroby typu C
(PZW-C) pegylowanym interferonem α (Peg-IFN) z ryba wiryną
powoduje tzw. trwałą odpowiedź wirusologiczną (sustained
virological response - SVR) u blisko 50% chorych. Odpowiedź
ta ściśle zależy od HCV i czynników genetycznych chorego.
Wykazano, że polimorfizm genu IL28B wiąże się z eradykacją
wirusa i SVR.
Cel: Zbadanie, czy wyniki leczenia PZW-C u chorych z regionu
Polski Południowej zależą od wariantów genetycznych IL28B,
a polimorfizm może być czynnikiem predykcyjnym SVR.
Materiał i metody: Sto czterdzieści dwie osoby z PZW-C spowodowanym genotypem 1b HCV leczono standardowo PegIFN z rybawiryną przez 48 tygodni. Polimorfizmy rs12979860
IL28B (C/T) badano metodą PCR-RFLP. HCV-RNA i aktywność
aminotransferazy alaninowej (ALT) w surowicy mierzono
przed leczeniem i po 12, 48 i 72 tygodniach terapii.
Wyniki: Wiremia HCV-RNA przed terapią i po 12-tygodniowym
leczeniu była wyższa u chorych z genotypem T/C i T/T. Trwałą
odpowiedź wirusologiczną osiągnęło istotnie więcej chorych
z genotypem C/C (71,1%) w porównaniu z 41,4% z genotypem
T/C i 23,5% T/T. Chorzy z genotypem C/C lepiej reagowali na
leczenie w porównaniu z osobami z genotypami T/C i T/T,
osiągali wyższe wskaźniki odpowiedzi wczesnej (12 tygodni),
na koniec leczenia (48 tygodni) i SVR. Aktywność ALT nie
różniła się istotnie podczas terapii pomiędzy grupami. Tolerancja leczenia była podobna i nie zależała od genotypów C/C,
T/C i T/T. Wnioski: Wyniki badania potwierdziły zależność odpowiedzi
na standardowe leczenie PZW-C spowodowanego genotypem 1b HCV od predyspozycji genetycznej chorego, jednak
w przeciwieństwie do niektórych doniesień złe rokowanie
obserwowano u homozygot T/T IL28B.Introduction: Treatment of chronic hepatitis C (CH-C) with
peginterferon α (Peg-IFN) and ribavirin leads to a sustained
virological response (SVR) in 50% of patients and depends on
HCV and host factors. Polymorphism of the IL28B gene is
associated with eradication of HCV and SVR.
Aim: The objective of this study was to examine patients from
the region of southern Poland and determine whether CH-C
therapy depends on the genetic variants of IL28B and
whether this polymorphism may predict SVR.
Material and methods: One hundred forty-two patients
with CH-C and the genotype 1b HCV were treated with PegIFN and ribavirin for 48 weeks. IL28B rs12979860 polymorphisms (C/T) were tested by PCR-RFLP. The HCV-RNA and
alanine aminotransferase (ALT) levels were measured
before treatment and after 12, 48 and 72 weeks.
Results: Viral load before and after 12 weeks of therapy was
higher in the genotypes T/C and T/T than in C/C. 71.1% of
patients with the genotype C/C achieved SVR vs. 41.4% with
the genotype T/C and 23.5% with T/T. Patients with the genotype C/C responded better to treatment as compared to subjects with the genotypes T/C and T/T, and achieved better
early response (12 weeks), at the end of treatment (48 weeks)
and SVR. Alanine aminotransferase activity was similar
among the groups. Tolerance of therapy was similar and independent of the genotypes.
Conclusions: The study confirmed the dependence of
response to standard treatment of CH-C caused by the genotype 1b HCV on the patient's genetic predisposition. In contrast to some other reports, poor prognosis was observed in
T/T homozygotes of IL28B
Markers of lipid peroxidation and antioxidant status in the serum and saliva of patients with active Crohn disease
- …