Liver osteodystrophy

Osteodystrofia wątrobowa, czyli zespół zaburzeń tkanki kostnej spowodowanych chorobą wątroby, jest częstym powikłaniem przewlekłych schorzeń tego narządu. Dochodzi do niej u ok. 20-100% pacjentów z przewlekłą chorobą wątroby zarówno w miąższowych, jak i cholestatycznych chorobach wątroby. Patogeneza zaburzeń tkanki kostnej jest złożona i nie do końca poznana. Wśród potencjalnych przyczyn osteodystrofii wątrobowej można wyróżnić zaburzenia wątrobowej hydroksylacji witaminy D, zmiany w zakresie receptora dla witaminy D, zwiększenie stężenia w surowicy parathormonu, niedobór insulinopodobnego czynnika wzrostu (IGF-1), hiperbilirubinemię, hipogonadyzm, niedobór osteoprotegeryn, jatrogenny wpływ farmakoterapii, zaburzenia wchłaniania witaminy D, wapnia i fosforu, do którego dochodzi wraz z pogarszaniem się czynności wątroby. Klinicznie najistotniejszymi następstwami osteodystrofii są bolesność oraz złamania kości. Kalcytriol - 1,25(OH)2D3 - jest aktywną formą witaminy D. Powstaje w wyniku dwustopniowej hydroksylacji - do pierwszej dochodzi w wątrobie, natomiast do drugiej w nerkach. Kalcytriol wpływa na komórki jelita cienkiego, czego efektem jest wzrost wchłaniania wapnia z pokarmu, oraz pobudza uwalnianie wapnia z kości do krwi. Zaburzenia metabolizmu witaminy D mogą być ważnym czynnikiem doprowadzającym do osteodystrofii. Ponieważ jednak korelacja między metabolizmem witaminy D a osteodystrofią wątrobową nie jest w pełni jasna, w artykule zwrócono uwagę na inne, hipotetyczne czynniki biorące udział w patogenezie osteodystrofii wątrobowej.Hepatic osteodystrophy, which is a disorder of bone metabolism, is a common side effect among patients with chronic liver diseases. It can be observed among approximately 20-100% of patients with chronic liver disease, both parenchymatous and cholestatic. The pathogenesis of hepatic osteodystrophy is complex and still unknown. Hypothetical causes of liver osteodystrophy can be impairment of vitamin D liver hydroxylation, vitamin D receptor, increased level of PTH in blood, decreased level of IGF-1, hyperbilirubinaemia, hypogonadism, decreased level of osteoprotegerin, effect of pharmacotherapy, impairment of digestion of vitamin D, calcium, phosphorus, present in chronic liver diseases. Clinically the most significant after-effects are bone tenderness and fractures. Calcitriol, 1,25(OH)2D3, is the active form of vitamin D. It is produced due to a two-step hydroxylation process, the first in the liver and the second in the kidneys. Calcitriol acts on the cells of the intestine to promote the absorption of calcium from food and on bone to mobilize calcium from the bone to the blood. Disturbances of vitamin D metabolism can be an important cause of liver osteodystrophy. However, the correlation between vitamin D and liver osteodystrophy is not very clear; thus we discuss in our article other hypothetical causes of liver osteodystrophy

Lyme disease : review

Lyme disease is a multi-organ animal-borne disease, caused by spirochetes of Borrelia burgdorferi (Bb), which typically affect the skin, nervous system, musculoskeletal system and heart. A history of confirmed exposure to tick bites, typical signs and symptoms of Lyme borreliosis and positive tests for anti-Bb antibodies, are the basis of a diagnosis. A two-step diagnosis is necessary: the first step is based on a high sensitivity ELISA test with positive results confirmed by a more specific Western blot assay. Antibiotic therapy is curative in most cases, but some patients develop chronic symptoms, which do not respond to antibiotics. The aim of this review is to summarize our current knowledge of the symptoms, clinical diagnosis and treatment of Lyme borreliosis

Decreased expression of the high mobility group box 1 (HMGB1) gene in peripheral blood in patients with mild or moderate clostridioides difficile infection

Cytokines are mediators of inflammation induced in the course of Clostridioides difficile infection (CDI). High Mobility Group Box 1 (HMGB1) is a cytokine playing an important role in the pathogenesis of numerous inflammatory and autoimmune diseases. The aim of the study was to assess the HMGB1 gene expression in the course of CDI. We have performed a prospective case-control study- including 55 adult patients, among them 27 with CDI, who were hospitalized from October 2018 to February 2020 and 28 healthy volunteers. We assessed: a complete blood count with differential leukocyte count, blood creatinine, albumin, and C-reactive protein (CRP) levels. Then, the expression of the HMGB1 gene was evaluated using quantitative Real-Time PCR. Patients with CDI were found to have a significant increase in white blood cells (WBC), neutrophil count, and CRP levels, they also exhibited decreased levels of albumin compared with controls. The HMGB1 gene expression was significantly lower among patients with CDI compared with the control group and significantly, inversely correlated with CRP level in blood. In conclusion, we have observed a decreased expression of the HMGB1 gene in peripheral blood of patients with mild or moderate CDI, which hypothetically could reflect their diminished capability to fight the pathogen

The effect of TCDD dioxin on the rat liver in biochemical and histological assessment

Eighteen male Wistar rats were divided into 3 groups of 6 animals each. Two groups received different intraperitoneal doses of TCDD (0.75 and 8 μg) in DMSO solution and the third group (control) received only DMSO on days 0, 7 and 14. On day 21 the animals were sacrificed, and then blood tests, pathological examination and CYP1A1 activity measurement were performed. In rats that received a high dose of dioxin (8 μg) hepatic lobules revealed parenchymal degeneration and vacuolization of hepatocytes was observed, and also an increased CYP reaction was found in central parts of lobules, around the central vein. The reaction in control and low dose groups was weak. The resorufin level was significantly (P<0.05) higher in the group receiving a low dose of dioxin as compared to the control group. The study confirmed that TCDD damages the rat liver in a dose-dependent manner. Administration of high TCDD doses causing major liver damage also damaged CYP1A1 (based on higher resorufin levels in epiluminescence). TCDD activates CYP1A1, which was confirmed by increased immunohistochemical reactivity of central areas of hepatic lobules

Identification of lipid derivatives in Hep G2 cells

Metabolism of polyunsaturated fatty acids results in biosynthesis of mediators with different physiological effects. These metabolites include prostaglandins, prostacyclins, isoprostanes and others that are important signalling molecules and regulate a variety of physiological and pathophysiological processes including inflammation. Prostaglandins and isoprostanes are produced by either non-enzymatic lipid peroxidation or by enzyme-induced peroxidation (cyclooxygenases and lipoxygenases). They are used as biomarkers of oxidative stress. The aim of our study was to assess the effect of eicosapentaenoic acid (EPA) supplementation with added benzo(a)pyrene (BaP) on HepG2 cells by using a UHPLC/MS-TOF method. This rapid and simple method was developed for the identification, separation and quantification of 8-iPGF3α, PGF3α, 8-isoPGF2α and 5-iPF2α in cultured cells. The UHPLC/MS-TOF method was validated. The calculated limit of detection was in the range of 0.16-0.50 ng/mL, precision (% RSD): 1.2-2.1% and recoveries better than 88%. This method empowered qualitative and quantitative analysis of the selected individual prostaglandins derived from arachidonic acid and eicosapentaenoic acid from cell extracts