Further evidence of altered redox status of hyperbilirubinaemic patients: role of bilirubin in Gilbert syndrome

Bilirubin is regarded as the most powerful endogenous antioxidant substance. It exhibits immunmodulator, inhibitor activities on kinases, yet it is clear that it can be potentially cytotoxic. Gilbert syndrome is characterised by hereditary, chronic, mild unconjugat-ed hyperbilirubinaemia. 12 Gilbert syndrome patients and 15 healthy controls were investigat-ed with special regard to reduction-oxidation status and free radical-antioxidant balance. Sera free SH-group concentration, H-donating ability, reducing power were measured spec-trophotometric methods. Total scavenger capacity, describing free radical-antioxidant balance, was determined by a newly developed chemiluminometric method in sera, plasma and erythrocytes. Patients with Gilbert syndrome showed a significant increase of non-enzymatic antioxidant capacity. Elevated free SH-group concentration, H-donating ability and reducing power were found in mild hyperbilirubinaemia compared with control group patients. On the other hand no significant differences were detected regarding free radical-antioxidant balance in sera, plasma and erythrocytes between the groups. On the basis of these results it can be supposed that elevated bilirubin concentration, via indirect or compensatory way, strengthens non-enzymatic antioxidant capacity, without changes in antioxidant-free radical balance. That is why further investigations are needed to clarify the consequences of elevated bilirubin concentration on cell redox homeostasis

Helicobacter pylori infection: New pathogenetic and clinical aspects

Helicobacter pylori (H. pylori) infects more than half of the world’s human population, but only 1% to 3% of infected people consequently develop gastric adenocarcinomas. The clinical outcome of the infection is determined by host genetic predisposition, bacterial virulence factors, and environmental factors. The association between H. pylori infection and chronic active gastritis, peptic ulcer disease, gastric cell carcinoma, and B cell mucosa-associated lymphoid tissue lymphoma has been well established. With the exception of unexplained iron deficiency anemia and idiopathic thrombocytopenic purpura, H. pylori infection has no proven role in extraintestinal diseases. On the other hand, there is data showing that H. pylori infection could be beneficial for some human diseases. The unpredictability of the long-term consequences of H. pylori infection and the economic challenge in eradicating it is why identification of high-risk individuals is crucial

A májfibrosis nem invazív jellemzésének lehetőségei a klinikai adatok tükrében

Liver cirrhosis is one of the leading causes of death worldwide. Liver biopsy is considered as the gold standard for the diagnosis of chronic liver diseases. Studies have focused on non-invasive markers for liver fibrosis because of the dangers and complications of liver biopsy. The authors review the non-invasive direct as well as indirect methods for liver fibrosis assessment and present the positive and negative predictive value, sensitivity and specificity of those. Clinical utilities of transient elastography (Fibrsocan) is also reviewed. Non-invasive methods are useful in the assessment of liver fibrosis, monitoring disease progression and therapeutic response. Their accuracy can be increased by the combined or sequential use of non-invasive markers

A májsejtrák célzott kezelésének újabb lehetőségei a molekuláris biológiai adatok ismeretében = New possibilities of targeted therapy in the treatment of hepatocellular carcinoma in view of molecular biology

A hepatocellularis carcinoma kórjóslata rossz. A felismeréskor a betegek 85%-a nem alkalmas a kuratív kezelésre, ezekben az esetekben a palliatív módozatok, a transarterialis kemoembolisatio, a rádiófrekvenciás ablatio és a szisztémás kemoterápia alkalmazhatóak. A szisztémás kemoterápia eredményei kiábrándítóak. Molekuláris biológiai ismereteink a célzott kezelési lehetőségek tárát bővíthetik a jövőben. Jelenleg a multikinázgátló sorafenib van csak törzskönyvezve hazánkban, de ígéretesek lehetnek még a VEGF-gátlók (bevacizumab, sunitinib), az EGFR-útvonal gátlása (erlotinib), valamint az mTOR-gátlók (rapamycin és származékai). Előnyös lehet a sorafenib vagy más érképződést gátló együttes adása helyi ablatív eljárásokkal (transarterialis kemoembolisatio, rádiófrekvenciás ablatio) vagy kuratív hepatectomiával. A jövő további lehetőségei közé tartoznak a Wnt-útvonalat módosítók, a retinoid vegyületek, a sejtciklusgátlók, a proteoszómagátlók és az epigenetikus kezelés. Orv. Hetil., 2010, 43, 1763–1768. | Hepatocellular carcinoma (HCC) has a poor prognosis. Approximately 85% of patients are not candidates for curative treatments at the time of diagnosis; hence palliative modalities (transcatheter arterial chemoembolisation, radiofrequency ablation, systemic chemotherapy) are used. Systemic chemotherapies have disappointing results. The increasing knowledge in the molecular biology of HCC will increase the possibilities of targeted therapy. The multi-tyrosine kinase inhibitor sorafenib is the only drug which has approved. The VEGF-inhibitors (bevacizumab, sunitinib), EGFR-blocker agents (erlotinib), as well as the inhibition of mTOR (rapamycin) are promising. Combination of sorafenib or other anti-angiogenic agents with local ablative procedure (transcatheter arterial chemoembolisation, radiofrequency ablation), or with curative hepatectomy also can be favorable. Alteration of Wnt pathway, retinoid compounds, inhibition of the cell cycle as well as the proteosome, and epigenetic therapy can be other potential promising targets in HCC. Orv. Hetil., 2010, 43, 1763–1768

A peptikus fekély: tények és kérdések – 2010 = Peptic ulcer: facts and questions – 2010

A peptikus fekélybetegség kóroktana és klinikai megjelenési formái átalakulóban vannak. A H. pylori -fertőzés mellett a nem szteroid gyulladáscsökkentők és a kis dózisú acetilszalicilsav-kezelés kóroki szerepe ismert. A H. pylori -pozitív fekélybetegség a baktérium eradikációjával gyógyítható. Az NSAID-fekély megelőzésére a savszekréció-gátló adását pedig a gyomor-bél rendszeri, valamint szív-ér rendszeri kockázati tényezők határozzák meg. A számos kóroki tényező és az új, hatékony kezelési módok alkalmazása ellenére továbbra is vannak megválaszolatlan kérdések. Előtérbe kerültek az NSAID- és a H. pylori- negatív fekélyek, amelyek száma növekszik, kezelésük tisztázásra vár. A H. pylori -eradikáció sikertelensége is gyakoribbá vált, az optimális kezelési mód hiányzik. | Etiology and clinical manifestation of the peptic ulcer keep changes nowadays. Helicobacter pylori-infection, nonsteroidal anti-inflammatory drugs and small dosage acetic acid treatment are the main etiological factors. Helicobacter pylori positive peptic ulcer can be treated with eradication of the bacterium. Prevention of the NSAID-ulcer and the prescription of the acid suppressive therapy depend on the gastrointestinal and cardiovascular risk factors of patient. Despite of the effective therapies, there are still questions to answer. The number of Helicobacter pylori and NSAID negative ulcers is likely to increase, their therapy must be clarified. There’s a fall in the eradication rate of Helicobacter pylori infection, the optimal treatment is missing

A nyelőcsőrák kockázati tényezői és lehetséges genetikai háttere = Epidemiology and pathogenesis of esophageal cancer, and the possibilities of its prevention

A nyelőcsőrák a hatodik leggyakoribb daganatos halálok, gyakorisága nő. A nyelőcsőrákok 95%-a laphámrák vagy adenocarcinoma. Bár a nyelőcsőlaphámrák és az adenocarcinoma szövettana és előfordulása különböző, számos kockázati tényezőjük (dohányzás, táplálkozási szokások), valamint a daganatkialakulás folyamata hasonló. A nyelőcsőrák több mint 90%-ban előrehaladott állapotban derül ki. A felismerés és a kezelés lehetőségeinek fejlődése ellenére kórjóslata rossz, az ötéves túlélés 10–13%. A kórélettani háttér pontosabb megértése a megelőzést segítheti, részben természetes hatóanyagok, részben nemszteroid gyulladáscsökkentők alkalmazásával. | Esophageal cancer is the sixth most common cancer mortality, with increasing incidence. 95% of the esophageal cancer is squamous cell carcinoma or adenocarcinoma. Although they differ in histology and epidemiology, some of their risk factors (smoking, dietary factors) and their pathogenesis are the same. More than 90% of esophageal cancer is diagnosed in late stage. Despite the development of diagnostic and therapeutic techniques, esophageal cancer has poor prognosis, with 5-year survival rates between 10–13%. Understanding the exact pathogenesis can help the prevention of this highly aggressive cancer, with the use of natural substances and nonsteroid inflammatory drugs

Nem alkoholos steatosis/steatohepatitis – 2010 = Non-alcoholic steatosis/steatohepatitis – 2010

A nem alkoholos eredetű zsírmáj és a steatohepatitis a kóros májműködés leggyakoribb oka. A szerzők áttekintik a kórkép fő kóroki tényezőit, kialakulásának lehetséges hátterét, klinikumát, valamint a kórisme felállításának nehézségeit. Nagy az igény olyan, nem invazív biomarkerek (TNF-α adiponektin, lipidperoxidáció termékei, citokeratin-18, hialuronsav), pontrendszerek (Fibrotest, APRI), vizsgálatok (Fibroscan) kidolgozására, amelyek a betegség előrehaladását, a gyulladást és a fibrosist jelzik. Mind ez idáig megfelelően hatékony kezelés nem ismert. A terápia részben a kiváltó tényezők eliminálását (testsúlycsökkentés), az anyagcserezavar (diabetes mellitus, hyperlipidaemia) kezelését célozza meg, részben a májvédelmet (antioxidánsok) helyezi előtérbe. Orv. Hetil., 2010, 47, 1940–1945. | Non-alcoholic steatosis/steatohepatitis is the most common etiology of abnormal liver function tests. Authors review the etiology, pathomechanism and clinical signs. Possibilities of the diagnosis are also summarized. There is an increasing need to find non-invasive biomarkers (TNF-α, adiponektin, end product of lipid peroxidation, cytokeratin-18, hyaluronic acid), score systems (Fibrotest, APRI), methods (Fibroscan), which would detect the progression of the disease, the development of inflammation and fibrosis. There is no proven specific therapy; the aim is the elimination of provoking factors (weight loss), treatment of diabetes mellitus and hyperlipidemia. Besides, liver protection (antioxidants) is important, as well. Orv. Hetil., 2010, 47, 1940–1945

Adatok az „önként vállalt gyermektelenség” csökkentésére gyulladásos bélbetegségben = Data for the Decrease of “Voluntary Childlessness” in Inflammatory Bowel Disease

Inflammatory bowel disease is a chronic disorder affecting young adults in their reproductive years, hence its populational consequences are not negligible. While fertility in inflammatory bowel disease is the same with the general population (except for male patients with sulphasalazine treatment and females with ileum-poch anal anastomosis), “voluntary childlessness” is higher, 14–18%. Patients require accurate counseling addressing fertility, pregnancy course and outcome. They need to be informed appropriately about risks and benefits of medications in inflammatory bowel disease in order to assist their decision making, decrease “voluntary childlessness” and improve compliance. Authors review the issues related to fertility, outcome of pregnancy, medical treatment options before and during pregnancy as well as during breastfeeding in inflammatory bowel disease. Orv. Hetil., 2012, 153, 1855–1862. </jats:p

Az idült májbetegségek progressziójához vezető folyamatok

As the result of various effects (viruses, metabolic diseases, nutritional factors, toxic agents, autoimmune processes) abnormal liver function, liver steatosis and connective tissue remodeling may develop. Progression of this process is complex including various pathways and a number of factors. The authors summarize the factors involved in the progression of chronic liver disease. They describe the role of cells and the produced inflammatory mediators and cytokines, as well as the relationship between the disease and the intestinal flora. They emphasize the role of oxidative stress, mitochondrial dysfunction and cell death in disease progression. Insulin resistance and micro-elements (iron, copper) in relation to liver damage are also discussed, and genetic and epigenetic aspects underlying disease progression are summarized. Discovery of novel treatment options, assessment of the effectiveness of treatment, as well as the success and proper timing of liver transplantation may depend on a better understanding of the process of disease progression