Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used in numerous areas of medicine. By inhibiting the prostaglandin synthesis pathway, they contribute to the development of injuries to the mucous membranes within the gastrointestinal tract, possibly leading to gastrointestinal bleeding. Proton pump inhibitors (PPIs) are used to prevent such events in high-risk groups. The bleeding risk is highest in patients above the age of 65, patients with a history of gastrointestinal bleeding, and patients with a history of peptic ulcer disease. The efficacy of bleeding prevention could not be proven in other groups. Notably, PPIs are associated with serious side effects, including acute kidney injury, malabsorption syndrome, and osteoporosis. Therefore, recommending the use of PPIs within the framework of prevention should be approached with caution. The widespread belief that IPP should be automatically prescribed together with NSAIDs is false and harmful to patients.
Niesteroidowe leki przeciwzapalne (NLPZ) są powszechnie stosowane w wielu obszarach medycyny. Jako leki hamujące szlak prostalglandyn przyczyniają się do powstawania uszkodzeń błony śluzowej przewodu pokarmowego, co może prowadzić do krwawienia. Zapobiega się mu, stosując w grupach wysokiego ryzyka profilaktycznie inhibitory pompy protonowej (IPP). Do pacjentów o ryzyku najwyższym należą osoby po 65. roku życia, po przebytym krwawieniu z przewodu pokarmowego i z chorobą wrzodową w wywiadach. W pozostałych przypadkach nie udowodniono skuteczności profilaktyki. Należy zauważyć, że IPP są obaczone poważnymi działaniami niepożądanymi, w tym ostrym uszkodzeniem nerek, zaburzeniami wchłaniania czy osteoporozą. Dlatego należy rozważnie podchodzić do zlecania IPP w ramach profilaktyki. Powszechny pogląd o konieczności automatycznego przepisywania IPP razem z NLPZ jest nieprawdziwy i szkodliwy dla pacjentów.
Historic buildings are constantly being exposed to numerous climatic changes such as damp and rainwater. Water migration into and out of the material's pores can lead to salt precipitation and the so-called efflorescence. The structure of the material may be seriously threatened by salt crystallization. A huge pressure is produced when salt hydrates occupy larger spaces, which leads at the end to cracking, detachment and material loss. Halophilic microorganisms have the ability to adapt to high salinity because of the mechanisms of inorganic salt (KCl or NaCl) accumulation in their cells at concentrations isotonic to the environment, or compatible solutes uptake or synthesis. In this study, we focused our attention on the determination of optimal growth conditions of halophilic microorganisms isolated from historical buildings in terms of salinity, pH and temperature ranges, as well as biochemical properties and antagonistic abilities. Halophilic microorganisms studied in this paper could be categorized as a halotolerant group, as they grow in the absence of NaCl, as well as tolerate higher salt concentrations (Staphylococcus succinus, Virgibacillus halodenitrificans). Halophilic microorganisms have been also observed (Halobacillus styriensis, H. hunanensis, H. naozhouensis, H. litoralis, Marinococcus halophilus and yeast Sterigmatomyces halophilus). With respect to their physiological characteristics, cultivation at a temperature of 25-30°C, pH 6-7, NaCl concentration for halotolerant and halophilic microorganisms, 0-10% and 15-30%, respectively, provides the most convenient conditions. Halophiles described in this study displayed lipolytic, glycolytic and proteolytic activities. Staphylococcus succinus and Marinococcus halophilus showed strong antagonistic potential towards bacteria from the Bacillus genus, while Halobacillus litoralis displayed an inhibiting ability against other halophiles.
Treatment of multiple sclerosis with interferon-beta involves the risk of the development of immunological response to this protein. The response consists in the production of antibodies that bind or neutralise interferon-beta. The binding antibodies are detectable in the majority of the treated patients and do not influence the efficacy of treatment. Simultaneously, large clinical studies provide evidence that the neutralising antibodies reduce and in high titres suppress the effect of interferon, which causes the frequency of exacerbations and the number of new and intensified outbreaks in magnetic resonance imaging to increase. What is more, it may even result in the accelerated progression of disability. The incidence of the neutralising antibodies depends on the preparation as well as the route of administration and concerns from 2 to 42% of the treated patients; it reaches its maximum between the 6th and the 24th month of treatment. The neutralising antibodies may be present temporarily (once they disappear, the efficacy of interferon returns to its initial level), yet a high titre predicts their long-term persistence, even after the drug has been discontinued. Various ways of detecting the neutralising antibodies have been devised – from methods that take advantage of a cytopathic effect to those based on the induction of a luciferase reporter gene. Reliable markers of the in vivo activity of interferon-beta that may complement marking of the antibodies are being sought. For many years, the issue of anti-interferon antibodies was accompanied by controversy that resulted from methodological difficulties in studying their clinical utility. At present, in view of the gathered data, European experts unanimously recommend a repeated screening examination of the neutralising antibody titre for patients treated with interferon and considering the results when making therapeutic decisions.
PL
Leczenie stwardnienia rozsianego interferonem beta wiąże się z ryzykiem rozwoju odpowiedzi immunologicznej przeciw temu białku. Polega ona na produkcji przeciwciał wiążących lub neutralizujących interferon beta. Przeciwciała wiążące są wykrywalne u większości leczonych i nie wpływają na skuteczność terapii. Jednocześnie duże badania kliniczne dostarczają dowodów na to, że przeciwciała neutralizujące zmniejszają, a w wysokich mianach znoszą działanie interferonu, co przekłada się na wzrost częstości rzutów oraz liczby nowych i wzmacniających się ognisk w badaniach rezonansu magnetycznego, a nawet przyspieszenie postępu niesprawności. Częstość występowania przeciwciał neutralizujących zależy od preparatu i drogi podania oraz dotyczy od 2 do 42% osób leczonych; maksimum osiąga między 6. a 24. miesiącem terapii. Przeciwciała neutralizujące mogą być obecne przejściowo (po ich zaniknięciu skuteczność interferonu powraca do poziomu wyjściowego), ale wysokie miano zapowiada ich wieloletnie utrzymywanie się, nawet po odstawieniu leku. Opracowano różne sposoby wykrywania przeciwciał neutralizujących – od metod wykorzystujących efekt cytopatyczny do tych opartych na indukcji genu reporterowego lucyferazy. Poszukuje się wiarygodnych markerów aktywności interferonu beta in vivo, które mogłyby uzupełniać oznaczenie przeciwciał. Przez wiele lat zagadnieniu przeciwciał przeciwinterferonowych towarzyszyły kontrowersje, które wynikały z trudności metodologicznych w badaniu ich znaczenia klinicznego. Obecnie, w świetle zgromadzonych danych, eksperci europejscy zgodnie zalecają powtarzane przesiewowe badanie miana przeciwciał neutralizujących u chorych leczonych interferonem i uwzględnienie wyników przy podejmowaniu decyzji terapeutycznych.
Introduction: The treatment of diverticulosis symptoms in patients with a history of diverticulitis is a challenge in everyday clinical practice. Aim: Efficacy assessment of a cyclic, year-long treatment with rifaximin-α in patients with symptomatic uncomplicated diverticular disease (SUDD) and a history of past diverticulitis. Material and methods: This study is a multicenter, retrospective, observational study involving 48 centers. The study group included patients who reported to the outpatient clinic within a month with SUDD symptoms, who had a history of diverticulitis, and who were given a cyclic rifaximin-α treatment of 2 x 400 mg/day for 7 days and then once a month for 12 months. Epidemiological and demographic data, the course of diverticulosis, the number of inflammation episodes and their diagnoses, complications, symptoms of SUDD, and its treatment were evaluated. The efficacy of rifaximin-α therapy was assessed on a 4-point scale (0 – no symptoms, 3 – severe symptoms) every 3 months, and analyzed: pain, tenderness, bloating, bowel movements, and recurrence of inflammation during the 12-month treatment. Results: 178 patients (67% women, median age 65 years [34–92]) were included in the study. The average duration of diverticulosis was 6.4 years (3–20), and 59% of patients had more than one episode of diverticulitis during this period. In total, 87% of patients had symptoms of SUDD after or between episodes of diverticulitis. Abdominal pain was the most common symptom (92%). An inflammation episode was diagnosed using imaging in 50.5% of cases, and the rest – based on typical clinical symptoms. As many as 46.2% of patients required hospitalization, and complications were diagnosed in 44% of cases. One hundred and seventy (95%) patients completed the 12-month rifaximin-α therapy. Changes in the severity of pain, abdominal tenderness, diarrhea, constipation, and bloating were assessed every 3 months. After 12 months of treatment with rifaximin-α, there was a statistically significant reduction in the severity of symptoms overall (median from 1.5 [0–3 points] to 0.2; P<0.001) and each symptom evaluated individually. Regardless of the previous diagnostic method of diverticulitis (imaging or typical clinical presentation) or its complications (e.g. perforation, abscess), treatment with rifaximin-α was equally effective. Conclusions: Cyclic therapy with rifaximin-α is effective in treating SUDD symptoms and in preventing the recurrence of symptoms, also in patients with a history of diverticulitis – regardless of how the diagnosis was made and disease complications. The extended treatment regimen leads to a gradual resolution of symptoms during 12 months of observation. Cyclic use of rifaximin-α is necessary to maintain symptom remission.