Ultra-spracované potraviny (UPF) sa často vyznačujú nízkou nutričnou kvalitou, vysokou energetickou hustotou a prítomnosťou prídavných látok, látok z obalov a zlúčenín, ktoré vznikajú počas výroby, spracovania a skladovania. UPF zahŕňa priemyselné receptúry a zvyčajne obsahuje mnoho zložiek. UPF obsahuje cukor, oleje, tuky, soľ, antioxidanty, stabilizátory a konzervačné látky, potravinárske prísady a emulgátory. Okrem nízkej výživovej hodnoty spracovanie potravín podporuje tvorbu škodlivých zlúčenín v potravinách. Potravinové prísady v rámci UPF, podporujú zápaly, poruchy funkcie pečene a metabolický syndróm, ktoré sú založené na zmenách mikrobiómu. Obezogény sú látky z prostredia, ktoré menia rovnováhu medzi príjmom a výdajom energie. Obezogény sú podskupinou environmentálnych chemických látok, ktoré pôsobia ako endokrinné disruptory ovplyvňujúce koncové metabolické ukazovatele. V posledných desaťročiach sa na celom svete dramaticky zvýšila spotreba ultra-spracovaných výrobkov. UPF sa na priemernom energetickom príjme podieľali viac ako 60 %. Priemerný obsah bielkovín, vlákniny, vitamínov a vápnika v strave výrazne klesá. Energetický príspevok UPF, zatiaľ čo obsah sacharidov, pridaného cukru a nasýtených tukov sa zvyšuje. Ultra-spracované potraviny sa podieľajú na väčšine pridaných cukrov v západnej strave. Fruktóza – najčastejší obezogén, sa spája so zvýšeným rizikom fibrózy pečene. V posledných rokoch pribúdajú dôkazy o škodlivom vplyve UPF. Konzumácia UPF sa spája s metabolickými zmenami, výskytom chronických ochorení a nadmernou úmrtnosťou. Existujú aj dôkazy o súvislosti s NAFLD, NASH a fibrózou. Vysoká spotreba UPF súvisí so škodlivými metabolickými a hepatálnymi parametrami v populácii NAFLD. Okrem toho kombinácia fajčenia a vysokého príjmu UPF môže zosilniť poškodenie pečene. Na základe dôkazov zo štúdií by sa vo výživových usmerneniach malo zvážiť odporúčanie znížiť príjem ultra- -spracovaných potravín na minimum a implementovať opatrenia v oblasti verejného zdravotníctva.
Ultra-processed foods (UPF) are often characterized by low nutritional quality, high energy density, and the presence of additives, substances from packaging, and compounds formed during production, processing, and storage. UPF includes industrial formulations, and usually contains many ingredients. UPF includes sugar, oils, fats, salt, antioxidants, stabilizers and preservatives, food additives, and emulsifiers. Beyond the poor nutritional value, food processing promotes the creation of harmful compounds in the food. Food additives within UPF, promote inflammation, liver dysfunction, and metabolic syndrome, which are based on changes in the microbiome. Obesogens are environmental substances that alter the balance between energy intake and energy expenditure. Obesogens are a subset of environmental chemicals that act as endocrine disruptors affecting metabolic endpoints. The consumption of ultra-processed products has increased dramatically worldwide in the last decades. UPF contributed more than 60% of the mean energy intake. The average content of protein, fiber, vitamins, and calcium in the diet decreases significantly. The roducy contribution of UPFs, while carbohydrate, added sugar, and saturated fat contents increase. Ultra-processed foods contribute most of the added sugars in the western diet. Fructose – the most frequent obesogen, is associated with an increased risk of liver fibrosis. In recent years, there has been growing evidence about the harmful effect of UPF. UPF consumption is associated with metabolic alterations, the incidence of chronic diseases, and excess mortality. There is also evidence for an association with NAFLD, NASH, and fibrosis. High UPF consumption is related to harmful metabolic and hepatic parameters in NAFLD population. Furthermore, the combination of smoking and high UPF intake may amplify liver damage. The evidence from studies, a recommendation to reduce ultra-processed food intake to a minimum should be considered in nutritional guidelines and implemented by public health policy measures.
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- lidé MeSH
- metabolický syndrom etiologie MeSH
- nealkoholová steatóza jater * etiologie MeSH
- průmyslově zpracované potraviny * škodlivé účinky MeSH
- Check Tag
- lidé MeSH
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- přehledy MeSH
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- abstrakt z konference MeSH
Východiská: Pneumatická dilatácia (PD) je stále obľúbenou liečbou achalázie pažeráka. Táto retrospektívna analýza informuje o našich 16-ročných skúsenostiach s pneumatickou dilatáciou pri liečbe pacientov s achaláziou. Pacienti a metódy: Za sebou nasledujúci pacienti s achaláziou, ktorí podstúpili endoskopickú balónovú dilatáciu, boli retrospektívne analyzovaní. Úspešnosť endoskopickej pneumatickej dilatácie bola definovaná tak, že okrem pneumatickej dilatácie nebola potrebná žiadna ďalšia liečba a celkové klinické Eckardtovo skóre muselo byť ≤ 3 (a zároveň každá jednotlivá položka < 2). Výsledky: V období január 2004 až december 2019 podstúpilo za sebou pneumatickú dilatáciu 140 pacientov s achaláziou (67 mužov [47,9 %], priemerný vek 54,9 ± 16,2 rokov). Medián sledovania pacientov od prvej dilatácie bol 125 mesiacov (6–263 mesiacov). Liečba pneumatickou dilatáciou (vrátane opakovaných PD) mala celkovo pozitívny efekt u 130 zo 140 pacientov (92,9 %), u 2 pacientov došlo počas prvej dilatácie k perforácii (1,4 %) a u 8 pacientov nebol efekt dostatočný (5,7 %). Zo 140 pacientov podstúpilo celkovo len jednu PD 107/ 140 (76,4 %), len dve PD podstúpilo 22/ 140 (15,7 %), celkovo len tri PD podstúpilo 8/ 140 (5,7 %) a celkovo 4 PD podstúpili 3/ 140 (2,1 %). Zlyhanie liečby sme pozorovali u 3 pacientov s 1 PD (37,5 %) oproti 5 pacientom s 2 a viac PD (62,5 %); p = 0,019. Záver: Endoskopická balónová dilatácia, začínajúca s 35-mm balónom, je z krátkodobého ako aj dlhodobého hľadiska efektívnou liečbou achalázie, s minimálnou morbiditou. Prípadný neúplný efekt dilatačnej terapie sa častejšie prejavuje už v skoršom období po úvodnej dilatačnej terapii.
Background: Pneumatic dilation (PD) is still a common treatment of oesophageal achalasia. This retrospective analysis informs about 16 years of experience with pneumatic dilation in the treatment of patients with achalasia. Patients and methods: Consecutive patients with achalasia treated with endoscopic balloon dilation therapy were analysed retrospectively. The success of endoscopic pneumatic dilation was defined as no treatment other than pneumatic dilation and the overall clinical Eckardt score ≤ 3 (and at the same time each individual item <2). Results: From January 2004 to December 2019, 140 patients with achalasia consecutively underwent pneumatic dilation (67 males [47.9%], mean age 54.9 ±16.2 years). The median follow-up since the first dilation was 125 months (range 6–263 months). Satisfactory results were observed in 130 patients (92.9%). Out of the remaining ten patients, two (1.4%) had periprocedural oesophageal perforation and in 8 (5.7%) patients the treatment eff ect was insufficient. Out of all patients, 107/ 140 (76.4%) had only one PD, 22/ 140 (15.7%) had two PDs, three PDs were performed in 8/ 140 (5.7%) and four PDs in 3/ 140 (2.1%). Treatment failure was more common in patients who had more pneumatic dilations (1 PD 37.5%, 2 and more PDs 62.5%; P = 0.019). Conclusions: Endoscopic balloon dilation, starting with a 35 mm balloon, is an effective treatment for achalasia in the short and long term, with minimal morbidity. The possible incomplete effect of dilation therapy is more often manifested in an earlier period after the initial dilation therapy.
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IgG4-related sclerosing cholangitis, a biliary manifestation of an IgG4-related disease, belongs to the spectrum of sclerosing cholangiopathies which result in biliary stenosis. It presents with signs of cholestasis and during differential diagnosis it should be distinguished from cholangiocarcinoma or from other forms of sclerosing cholangitis (primary and secondary sclerosing cholangitis). Despite increasing information and recently established diagnostic criteria, IgG4-related sclerosing cholangitis remains underdiagnosed in routine clinical practice. The diagnosis is based on a combination of the clinical picture, laboratory parameters, histological findings, and a cholangiogram. Increased serum IgG4 levels are nonspecific but are indeed a part of the diagnostic criteria proposed by the Japan Biliary Association and the HISORt criteria for IgG4-SC. High serum IgG4 retains clinical utility depending on the magnitude of elevation. Approximately 90% of patients have concomitant autoimmune pancreatitis, while 10% present with isolated biliary involvement only. About 26% of patients have other organ involvement, such as IgG4-related dacryoadenitis/sialadenitis, IgG4-related retroperitoneal fibrosis, or IgG4-related renal lesions. A full-blown histological finding characterized by IgG4-enriched lymphoplasmacytic infiltrates, obliterative phlebitis, and storiform fibrosis is difficult to capture in practice because of its subepithelial localization. However, the histological yield is increased by immunohistochemistry, with evidence of IgG4-positive plasma cells. Based on a cholangiogram, IgG-4 related sclerosing cholangitis is classified into four subtypes according to the localization of stenoses. The first-line treatment is corticosteroids. The aim of the initial treatment is to induce clinical and laboratory remission and cholangiogram normalization. Even though 30% of patients have a recurrent course, in the literature data, there is no consensus on chronic immunosuppressive maintenance therapy. The disease has a good prognosis when diagnosed early.
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