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    Ameliorative Effects of Larazotide Acetate on Intestinal Permeability and Bacterial Translocation in Acute Pancreatitis Model in Rats
    (Springer, 2024) Karahan, Dogu; Harputluoglu, Muhsin Murat Muhip; Gul, Mehmet; Gunduz, Ayten; Ozyalin, Fatma; Inceoglu, Feyza; Tikici, Deniz
    Background Intestinal barrier dysfunction in acute pancreatitis (AP) may progress to systemic inflammatory response syndrome (SIRS) and multi-organ failures by causing bacterial translocation. Larazotide acetate (LA) is a molecule that acts as a tight junction (TJ) regulator by blocking zonulin (Zo) receptors in the intestine. Aims In our study, we aimed to investigate the effects of LA on intestinal barrier dysfunction and bacterial translocation in the AP model in rats. Methods Thirty-two male Sprague-Dawley rats were divided into 4 groups; control, larazotide (LAR), AP, and AP + LAR. The AP model was created by administering 250 mg/100 g bm L-Arginine intraperitoneally 2 times with an hour interval. AP + LAR group received prophylactic 0.01 mg/mL LA orally for 7 days before the first dose of L-Arginine. For intestinal permeability analysis, fluorescein isothiocyanate-dextran (FITC-Dextran) was applied to rats by gavage. The positivity of any of the liver, small intestine mesentery, and spleen cultures were defined as bacterial translocation. Histopathologically damage and zonulin immunoreactivity in the intestine were investigated. Results Compared to the control group, the intestinal damage scores, anti-Zo-1 immunoreactivity H-Score, serum FITC-Dextran levels and bacterial translocation frequency (100% versus 0%) in the AP group were significantly higher (all p < 0.01). Intestinal damage scores, anti-Zo-1 immunoreactivity H-score, serum FITC-Dextran levels, and bacterial translocation frequency (50% versus 100%) were significantly lower in the AP + LAR group compared to the AP group (all p < 0.01). Conclusions Our findings show that LA reduces the increased intestinal permeability and intestinal damage by its effect on Zo in the AP model in rats, and decreases the frequency of bacterial translocation as a result of these positive effects.
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    Ecstasy induced acute hepatic failure. Case reports
    (Univ Catholique Louvain-Ucl, 2015) Atayan, Yahya; Cagin, Yasir Furkan; Erdogan, Mehmet Ali; Harputluoglu, Muhsin Murat Muhip; Bilgic, Yilmaz
    3,4-methylenedioxymethamphetamine (MDMA), an amphetamine derivative known as ecstasy, has stimulating and hallucinogenic properties. It has become a substance that is widely used especially by young people. Hepatotoxicity is one of the rare side effects of this substance and can be fatal. Ecstasy-induced fulminant hepatitis has been reported in case reports. The clinical course and the prognosis of the cases may differ. In this article, two cases in whom ecstasy-induced fulminant hepatic failure had developed and who were treated with liver transplantation, and one case which recovered with treatment, have been presented.
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    Fingolimod induced fulminant liver failure requiring liver transplantation: A case report
    (Kare Publ, 2023) Caliskan, Ali Riza; Harputluoglu, Muhsin Murat Muhip; Samdanci, Emine; Cirik, Salih; Yilmaz, Sezai
    Fingolimod has been used for about ten years to treat multiple recurrent sclerosis. It has been reported that Fingolimod causes an elevation in liver enzymes. In this case report, the clinical and laboratory parameters improved after discontinuation of the drug. However, there is no publication in the literature regarding acute liver failure and liver transplantation following Fingolimod treatment. In this article, we presented a 33 - year - old female patient who developed acute liver failure and underwent liver transplantation after Fingolimod treatment for recurrent multiple sclerosis.