@article{MTMT:34856127,
	title = {A Case Report of Hyperhemolytic Syndrome in Sickle Cell Disease, with a Special Focus on Avoiding the Use of Transfusions},
	url = {https://m2.mtmt.hu/api/publication/34856127},
	author = {Obajed Al-Ali, Omar and Pfliegler, György and Magyari, Ferenc and Borics, Fanni and Pinczés, László Imre and Illés, Árpád and Brúgós, Boglárka Csilla},
	doi = {10.3390/thalassrep14010003},
	journal-iso = {THALASS REP},
	journal = {THALASSEMIA REPORTS},
	volume = {14},
	unique-id = {34856127},
	issn = {2039-4357},
	abstract = {In patients with sickle cell disease (SCD), transfusions pose risks like delayed hemolytic transfusion reaction (DHTR) and hyperhemolytic syndrome (HHS). We present the case of a 61-year-old Nigerian male patient with SCD, developing hyperhemolytic syndrome (HHS) post-orthopedic surgery due to alloimmunization from blood transfusions. Surgery induced massive hemorrhage, requiring RBC transfusions. Postoperatively, he developed HHS with jaundice, hemoglobinuria, and fever. Despite additional transfusions, his condition worsened, leading to hematological consultation on postoperative day +9. Laboratory findings showed positive DAT and multiple alloantibodies. The diagnosis of HHS was established and treatment involved high-dose methylprednisolone, intravenous immunoglobulin (IVIG), and erythropoietin. The patient was discharged on postoperative day +24 with stable hemoglobin levels, tapering doses of methylprednisolone, and continuous administration of hydroxyurea prescribed. HHS pathogenesis involves extensive intravascular hemolysis, exacerbated by alloimmunization. Diagnostic challenges and therapy selection complexity underscore the need for cautious transfusion strategies in HHS, reserving them for hemodynamic instability or hypoxia. This case highlights promptly recognizing and managing HHS in SCD for improved outcomes and avoiding unnecessary transfusions.},
	year = {2024},
	eissn = {2039-4365},
	pages = {18-25},
	orcid-numbers = {Pinczés, László Imre/0000-0003-0453-1709}
}

@article{MTMT:34855342,
	title = {Can we define difficult-to-treat systemic sclerosis?},
	url = {https://m2.mtmt.hu/api/publication/34855342},
	author = {Szűcs, Gabriella and Szekanecz, Zoltán and Szamosi, Szilvia},
	doi = {10.1080/1744666X.2024.2352450},
	journal-iso = {EXPERT REV CLIN IMMUNOL},
	journal = {EXPERT REVIEW OF CLINICAL IMMUNOLOGY},
	unique-id = {34855342},
	issn = {1744-666X},
	year = {2024},
	eissn = {1744-8409},
	pages = {1-17}
}

@article{MTMT:34845388,
	title = {Monogénesen öröklődő és szerzett autoinflammatoricus betegségek},
	url = {https://m2.mtmt.hu/api/publication/34845388},
	author = {Szekanecz, Zoltán and Szamosi, Szilvia and Benkő, Szilvia and Szűcs, Gabriella},
	doi = {10.1556/650.2024.33038},
	journal-iso = {ORV HETIL},
	journal = {ORVOSI HETILAP},
	volume = {165},
	unique-id = {34845388},
	issn = {0030-6002},
	abstract = {Az autoinflammatio a természetes (innate) immunitás zavara, mely veleszületett, monogénes vagy szerzett lehet. A monogénes autoinflammatoricus kórképek közé tartoznak az inflammasomopathiák, az actinopathiák, az endoplazmatikus reticulum stresszt okozó mutációk, az NFκB-hez társult betegségek, az interferonopathiák, az endogén antagonisták génjeinek mutációi és a DADA2. A szerzett autoinflammatoricus betegségek közé számos gyulladásos reumatológiai kórképet, bél-, bőr- és csontbetegséget, valamint egyéb kórképeket (például VEXAS, IgG4-gyel társult betegség, recurrens pericarditis, 2-es típusú diabetes, interstitialis tüdőbetegség) sorolhatunk. Ebben az összefoglalóban áttekintjük az autoinflammatio koncepcióját és főbb mechanizmusait, a legfontosabb monogénes és szerzett autoinflammatoricus kórképeket, az immundeficientiák autoinflammatióban játszott szerepét, valamint a szóba jövő terápiás lehetőségeket. Autoinflammation is a disorder of natural (innate) immunity, which can be monogenic, or acquired. Monogenic autoinflammatory diseases include inflammasomopathies, actinopathies, endoplasmic reticulum stress mutations, NFκB-associated diseases, interferonopathies, mutations in endogenous antagonist genes, and DADA2. Acquired autoinflammatory diseases include numerous inflammatory rheumatological diseases, intestinal, skin and bone diseases, as well as other conditions (e.g., VEXAS, IgG4-related disease, recurrent pericarditis, type 2 diabetes, interstitial lung disease). In this summary, we review the concept and main mechanisms of autoinflammation, the most important monogenic and acquired autoinflammatory conditions, the role of inborn errors of immunity in autoinflammation, as well as the possible therapeutic options.},
	keywords = {innate immunity; inflammasome; Autoinflammatory diseases; NFκB; AUTOINFLAMMATION; Interferonopathy; inborn errors of immunity; természetes immunitás; autoinflammatio; autoinflammatoricus betegségek; inflammasomopathiák; interferonopathiák; immundeficientiák},
	year = {2024},
	eissn = {1788-6120},
	pages = {683-697}
}

@article{MTMT:34843175,
	title = {Optimizing thiopurine therapy in autoimmune hepatitis : a multi-center study on monitoring metabolite profiles and co-therapy with allopurinol},
	url = {https://m2.mtmt.hu/api/publication/34843175},
	author = {Jan, Philipp Weltzsch and Claudius, Bartel and Moritz, Waldmann and Thomas, Renné and Stephanie, Schulze and Benedetta, Terziroli Beretta-Piccoli and Papp, Mária and Ye, Oo and Vincenzo, Ronca and Marcial, Sebode and Ansgar, Lohse and Christoph, Schramm and Johannes, Hartl},
	journal-iso = {HEPATOLOGY},
	journal = {HEPATOLOGY},
	unique-id = {34843175},
	issn = {0270-9139},
	year = {2024},
	eissn = {1527-3350},
	orcid-numbers = {Papp, Mária/0000-0003-3662-4010}
}

@article{MTMT:34836559,
	title = {Non-pancreatic hyperlipasemia : a puzzling clinical entity},
	url = {https://m2.mtmt.hu/api/publication/34836559},
	author = {Krisztina, Eszter Feher and Tornai, Dávid and Vitális, Zsuzsanna and Dávida, László and Sipeki, Nóra and Papp, Mária},
	journal-iso = {WORLD J LGASTROENTEROL},
	journal = {WORLD JOURNAL OF GASTROENTEROLOGY},
	volume = {30},
	unique-id = {34836559},
	issn = {1007-9327},
	year = {2024},
	eissn = {2219-2840},
	pages = {1-15},
	orcid-numbers = {Tornai, Dávid/0000-0002-1335-5498; Vitális, Zsuzsanna/0000-0001-8198-5312; Sipeki, Nóra/0000-0002-6806-2991; Papp, Mária/0000-0003-3662-4010}
}

@article{MTMT:34836389,
	title = {Autoinflammatio és autoinflammatorikus kórképek},
	url = {https://m2.mtmt.hu/api/publication/34836389},
	author = {Szekanecz, Zoltán and Szamosi, Szilvia and Benkő, Szilvia and Szűcs, Gabriella},
	journal-iso = {IMMUNOLÓGIAI SZEMLE},
	journal = {IMMUNOLÓGIAI SZEMLE},
	unique-id = {34836389},
	issn = {2061-0203},
	year = {2024}
}

@article{MTMT:34831051,
	title = {A rheumatoid arthritis etiopatogenezise - újdonságok},
	url = {https://m2.mtmt.hu/api/publication/34831051},
	author = {Szekanecz, Zoltán and Kacsándi, Dorottya and Soós, Boglárka},
	journal-iso = {IMMUNOLÓGIAI SZEMLE},
	journal = {IMMUNOLÓGIAI SZEMLE},
	volume = {16},
	unique-id = {34831051},
	issn = {2061-0203},
	year = {2024},
	pages = {4-14}
}

@article{MTMT:34829474,
	title = {A JAK-gátlók alkalmazásának jövőbeli lehetőségei krónikus gyulladásos kórképekben},
	url = {https://m2.mtmt.hu/api/publication/34829474},
	author = {Szekanecz, Zoltán},
	journal-iso = {ORVOSTOVÁBBKÉPZŐ SZLE},
	journal = {ORVOSTOVÁBBKÉPZŐ SZEMLE},
	unique-id = {34829474},
	issn = {1218-2583},
	year = {2024}
}

@article{MTMT:34820283,
	title = {Efficacy and safety of avacopan in patients with ANCA-associated vasculitis receiving rituximab in a randomised trial},
	url = {https://m2.mtmt.hu/api/publication/34820283},
	author = {Geetha, Duvuru and Dua, Anisha and Yue, Huibin and Springer, Jason and Salvarani, Carlo and Jayne, David and Merkel, Peter and Szűcs, Gabriella},
	doi = {10.1136/ard-2023-224816},
	journal-iso = {ANN RHEUM DIS},
	journal = {ANNALS OF THE RHEUMATIC DISEASES},
	volume = {83},
	unique-id = {34820283},
	issn = {0003-4967},
	year = {2024},
	eissn = {1468-2060},
	pages = {223-232},
	orcid-numbers = {Geetha, Duvuru/0000-0001-8353-5542; Dua, Anisha/0000-0002-3508-9290; Springer, Jason/0000-0002-3903-6049; Salvarani, Carlo/0000-0001-5426-5133; Jayne, David/0000-0002-1712-0637; Merkel, Peter/0000-0001-9284-7345}
}

@article{MTMT:34818887,
	title = {Eculizumab Treatment of Massive Hemolysis Occurring in a Rare Co-Existence of Paroxysmal Nocturnal Hemoglobinuria and Myasthenia Gravis},
	url = {https://m2.mtmt.hu/api/publication/34818887},
	author = {Bicskó, Ráhel Réka and Illés, Árpád and Hevessy Zsuzsanna, Dóra and Ivády, Gergely and Kerekes, György and Méhes, Gábor and Csépány, Tünde and Gergely, Lajos},
	doi = {10.3390/hematolrep16020025},
	journal-iso = {HEMATOL REP},
	journal = {HEMATOLOGY REPORTS},
	volume = {16},
	unique-id = {34818887},
	issn = {2038-8322},
	abstract = {The co-occurrence of myasthenia gravis (MG) and paroxysmal nocturnal hemoglobinuria (PNH) is rare; only one case has been published so far. We report a 63-year-old Caucasian female patient who was diagnosed with MG at the age of 43. Thymoma was also detected, and so it was surgically resected, which resulted in reasonable disease control for nearly 20 years. Slight hemolysis began to emerge, and then myasthenia symptoms progressed, so immunosuppressive therapy was started. Due to progressive disease and respiratory failure, the patient underwent plasmapheresis, and ventilatory support was stopped. Marked hemolysis was present, and diagnostic tests confirmed PNH with type III PNH cells. Her myasthenia symptoms aggravated, mechanical ventilation had to be started again, and due to the respiratory acidosis, massive hemolysis occurred. After two plasmapheresis sessions, the patient received eculizumab at 600 mg, resulting in prompt hemolysis control. After the second dose of the treatment, the patient was extubated. Still, due to their inability to cough, she developed another respiratory failure and pneumonia–sepsis, resulting in the patient’s death. This case highlights the rare association between these two serious diseases and similar immune-mediated pathophysiology mechanisms involving the complement system.},
	year = {2024},
	eissn = {2038-8330},
	pages = {255-259},
	orcid-numbers = {Csépány, Tünde/0000-0002-8305-3209}
}