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1.
Eur J Pediatr ; 183(2): 515-522, 2024 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-37947925

RESUMO

We would like to provide an updated comprehensive perspective and identify the components linked to chronic spontaneous urticaria (CSU) without specific triggers in autoimmune atrophic gastritis (AAG). AAG is an organ-specific autoimmune disease that affects the corpus-fundus gastric mucosa. Although we lack a unified explanation of the underlying pathways, when considering all paediatric patients reported in the literature, alterations result in gastric neuroendocrine enterochromaffin-like (ECL) cell proliferation and paracrine release of histamine. Several mechanisms have been proposed for the pathogenesis of CSU, with much evidence pointing towards AAG and ECL cell responses, which may be implicated as potential factors contributing to CSU. The excessive production/release of histamine into the bloodstream could cause or trigger exacerbations of CSU in AAG, independent of Helicobacter pylori; thus, the release of histamine from ECL cells may be the primary modulator. CONCLUSION: Considering the understanding of these interactions, recognising the respective roles of AAG in the pathogenesis of CSU may strongly impact the diagnostic workup and management of unexplained/refractory CSU and may inform future research and interventions in the paediatric population. WHAT IS KNOWN: • Autoimmune atrophic gastritis is a chronic immune-mediated inflammatory disease characterised by the destruction of the oxyntic mucosa in the gastric body and fundus, mucosal atrophy, and metaplastic changes. • Autoimmune atrophic gastritis in paediatric patients is important because of the poor outcome and risk of malignancy and possibly underestimated entities primarily reported in single-case reports. WHAT IS NEW: • Upper gastrointestinal inflammatory disorders, independent of H. pylori, have been implicated as potential inducing factors in the development of chronic spontaneous urticaria. • If a paediatric patient presents with symptoms such as anaemia, reduced vitamin B12 levels, recurrent urticaria with no other detectable aetiology, positive anti-parietal cell antibodies, and elevated gastrin levels, autoimmune atrophic gastritis should be considered a possible cause of chronic urticaria.


Assuntos
Doenças Autoimunes , Urticária Crônica , Gastrite Atrófica , Gastrite , Infecções por Helicobacter , Helicobacter pylori , Humanos , Criança , Gastrite Atrófica/complicações , Gastrite Atrófica/patologia , Histamina , Gastrite/complicações , Gastrite/diagnóstico , Mucosa Gástrica/patologia , Urticária Crônica/etiologia , Urticária Crônica/patologia , Doenças Autoimunes/complicações , Doenças Autoimunes/diagnóstico , Doença Crônica , Infecções por Helicobacter/complicações
2.
Carbohydr Polym ; 272: 118461, 2021 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-34420721

RESUMO

The molecular weight (Mw) of dextran derivatives, such as regioselectively oxidized dicarboxydextran (DXA), is greatly influencing their faith in an organism, which could be possibly used to improve anticancer drug delivery. Here we present a modified method of sulfonation-induced chain scission allowing direct and accurate control over the Mw of DXA without increasing its polydispersity. Prepared DXA derivatives (Mw = 10-185 kDa) have been conjugated to cisplatin and the Mw of the carrier found to have a significant impact on cisplatin release rates, in vitro cytotoxicity, and migrastatic potential. Conjugates with the high-Mw DXA showed particularly increased anticancer efficacy. The best conjugate was four times more effective against malignant prostatic cell lines than free cisplatin and significantly inhibited the ovarian cancer cell migration. This was traced to the characteristics of spontaneously formed cisplatin-crosslinked DXA nanogels influenced by Mw of DXA and amount of loaded cisplatin.


Assuntos
Antineoplásicos/farmacologia , Cisplatino/farmacologia , Dextranos/química , Portadores de Fármacos/química , Neoplasias/tratamento farmacológico , Células A549 , Adenocarcinoma/tratamento farmacológico , Adenocarcinoma/metabolismo , Antineoplásicos/química , Movimento Celular/efeitos dos fármacos , Cisplatino/química , Sistemas de Liberação de Medicamentos/métodos , Feminino , Humanos , Masculino , Peso Molecular , Nanogéis/química , Neoplasias/metabolismo , Neoplasias Ovarianas/tratamento farmacológico , Neoplasias Ovarianas/metabolismo , Oxirredução , Neoplasias da Próstata/tratamento farmacológico , Neoplasias da Próstata/metabolismo
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