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1.
Visc Med ; 33(3): 221-226, 2017 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-28785572

RESUMO

BACKGROUND: The aim of this study was to analyze the admissions and the management of peptic ulcer disease (PUD) in a tertiary care surgical center. METHODS: We evaluated the medical records of all patients admitted to the University Hospital of Tübingen, Germany, for treatment of PUD during 1989-2008. Patients were included into the study if the diagnosis was verified endoscopically or surgically. Annual number of admissions, length of hospitalization, mortality rate, age, rate of non-steroidal anti-inflammatory drugs (NSAIDs) and proton pump inhibitor (PPI) medication, rate of Helicobacter pylori infection, and complications of PUD and surgery performed were recorded. Data were analyzed by descriptive analyses, Pearson's chi-square test, and regression analysis. RESULTS: This study included 614 admissions. The number of annual admissions (31 ± 12), the length of hospitalization (9 ± 3 days), and the mortality rate (5 ± 4% per year) remained constant, whereas the age increased (1989: 52 ± 14 years vs. 2008: 67 ± 16 years). The rates of patients with H. pylori infection (47 ± 28% per year), NSAIDs treatment (29 ± 15% per year), and PPI treatment (31 ± 27% per year) remained constant. The most frequent PUD complication was hemorrhage (42 ± 16% per year), followed by perforation (9 ± 8% per year). During 1999-2008, more hemorrhages (125 vs. 121; p < 0.05) and perforations (40 vs. 21; p < 0.05) were registered than during 1989-1998. The rate of emergency surgery increased from 70% during 1989-1998 to 87% during 1999-2008. In contrast, elective surgery decreased from 21% during 1989-1998 to 7% during 1999-2008. Ulcer excision and oversewing was the most frequent surgical procedure performed (59%), with decreasing rates of acid-reducing surgery. CONCLUSION: Despite recent advances in PUD management, ulcer hemorrhage and perforation remain a significant health burden and a surgical disease.

2.
World J Gastroenterol ; 20(17): 4883-91, 2014 May 07.
Artigo em Inglês | MEDLINE | ID: mdl-24803799

RESUMO

The laparoscopic technique was introduced in gastrointestinal surgery in the mid 1980s. Since then, the development of this technique has been extraordinary. Triggered by technical innovations (stapling devices or coagulation/dissecting devices), nowadays any type of gastrointestinal resection has been successfully performed laparoscopically and can be performed laparoscopically dependent on the patient's condition. This summary gives an overview over 30 years of laparoscopic surgery with focus on today's indications and evidence. Main indications remain the more common procedures, e.g., appendectomy, cholecystectomy, bariatric procedures or colorectal resections. For all these indications, the laparoscopic approach has become the gold standard with less perioperative morbidity. Regarding oncological outcome there have been several high-quality randomized controlled trials which demonstrated equivalency between laparoscopic and open colorectal resections. Less common procedures like esophagectomy, oncological gastrectomy, liver and pancreatic resections can be performed successfully as well by an experienced surgeon. However, the evidence for these special indications is poor and a general recommendation cannot be given. In conclusion, laparoscopic surgery has revolutionized the field of gastrointestinal surgery by reducing perioperative morbidity without disregarding surgical principles especially in oncological surgery.


Assuntos
Doenças do Sistema Digestório/cirurgia , Neoplasias do Sistema Digestório/cirurgia , Procedimentos Cirúrgicos do Sistema Digestório/métodos , Laparoscopia , Doenças do Sistema Digestório/diagnóstico , Doenças do Sistema Digestório/mortalidade , Neoplasias do Sistema Digestório/diagnóstico , Neoplasias do Sistema Digestório/mortalidade , Procedimentos Cirúrgicos do Sistema Digestório/efeitos adversos , Procedimentos Cirúrgicos do Sistema Digestório/mortalidade , Medicina Baseada em Evidências , Humanos , Laparoscopia/efeitos adversos , Laparoscopia/mortalidade , Fatores de Risco , Resultado do Tratamento
3.
Cell Physiol Biochem ; 32(6): 1878-90, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-24356325

RESUMO

BACKGROUND/AIMS: Cholecystokinin 1-receptor (CCK1-R) activation by long chain fatty acid (LCFA) absorption stimulates vago-vagal reflex pathways in the brain stem. The present study determines whether this reflex also activates the cholinergic anti-inflammatory pathway, a pathway known to modulate cytokine release during endotoxemia. METHODS: Mesenteric lymph was obtained from wild type (WT) and CCK1-R knockout (CCK1-R(-/-)) mice intraperitoneally challenged with Lipopolysaccharid (LPS) (endotoxemic lymph, EL) and intestinally infused with vehicle or LCFA-enriched solution. The lymph was analyzed for TNFα, IL-6 and IL-10 concentration and administered to healthy recipient mice via jugular infusion. Alveolar wall thickness, myeloperoxidase (MPO) and TUNEL positive cells were determined in lung tissue of recipient mice. RESULTS: LCFA infusion in WT mice reduced TNFα concentration in EL by 49% compared to vehicle infusion, but had no effect in CCK1-R(-/-) mice. EL significantly increased the alveolar wall thickness, the number of MPO-positive and TUNEL-positive cells compared to control lymph administration. LCFA infusion in WT, but not in CCK1R(-/-) mice, significantly reduced these pathological effects of EL. CONCLUSION: During endotoxemia enteral LCFA absorption reduces TNFα release into mesenteric lymph and attenuates histomorphologic parameters of lung dysfunction. Failure to elicit this effect in CCK1R(-/-) mice demonstrates that anti-inflammatory properties of LCFAs are mediated through CCK1-Rs.


Assuntos
Pulmão/patologia , Receptor de Colecistocinina A/metabolismo , Animais , Endotoxemia/induzido quimicamente , Endotoxemia/metabolismo , Endotoxemia/patologia , Ácidos Graxos Insaturados , Interleucina-10/análise , Interleucina-6/análise , Lipopolissacarídeos , Linfonodos/efeitos dos fármacos , Linfonodos/metabolismo , Masculino , Camundongos , Camundongos Knockout , Peroxidase/metabolismo , Receptor de Colecistocinina A/deficiência , Receptor de Colecistocinina A/genética , Fator de Necrose Tumoral alfa/análise
4.
Cell Physiol Biochem ; 28(4): 753-60, 2011.
Artigo em Inglês | MEDLINE | ID: mdl-22178887

RESUMO

BACKGROUND: Sepsis is a common problem in intensive care patients leading to multi-organ failure and gastrointestinal paralysis. AIM: The aim of the study was to investigate whether the gastrointestinal tract is not only the target but also the source of inflammatory mediators inhibiting gastrointestinal motility. METHODS: Mesenteric lymph was obtained from rats in which a sepsis was induced by lipopolysaccharide (LPS) intraperitoneally. Gastrointestinal motility was recorded following mesenteric lymph- or TNFα infusion into the jugular vein of separate healthy recipient rats using the strain gauge transducer technique. RESULTS: Infusion of sepsis lymph significantly impairs gastric and colonic motility, decreasing the motility-index in the stomach and colon by about 57% and 21% respectively in comparison to baseline motility. Among other inflammatory mediators, TNFα plays an important role in mediating the inhibitory effect of mesenteric lymph on gastrointestinal motility during sepsis. CONCLUSIONS: The gastrointestinal tract is the source and the target of inflammatory mediators released during sepsis causing paralytic ileus.


Assuntos
Motilidade Gastrointestinal/fisiologia , Mediadores da Inflamação/metabolismo , Mucosa Intestinal/patologia , Sepse/fisiopatologia , Animais , Motilidade Gastrointestinal/efeitos dos fármacos , Mucosa Intestinal/metabolismo , Lipopolissacarídeos/toxicidade , Linfa/metabolismo , Masculino , Mesentério/metabolismo , Ratos , Ratos Sprague-Dawley , Sepse/metabolismo , Fator de Necrose Tumoral alfa/metabolismo
5.
J Gastrointest Surg ; 15(5): 853-9, 2011 May.
Artigo em Inglês | MEDLINE | ID: mdl-21384238

RESUMO

BACKGROUND: Immune cells and inflammatory mediators are released from the gastrointestinal tract into the mesenteric lymph during sepsis causing distant organ dysfunction. Recently, it was demonstrated that macrophages in the gut wall are controlled by the vagus nerve, the so-called cholinergic anti-inflammatory pathway. AIM: This study aims to investigate whether an enteral diet with lipid prevents the activation of leukocytes in the gut wall. METHODS: Mesenteric lymph was obtained from rats, receiving an enteral infusion of glucose or glucose + lipid before and after lipopolysaccharide (LPS) injection. Immune cells in mesenteric lymph were analyzed with fluorescence-activated cell sorting before and after LPS injection. Mesenteric lymph leukocytes from rats receiving enteral glucose with or without lipid were stimulated in vitro with LPS and tumor necrosis factor (TNF)α was measured in the supernatant. RESULTS: The release of macrophages from the gut during sepsis was not significantly different in animals enterally treated with glucose or lipid. However, the release of TNFα from mesenteric lymph leukocytes after in vitro LPS stimulation was more than 3-fold higher in the glucose group compared to the lipid-treated group. CONCLUSIONS: During sepsis, activated macrophages are released from the gut into mesenteric lymph. However, an enteral diet with lipid is able to suppress the inflammatory cytokine release from mesenteric lymph leukocytes.


Assuntos
Nutrição Enteral/métodos , Ácidos Graxos Ômega-3/uso terapêutico , Imunidade Celular , Mucosa Intestinal/imunologia , Ativação de Macrófagos/efeitos dos fármacos , Macrófagos/imunologia , Mesentério/imunologia , Animais , Modelos Animais de Doenças , Ácidos Graxos Ômega-3/administração & dosagem , Mucosa Intestinal/efeitos dos fármacos , Mucosa Intestinal/patologia , Linfa/imunologia , Macrófagos/efeitos dos fármacos , Masculino , Mesentério/patologia , Ratos , Ratos Sprague-Dawley , Sepse/imunologia , Sepse/patologia , Sepse/prevenção & controle
6.
J Neurosci Res ; 86(3): 660-7, 2008 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-17893916

RESUMO

Astroglia terminate glutamatergic neurotransmission and prevent excitotoxic extracellular glutamate concentration by clearing synaptically released glutamate through the high-affinity, sodium-dependent glutamate transporters GLT-1 and GLAST. Many brain injures are associated with the disturbed expression of glial glutamate transporters and a subsequent increase of extracellular glutamate to neurotoxic levels. We have now followed up initial hints pointing to endothelins, a family of injury-regulated peptides, as mediators of this injury-induced loss of glial glutamate transporter expression. We observed that, in line with such a role, endothelins not only act as potent inhibitors of basal and exogenously (dbcAMP)-induced expression of GLT-1 in cortical astrocytes as shown before, but likewise inhibit expression of GLT-1 or GLAST in astrocytes cultured from the diencephalon, mesencephalon, cerebellum, and spinal cord. We further demonstrate that endothelins equally inhibit GLT-1 expression in cortical slice cultures, a culture system closely resembling the in vivo situation. Although brain injuries are usually associated with an increase in the expression of the glutamate-converting enzyme glutamine synthetase, cultured cortical astrocytes maintained with endothelins showed an almost complete loss of glutamine synthetase. Interestingly, the inhibitory effects of endothelins on the expression of glutamine synthetase, but not of glutamate transporters, was overridden by high extracellular glutamate, indicating that the primarily inhibitory action of endothelins on the various components of glial glutamate turnover dissociates in the injured brain.


Assuntos
Sistema X-AG de Transporte de Aminoácidos/metabolismo , Lesões Encefálicas/metabolismo , Endotelinas/metabolismo , Ácido Glutâmico/metabolismo , Neuroglia/metabolismo , Traumatismos da Medula Espinal/metabolismo , Animais , Animais Recém-Nascidos , Astrócitos/metabolismo , Encéfalo/metabolismo , Encéfalo/patologia , Lesões Encefálicas/patologia , Bucladesina/farmacologia , Células Cultivadas , Córtex Cerebral/metabolismo , Córtex Cerebral/patologia , Transportador 1 de Aminoácido Excitatório/antagonistas & inibidores , Transportador 2 de Aminoácido Excitatório/antagonistas & inibidores , Líquido Extracelular/metabolismo , Glutamato-Amônia Ligase/antagonistas & inibidores , Técnicas In Vitro , Ratos , Ratos Sprague-Dawley , Medula Espinal/metabolismo , Medula Espinal/patologia , Traumatismos da Medula Espinal/patologia
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