ABSTRACT
Resumen La gastropatía isquémica es una entidad rara, cuya etiología más frecuente es la obstrucción al flujo sanguíneo secundaria a aterosclerosis. Sus manifestaciones clínicas y endoscópicas son inespe cíficas, pudiendo simular afecciones más prevalentes. La sospecha clínica en pacientes con factores de riesgo cardiovascular permite un diagnóstico precoz y tratamiento adecuado. Presentamos el caso de una paciente con gastropatía isquémica crónica que se manifestó con dolor abdominal, pérdida de peso y hallazgos endoscópicos compatibles con linitis plástica. Se arribó al diagnóstico con una biopsia endoscópica en bloque luego de haber obtenido dos biopsias previas no concluyentes.
Abstract Chronic ischemic gastropathy is a rare entity, being the atheroesclerotic vascular the most prevalent cause. Clinical and endoscopic manifestations are unspecific and may simulate more frequent pathologies. Cardio vascular risk factors allow us to diagnose and treat these patients earlier. We present the case of a patient with chronic ischemic gastropathy that manifested abdominal pain, weight loss and endoscopic findings as a simula tor of linitis plastica. The diagnosis was made with an endoscopic block biopsy after two inconclusive biopsies.
ABSTRACT
Gastric volvulus is nothing but the torsion of stomach in thoracic cavity by more than 1800 along its transverse or longitudinal axis. A very rare case occurring both in male and female. The term first described by Berti after doing an autopsy of a female, in 1886. We found a case of 65 years old male with history of dyspepsia since, 1 year with history of vomiting and pain abdomen since, 1 day. On evaluation, clinically gurgling sound heard on left side chest and with investigations like USG and CT whole abdomen, we came to know about mesentrico axial volvulus which is more common in children. Acute gastric volvulus cases have high mortality rate also requires emergency surgery. Gastric volvulus is very rare with variable and non-specific clinical presentations, hence high level of suspicion for radiologic diagnosis may require. Acute gastric volvulus is a potentially life-threatening occurrence with a good outcome when treated in a timely fashion. Chronic volvulus may be more difficult to recognize. Timely diagnosis with proper treatment can potentially decreases morbidity and mortality of the patient.
ABSTRACT
INTRODUCTION: Gastric ischemia represents an important medical challenge in pathology and surgical practice. OBJECTIVE: The purpose of this study was to assess the effects of acute gastric ischemia on different regions of the stomach. METHOD: Rabbit stomachs were subjected to devascularization of the greater and lesser curvatures for 3, 6 and 12 hours. After these periods, the stomachs were removed for macro and microscopic analysis. RESULTS: Hemorrhagic necrosis was more marked in the gastric fundus and body. In contrast, the antropylorus remained preserved in 100% of the rabbits after 3 hours of ischemia (group I), and in 80% of the rabbits after 6 and 12 hours of ischemia (groups II and III). Necrosis of the gastric body and fundus mucosa were observed in all animals after 6 and 12 hours of ischemia. CONCLUSION: We concluded that this experimental model of acute gastric ischemia was effective in producing hemorrhagic necrosis of the gastric fundus and body in rabbits even within a short period of time. Furthermore, the antropyloric region was preserved in most animals.
INTRODUÇÃO: Isquemia gástrica representa um importante desafio médico nas áreas de Patologia e Cirurgia. O objetivo do presente trabalho foi avaliar os efeitos da isquemia gástrica aguda nas diferentes regiões do estômago. MÉTODO: Estômagos de coelhos foram submetidos à completa desvascularização das curvaturas maior e menor durante 3, 6 e 12 horas. Após esses períodos de tempo, os órgãos foram removidos para análise macro e microscópica. RESULTADOS: Necrose hemorrágica foi mais evidente nas regiões de corpo e fundo. Por outro lado, a região antropilórica manteve-se preservada em 100% dos coelhos após 3 horas de isquemia (grupo I), e em 80% dos coelhos após 6 e 12 horas de isquemia (grupos II e III). Necrose da camada mucosa do corpo e do fundo gástricos foi observada em todos os animais após 6 e 12 horas de isquemia. CONCLUSÃO: Conclui-se que esse modelo de isquemia gástrica aguda foi eficaz para produzir necrose hemorrágica do corpo e fundo de coelhos mesmo por um curto período de tempo. Além disso, a região antropilórica manteve-se preservada na maioria dos animais.
ABSTRACT
Necrotizing gastritis is an infrequent severe pathology. The rich vascular supply and intramural arterial anastomosis protects stomach from vascular disease and embolism. Gastric infarction and necrosis presents as an acute abdominal emergency that requires rapid resolution, which in general includes surgery. Other important etiologies reported are chemical agents, mechanical distention, postoperative, bulimia and infectious diseases. In this article, we report a case of necrotizing gastritis in a 29 years-old male patient, with chronic consumption of NSAIDs for low back pain. He was admitted in the emergency room due to acute abdominal pain that appeared, after alcohol and raw fish consumption. Antral wall thickening was observed in the abdominal computed tomography. Upper gastric endoscopy showed necrosis of antral mucosa and biopsies confirmed necrotizing gastritis. He received medical therapy with antibiotics and proton pump inhibitors with an excellent response with clinical and endoscopic resolution in one month.
La gastritis necrotizante es una patología infrecuente muy grave. Esto se debe en parte a la rica irrigación y a las anastomosis arteriales intramurales que protegen al estómago de enfermedades vasculares y embolias. El infarto gástrico se presenta como una urgencia abdominal, que requiere resolución precoz, frecuentemente quirúrgica. Otras etiología importantes reportadas incluyen agentes químicos, factores mecánicos, bulimia e infecciones. En este artículo se presenta el caso de un paciente de 29 años, sexo masculino, con antecedentes de uso crónico de anti-inflamatorios no esteroidales (AINES), que ingresa a urgencia con dolor abdominal agudo, posterior al consumo de alcohol y pescado crudo. Destaca un engrosamiento antral marcado, sin neumatosis en la tomografía computada de abdomen. En la endoscopia digestiva alta se observa extensa necrosis de la mucosa antral y se confirma el diagnóstico de gastritis necrotizante por biopsias. El paciente tuvo una excelente respuesta a tratamiento con reposo intestinal, antibióticos e inhibidores de bomba de protones. Luego de 1 mes, presentó recuperación completa clínica y endoscopía.
Subject(s)
Humans , Male , Adult , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Gastritis/diagnosis , Gastritis/chemically induced , Alcoholism/complications , Biopsy , Endoscopy, Gastrointestinal , Gastritis/therapy , Necrosis , Tomography, X-Ray ComputedABSTRACT
Objective To observe the effect of microinjection of oxytocin(OT) into paraventricular nucleus(PVN) on gastric ischemia-reperfusion(GI-R) injury and its molecular mechanism.Methods GI-R injury was induced in rats by clamping the celiac artery for 30 min and followed by reperfusing for 1 h.A cannula was inserted into the unilateral PVN for microinjection of OT.The gastric mucosal injury index was counted grossly.The expressions of Akt and caspase-3 in rat gastric mucosa were examined by Western blot and by immunohistochemistry.Results Microinjection of OT into PVN dose-dependently allevated gastric mucosal injury subjected to GI-R.Microinjection OT into PVN significantly increased the expression of Akt protein and decreased the level of caspase-3 in gastric mucosal following GI-R.The effects of OT were prevented by pretreatment with OT receptor antagonist atosiban into the lateral cerebral ventricle.Conclusion Microinjection of OT into PVN significantly protected against GI-R injury.These effects of OT are mediated by its receptors.The mechanisms are mediated by increasing Akt expression,which in turn inhibits caspase-3 expression.
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Objective To observe the effects of electrical stimulation of paraventricular nucleus(PVN) on gastric mucosal cellular apoptosis,proliferation,and expression of BCL-2,BAX induced by gastric ischemia-reperfusion(GI-R) and the potential mechanisms of protection of PVN on GI-R injury.Methods After electrical stimulation of PVN,the experimental model of GI-R were established by clamping the celiac artery for 30 min and then reperfusing the artery for 30 min,1 h,3 h,or 6 h respectively.We used immunohistochemistry to detect the gastric mucosal cells apoptosis,proliferation and the expression of BCL-2,BAX.Results Compared with GI-R group,the electrical stimulation of PVN markedly decreased gastric mucosal cellular apoptosis,increased the proliferation,and promoted the protein expression of BCL-2,but markedly inhibited the protein expression of BAX at 30 min,1 h,3 h after reperfusion respectively.Conclusion The protective effect of PVN on GI-R injury is associated with up-regulation of expression of BCL-2 and down-regulation expression of BAX,and so inhibited gastric mucosal cellular apoptosis and promoted proliferation.
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AIM: To determine the effect of electrical stimulation of lateral hypothalamic area(LHA) on gastric ischemia-reperfusion injury(GI-RI) in rats and to analyse its possible neuroregulatory mechanisms. METHODS: The methods of electrical stimulation(ES), chemical stimulation, electrolytic lesion(EL) and denervation were used to investigate the effect of LHA ES on gastric mucosal injury in rats subjected to 30 min gastric ischemia followed by 60 min reperfusion and to analyse the role of dorsal vagal complex(DVC), vagus and sympathetic nerve in this effect. RESULTS: ①Electrical stimulation of LHA and microinjection of L-glutamic acid into LHA obviously aggravated GI-RI; ②Electrolytic lesion of the LHA attenuated the GI-RI;③DVC lesion eliminated the effect of electrical stimulation of LHA on GI-RI; ④Vagotomy or sympathectomy eliminated the effect of electrical stimulation of LHA on GI-RI too.CONCLUSION: These results indicate that the LHA is a specific area in the CNS for exerting aggravative effects on the GI-RI; the DVC, vagus and sympathetic nerve may be involved in regulatory effects of LHA on GI-RI.