Appendiceal adenocarcinoma presenting as left-sided large bowel obstruction,a case report and literature review

Background

appendiceal tumours are rare, they may be encountered unexpectedly in any acute or elective abdominal operation, many of these tumours are not appreciated intraoperatively and are diagnosed only during formal histopathological analysis of an appendicectomy specimen. Herein we present a case of appendiceal adenocarcinoma presenting as left-sided large bowel obstruction, we also review the literature of unusual presentations of appendiceal tumours.

Case Presentation

we report a case of left sided large bowel obstruction found to be secondary to an appendiceal adenocarcinoma. The patient presented with abdominal pain, distension and constipation, CT scan showed large bowel obstruction thought to be due to a sigmoid tumour, on laparotomy the appendix was also noted to be abnormal. A low Hartman's was performed with en-bloc total hysterectomy and bilateral salpigo-oophorectomy. A separate ileocaecal resection with end ileostomy was also performed, pathology specimens showed that the primary neoplasm was the appendix with metastasis to the distal sigmoid.

Conclusion

appendiceal tumours are rare, they usually present as acute appendicitis, other presentations are far less common.

     

Glutamine in the pathogenesis of acute hepatic encephalopathy

Hepatic encephalopathy (HE) is the major neurological disorder associated with liver disease. It presents in chronic and acute forms, and astrocytes are the major neural cells involved. While the principal etiological factor in the pathogenesis of HE is increased levels of blood and brain ammonia, glutamine, a byproduct of ammonia metabolism, has also been implicated in its pathogenesis. This article reviews the current status of glutamine in the pathogenesis of HE, particularly its involvement in some of the events triggered by ammonia, including mitochondrial dysfunction, generation of oxidative stress, and alterations in signaling mechanisms, including activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappaB (NF-κB). Mechanisms by which glutamine contributes to astrocyte swelling/brain edema associated with acute liver failure (ALF) will also be described.     

Ultrastructural characterization of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-induced cell death in embryonic dopaminergic neurons

Developing neuronal populations undergo significant attrition by natural cell death. Dopaminergic neurons in the substantia nigra pars compacta undergo apoptosis during synaptogenesis. Following this time window, destruction of the anatomic target of dopaminergic neurons results in dopaminergic cell death but the morphology is no longer apoptotic. We describe ultrastructural changes that appear unique to dying embryonic dopaminergic neurons. In primary cultures of mesencephalon, death of dopaminergic neurons is triggered by activation of glutamate receptors sensitive to alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and differs ultrastructurally from both neuronal apoptosis or typical excitotoxicity. AMPA causes morphological changes selectively in dopaminergic neurons, without affecting other neurons in the same culture dishes. Two hours after the onset of treatment swelling of Golgi complexes is apparent. At 3 h, dopaminergic neurons display loss of membrane asymmetry (coinciding with commitment to die), as well as nuclear membrane invagination, irregular aggregation of chromatin, and mitochondrial swelling. Nuclear changes continue to worsen until loss of cytoplasmic structures and cell death begins to occur after 12 h. These changes are different from those described in neurons undergoing either apoptosis or excitotoxic death, but are similar to ultrastructural changes observed in spontaneous death of dopaminergic neurons in the natural mutant weaver mouse.     

Suppression of ammonia-induced swelling by aspartate but not by ornithine in primary cultures of rat astrocytes

Cerebral edema with a rise in intracranial pressure is the hallmark of fulminant hepatic failure (FHF) and acute hyperammonemic (HA) states and is characterized by a poor survival rate. Astrocytes are the cells in brain which are swollen in these conditions. Several hypotheses have been proposed to explain the mechanism of cerebral edema in FHF and treatment strategies have evolved based on these putative mechanisms. Treatment with a mixture of ornithine and aspartate has been proven to be clinically beneficial as it reduces edema and improves the neurological status. It has been suggested that these two amino acids generate the glutamate required for the synthesis of glutamine and that they also enhance urea synthesis in surviving hepatocytes in FHF and HA. Presently, we report that of these two amino acids, only aspartate is effective in suppressing ammonia-induced swelling in primary cultures of astrocytes, while ornithine is ineffective. These results are discussed in relation to the metabolism of aspartate and ornithine in astrocytes, with an emphasis on glutamine synthesis and the malate-aspartate shuttle (MAS). We propose that the ability of aspartate to generate glutamate in the cytosol for glutamine synthesis and oxaloacetate in mitochondria to support the citric acid cycle play a role in its ability to reduce ammonia-induced swelling in astrocytes.