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Query: UMLS:C0042961 (volvulus)
4,305 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Corneal inflammation (keratitis) is a major cause of visual impairment in Onchocerca volvulus infection. Previous studies showed that onchocercal keratitis can be induced in mice following s.c. immunization and intracorneal injection with soluble O. volvulus Ags (OvAg), and that the inflammatory response is dependent on T cells and IL-4. Since recombinant IL-12 impairs IL-4-dependent, Th2-mediated responses in other parasitic infections and in models of allergic asthma, the present study was undertaken to determine the effect of IL-12 on onchocercal keratitis. Mice were injected i.p. with IL-12 or saline at the time of initial sensitization to OvAg. Surprisingly, IL-12 treatment caused significant exacerbation of corneal pathology, which was associated with increased eosinophil and mononuclear cell infiltration into the corneal stroma. Consistent with the well-documented effect of IL-12 on Th1 cell development, corneas of IL-12-treated animals had elevated expression of the Th1 cytokine IFN-gamma and diminished expression of the Th2 cytokines IL-4, IL-5, IL-10, and IL-13. However, corneas from these animals also had marked elevation of alpha- and beta-chemokines known to be active on eosinophils and mononuclear cells, including IFN-gamma-inducible protein (IP)-10, macrophage inflammatory protein-1alpha, macrophage inflammatory protein-1beta, JE/monocyte chemotactic protein-1, RANTES (regulated upon activation, normal T expressed and secreted), and eotaxin. Together, these data indicate that IL-12 exacerbates OvAg-mediated corneal pathology by enhancing chemokine expression and recruitment of inflammatory cells.
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PMID:IL-12 exacerbates helminth-mediated corneal pathology by augmenting inflammatory cell recruitment and chemokine expression. 899

This review illustrates the changing paradigms in the understanding of the pathogenesis of pneumatosis intestinalis. Although many theories have been evoked, pragmatically there appear to be four major clinical and diagnostic imaging considerations. The most common and most emergent life-threatening cause of intramural bowel gas is the result of bowel necrosis due to bowel ischemia, infarction, necrotizing enterocolitis, neutropenic colitis, volvulus, and sepsis. In the stomach, intramural gas can be caused by emphysematous gastritis or ingestion of caustic agents. These situations represent surgical emergencies. Pneumatosis is found secondary to mucosal disruption presumably due to over-distention from peptic ulcer, pyloric stenosis, annular pancreas, and even to more distal obstruction. Disruption can also be caused by ulceration, erosions, or trauma, including the trauma of child abuse. Disruption can also be iatrogenic from intracatheter jejunal feeding tubes, stent perforation, sclerotherapy, or surgical or endoscopic trauma. In these cases, the gas may be focal or linear. Treatment depends on the extent of the disruption and the underlying cause. A more subtle form of mucosal disruption may occur due to mucosal erosions and also to defects in intestinal crypts secondary to acute and subclinical enteritides that allow intraluminal bacterial gas under pressure to percolate into the bowel wall layers, particularly the submucosa (29). Pneumatosis, often linear or cystic in appearance, is seen with increased frequency in patients who are immunocompromised because of steroids, chemotherapy, radiation therapy, or AIDS. In these cases, the pneumatosis may result from intraluminal bacterial gas entering the bowel wall due to increased mucosal permeability caused by defects in bowel wall lymphoid tissue. Clinical and imaging findings are important in the differentiation of this transient pneumatosis from fulminant life-threatening causes in this subset of patients. A pulmonary cause must still be considered in cases of chronic obstructive pulmonary disease, asthma, and cystic fibrosis. It can occur with barotrauma and after chest tube placement. It may relate to increased intrathoracic pressure associated with retching and vomiting. The possibility remains that occasionally the origin of pneumatosis intestinalis will remain cryptogenic--caused but unexplained.
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PMID:Pneumatosis intestinalis: a review. 953 Feb 94

Gastric volvulus was first described by Berti in 1966. Whereas acute gastric volvulus is very rare, chronic gastric volvulus on the other hand is being diagnosed with increasing frequency. This is attributed to the liberal use of barium meal for the evaluation of infants and children with repeated attacks of vomiting and recurrent chest infection. This report describes our experience in the management of 36 infants and children with acute and chronic gastric volvulus. Their medical records were retrospectively reviewed for: age at diagnosis, sex, symptomatology, diagnosis, treatment and outcome. There were 22 males and 14 females. Their ages at presentation ranged from 1 week to 2.5 years (mean 6.7 months). Their symptomatology included repeated attacks of vomiting (30 patients), recurrent chest infection and asthma like symptoms (6 patients), failure to thrive (6 patients), chocking with feeds (3 patients), loose bowel motion (3 patients) and apnoea attack (1 patient). Two presented acutely with intrathoracic gastric volvulus. One of them had recurrent left diaphragmatic hernia while the other had a large paraesophageal hernia. The remaining patients had chronic intraabdominal gastric volvulus. Radiologically, all had organo-axial gastric volvulus except one who had mesenterico-axial gastric volvulus and 33 (97%) of them had demonstrable gastroesophageal reflux. Eleven were treated conservatively because their symptoms were mild to moderate and settled. The two patients with intrathoracic gastric volvulus underwent reduction of the contents, repair of the defect and anterior gastropexy. The remaining patients underwent gastropexy, both fundal and anterior. Intraoperatively, two were found to have diaphragmatic hernia, nine had mobile (non-fixed) spleen, and eight showed mobile stomach with lax ligaments. Post-operatively, all did well and showed good improvement with disappearance of their symptoms and increase in weight. Acute gastric volvulus is very rare. Prompt clinical suspicion and radiological assessment are essential to treat this life-threatening condition. Chronic gastric volvulus on the other hand is more common but under diagnosed. It should be included in the differential diagnosis of infants and children with repeated attacks of chest infection, vomiting and failure to thrive. Barium meal should form part of their investigations. The treatment of chronic gastric volvulus depends on their symptomatology. Those with mild to moderate symptoms should be treated conservatively, while those with persistent and severe symptoms should undergo anterior (to the abdominal wall) and fundal (to the diaphragm) gastropexy without fundoplication.
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PMID:Acute and chronic gastric volvulus in infants and children: who should be treated surgically? 1787 14