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Síndrome de Sturge-Weber; Angiomatose de Sturge-Weber; Doença de Sturge-Weber.

Microcirculatory disturbances and leukocyte activation are main events in the pathogenesis of acute pancreatitis (AP) that is characterized by inflammatory up-regulation. Nitric oxide-donating nonsteroidal anti-inflammatory drugs (NO-NSAIDs) regulate vascular function and mitigate inflammation. To investigate the influence of NO-NSAIDs on AP. AP was induced by the biliopancreatic duct outlet exclusion-closed duodenal loops model. Treatment with NO-flurbiprofen, NO-ibuprofen, NO-aspirin, or their parental drugs was done (i) 1 h before, (ii) 1 h after, (iii) 1 h before and 4 h after, or (iv) 4 h after surgery. The degree of severity was evaluated using biochemical and histopathological analyses. NO-NSAIDs given before and during the first hour of the noxia decreased blood levels of amylase, lipase, C-reactive protein, IL-6, IL-10, heat shock protein 72, prostaglandin E2 inactive metabolite, and 8-isoprostane, as well as pancreatic and lung myeloperoxidase and cyclooxygenase. Acinar and fat necrosis, hemorrhage, and leukocyte infiltrate were also reduced. The best protection was achieved when treatment was performed 1 h before and 4 h after triggering AP. NO-flurbiprofen was the most effective drug. AP severity was significantly ameliorated by NO-NSAIDs being the administration time essential to achieve optimal pancreatic protection that may result to be useful in the prevention of postendoscopic severe AP.

Severe acute pancreatitis may be triggered by an extrapancreatic insult at the peri-Vaterian duodenum such as that occurring in the short-term, 20 min closed duodenal loop model in Wistar rat, which mimics biliary acute pancreatitis or that following endoscopy. Glucocorticoids are immunological modulators whose therapeutic value is worth investigating. Wistar male rats were used under standardized conditions. Acute pancreatitis was induced by instillation of a 7% sodium tauraocholate solution with 5 drops of methylene blue to monitor absence of duodenal bilio pancreatic reflux into the peri-Vaterian duodenum for 20 min. Detection of biliopancreatic reflux with methylene blue was an exclusion criterion. Different doses and times of administration of subcutaneous hydrocortisone were evaluated. Biochemical assays were carried out in blood samples and pancreatic and lung tissue, while histpathological studies were done in the pancreas, lung liver, duodenum, spleen, kidneys, suprarenal glands, and stomach. Animals subjected to the experimental model developed severe acute pancreatitis. According to the dose and time ofadministration, hydrocortisone therapy was effective and beneficial at a dose of 4 mg/kg give 30 min before inducing acute pancreatitis. It was ineffective when doses were 4 mg/kg and given either before or after. Thus, the proposed model is valid and useful to study the initiation mechanism of acute pancreatitis caused extrapancreatically while its amelioration by glucocorticoid is related the dose and time factor to achieve therapeutical results.

Leukocyte activation, inflammatory up-regulation, and microcirculatory disruption associated with ischemia-reperfusion injury are hallmarks in the pathogenesis of acute pancreatitis (AP). NO donors ensure microvascular integrity, while glucocorticoids act as anti-inflammatory and immune modulator drugs. AP was induced by the biliopancreatic duct outlet exclusion-closed duodenal loops (BPDOE-CDLs) model. Treatment with hydrocortisone (6 mg/kg) or prednisolone (0.5 mg/kg) alone or together with DETA-NO (0.5 mg/kg) was done (a)1 hr pre or (b)1 hr post, or (c) 1 hr pre and 4 hr post ,or (d) 4 hr post triggering AP. NOS inhibition by l-NAME (15 mg/kg) and glucocorticoid receptor blockage by mifepristone (3 mg/kg) was considered. AP severity was assessed by biochemical and histopathological analyses. Treatment with glucocorticoids together with DETA-NO 1 hr pre and 4 hr post BPDOE-CDLs reduced serum amylase, lipase, C-reactive protein, IL-6, IL-10, hsp72, and 8-isoprostane as well as pancreatic and lung myeloperoxidase. Acinar and fat necrosis, hemorrhage, and neutrophil infiltrate were also decreased. Hydrocortisone together with DETA-NO rendered the best results. We conclude that AP severity was significantly diminished by glucocorticoids associated with DETA-NO, with the optimal dose and time point of administration being crucial to provide adequate protection against AP.

Background and Aims: In the general adaptation syndrome, gastric lesions are the first manifestation of stress. We hypothesized that acute pancreatitis (AP), an inflammatory acute disease, will be exacerbated if unchained following stress. Visceral hypersensitivity will be enhanced due to catecholaminergic discharges leading to an over-induction of the intrapancreatic cholinergic tone with increased response of the pancreocyte to cholecystokinin (CCK). Our aim was to investigate the influence of stress before AP on the later AP, and the effect of AP on underlying diseases such as gastric ulceration. Methods: The model of stress induced by restraint was followed by the bilio-pancreatic duct outlet exclusion closed duodenal loops model. The effect of autonomous arc reflex (AAR) interruption by anesthetics after stress but before AP was assessed. The participation of the vagal and sympathetic pathways and involvement of CCK-A receptors were considered. The degree of severity was evaluated using biochemical and histopathological analyses. Results: Induction of AP after stress was more severe than in its absence. Acinar and fat necrosis, hemorrhage and neutrophil infiltrate foci were evenly distributed, being significantly greater in size and number after stress. Gastric ulceration evolved to ulcer, hemorrhage and gastric necrosis after AP triggering. Serum amylase, lipase, C-reactive protein, IL-6, IL-10 and plasmatic hsp72 as well as pancreatic and lung myeloperoxidase were significantly elevated in AP after stress while pancreatic amylase and lipase were significantly reduced. AAR blockage ameliorated AP after stress. Conclusions: Stress aggravates pancreatic pathology while AP deteriorates gastric pathology, and anesthetic treatment was beneficial for both. Restraint in other animal models can be useful to study the influence of stress in the evolution of other diseases.

Severe acute pancreatitis may be triggered by an extrapancreatic insult at the peri-Vaterian duodenum such as that occurring in the short-term, 20 min closed duodenal loop model in Wistar rat, which mimics biliary acute pancreatitis or that following endoscopy. Glucocorticoids are immunological modulators whose therapeutic value is worth investigating. Wistar male rats were used under standardized conditions. Acute pancreatitis was induced by instillation of a 7% sodium tauraocholate solution with 5 drops of methylene blue to monitor absence of duodenal bilio pancreatic reflux into the peri-Vaterian duodenum for 20 min. Detection of biliopancreatic reflux with methylene blue was an exclusion criterion. Different doses and times of administration of subcutaneous hydrocortisone were evaluated. Biochemical assays were carried out in blood samples and pancreatic and lung tissue, while histpathological studies were done in the pancreas, lung liver, duodenum, spleen, kidneys, suprarenal glands, and stomach. Animals subjected to the experimental model developed severe acute pancreatitis. According to the dose and time of administration, hydrocortisone therapy was effective and beneficial at a dose of 4 mg/kg give 30 min before inducing acute pancreatitis. It was ineffective when doses were4 mg/kg and given before sodium taurocholate harmful when the dose was4 mg/kg and given either before or after. Thus, the proposed model is valid and useful to study the initiation mechanism of acute pancreatitis caused extrapancreatically while its amelioration by glucocorticoid is related the dose and time factor to achieve therapeutical results.

Background and Aims: Biliary acute pancreatitis or postendoscopic iatrogenia acute pancreatitis (AP) are likely triggered by autonomous arc reflexes (AAR) initiated in the peri-Vaterian duodenum (PV-D). The bilio-pancreatic duct outlet exclusion closed duodenal loops (BPDOE-CDL) model mimics these circumstances. Our aim was to validate this model and evaluate the role of AAR via their interruption with local anesthetics. Methods: Severe AP was induced in Wistar rats with the BPDOE-CDL model: extra-pancreatic insult was provoked in the PV-D by distension with 8% sodium taurocholate and methylene blue for 45 min to show the absence of duodenum pancreatic reflux. Treated experimental groups received a 2% lidocaine chlorhydrate gel instilled into the PV-D prior to triggering the AP, or before and after at the celiac-ganglia complex, or at both sites. The degree of severity was evaluated using biochemical and histopathological analysis. Results: Induction of AP by BPDOE- CDL was severe, with acinar and fat necrosis and hemorrhage with a greater foci number in the cephalic segment. Groups pretreated with local anesthetic developed mild or moderate AP characterized by edema and leukocyte infiltrate. Serum amylase, lipase and CRP were significantly reduced in all treated groups. Other blood metabolites and pancreatic myeloperoxidase, amylase and lipase, were significantly decreased. Conclusion: The BPDOE-CDL model was validated, emphasizing the importance of AAR as extrapancreatic initiators of AP. The interruption of AAR by lidocaine chlorhydrate prevented excessive pancreatic inflammation and diminished hemorrhage and necrosis and may prove a useful prophylactic procedure to prevent postendoscopic severe AP.

In previous in vivo studies we have reported that atrial natriuretic factor enhanced induced salivary secretion and increased isoproterenol-induced amylase release in the rat suggesting that, ANF effect could be mediated by phosphatidylinositol hydrolysis. In the present work, the effect of ANF on rat parotid tissue incubated in vitro was investigated with the aim to assess whether the phosphoinositol pathway was involved in ANF intracellular signaling in the parotid gland. Results showed that ANF induced a dose dependent increase in amylase fractional release, which was lower than that evoked by any concentration of isoproterenol. Furthermore 100 nM ANF enhanced isoproterenol-evoked amylase release. The effect of ANF was not affected in the presence of propranolol suggesting the noninvolvement of the β adrenergic receptor, which is the main stimulus for the output of the enzyme in the parotid gland. However, ANF increased phosphatidylinositol hydrolysis, which implies an increase in intracellular calcium, which is necessary for the achievement of maximal response in amylase release. This effect was abolished in the presence of neomycin supporting ANF direct stimulation of phospholipase C. These results suggest the involvement of the C type natriuretic peptide receptor coupled to phospholipase C in ANF evoked amylase release and ANF enhancement of the isoproterenol-induced output of the enzyme.

D-Lactic acidosis associated with encephalopathy is a clinical condition that occurs in patients with short bowel syndrome. We studied the fecal flora and the composition of fecal water of a child who developed this unusual disorder. Bacteriological studies showed that the patient's stool contained a marked predominance of gram-positive anaerobes. Two strains were identified, Lactobacillus plantarum and Lactobacillus salivarius, as the main bacteria isolated. Fecal water showed pH 4.8 and total lactic acid (sum of L- and D-lactic acids) was the principal organic anion found in the feces. We also incubated the patient's stool in a continuous culture with a view to determining the effect of the pH on the production of volatile fatty acids (VFA) and L- and D-lactic acids. The culture was maintained at pH 5.0, 5.5, 6.0, and 6.5 for four consecutive periods of four days each. We then studied the culture for a further four days at pH 5.0 once again. This study showed that with the progressive rise of the pH from 5.0 to 6.5 L- and D-lactic acids decreased and VFA production increased. D-Lactic acid formation was inhibited at pH 6.5, but when the culture was returned to pH 5.0, it increased to a high level again. These results suggest that the pH plays an important role in the ecological changes in the colonic bacteria that result in D-lactic acid production.

s / Pancreatology 12 (2012) 502–597 535 mural nodules, dilatedmainpancreatic duct or positive cytology) pancreatic sphincterotomy (PS) can be considered as an alternative treatment to reduce attacks of acute pancreatitis by facilitating drainage of mucus through the papilla. Aim: Reduce the frequency of acute pancreatitis attacks performing PS in patients affected by symptomatic SB-IPMN without radiological evidence of malignancy or in patients with MD-IPMN unfit for surgery. Patients and methods: From October 2010 to June 2011, 6 patients (3 male, mean age 53 14,23years) with IPMN (2 with mixed form: MD + SB-IPMN and 4 with SB-IPMN) diagnosed by MRCP with secretin stimulaton underwent PS. Pancreas divisum was diagnosed in 1 patient. In 5 patients IPMN was localized in the head of the pancreas whereas 1 patient was affected by mixed-IPMN haed and body. Mean diameter of cystic lesions was 18,8 10,64 mm. All patients were symptomatic for acute pancreatitis: 5 cases mild acute pancreatitis and 1 case severe acute pancreatitis Results: In 5 out of six patients pancreatography showed cystic lesions communicating with main pancreatic duct and confirmed pancreas divisum in 1; in one case with mixed type-IPMN visualization of cystic lesion localized in the body was not obtained. Six PS were performed (5 major papilla and 1 minor papilla). Mucus go out after sphincterotomy in only 2 cases (mixed-IPMN). Mortality of procedure was 0% and morbidity was 16% (one patient presented self-limiting bleeding post-ERCP, 5 days after sphincterotomy). Duration of follow-up was 8 months (range1-8 months). Two patients presented recurrent pancreatitis and underwent to DCP: one was affected bymixed-IPMN and the other by SB-IPMN (head localization). Conclusion: PS can represent an alternative treatment for symptomatic benign SB-IPMN or MD-IPMN unfit for surgery. Scheduled and regular follow-up with non invasive radiological techniques is mandatory in treated patients.

Luminal proteolytic activity (PA) of different colonic segments was ascertained in animals subjected to pancreatic duct ligation (PDL) and in control rats. The PDL rats revealed a significant PA reduction in the cecum, proximal colon (P < 0.01), and distal colon (P < 0.05). Proteolytic activity, trypsin, and chymotrypsin activity in control rats diminished progressively from the cecum to the distal colon. Conversely in PDL rats, we found maximal PA in distal colon. The conclusion is drawn that a significant proportion of colonie proteolytic activity can be attributed to pancreatic proteases with a maximal contribution at cecum level.

AIM: To investigate the severity of acute pancreatitis (AP) is associated to the intensity of leukocyte activation, inflammatory up-regulation and microcirculatory disruption associated to ischemia-reperfusion injury. Microvascular integrity and inhibition of pro-inflammatory mediators are key-factors in the evolution of AP. Relaxin is an insulin-like hormone that has been attributed vasorelaxant properties via the nitric oxide pathway while behaving as a glucocorticoid receptor agonist. METHODS: AP was induced by the bilio-pancreatic duct-outlet-exclusion closed-duodenal-loops model. Treatment with relaxin was done at different time-points. Nitric oxide synthase inhibition by L-NAME and glucocorticoid receptor (GR) blockage by mifepristone was considered. AP severity was assessed by biochemical and histopathological analyses. RESULTS: Treatment with relaxin reduced serum amylase, lipase, C-reactive protein, IL-6, IL-10, hsp72, LDH and 8-isoprostane as well as pancreatic and lung myeloperoxidase. Acinar and fat necrosis, hemorrhage and neutrophil infiltrate were also decreased. ATP depletion and ADP/ATP ratio were reduced while caspases 2-3-8 and 9 activities were increased. L-NAME and mifepristone decreased the efficiency of relaxin. CONCLUSION: Relaxin resulted beneficial in the treatment of AP combining the properties of a GR agonist while preserving the microcirculation and favoring apoptosis over necrosis.