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1
Content available remote Coexistence of pancreatic tuberculosis with systemic brucellosis: a case report
100%
EN
Isolated pancreatic tuberculosis is an extremely rare clinical entity and is difficult to diagnose particularly in immunocompetent individuals. Clinical findings and symptomatology of brucellosis are often similar to tuberculosis thus making the differentiation amongst the two entities difficult. We report a case of pancreatic tuberculosis with systemic brucellosis in a 29 year old veterinarian who presented with epigastric pain and loss of appetite. Initial investigations revealed leukocytosis with moderately elevated transaminase, gamma glutamyl transferase, amylase and lipase levels. Imaging studies revealed an anechoic multiloculated cyst in the body and tail of the pancreas. Given the patient’s occupational risk coupled with the presence of a positive Brucella agglutination test (with a titer of 1:320); a diagnosis of pancreatitis secondary to brucellosis was given. In addition to standard pancreatitis therapy of bowel rest with intravenous fluid/electrolyte replacement, anti-brucellosis therapy was also administered. The patient’s initial response to therapy was positive however, 6 weeks into therapy, his abdominal pain recurred and repeat CT scan revealed the development of a pseudocyst in the pancreas. After failing a second attempt at conservative supportive therapy, the patient underwent an explorative laparotomy. Histological examination of the resected pancreatic specimen showed necrosis and was positive for tuberculosis by polymerase chain reaction. Herein, we describe the first case reported in the medical literature of the coexistence of systemic brucellosis with pancreatic tuberculosis. We suggest that the possibility of the coexistence of brucellosis with tuberculosis be kept in mind when assessing pancreatitis patients in endemic regions and in individuals with occupational risk hazards.
2
100%
EN
The molecular principles that lead to chronic pancreatitis are incompletely understood. Trypsin(ogen) plays a key role in the development of pancreatitis. Since the production of trypsin(ogen) by acinary pancreatic cells is paralleled by the expression of vigilin we hypothesised that vigilin may be involved in the onset of pancreatitis. Vigilin is a ubiquitous protein and has apparently high affinity to RNA. In the present study experimental pancreatitis was induced in male rats by a single intravenous application of dibutyltin dichloride (DBTC). Sections of rat pancreas were immunostained with an affinity-purified polyclonal antiserum against vigilin or trypsin(ogen). The changes in vigilin and trypsin(ogen) protein expression were determined by immunoblotting and subsequent sequence analysis of the amino acids. Induction of pancreatitis by DBTC caused alterations in the distribution and the amount of both vigilin and trypsin(ogen) as shown by immunohistochemical and immunoblot analysis. Furthermore we could demonstrate that anionic trypsinogen expression is up-regulated in DBTC-induced chronic pancreatitis. The obtained results suggest that vigilin as well as trypsin(ogen) are involved in the pathogenesis of pancreatitis and that the long-time DBTC-induced pancreatitis is a useful model for study of chronic pancreatitis.
4
Content available remote Hypercalcemia: A rare cause of cerebral infarction
100%
Open Medicine
|
2008
|
tom 3
|
nr 4
514-516
EN
Hypercalcemia is a definite but rare cause of acute pancreatitis. It is often overlooked in the presence of more common etiological factors such as gallstones, alcohol and trauma. Cerebral infarction secondary to hypercalcemia has also been described. We have done a literature review to explore the possible pathological processes causing cerebral infarction in hypercalcemic patients.
5
Content available remote Biological markers of severity in acute pancreatitis
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6
Content available remote Nutrition in acute pancreatitis: a review
88%
EN
We perform an update about nutritional measures that have been adopted in patients with acute pancreatitis (AP). The nutritional support is an essential part of treatment in AP. When the AP is mild or moderate, there is no doubt that is not necessary to use an artificial nutritional support, and it is recommended that oral nutritional support should begin as soon as possible. If the AP is severe, the best way to provide nutritional support is through enteral nutritional (EN) because it reduces infection, length of hospitalization and mortality rate. Parenteral nutrition (PN) should be used only when EN is Impossible. However, there is no scientific evidence for recommending the most optimal route necessary to administer this type of nutritional support; we seek to uncover whether this is by gastric or jejunal route and the proper formula to use. There is an international agreement that the nutritional support should begin quickly, within the first 24 and 72 hours of hospitalization. As conclusion, more research needs to be done concerning nutritional support in AP, and many questions are not been answered yet.
7
Content available remote Acute pancreatitis after nifedipine and acetaminophen poisoning - case report
88%
EN
The incidence of drug-induced pancreatitis is rare. There have been several reports of acute pancreatitis as a complication in acute poisoning with drugs or toxins. We present a case of a young woman with acute pancreatitis secondary to an overdose of nifedipine and acetaminophen in a suicide attempt. We excluded other causes of acute pancreatitis by clinical history, serum toxicology, serology, and abdominal imaging. The most likely underlying pathophysiological mechanism was ischemic injury of the pancreas secondary to severe collapse induced by nifedipine and possible acetaminophen-induced direct pancreatotoxicity. The pancreatitis resolved with treatment that included continuous veno-venous haemofiltration in an intensive care unit. Emergency and intensive care units should be aware of this unusual complication of such poisoning. To our knowledge, this is the first reported association between massive nifedipine overdose and acute pancreatitis.
8
Content available remote Classifications of acute pancreatitis: to Atlanta and beyond
75%
EN
Until Atlanta Classification (AC) made in 1992, there was not any classification of acute pancreatitis (AP). Last twenty years AC let us compare results and papers. But the increasing understanding of the pathophysiology of AP, improvements in diagnostic methods and the development of minimally invasive tools for radiological, endoscopic and surgical management of local complications, several authors have called for the AC to be reviewed. Last months, two new classifications of AP have been published. We made a historical review of AC, the two new classifications and a comparison between them.
9
Content available remote Evidence-based management of pancreatitis
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10
Content available remote Quality assurance of sphincterotomy: A prospective single-centre survey
75%
EN
Quality assurance becomes an increasingly important part of clinical medicine and of the field of endoscopy. Endoscopic sphincterotomy is associated with a fairly high complication rate. We aimed to assess our quality of sphincterotomy for benchmarking by using a prospective electronic database registry, and to identify potential risk factors for post-interventional complications. Over 2 years, 471 sphincterotomies were performed in a single tertiary referral centre. Patient- and procedure-related variables were prospectively recorded with the support of a multi-centre international sphincterotomy registry. Multivariate analysis was performed. The overall post-interventional complication rate was 9.3%. Pancreatitis happened in 5.5%, bleeding in 2.1%, perforation in 1.3%, and cholangitis in 0.4%. In the multivariate analysis following variables remained highly significant and predictive for complications: ‘papilla only in lateral view’ (p=0.001), antiplatelet therapy (p=0.024), and opacification with contrast up to the pancreatic tail (p=0.001). The primary success rate of sphincterotomy was 95.1%. The rate of post-interventional pancreatitis did not differ significantly regardless of the presence of prophylactic pancreatic stent (p=0.56). The outcome of sphincterotomy in our centre matches with literature data. The extent of pancreatic duct opacification has an influence on the pancreatitis rate. Prevention of pancreatitis by inserting pancreatic stents is not confirmed.
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