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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatitis is a common disease in the United States, with the most likely etiologies being biliary tract disease and alcohol use. Infections with parasites such as Ascaris lumbricoides comprise a small percentage of pancreatitis cases in the United States, but they are a common etiology in developing countries. In the United States, the incidence of pancreatic and biliary ascariasis has been increasing because of the migration of people from endemic countries, as well as increased travel by Americans to such countries. Patients treated for this roundworm can have reinvasion for the same reasons. We report the case of a patient with two episodes of pancreatitis due to A. lumbricoides 2 years apart.
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PMID:Pancreatitis due to Ascaris lumbricoides: second occurrence after 2 years. 1121 51

Infections of the liver and biliary tract are common during the course of AIDS. A variety of viral, bacterial, fungal, and other opportunistic infections can present with hepatobiliary involvement as either the primary site of infection or secondary to a disseminated process. Coinfection with hepatitis B and C are particularly common due to the shared means of transmission of these viruses with HIV. The typical presenting features of hepatobiliary infections are right upper quadrant (RUQ) pain and abnormal liver function tests. Initial evaluation should include an RUQ ultrasonogram, which will usually identify abnormalities in the biliary tract and may demonstrate some parenchymal abnormalities as well. A liver biopsy is necessary to determine the etiology of focal hepatic lesions or opportunistic infections within hepatic parenchyma when other less invasive tests are negative or inconclusive. Special stains and culture techniques are required to identify specific organisms in the biopsy specimen. HIV-related biliary disorders include acalculous cholecystitis, which is a potentially serious condition requiring prompt recognition and gallbladder decompression. AIDS-cholangiopathy is a form of cholangitis involving the intra- and/or extrahepatic biliary tree. Endoscopic retrograde cholangio-pancreatography (ERCP) is the test of choice, demonstrating the stricturing, dilatation, and beading of bile ducts seen in this condition. Endoscopic sphincterotomy of the papilla of Vater may provide symptomatic relief for patients with papillary stenosis. Opportunistic infections of the pancreas have been reported. Evaluation should include a computerized tomogram of the abdomen and possible pancreatic tissue aspiration or biopsy. Management of pancreatitis is supportive.
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PMID:Hepatobiliary and pancreatic infections in AIDS: Part one. 1136 70

Acute pancreatitis is a common cause for presentation to emergency departments. Common causes in Western societies include biliary pancreatitis and alcohol (the latter in the setting of chronic pancreatitis). Acute pancreatitis also follows endoscopic retrograde pancreatography in 5 to 10% of patients, a group that could potentially benefit from prophylactic treatment. Although episodes of pancreatitis usually run a relatively benign course, up to 20% of patients have more severe disease, and this group has significant morbidity and mortality. Therefore, attempts have been made to identify, at or soon after presentation, those patients likely to have a poor outcome and to channel resources to this group. The mainstay of treatment is aggressive support and monitoring of those patients likely to have a poor outcome. Pharmacotherapy for acute pancreatitis (both prophylactic and in the acute setting) has been generally disappointing. Efforts initially focused on protease inhibitors, of which gabexate shows some promise as a prophylactic agent. Agents that suppress pancreatic secretion have produced disappointing results in human studies. Infection of pancreatic necrosis is associated with high mortality and requires surgical intervention. In view of the seriousness of infected necrosis, the use of prophylactic antibacterials such as carbapenems and quinolones has been advocated in the setting of pancreatic necrosis. Similarly, data are accumulating to support the use of prophylactic antifungal therapy. Recently, it has become apparent that the intense inflammatory response associated with acute pancreatitis is responsible for much of the local and systemic damage. With this realisation, future efforts in pharmacotherapy are likely to focus on suppression or antagonism of pro-inflammatory cytokines and other inflammatory mediators. Similarly, animal studies have demonstrated the importance of oxidative stress in acute pancreatitis, although to date there is a paucity of information regarding the efficacy of antioxidants. Although the clinical course for most patients with acute pancreatitis is mild, severe acute pancreatitis continues to be a clinical challenge, requiring a multidisciplinary approach of physician, intensivist and surgeon.
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PMID:Optimising outcomes in acute pancreatitis. 1157 95

Although necrotizing pancreatitis remains a devastating disease, progress during the past 2 decades has significantly reduced morbidity and mortality. Early recognition of severe disease, using scoring systems or clinical signs, is essential to successful therapy. Standard therapy for patients with severe disease includes early invasive monitoring and resuscitation, prophylactic antibiotics, nutrition, and serial CT scanning and FNA to identify infected necrosis. Recent data suggest that with few exceptions, patients with pancreatic necrosis can be managed with a conservative strategy, reserving surgery or other forms of intervention for documented infection. Such a policy must be flexible, however. Infection may develop late after weeks of sterility, and repeated FNAs are necessary. Conservative management produces a subset of patients with persistent pain, malaise, and an inability to tolerate a diet or return to activities of daily life. These patients with organized necrosis do well with delayed debridement. Although there may still be a subset of patients with sterile necrosis who might benefit from earlier debridement, we have not yet identified a marker for this group.
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PMID:Current management of necrotizing pancreatitis. 1246 48

The clinical course of acute pancreatitis varies from a mild, transitory illness to a severe, rapidly fatal disease. In about 80% to 90% of cases pancreatitis presents as a mild, self-limiting disease with low morbidity and mortality. Unlike mild pancreatitis, necrotizing pancreatitis develops in about 15% of patients, with infection of pancreatic and peripancreatic necrosis representing the single most important risk factor for a fatal outcome. Infection of pancreatic necrosis in the natural course develops in the second and third week after onset of the disease and is reported in 40% to 70% of patients with necrotizing pancreatitis. Just recently, prevention of infection by prophylactic antibiotic treatment and assessment of the infection status of pancreatic necrosis by fine-needle aspiration have been established in the management of severe pancreatitis. Because medical treatment alone will result in a mortality rate of almost 100% in patients with signs of local and systemic septic complications, patients with infected necrosis must undergo surgical intervention, which consists of an organ-preserving necrosectomy combined with a postoperative closed lavage concept that maximizes further evacuation of infected debris and exudate. However, intensive care treatment, including prophylactic antibiotics, reduces the infection rate and delays the need for surgery in most patients until the third or fourth week after the onset of symptoms. At that time, debridement of necrosis is technically easier to perform, due to better demarcation between viable and necrotic tissue compared with necrosectomy earlier in the disease. In contrast, surgery is rarely needed in the presence of sterile pancreatic necrosis. In those patients the conservative approach is supported by the present data.
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PMID:Management of infection in acute pancreatitis. 1248 63

Infections with the group B coxsackieviruses either can be asymptomatic or can lead to debilitating chronic diseases. To elucidate the mechanism by which these viruses cause chronic disease, we developed a mouse model of chronic pancreatitis by using a virulent variant of coxsackievirus B4, CVB4-V. Infection with CVB4-V results in an early, severe pancreatitis, which can lead to mortality or progress to chronic pancreatitis. Chronic pancreatitis, in this model, is due to immunopathological mechanisms. We investigated whether interleukin-12 (IL-12) could modulate the outcome of CVB4-V infection. Eighty-five percent of the infected mice treated with 500 ng of IL-12 survived, whereas all untreated mice succumbed. To understand the mechanism underlying the beneficial effect of IL-12, we investigated the role of gamma interferon (IFN-gamma). Three lines of evidence suggest that the protective effect of IL-12 is due to IFN-gamma. First, administration of IL-12 increased the production of endogenous IFN-gamma in CVB4-V-infected mice. Both NK and NKT cells were identified as the source of IFN-gamma. Second, IFN-gamma knockout mice treated with IL-12 succumbed to infection with CVB4-V. Third, wild-type mice treated with IFN-gamma survived infection with CVB4-V. Due to the antiviral effects of IFN-gamma, we examined whether IL-12 treatment affected viral replication. Administration of IL-12 did not decrease viral replication in the pancreas, but it did prevent extensive tissue damage and the subsequent development of chronic pancreatitis. The data suggest that IL-12 treatment during CVB4-V infection is able to suppress the immunopathological mechanisms that lead to chronic disease.
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PMID:Exogenous interleukin-12 protects against lethal infection with coxsackievirus B4. 1285 96

Pancreatitis is clearly associated with alcohol abuse, but only a relatively small percentage of people who abuse alcohol develops obvious pancreatitis. These observations have led to the concept that the development of alcoholic pancreatitis requires cofactors. Although diet and smoking have been studied, a clear cofactor has not been identified. The study results presented in this paper were obtained to determine whether viral infection of the pancreas would be a cofactor for alcoholic pancreatitis similar to the role of hepatitis virus infections in the development of alcoholic liver disease. To test this hypothesis, mice were fed ethanol with a liquid diet protocol and infected with coxsackievirus B3 (CVB3). It was found that consumption of alcohol alone did not result in pancreatitis as determined by serum levels of amylase or histologic changes in the pancreas. Two strains of CVB3 that are tropic for the pancreas were used; a virulent and an avirulent strain. Infection of alcohol-fed animals with the virulent CVB3 strain 28 resulted in a more severe pancreatitis than the pancreatitis noted in control animals. Alcohol-fed mice infected with the avirulent strain (GA) showed severe pancreatitis, whereas the infection of control mice did not result in obvious pathologic effects in the pancreas. This model allows mechanistic studies to define the role of viral infection as a cofactor for alcoholic pancreatitis.
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PMID:Animal model of alcoholic pancreatitis: role of viral infections. 1457 91

Infection associated with systemic inflammatory response syndrome (SIRS) is a major cause of morbidity and mortality in patients with major surgery, polytrauma, and severe burn injury. In previous studies, mice with severe pancreatitis (a mouse model of SIRS, SIRS mice) have been shown to be greatly susceptible to various infections. In the present study, a mechanism involved in the impaired resistance of SIRS mice to infectious complications was investigated. Sera from SIRS mice impaired the resistance of normal mice to infectious complications induced by cecal ligation and puncture (CLP). CC chemokine ligand 2 (CCL2) was detected in sera of SIRS mice. Resident macrophages (RMphi) cultured with SIRS mouse sera converted to alternatively activated macrophages (AAMphi), which were also demonstrated in mice treated with recombinant murine CCL2. However, AAMphi were not demonstrated in mice injected with SIRS mouse sera and anti-CCL2 monoclonal antibody (mAb) in combination. Furthermore, normal mice that received SIRS mouse sera and anti-CCL2 mAb resisted CLP-induced infectious complications. These results indicate that the resistance of SIRS mice to infectious complications is impaired by AAMphi generated from RMphi in response to SIRS-associated CCL2 production.
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PMID:CCL2, a product of mice early after systemic inflammatory response syndrome (SIRS), induces alternatively activated macrophages capable of impairing antibacterial resistance of SIRS mice. 1512 72

Here we report the first German case of necrotizing pancreatitis, peritonitis, and septic shock caused by linezolid-resistant Enterococcus faecium and Enterococcus faecalis.
Infection 2004 Jun
PMID:Linezolid-resistant Enterococcus faecium and Enterococcus faecalis isolated from a septic patient: report of first isolates in Germany. 1518 81

Histopathological and functional changes in the pancreas were studied in 94 hamsters infected and reinfected with Trypanosoma cruzi VIC strain and in 73 non-infected normal controls. Infection in each animal was verified by microhematocrit, hemoculture, specific peroxidase anti-peroxidase, polymerase chain reaction and seroagglutination. Blood glucose and insulin were determined. The number of islets per section and the number of islet cells marked with antibodies were counted. Insulitis, neuritis, fibrosis, atrophy and inflammatory infiltrates were evaluated. Experimental chagasic infection caused pancreatitis similar to human Chagas' disease, involving acini, islets and nerves, with atrophy and fibrosis, although without correlation to the number of reinfections. Erratic blood glucose levels and a tendency to hypoinsulinemia were observed in infected animals. During the acute phase, the number of somatostatin and pancreatic polipeptide producer islet cells was lower in infected hamsters, which was eventually related to changes in blood sugar levels and hypoinsulinemia. Our findings favor the hypothesis of the existence of an endocrine form of chronic chagasic infection.
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PMID:Functional and histopathological study of the pancreas in hamsters (Mesocricetus auratus) infected and reinfected with Trypanosoma cruzi. 1532 22


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