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

Two patients died of psittacosis after presenting with generalised toxaemia, acute renal failure, and evidence of pancreatitis. Death was attributed to the virulence of the chlamydial strain and the delay in antemortem diagnosis. In one case Chlamydia psittaci was isolated from necropsy lung tissue. A third case of psittacosis suggested person-to-person or fomite spread, which is rarely reported. Infection was acquired from an apparently healthy, imported and quarantined cockatiel. Import restrictions on psittacines should thus be tightened and psittacosis should be made a notifiable disease.
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PMID:Fulminant psittacosis. 8 4

Infection of pregnant or non-pregnant mice with Coxsackieviruses B1, B3, B4 or B5 produced a severe pancreatitis consisting of a degeneration of the acinar cells, loss of zymogen granules, infiltration of mononuclear and plasma cells and a replacement of the exocrine tissue with fatty tissue. Coxsackieviruses B2 and B6 did not cause these changes in the period up to 6 weeks following virus injection. Suckling mice did not appear to be more susceptible to pancreatic damage due to these two viruses. Sequential studies on the development of Coxsackievirus B-induced pancreatic lesions indicated that although the changes due to B1, B3, B4 or B5 were similar in type, B3 and B4 exhibited a more rapid action in the tissue and more severe lesions than either B1 or B5. In this work, none of the Coxsackie B viruses examined elicited pathological changes in the islets of Langerhans detectable with the light microscope.
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PMID:Pathological changes in the pancreas of mice following infection with Coxsackie B viruses. 78

Acute pancreatitis was studied by electron microscopy after retrograde infusion of either trypsin, and/or beta-glucuronidase into the canine pancreatic duct. Marked changes were induced by the mixture of trypsin and beta-glucuronidase. (1) The acinar cells were initially excavated from the acinar lumen and formed cystic bodies in themselves. The cystic bodies were then disrupted at their marginal membranes, and the acinar cells were filled with a large amount of fibrillar materials which originated from the contents of the cystic bodies. At this time, the luminal margin of the acinar cells completely disappeared. (2) The cellular organellas and the intracellular fibrillar materials in the acinar cells were discharged into the interstitial space through the disrupted basal lamina. Infection in the pancreatic ductal system was considered to play an important role in the pathogenesis of acute hemorrhagic pancreatitis.
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PMID:Ultrastructural studies of experimental acute pancreatitis. 97 83

Fifty-two cases of acute renal failure at Livingstone Hospital were studied. Twenty-two cases were obstetric, 10 surgical and 20 medical. The aetiological factors are tabulated and the pathophysiology is reported. Clinical features and biochemical abnormalities are presented. Infection was the commonest associated factor, followed by hypotension and volume problems, coagulation disorders, jaundice and hepatic failure, respiratory failure, pancreatitis and typhoid fever. In 7 of the medical cases the aetiology was unknown and was assumed to be toxic. A case history of a patient with leptospirosis, acute renal failure, liver failure and pancreatitis is presented. The mortality in this series was 32%.
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PMID:Acute renal failure. Experience with 52 patients treated at Livingstone Hospital. 125 Dec 80

Because pancreatitis has been reported frequently in adults with human immunodeficiency virus infection, we sought to determine the incidence of pancreatitis in children with acquired immunodeficiency syndrome by reviewing all records of children with AIDS, their serum amylase and lipase levels, and the factors associated with pancreatitis through a case-control analysis. During a 6-year period pancreatitis developed in 9 (17%) of 53 pediatric patients with AIDS. Six children had vertical transmission of infection and three patients had acquired HIV infection through contaminated blood products. Pancreatitis developed at a median age of 5.2 years (range 1.2 to 20 years). All patients had vomiting and abdominal pain. When the patients were first seen, lipase values were elevated more than amylase values (p = 0.028). Amylase and lipase levels declined at comparable rates. In the case-control analysis, pentamidine isethionate was significantly associated with pancreatitis (p = 0.02); the risk was greater in patients who received pentamidine isethionate and had absolute CD4 T-lymphocyte counts less than 100 cells/mm3 (p = 0.001). Infections associated with the onset of pancreatitis included cytomegalovirus (4), Cryptosporidium (1), Pneumocystis carinii pneumonia (3), and Mycobacterium avium intracellulare (1). Coinfection with cytomegalovirus was associated with a protracted course in four children. Ultrasonographic examination demonstrated biliary ductal dilatation 6 months after the onset of pancreatitis in one child. Seven children have died at a mean of 8 months after the initial onset of pancreatitis; the one living child has survived 5 months from the onset of pancreatitis. We conclude that pancreatitis is common in pediatric patients with AIDS and may be related to pentamidine isethionate exposure, especially when absolute CD4 T-lymphocyte counts are less than 100 cells/mm3. Serum amylase levels do not always accurately predict the onset of pancreatitis; serum lipase levels should be measured in children with symptoms. The onset of pancreatitis in an HIV-infected child is a poor prognostic indicator.
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PMID:Pancreatitis in pediatric human immunodeficiency virus infection. 137 Sep 62

Infections accompanying severe pancreatitis are secondary and of three types: infected pancreatic necrosis, infected pseudocyst (including peripancreatic fluid collection), and pancreatic abscess. The first is an earlier, more morbid process, with antibiotics supportive and surgical debridement necessary. The latter two processes occur later in the course of pancreatitis and are less morbid. Antibiotics are supportive and invasive-nonsurgical drainage methods are possible. The decision for intervention is based first on clinical toxicity as determined by an overall assessment by the clinician. The presence of parenchymal necrosis is best determined by the dynamic bolus CT scan. The presence of infection is best determined by percutaneous CT-guided aspiration. Infected necrosis is fatal unless treated with operative intervention. A peripancreatic fluid collection, pseudocyst, or pancreatic abscess needs to be treated if symptomatic. If infected, as determined by CT-guided needle aspiration, then they should be drained. Radiologic or endoscopic invasive-nonsurgical methods are tried initially and then surgery is attempted if they fail. The nonsurgical methods are most successful with pancreatitis of a nonbiliary or a nonalcohol etiology.
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PMID:Infections complicating severe pancreatitis. 143 Oct 40

Findings from 44 autopsy examinations of cardiac transplant patients during a 10-year period were reviewed. The autopsy rate was 85%. One half of the autopsy patients underwent original transplantation for ischemic heart disease and 34% for cardiomyopathy. Survival after transplantation ranged from 0 (intraoperative) to 91 months. Rejection (including hyperacute rejection) was responsible for 41% of deaths, followed by infection (25%), and intraoperative deaths at first transplantation (9%). Most of the remaining complications were related to surgery or artificial heart support, accelerated allograft atherosclerosis, and lymphoma. Infections were not only responsible for a substantial percentage of deaths but were also a co-morbid finding in a number of patients who died primarily of other causes. Pulmonary infections represented the most common anatomic site. Twenty-five percent of the autopsy patients had gastrointestinal and/or pancreatic abnormalities, principally mucosal inflammation, erosions or hemorrhage, and pancreatitis. Review of premortem rejection history indicated that 64% of patients who died of or with rejection at autopsy had had an episode of rejection 3 weeks after transplantation and/or at least one episode of severe rejection.
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PMID:Autopsy findings in cardiac transplant patients. A 10-year experience. 154 52

To compare the effectiveness of cystgastrostomy and cystjejunostomy for treatment of pancreatic pseudocysts, 39 patients with cystgastrostomy were compared to 59 patients with cystjejunostomy. The groups were comparable in age, sex, cause of pancreatitis, pseudocyst location, symptoms, and preoperative serum amylase level. Cysts treated with cystgastrostomy were larger (mean diameter, 11.1 +/- 0.9 cm) than cysts treated by cystjejunostomy (mean diameter, 6.7 +/- 0.7 cm) (p less than 0.05). Mean duration of surgery was 148 +/- 11 minutes for cystgastrostomy versus 265 +/- 15 minutes for cystjejunostomy (p less than 0.05). Mean blood loss was 397 +/- 82 ml for cystgastrostomy versus 703 +/- 80 ml for cystjejunostomy (p less than 0.05) Mean intraoperative fluid requirements were 2640 +/- 313 ml for cystgastrostomy and 4403 +/- 362 ml for cystjejunostomy (p less than 0.05). Cyst recurrence was 10% for cystgastrostomy versus 7% for cystgastrostomy. Postoperative gastrointestinal bleeding occurred in 8% of patients with cystgastrostomy and in 2% of patients with cystjejunostomy. Infection problems with cystjejunostomy included two wound infections and one case of septicemia; infection problems with cystjejunostomy included five intraabdominal abscesses, two wound infections, and one case of pneumonia. Two patients died with cystgastrostomy (both from gastrointestinal bleeding); two patients died with cystjejunostomy (one from intraabdominal sepsis and one from pulmonary embolus). Cystgastrostomy was used for significantly larger pseudocysts and was associated with significantly less blood loss and operating time than cystjejunostomy (p less than 0.05). Morbidity and mortality from cystgastrostomy and cystjejunostomy were comparable, although gastrointestinal bleeding was more common with cystgastrostomy and intraabdominal abscess was more common with cystjejunostomy. Since cystgastrostomy can usually be performed more quickly and with less blood loss, it should be considered whenever anatomically feasible.
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PMID:Are cystgastrostomy and cystjejunostomy equivalent operations for pancreatic pseudocysts? 221 73

Coxsackie B viruses are known etiological agents of pancreatic diseases, including diabetes. The pathogenesis of these infections is influenced by both host and viral factors. In this report, we examined whether the outcome of Coxsackie B4 virus infection is dependent on the genes within the major histocompatibility complex (MHC). We generated a pancreatic variant, CB4-V and established an animal model system of pancreatitis with concurrent hypoglycemia in mice. Infection of various B10 H-2 congenic strains of mice revealed that the development of hypoglycemia with accompanying pancreatitis was independent of the MHC haplotype. However, the severity of the disease as monitored by the extent and duration of hypoglycemia and by mortality rate was found to be associated with the H-2 haplotype, specifically the H-2Kq locus. Pancreatic damage induced by CB4-V appeared to be both immune-mediated and viral-mediated. Histological examination of pancreatic tissue from infected B10 H-2 congenic mice revealed an association between acute destruction of the exocrine pancreas and lymphocytic infiltration. This infiltration may correlate with immune-mediated destruction of the infected pancreatic tissue. Since preferential replication of CB4-V was not observed in the most susceptible B10 mouse strain, direct viral destruction may not be the major mechanism of pancreatic injury.
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PMID:Severity of disease induced by a pancreatropic Coxsackie B4 virus correlates with the H-2Kq locus of the major histocompatibility complex. 256 Feb 95

Infection with 100 Opisthorchis viverrini (OP) metacercariae prior to two injections of dihydroxy-di-n-propyl nitrosamine (DHPN) (1000 mg/kg body weight) brought about significant enhancement of resultant preneoplastic lesion development in Syrian hamster liver and pancreas tissue. Thus combined treatment with carcinogen and parasite was associated with pancreatic atypical (dysplastic) foci, hepatocellular nodules, cholangiofibrosis and cholangiocarcinomas. No such lesions were observed in carcinogen alone, parasite alone or untreated control groups. In addition, parasite induced hyperplastic gall bladder epithelium was found to include areas of putative preneoplastic cells only in the DHPN-OP combined group. The results strongly suggest that pancreatitis and biliary cirrhosis associated with liver fluke infestation are responsible for the observed enhancement of carcinogenesis, and that the resultant increased proliferation plays a major role in tumorigenesis.
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PMID:Enhancement of DHPN induced hepatocellular, cholangiocellular and pancreatic carcinogenesis by Opisthorchis viverrini infestation in Syrian golden hamsters. 283 5


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