Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Type-8 avian adenoviruses were isolated from chickens in a commerical flock suffering an outbreak of inclusion body hepatitis. Serum-neutralizing titer to this type, but not to 7 other types of avian adenovirus, was more than 4 times as high in convalescing chickens as in chickens from the flock bled 2 weeks previously, during the disease outbreak. A disease similar to that in the commercial flock and to inclusion body hepatitis as described in the literature was produced by intra-abdominal inoculation of a type-8 isolant, AMG 5 (2a), into 1-day-old specific-pathogen-free chicks. Pathologic features of the disease included necrotizing hepatitis, pancreatitis, and severe lymphoid depletion of the bursa of Fabricius, thymus, and spleen. It was concluded that type-8 avian adenoviruses were involved in the etiology of the naturally occurring outbreak of inclusion body hepatitis.
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PMID:Involvement of a type-8 avian adenovirus in the etiology of inclusion body hepatitis. 19 Sep 94

Twenty 1-day-old specific-pathogen-free chickens each were given an intraabdominal inoculation of either a type-8 avian adenovirus, [AMG 5 (2a], or a type-5 avian adenovirus, inclusion body hepatitis virus (IBHV). The diseases produced were similar. High (60-100%) mortality and statistically significant depression of body weights occurred in both infections. There were necrotizing hepatitis and pancreatitis, lymphoid depletion in the spleen, bursa of Fabricius and thymus, hydropericardium, nephritis and enteritis. Intranuclear inclusions occurred in affected organs. Fluorescent-antibody staining, the Feulgen reaction for deoxyribonucleic acid and electron microscopic studies, as well as studies from the literature, indicated that basophilic inclusions consisted of assembled adenovirions.
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PMID:Comparative study of experimental inclusion body hepatitis of chickens caused by two serotypes of avian adenovirus. 20 21

Genetic resistance of C3H/RV mice to lethal infection with Banzi virus (flavivirus) was severely compromised by immunosuppression with cyclophosphamide, sublethal X-irradiation, or thymus (T-) cell depletion. The mortality rate among immunosuppressed mice was usually 100%, but average survival times were shorter for mice treated with cyclophosphamide or for X-irradiated mice (10 days) than for T-cell-depleted mice (17 days). Mice treated with cyclophosphamide had high titers of virus in brain, lymphoid tissues, pancreas, and serum. Viral antigen was widespread in brain and pancreas, and mice developed nonsuppurative meningoencephalitis and pancreatitis. Yields of virus, spread of viral antigen, and lesions in T-cell-depleted mice were similar but less severe. Mice treated with cyclophosphamide did not have detectable hemagglutination-inhibiting antibody. T-cell-depleted mice developed hemagglutination-inhibiting antibody but were not protected from lethal infection. These results indicate that genetic resistance of C3H/RV mice to Banzi virus requires immunological factors, and that T-cells play a significant role in resistance to infection with Banzi virus.
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PMID:Genetic resistance to lethal flavivrus encephalitis. II. Effect of immunosuppression. 78 45

Interleukin-2 (IL-2) is increasingly used to treat patients with cancers refractory to conventional treatment. Flu-like syndromes are extremely frequent but usually mild. A variety of skin complications (mostly erythema and mucositis) have been reported. Life-threatening skin reactions have also been described. Acute reactivation of psoriasis can also occur. Immediate hypersensitivity reactions have so far not been described, but IL-2 treatment has been shown to predispose to acute hypersensitivity reactions to iodine-containing contrast media. Hypothyroidism is the major endocrine complication and antithyroid antibodies have been detected in approximately 50% of patients. Neurological and psychiatric disturbances with moderate or severe mental status changes are common and sometimes treatment-limiting. The occurrence of peritumoural oedema in patients with brain metastases can also be a major practical problem. Musculoskeletal disorders are transient and resolve spontaneously. The vascular leak syndrome is the most frequent and severe complication of IL-2 of which weight gain, generalised oedema, hypotension and impaired renal function are the main features. Even though a damaging effect on vascular endothelium cells by various cytokines released by activated lymphoid cells or mediated by non-lymphocyte-dependent factors has been proposed to be involved, the mechanism remains unclear. Other cardiovascular injuries, possibly life-threatening, including myocarditis, angina pectoris and myocardial infarction, can occur during the first days of treatment. Supraventricular arrhythmias are the most common rhythmic disorder. Decreases in myocardial contractility and haemodynamic pattern similar to those of septic shock have been encountered in most cases. Acute renal dysfunction is common but resolves with symptomatic management. Intrahepatic cholestasis with hyperbilirubinaemia is observed in most patients but permanent liver damage has not been described. Several cases of pancreatitis have been reported. Anaemia, thrombocytopenia, lymphocytopenia and eosinophilia are frequent and occur in most if not all patients. Some data suggest a high incidence of infectious complications, particularly in patients with surgically tunnelled catheters, but marked flu-like syndromes may be confounding. Finally, death directly related to IL-2 treatment has been noted in less than 1% of all patients. Investigations are under way to minimise IL-2 toxicity with varying dose regimens and combined treatments.
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PMID:Clinical toxicity of interleukin-2. 141 98

An autopsy case of chronic pancreatitis associated with unusual chronic thyroiditis in a 54-year-old woman is presented. Microscopically, the pancreas was densely infiltrated by lymphocytes and its exocrine parenchyma was completely replaced by sclerotic tissue. The thyroid gland was also infiltrated by lymphocytes, but no lymphoid follicles were observed. These morphological changes are rare findings with respect to the severity of inflammation and the association of the affected organs. Further findings suggested involvement of an autoimmune mechanism in the pathogenesis of these lesions. Using the avidin-biotin-conjugate technique and antibodies (Abs) against T lymphocyte and HLA-DR antigens (Ags), immunological aspects of the lesions were studied. Most of these infiltrating lymphocytes were revealed to be T lymphocytes, and HLA-DR Ags were observed on the epithelial cells of the pancreatic ducts and thyroid follicles. As a control, 45 surgical specimens of pancreas and thyroid gland were studied for detection of HLA-DR expression on the epithelial cells. One case of chronic pancreatitis was revealed to express HLA-DR Ag on the epithelium. The patient was a 44-year-old woman who had silently developed pancreatic cyst due to chronic inflammation. This finding also suggests a role of autoimmunity in the pathogenesis of chronic idiopathic pancreatitis.
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PMID:Expression of histocompatibility antigen HLA-DR on the epithelial cells of the pancreatic duct and thyroid follicle. An autopsy case. 239 38

Infectious mononucleosis, a systemic illness caused by the Epstein-Barr virus, is seen frequently by primary care physicians. Mononucleosis affects several organ systems, and, within the abdomen, there can be splenic involvement, hepatitis, mesenteric lymphadenopathy, hyperplasia of gut-associated lymphoid tissue, pancreatitis, and transient malabsorption. Life-threatening abdominal complications require prompt recognition and intervention. Other abdominal complications, though worrisome, are usually short-lived and resolve without sequelae.
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PMID:Abdominal complications of infectious mononucleosis. 305 95

A primate lymphotropic lentivirus was isolated on the human T-cell line HuT 78 after cocultivation of a lymph node from a pig-tailed macaque (Macaca nemestrina) that had died with malignant lymphoma. This isolate, originally designated M. nemestrina immunodeficiency virus (MnIV) and now classified as simian immunodeficiency virus (SIV/Mne), was inoculated intravenously into three juvenile rhesus monkeys (Macaca mulatta), three juvenile pig-tailed macaques (M. nemestrina), and two juvenile baboons (Papio cynocephalus). All six macaques became viremic by 3 weeks after inoculation, whereas neither of the baboons developed viremia. One pig-tailed macaque died at 15 weeks with suppurative peritonitis secondary to ulcerative, necrotizing colitis. Immunologic abnormalities included a marked decrease in CD4+ peripheral blood lymphocytes. Although five macaques mounted an antibody response to SIV/Mne, the animal that died at 15 weeks remained antibody negative. Three other macaques (two rhesus and one pig-tailed) died 66 to 87 weeks after inoculation after exhibiting progressive weight loss, anemia, and diarrhea. Histopathologic findings at necropsy included various manifestations of immune deficiency, nephropathy, subacute encephalitis, pancreatitis, adenocarcinoma, and lymphoid atrophy. SIV/Mne could be readily isolated from the spleens and lymph nodes of all necropsied macaques, and from the cerebrospinal fluid, brains, bone marrow, livers, and pancreas of some of the animals. SIV antigens were localized by avidin-biotin immunohistochemistry to pancreatic islet cells and to bone marrow endothelial cells. The data suggest that African baboons may be resistant to infection by SIV/Mne, whereas Asian macaques are susceptible to infection with this pathogenic primate lentivirus.
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PMID:Inoculation of baboons and macaques with simian immunodeficiency virus/Mne, a primate lentivirus closely related to human immunodeficiency virus type 2. 328 32

Approximately 3,000 microslides of hematoxylin and eosin (HE)-stained sections of pancreas from 1,000 nonhuman primates were reviewed. Sections were from 557 females and 443 males; 658 were adults of unknown age and 342 were laboratory-born animals of known age. The latter included 94 animals less than one year old, 92 from one to five years old, and 156 from five to more than 20 years old. There were 326 squirrel monkeys, 319 rhesus monkeys, 100 great apes, 123 other macaques, 61 other Old World monkeys, 39 other New World monkeys, and 32 prosimians. Pancreatic lesions of varied severity found in 187 (18.7%) of these nonhuman primates included focal parenchymal or periductal accumulations of mononuclear inflammatory cells with varied degrees of periductal fibrosis in 77; hyalinized islets (amyloidosis) in 29; acute or chronic diffuse pancreatitis in 18; chronic focal pancreatitis with or without ductal hyperplasia in ten; neoplasms in 11; hemorrhage of the parenchyma or islets in eight; parasites in seven; lymphoid or ectopic splenic nodules of the parenchyma in six; acinar ectasia in six; focal parenchymal fat in six; ectopic pancreas in four; parenchymal cysts without fibrosis in three; acinar cell atrophy in one; and cystic fibrosis-like changes in one.
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PMID:A survey of pancreatic lesions in nonhuman primates. 615 9

A total of 145 BB Wistar diabetic rats, 46 of their nondiabetic siblings, and 43 outbred Wistar rats were autopsied and the frequency of lesions in all organ systems were determined. Common strain-related lesions included pulmonary infections, granulomas, lymphoid hyperplasia, lymphomas, lymphocytopenia, eosinophilia, supradiaphragmatic accessory lobes of the liver, and prostatic atrophy. These suggest some basic strain-related abnormalities of the immune system that were selected by the process of inbreeding. Diabetes-related lesions were insulitis, testicular atrophy, cataracts, hepatic fatty change, pancreatitis, lymphocytic thyroiditis, hypoglycemic brain damage, central pontine myelinolysis, stomach erosions, and idiopathic megacolon. Many of these are sequelae of human juvenile-onset diabetes and support the validity of the BB Wistar rat as an animal model for human diabetes mellitus. The absence of several important sequelae of the human disease (i.e., diabetic nephropathy, atherosclerosis, and severe microangiopathy) suggests a degree of infidelity as a model for human diabetes mellitus. Nonspecific lesions occurring in all three groups of rats included myocardial degeneration and fibrosis, splenic extramedullary hematopoiesis, and chronic progressive glomerulonephropathy.
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PMID:Pathological lesions in the spontaneously diabetic BB Wistar rat: a comprehensive autopsy study. 634 94

Approximately 3,000 microslides of hematoxylin and eosin (HE)-stained sections of pancreas from 1,000 nonhuman primates were reviewed. Sections were from 557 females and 443 males; 658 were adults of unknown age and 342 were laboratory-born animals of known age. The latter included 94 animals less than one year old, 92 from one to five years old, and 156 from five to more than 20 years old. There were 326 squirrel monkeys, 319 rhesus monkeys, 100 great apes, 123 other macaques, 61 other Old World monkeys, 39 other New World monkeys, and 32 prosimians. Pancreatic lesions of varied severity found in 187 (18.7%) of these nonhuman primates included focal parenchymal or periductal accumulations of mononuclear inflammatory cells with varied degrees of periductal fibrosis in 77; hyalinized islets (amyloidosis) in 29; acute or chronic diffuse pancreatitis in 18; chronic focal pancreatitis with or without ductal hyperplasia in ten; neoplasms in 11; hemorrhage of the parenchyma or islets in eight; parasites in seven; lymphoid or ectopic splenic nodules of the parenchyma in six; acinar ectasia in six; focal parenchymal fat in six; ectopic pancreas in four; parenchymal cysts without fibrosis in three; acinar cell atrophy in one; and cystic fibrosis-like changes in one.
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PMID:A survey of pancreatic lesions in nonhuman primates. 681 73


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