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)

In the annuals of autopsy records in Japan, edited by the Japanese Society of Pathology and covering 20 years, from 1958 to 1977, 377841 autopsy cases are registered with a short summary of the pathology findings. Of these, 434 cases with idiopathic, interstitial, viral, non-specific (NSM) and giant cell (GCM) myocarditis were found. The incidences of NSM and GCM were 0.11 and 0.007%, respectively. The annual incidence of NSM showed periodic fluctuations with in 5-year intervals and increased remarkably after 1974. Incidence of GCM showed a similar fluctuation but with a one to two year delay of peaks. The male to female ratio was 1.2: 1 and the age distribution had two peaked patterns for both sexes, though these peaks were scattered widely from neonate to elderly patients. The regional distribution of NSM showed a concentration in the middle portion of Honshu and its regional annual incidence had propagation waves from the central area to peripheral areas. The same tendency was observed in GCM cases. Hokkaido was characterized by a low incidence of NSM and no GCM. Complications of myocarditis included pancreatitis, pneumonitis, interstitial nephritis, meningoencephalitis, hepatitis, hepatic cirrhosis and a considerable incidence of malignancies. Antibiotics, antineoplastic agents, steroids and irradiation therapy were the main forms of treatment applied before or after the start of myocarditis.
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PMID:Twenty year autopsy statistics of myocarditis incidence in Japan. 382 May 37

The symptoms and signs of 51 patients with a history of scorpion sting were studied. Acute pulmonary oedema with peripheral circulatory failure due to myocarditis developed in 10. Pulmonary oedema appeared within thirty minutes to ten hours after the sting. 5 out of 7 male patients in whom pulmonary oedema subsequently developed presented with priapism. Profuse sweating, mydriasis, vomiting, and peripheral circulatory failure were also seen, and, in 1 patient, the clinical picture was suggestive on pancreatitis. The remaining 40 patients has severe local pain only and no subsequent cardiac manifestations. There appears to be a positive correlation between occurrence of priapism in a male and the later development of cardiac manifestations after a scorpion sting.
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PMID:Diagnostic cardiac premonitory signs and symptoms of red scorpion sting. 612 Apr 3

Systemic pathological alterations were studied in thirty-seven autopsied patients with Kawasaki disease. Systemic vasculitis was the most characteristic pathological finding and was present in all the patients. In addition to the vasculitis, there was a high incidence of inflammatory lesions in various organs and tissues: in the heart, endocarditis, myocarditis, and pericarditis; in the digestive system, stomatitis, sialoduct-adenitis, catarrhal enteritis, hepatitis, cholangitis, pancreatitis, and pancreas ductitis; in the respiratory system, bronchitis and segmental interstitial pneumonia; in the urinary system, focal interstitial nephritis, cystitis, and prostatitis; in the nervous system, aseptic leptomeningitis, choriomeningitis, gangliontis, and neuritis; in the hematopoietic system, lymphadenitis, splenitis, and thymitis. Dermatitis, panniculitis or myositis were also observed in some patients. Therefore, Kawasaki disease is a systemic inflammatory disease which mainly affects the cardiovascular system. These systemic inflammatory lesions are considered to correspond to the variegated clinical manifestaitions. The relationship between Kawasaki disease and infantile polyarteritis nodosa (IPN) were discussed, based on the clinicopathological characteristics.
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PMID:General pathology of Kawasaki disease. On the morphological alterations corresponding to the clinical manifestations. 744 9

The B7-CD28/CTLA-4 costimulatory pathway can provide a signal pivotal for T cell activation. Signaling through this pathway is complex due to the presence of two B7 family members, B7-1 and B7-2, and two counterreceptors, CD28 and CTLA-4. Studies with anti-CTLA-4 monoclonal antibodies have suggested both positive and negative roles for CTLA-4 in T cell activation. To elucidate the in vivo function of CTLA-4, we generated CTLA-4-deficient mice. These mice rapidly develop lymphoproliferative disease with multiorgan lymphocytic infiltration and tissue destruction, with particularly severe myocarditis and pancreatitis, and die by 3-4 weeks of age. The phenotype of the CTLA-4-deficient mouse strain is supported by studies that have suggested a negative role for CTLA-4 in T cell activation. The severe phenotype of mice lacking CTLA-4 implies a critical role for CTLA-4 in down-regulating T cell activation and maintaining immunologic homeostasis. In the absence of CTLA-4, peripheral T cells are activated, can spontaneously proliferate, and may mediate lethal tissue injury.
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PMID:Loss of CTLA-4 leads to massive lymphoproliferation and fatal multiorgan tissue destruction, revealing a critical negative regulatory role of CTLA-4. 758 44

Within a space of four months, between March to June 1993, medico-legal autopsies on 9 sudden infant deaths from natural causes were conducted at the Department of Forensic Medicine. Of these, 6 were due to unspecified interstitial pneumonitis or myocarditis (consistent with viral aetiologies), while 1 was attributed to adenovirus infection. The remaining 2 were due to fulminant Coxsackie virus (type B1) infection, where the post-mortem findings included leptomeningitis, myocarditis, florid interstitial pneumonitis, pancreatitis and focal hepatic necrosis. Coxsackie B viruses are often implicated in perinatal disease and, together with other viral infections, should be considered in the investigation of all sudden infant deaths.
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PMID:Acute fulminant, fatal coxsackie B virus infection: a report of two cases. 774 14

Nine autopsy cases of disseminated toxoplasmosis in New York are reported. Brain were involved in 9 cases, heart in 8, lung in 4, and pancreas, GI tract, thyroid, lymph nodes and urogenital organs were also involved. There were toxoplasma encephalitis in 9 cases, myocarditis in 4, pneumonia in 3 and pancreatitis in 2. Only toxoplasma encephalitis and pneumonia produced signs and symptoms leading to diagnosis by CT scan of brain, toxoplasma antibody titer and confirmed by smears, bone marrow biopsy and autopsy based on recognition of encysted toxoplasma. The authors classified the lesions as static (latent), necrotic, infiltrative and proliferative status, with the emphasis on the diagnostic significance of identification of toxoplasma, especially its encysted form.
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PMID:[AIDS complicated with disseminated toxoplasmosis: a pathological study of 9 autopsy cases]. 795 57

The D variant of encephalomyocarditis virus (EMCV-D) is used in the murine model to study virus-induced, acute-onset diabetes mellitus (IDDM) and myocarditis. In this model, viral replication and disease occur within seven days post infection (p.i.), and by Day 10 p.i., no infectious virus is detectable. The present study examined the possibility that EMCV-D persists in ICR-Swiss mice after the acute infection is resolved. The data show that viral antigen is detected at 28 days p.i. within the pancreatic islets of 8/10 males and 13/14 females, and within the heart valves of all animals tested. Histologic examination of the organs at 28 days p.i. suggests the development of chronic obstructive pancreatitis, and shows almost fully healed lesions in the myocardium. These observations indicate that the murine model for the study of EMCV-D induced IDDM may be extended to investigate chronic pancreatitis and heart-valve disease.
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PMID:Persistence of the D variant of encephalomyocarditis virus in the ICR-Swiss mouse. 810 61

A transfection-reactivated Coxsackievirus B3 (rCVB3), from a full-length cDNA clone of Nancy strain, has previously been shown to be as cardiovirulent as the wild-type virus. Myocarditis induced by this genetically defined virus was compared in SWR mice with the traditional Balb/c model. SWR mice inoculated with rCVB3 developed more severe myocarditis but less severe pancreatitis than Balb/c mice. In contrast to the poor general health and frequent mortality of Balb/c mice following CVB3 infection, the body weight of SWR mice was not affected by CVB3 inoculation and no mortality occurred at titres of 10(2)-10(7) plaque forming units (PFU). Typical myocarditis developed in SWR mice 7 days post infection. Myocarditic foci consisting of necrotic myocardial fibres and mononuclear cell infiltrates resolved by day 30, similar to that observed in Balb/c. However, SWR mice were more sensitive to rCVB3-induced myocarditis than were Balb/c mice: mild myocarditis was induced (4/4) by as low as 10(2) PFU of the virus (ID50 < 10(1.5) PFU), and more severe myocarditis was seen at higher PFU of virus in a dose-dependent manner. The SWR model was tested with attenuated variants derived from cardiovirulent rCVB3. The ID50 for myocarditis was 10(7) PFU for a large plaque-size attenuant and 10(6) PFU for a minute plaque-size attenuant, indicating loss of cardiovirulence by a factor of more than 10(4)-10(5). rCVB3-induced SWR mouse is a sensitive and reliable model for myocarditis. It is useful in assessing the cardiovirulence of different CVB3 variants and evaluating the efficacies of anti-viral therapies. It will allow follow-up study after high dose infection with cardiovirulent rCVB3.
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PMID:Characterization of a murine model of myocarditis induced by a reactivated coxsackievirus B3. 819 11

Balb/c weanling mice were intraperitoneally inoculated with a myocarditic variant of coxsackievirus B3, with the aim of characterizing more thoroughly the features of virus-induced cell injury in pancreas and heart, as well as to compare ultrastructural alterations with histological and virological findings. During the first week post-infection (pi), all animals developed acinar pancreatitis, followed by focal myocarditis. At electron microscopy, acinar cells showed patent distortion, including marked loss of organelles and zymogen granules, together with gross dilatation of rough endoplasmic reticulum. Cardiac cells presented severe cytoskeletal changes, as myofibrillar collapse with a haphazard arrangement, concomitant with a decrease in myofibril number; besides, irregular pattern of nuclear chromatin and increased presence of swollen mitochondria were often observed. As the few initially detected lymphocytes tended to disappear in necrotic foci, there was an increase in fibroblast number concurrent with progressive scarring. Ultrastructural changes in both pancreas and heart correlated with local viral replication, suggesting that cell damage is attributable to direct viral action.
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PMID:Ultrastructural study of cell injury induced by coxsackievirus B3 in pancreatic and cardiac tissues. 820 11

The ability of two coxsackievirus B3 (CBV3) variants to induce myocarditis in BALB/c mice was studied and plaque-forming assay, polymerase chain reaction (PCR), in situ hybridization, and immunohistochemistry were compared for detecting viruses and viral components in the myocardium. The virological findings were related to histopathologic and ultrastructural changes in the myocardium. CBV3-W induced severe myocarditis characterized by massive myocyte necrosis. Widely distributed myocyte damage clearly preceded modest inflammatory infiltrates in the myocardium. In contrast, CBV3-M1 induced mild myocardial injury. Both variants caused fulminant pancreatitis with nearly complete necrosis of the exocrine pancreas. CBV3 RNA was identified by PCR in the myocardium of CBV3-W-infected mice until the end of the follow-up period of 14 days. Moreover, semiquantitative results were obtained when the PCR/hybridization results were analyzed by a phosphor imaging system. Immunohistochemistry and in situ hybridization from formaldehyde-fixed, paraffin-embedded specimens were highly similar in detecting viral components during the early stages of the myocardial injury. The results indicate that: (i) direct viral damage plays an essential role in acute murine CBV3-induced myocarditis, (ii) PCR appears a useful and sensitive diagnostic method in acute myocarditis, and (iii) immunohistochemistry as a specific and relatively rapid method might be practicable also in studying the early stages of acute myocarditis from archival clinical material.
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PMID:Experimental myocarditis induced by two different coxsackievirus B3 variants: aspects of pathogenesis and comparison of diagnostic methods. 855 Dec 77


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