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)

Diagnostic re-evaluation of measurement of electric skin resistance (ESR), skin temperature (ST) and deeper tenderness (DT) was performed in patients with abdominal pain due to pancreatitis, cholecystopathy and duodenal ulcer. These determinations were conducted when the pain was complained of and after the pain ceased by paravertebral anesthesia. ESR was decreased on the opposite tender points of the abdominal walls as compared with those values of the healthy abdominal walls. On the contrary, ESR was increased on the suffered body areas in patients with active myelitis. ESR was decreased on the abdominal walls where visceral pain was induced by inflation of a balloon attached to the apex of a Miller-Abbott double lumen tube. DT tended to show decrease, while ST a slight increase, when the pain was evoked. However, in these pain induced experiments, ST changes were not so remarkable as those of ESR. A viscero-cutaneous reflex machanism and the predominance of sympathetic nerve control might be possible causes to produce these changes. Several important factors influencing the determination of the ESR were also discussed.
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PMID:A diagnostic re-evaluation of electric skin resistance, skin temperature and deeper tenderness in patients with abdominal pain. 96 22

Primary infection with varicella zoster is characterzed by a generalized vesicular rash usually without significant systemic illness. Encephalitis, pneumonitis, pancreatitis, nephritis, Reye and Guillan-Barre syndrome transvers myelitis, myocarditis have been reported before, but there is not any case having all these system to be involved during the same infection in a sequential manner ending up with multiorgan failure. We wanted to represent 21-month-old boy had a multiorgan failure due to varicella zoster infection.
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PMID:Complications of varicella zoster. 1192 39

Paramyxovirus-1 (PMV-1) infection was diagnosed in racing pigeons in Ontario during 1985, but it was not until January 1989, that the virus was isolated from feral pigeons (Columba livia) in this province. During an 18 month period beginning January 1988, a total of 43 feral pigeons was submitted to the Wildlife Diseases Laboratory, Pathology Department, Ontario Veterinary College. A history of neurological signs accompanied most of the birds. Tissues from 29 birds were submitted for PMV-1 isolation. Allantoic inoculation of embryonated chicken eggs yielded PMV-1 in 10 of the pigeons submitted. On the basis of histological criteria, we believe that 12 other birds were also infected with PMV-1.Gross pathological changes were unremarkable. Lymphplasmacytic interstitial nephritis was observed histologically in all birds from which PMV-1 was isolated. Other lesions seen, in decreasing frequency of occurrence, were lymphoplasmacytic interstitial hepatitis and multifocal hepatic necrosis, lymphoplasmacytic interstitial pancreatitis, nonsuppurative encephalitis and myelitis.The existence of PMV-1 in feral pigeons poses a potential threat to the poultry population since there is ample opportunity for mingling with poultry under open housing management. There is also a concern that pigeons may harbor the virus, perhaps in the kidney, and become chronic carriers and potential long-term disseminators of the disease.
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PMID:Paramyxovirus-1 in feral pigeons (Columba livia) in Ontario. 1742 32

The areas of Europe in which West Nile virus (WNV)-transmission to humans is observed have expanded over the last few years, with endemic circulation amongst animals of southern Europe. This situation calls for heightened vigilance to the clinical presentation of WNV infection in humans. The average incubation period lasts 2-6 days. Of those infected, 20% will experience a mild, non-specific disease presentation such as high fever, headache, myalgia, possibly with rash and lymphadenopathy; <1% will develop severe neurological symptoms. Rare complications include: myelitis, optic neuritis, rhombencephalitis, polyradiculitis, myocarditis, pancreatitis and fulminant hepatitis. Clinicians should take WNV infection into consideration when making a differential diagnosis for such symptoms in patients who have returned from areas with potential virus circulation. Given the increase in the spread of WNV within Europe, this now holds true for continental travellers as well as those destined for the Americas, Africa and Asia. It is important to include the patient's travel history, clinical symptoms and any occurrences of vaccination against viruses causing Japanese encephalitis, tick-borne encephalitis and yellow fever into the diagnostic workup, as the antibodies against these diseases show cross-reactivity.
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PMID:[West Nile virus expanding in Europe]. 2196 90

Infection with varicella zoster virus (VZV) causes varicella (chickenpox), which can be severe in immunocompromised individuals, infants and adults. Primary infection is followed by latency in ganglionic neurons. During this period, no virus particles are produced and no obvious neuronal damage occurs. Reactivation of the virus leads to virus replication, which causes zoster (shingles) in tissues innervated by the involved neurons, inflammation and cell death - a process that can lead to persistent radicular pain (postherpetic neuralgia). The pathogenesis of postherpetic neuralgia is unknown and it is difficult to treat. Furthermore, other zoster complications can develop, including myelitis, cranial nerve palsies, meningitis, stroke (vasculopathy), retinitis, and gastroenterological infections such as ulcers, pancreatitis and hepatitis. VZV is the only human herpesvirus for which highly effective vaccines are available. After varicella or vaccination, both wild-type and vaccine-type VZV establish latency, and long-term immunity to varicella develops. However, immunity does not protect against reactivation. Thus, two vaccines are used: one to prevent varicella and one to prevent zoster. In this Primer we discuss the pathogenesis, diagnosis, treatment, and prevention of VZV infections, with an emphasis on the molecular events that regulate these diseases. For an illustrated summary of this Primer, visit: http://go.nature.com/14xVI1.
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PMID:Varicella zoster virus infection. 2718 65