pancreatitis/nikotiin

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Nicotine ameliorates experimental severe acute pancreatitis via enhancing immunoregulation of CD4+ CD25+ regulatory T cells.

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OBJECTIVE Activation of "nicotinic anti-inflammatory pathway" could reduce severity of inflammation and injury induced by acute pancreatitis. However, the role of regulatory T (Treg) cells in this pathway is unclear. METHODS Severe acute pancreatitis (SAP) was induced in mice through retrograde

Tobacco smoking and the risk of pancreatitis: A systematic review and meta-analysis of prospective studies.

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Tobacco smoking has been associated with increased risk of pancreatitis in several studies, however, not all studies have found an association and it is unclear whether there is a dose-response relationship between increasing amount of tobacco smoked and pancreatitis risk. We conducted

Effects of Nicotine and Vagus Nerve in Severe Acute Pancreatitis-Associated Lung Injury in Rats.

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OBJECTIVE The cholinergic anti-inflammatory pathway has been elucidated as a regulator of inflammatory responses in several experimental models of diseases. This regulatory mechanism is mediated by acetylcholine, released from efferent vagus nerve, interacts with α7 nicotinic acetylcholine receptors

An exploratory study on the development of an animal model of acute pancreatitis following nicotine exposure.

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Cigarette smoking is known to be a major risk factor for pancreatic cancer and pancreatitis is believed to be a predisposed condition for pancreatic cancer. As of this date, there is no established experimental animal model to conduct detailed studies on these two deadly diseases. Our aim is to

Consumption of alcohol and tobacco and other risk factors for pancreatitis.

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Histories of alcohol and tobacco consumption and other potential risk factors were obtained from 98 patients with pancreatitis and 451 comparison patients at 11 large hospitals in Eastern Massachusetts and Rhode Island between 1975 and 1979. The great majority of the patients with pancreatitis had

Meta-analysis: Tobacco smoking may enhance the risk of acute pancreatitis.

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OBJECTIVE Questions remain unclear about the association of smoking status and the development of acute pancreatitis (AP). We performed a meta-analysis of observational studies explore this association. METHODS A computerized literature search was performed in MEDLINE and EMBASE through November 30,

Is tobacco a risk factor for chronic pancreatitis and alcoholic cirrhosis?

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In a case control study alcohol intake and tobacco use were assessed between 1975 and 1987 in 103 male patients suffering from alcoholic cirrhosis of the liver, in 145 patients with chronic pancreatitis, and in 264 control subjects. The patients with chronic pancreatitis were significantly younger

Tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone initiates and enhances pancreatitis responses.

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Clinical studies indicate that cigarette smoking increases the risk for developing acute pancreatitis. The nicotine metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a major cigarette smoke toxin. We hypothesized that NNK could sensitize to pancreatitis and examined its effects in

[Influence of tobacco smoking on lipase activity in patients with pancreatitis].

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The aim of this study is to prove the influence of tobacco smoking on lipase activity in the blood of smoking and non-smoking health persons and in smoking and non-smoking patients with diagnosed acute (AP), chronic exaggerated (CEP) and chronic pancreatitis (CP). The blood has been collected from

[Effect of tobacco smoking on amylase activity in patients with pancreatitis].

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The pancreas is one of the first organs pathologically affected by the tobacco smoking. However, the mechanism of development of these changes is not eventually recognised. It has been demonstrated that nicotine influences exogenous function of pancreas. The aim of this study is to prove the

Does tobacco influence the natural history of autoimmune pancreatitis?

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Tobacco recently appeared as a major independent factor adversely influencing the natural course of alcoholic chronic pancreatitis. However, the role of tobacco in patients with autoimmune pancreatitis (AIP) has never been studied. Type 2 AIP is associated with inflammatory bowel disease, especially

Tobacco, ethanol, coffee, pancreatitis, diabetes mellitus, and cholelithiasis as risk factors for pancreatic carcinoma.

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A hospital-based case-control study of pancreatic cancer was conducted in Athens in 1991-92. One hundred and eighty-one patients operated on for cancer of the exocrine pancreas in eight teaching hospitals formed the case series, whereas hospital patient controls and hospital visitor controls formed

[Acute nonalcoholic nonbiliary pancreatitis. Difficulties in diagnosis and possibility of nicotine toxicity].

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BACKGROUND The possibility of nicotine toxicity, although rare, should be considered in cases of acute edematous pancreatitis. METHODS A 30-year-old woman was hospitalized to identify the cause of an initial episode of acute edematous pancreatitis. The observation of native anti-DNA and

Pathophysiological Events Associated With Pancreatitis in Response to Tobacco: An In Vitro Comparative Study With Ethanol in Primary Acinar Cell Culture.

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OBJECTIVE The aim of this study was to comparatively analyze the effects of different concentrations of cigarette smoke condensate (CSC, a standardized tobacco extract) and ethanol on intracellular enzyme activation, cell necrosis, alteration of cytosolic calcium concentration ([Ca]c), and amylase

Relationship of pancreas volume to tobacco smoking and alcohol consumption following pancreatitis.

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Tobacco smoking and alcohol consumption are established risk factors for diseases of the pancreas. With the recent advances in imaging modalities (such as magnetic resonance (MR) imaging), opportunities have arisen to study pancreas size, in both health and disease. Studies

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