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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe hypophosphatemia (<1.0 mg/dl) is a rarely reported complication of acute pancreatitis; when it does occur, it is typically attributed to alcohol abuse rather than the pancreatitis itself (1-5). In the literature, pancreatitis is not cited as a cause of hypophosphatemia (5, 6-16). Both pancreatitis and hypophosphatemia have widespread ramifications on human physiology, affecting hematologic, neural, hepatic, endocrine, respiratory, and renal systems. Given the possible synergistic consequences of pancreatitis and low serum phosphate, we emphasize the importance of recognizing hypophosphatemia as a complication of pancreatic inflammation.Herein, we report a case of acute pancreatitis unrelated to alcohol abuse associated with severe hypophosphatemia and review the pathophysiology.
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PMID:Severe hypophosphatemia associated with gallstone pancreatitis: a case report and review of the literature. 1664 27

Pancreatitis is a severe and frequently lethal disorder, a major cause of which is alcohol abuse. Parenchymal cell death is a major complication of pancreatitis. In experimental models of (non-alcoholic) acute pancreatitis, acinar cells have been shown to die through both necrosis and apoptosis, the two principal pathways of cell death. The severity of experimental acute pancreatitis correlates directly with the extent of necrosis and inversely with apoptosis. Thus, understanding the regulation of apoptosis and necrosis, and whether it is possible to manipulate the pattern of death responses, is becoming exceedingly important in investigations of the pathogenesis and treatment of pancreatitis. The effects of alcohol on cell death responses of pancreatitis, and the mechanisms that may mediate these effects, are just starting to be explored. This paper reviews the signaling pathways mediating the balance between apoptosis and necrosis in acute pancreatitis, and alcohol's effects on cell death responses in pancreatitis.
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PMID:Cell death in pancreatitis: effects of alcohol. 1695 57

Acute pancreatitis represents the 0.15-1.5% of all diagnoses in the Emergency Room. Biliary diseases and alcohol abuse are the two mainly etiological factors of this illness in Italy. From a clinical point of view, the course of alcoholic and biliary acute pancreatitis is the same; however, because the endoscopic retrograde cholangiopancreatography associated with endoscopic sphincterotomy can prevent further complications in patients with severe biliary pancreatitis, it is important to early recognize the biliary origin of the disease. On the other hand, the identification of alcoholic origin of pancreatitis can prevent interventional procedures not useful in this kind of patients. In this paper we will assess the markers able to early identify the etiology of this acute illness such as the liver function tests and the lipase/amylase ratio.
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PMID:[Lipase/amylase ratio and liver function tests for the etiological assessment of acute pancreatitis: facts and fiction]. 1701

Normal physiological regulation depends on Ca(2+) microdomains, because there is a need to spatially separate Ca(2+) regulation of different cellular processes. It is only possible to generate local Ca(2+) signals transiently; so, there is an important functional link between Ca(2+) spiking and microdomains. The pancreatic acinar cell provides a useful cell biological model, because of its clear structural and functional polarization. Although local Ca(2+) spiking in the apical (granular) microdomain regulates fluid and enzyme secretion, prolonged global elevations of the cytosolic Ca(2+) concentration are associated with the human disease acute pancreatitis, in which proteases in the granular region become inappropriately activated and digest the pancreas and its surroundings. A major cause of pancreatitis is alcohol abuse and it has now been established that fatty acid ethyl esters and fatty acids, non-oxidative alcohol metabolites, are principally responsible for causing the acinar cell damage. The fatty acid ethyl esters release Ca(2+) from the endoplasmic reticulum and the fatty acids inhibit markedly mitochondrial ATP generation, which prevents the acinar cell from disposing of the excess Ca(2+) in the cytosol. Because of the abolition of ATP-dependent Ca(2+) pump activity, all intracellular Ca(2+) concentration gradients disappear and the most important part of the normal regulatory machinery is thereby destroyed. The end stage is necrosis.
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PMID:Failure of calcium microdomain generation and pathological consequences. 1704 97

Hypertriglyceridaemia is a well known risk factor for acute pancreatitis. Hypertriglyceridaemia may be primary in origin or secondary to alcohol abuse, diabetes mellitus, pregnancy or use of drugs. In this case report, the cause of acute pancreatitis was tamoxifen. We report on a patient with tamoxifen-induced acute pancreatitis and hypertriglyceridaemia who was successfully treated with insulin infusion and long-term gemfibrozil.
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PMID:Tamoxifen-induced severe hypertriglyceridaemia and acute pancreatitis. 1716 63

Secondary hyperparathyroidism is highly prevalent in patients with end-stage renal disease. After successful kidney transplantation, however, parathyroid glands gradually involute to normal size with subsequent normalization of intact parathyroid hormone (PTH), serum calcium, and phosphorous concentrations. This report describes a 48-year-old diabetic end-stage renal disease patient who underwent a successful cadaveric kidney transplant. Serum calcium and phosphorous concentrations normalized within 6 months. Three years later, he presented with complaints of proximal muscle weakness that was progressively worsening. Physical examination revealed temporal wasting and proximal muscle weakness. Detailed neurologic examination was unremarkable except for decreased vibratory sensation in both feet. Laboratory data showed stable allograft function (serum creatinine, 1.3 mg/dL), hypocalcemia, and hypophosphatemia with markedly elevated alkaline phosphatase level (726 IU/L) and intact PTH level (947 pg/mL). Further laboratory evaluation revealed poor nutritional status and severe deficiency of 25(OH)D (4.0 ng/mL). Past medical history included remote episodes of acute pancreatitis due to prior alcohol abuse. Computed tomography of the abdomen showed calcific atrophic pancreas, and steatorrhea was confirmed on stool studies. Decreased bone mineral density was noted by computed tomography bone density scan. Secondary hyperparathyroidism and osteomalacia had developed due to severe vitamin D deficiency, occurring as a result of previously unrecognized, minimally symptomatic pancreatic exocrine insufficiency. Treatment with vitamin D, calcium, and pancreatic enzyme replacement led to remarkable resolution of clinical symptoms and secondary hyperparathyroidism (intact PTH, 65 pg/mL after therapy) and resulted in significant improvement in bone mineralization. Factors associated with vitamin D deficiency in the chronic kidney disease and post-transplant patient population are reviewed.
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PMID:Osteomalacia and secondary hyperparathyroidism after kidney transplantation: Relationship to vitamin D deficiency. 1722 Jun 96

The pancreas develops from ventral and dorsal buds, which undergo fusion. Failure to fuse results in pancreas divisum, which is defined by separate pancreatic ductal systems draining into the duodenum. Risk of developing pancreatitis is increased in pancreas divisum. MR cholangiopancreatography (MRCP) is the technique of choice for detecting it non-invasively. Annular pancreas is the result of incomplete rotation of the pancreatic bud around the duodenum with the persistence of parenchyma or a fibrous band encircling (stenosing) the duodenum. Acute pancreatitis is usually caused by bile duct stones or alcohol abuse. Contrast-enhanced multi-detector row CT is the method of choice to assess the extent of this disease. In acute pancreatitis, the role of MRCP is mainly limited to finding bile duct stones in patients with suspected biliary pancreatitis. Chronic pancreatitis results in relentless and irreversible loss of exocrine (and sometimes endocrine) function of the pancreas. MDCT even shows subtle calcifications. MRCP is the method of choice for non-invasive assessment of the duct. Inflammatory pseudotumor in chronic pancreatitis and groove pancreatitis are difficult to differentiate from pancreatic cancer. In these cases, multiple imaging methods such as MDCT, MRI and endosonography including biopsy may be used to make a diagnosis.
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PMID:[Pancreas. Congenital changes, acute and chronic pancreatitis]. 1746 82

This paper provides a summary of the effects of alcohol abuse on the pathobiologic responses that occur during acute and chronic pancreatitis considering both the human disease and animal/tissue models. The effects are multiple and include ones on cell death leading to necrosis; on inflammation resulting in a sensitized response to pancreatic stress; and fibrosis through effects of ethanol on pancreatic stellate cells and the plasminogen system. Although the effects of alcohol are multiple and complex, it is likely that a combination of a few key effects on these pathobiologic responses drive the increased sensitivity of the pancreas to acute pancreatitis with pancreatic stress and the promotion of chronic pancreatitis with pancreatic injury occurring during acute pancreatitis.
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PMID:Pathobiology of alcoholic pancreatitis. 1759 22

The etiology of an attack of acute pancreatitis (AP) is highly variable. It is important to identify the causing factor, because it can have an effect on the specific treatment of AP. Furthermore, in some cases relapses of AP can be prevented when the causing factor is eliminated. The most common etiology of AP is alcohol abuse and gallstone disease (>80% of all cases). What diagnostic measures should be undertaken before an attack of AP is considered as idiopathic? Important factor in the etiologic diagnostic work-up is the availability, safety, and cost-effectiveness of suitable methods. Further, the relevance of the findings has to be assessed. In some cases also the age of the patient and number of attacks of AP (first vs. recurring) have effects on efforts to detect the causing factor of AP. This review focuses on the search for other etiologic factors once alcohol and gallstones have been excluded.
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PMID:Non-alcoholic etiologies of acute pancreatitis - exclusion of other etiologic factors besides alcohol and gallstones. 1759 26

Although alcohol abuse is the major cause of chronic pancreatitis, the pathogenesis of alcoholic chronic pancreatitis (ACP) remains obscure. A critical obstacle to understanding the mechanism of ACP is lack of animal models. Our objective was to develop one such model. Rats were pair-fed for 8 wk ethanol or control Lieber-DeCarli liquid diet. For the last 2 wk, they received cyclosporin A (CsA; 20 mg/kg once daily) or vehicle. After 1 wk on CsA, one episode of acute pancreatitis was induced by four 20 microg/kg injections of cerulein (Cer); controls received saline. Pancreas was analyzed 1 wk after the acute pancreatitis. CsA or Cer treatments alone did not result in pancreatic injury in either control (C)- or ethanol (E)-fed rats. We found, however, that alcohol dramatically aggravated pathological effect of the combined CsA+Cer treatment on pancreas, resulting in massive loss of acinar cells, persistent inflammatory infiltration, and fibrosis. Macrophages were prominent in the inflammatory infiltrate. Compared with control-fed C+CsA+Cer rats, their ethanol-fed E+CsA+Cer counterparts showed marked increases in pancreatic NF-kappaB activation and cytokine/chemokine mRNA expression, collagen and fibronectin, the expression and activities of matrix metalloproteinase-2 and -9, and activation of pancreatic stellate cells. Thus we have developed a model of alcohol-mediated postacute pancreatitis that reproduces three key responses of human ACP: loss of parenchyma, sustained inflammation, and fibrosis. The results indicate that alcohol impairs recovery from acute pancreatitis, suggesting a mechanism by which alcohol sensitizes pancreas to chronic injury.
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PMID:A rat model reproducing key pathological responses of alcoholic chronic pancreatitis. 1788 79


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