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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three aspects of the pathophysiology of acute pancreatitis are discussed: 1. the initiating mechanisms, 2. the mechanisms of the fat necrosis, 3. the processes leading to shock phenomena. It is pointed out that the intraglandular activation of the precursors for both lipolytic and proteolytic enzymes seems to be essential for the initiating mechanisms of the disease. The role of the hormone dependent lipolytic enzyme of the fat tissue is discussed in relation to the occurrence of extrapancreatic fat necrosis. The role of the vaso-active compounds, such as plasma kinins and histamine for the occurrence of shock during acute hemorrhagic pancreatitis is pointed out.
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PMID:[Acute pancreatitis. Aspects of the pathophysiology (author's transl)]. 6 82

Drug histories were taken from 100 patients in their first attack of acute pancreatitis, and each was matched with a control subject of the same sex who was admitted to hospital as an emergency with acute abdominal pain, whose serum-amylase was within the normal range, and whose age was within three years of the pancreatitis patient's. The major differences between the patient groups was in the use of cardiovascular agents, and this was primarily due to a statistically significant excess of diuretic takers among the pancreatitis patients. There was an associated excess of intake of digoxin and antihypertensive and anti-anginal agents, but neither difference was statistically significant. Other categories of drugs showed no substantial differences. The difference between the pancreatitic patients and controls is almost entirely accounted for by takers of cyclopenthiazide with potassium chloride and of frusemide, especially the former. Further clinical and experimental evidence is required before the role of diuretics and/or potassium chloride in causing acute pancreatitis can be determined.
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PMID:Drug-associated primary acute pancreatitis. 7 39

The application of transcutaneous electrical nerve stimulation (TENS) to the abdomen produced prompt and sustained relief of the pain associated with pancreatitis in five patients and in another patient with probable acute pancreatitis. The disorder was acute in two patients and recurrent in four. Multiple hospitalizations, including the need for analgesics and opiates, had been required during previous attacks in five patients. In view of the simple and noninvasive nature of such treatment, more extensive clinical trials appear to be warranted. Some of the possible mechanisms of action for TENS analgesia are reviewed.
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PMID:Transcutaneous electrical nerve stimulation in the management of pancreatitis pain. 7 40

Recent data seem to support a tubular defect as the mechanism of the elevated renal clearance of amylase relative to creatinine in acute pancreatitis. Glucagon has been proposed by some to be an important factor in this phenomenon. To examine the role of glucagon as this "tubular dysfunction factor", we investigated the effect of intravenously infused glucagon on the fractional excretion of amylase and the tubular handling of a low molecular weight protein, beta2 microglobulin, in normal, healthy volunteers. At glucagon levels far in excess of those seen in pancreatitis, the clearance ratio of beta2 microglobulin relative to creatinine increased, whereas the clearance ratio of amylase relative to creatinine did not increase above the normal range. The dissociation between beta2 microglobulin clearance and amylase clearance allows one to question the theory that tubular dysfunction is the mechanism of the elevated renal clearance of amylase relative to creatinine in acute pancreatitis. Glucagon does not appear to be the sole factor responsible for the elevation of renal clearance of amylase relative to creatinine in acute pancreatitis.
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PMID:Effect of glucagon infusion on the renal clearance of amylase relative to creatinine. 8 90

Intraductal administration of enterokinase in rats produced hyperamylasemia and acute hemorrhagic pancreatitis. The experimental pancreatitis and hyperamylasemia could be prevented by the concomitant intraductal injection of fluorouracil, pituitrin, or chlorophyll-a. The clinical implication of the study is that these agents, if given intraductally, may be useful in the prevention of iatrogenic hyperamylasemia and acute pancreatitis that may occur after endoscopic retrograde pancreatocholangiography.
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PMID:Effect of chlorophyll-a, fluorouracil, and pituitrin on experimental acute pancreatitis. 8 61

The renal handling of beta-2-microglobulin, amylase and albumin was studied in patients with acute pancreatitis. The data were compared with results obtained from patients with glomerular proteinuria and from patients with tubular proteinuria. Initially during acute pancreatitis, the clearance ratio (clearance protein/clearance creatinine) for beta-2-microglobulin was increased dramatically (77-fold) compared to normals. After four to seven days this ratio had fallen and was elevated only 7-fold. The corresponding figures for amylase were 3.3 and 1.8 times and for albumin 9 and 5 times respectively. In glomerular disease, the clearance ratios for beta-2-microglobulin, amylase and albumin were increased 6, 1.1, and 154 times and in tubular disease 448, 1.1, and 28 times, respectively. The electrophoretic pattern of the urinary proteins during pancreatitis was mostly normal. In a few cases, slight tubular proteinuria was noticed. Amylase activity in serum and urine from patients with pancreatitis was found to sediment, (S20,W = 4.6) in a sucrose gradient, identical to amylase from normal serum and urine. The marked increase in the excretion of beta-2-microglobulin probably reflects interference of the kidney function at the proximal tubular level. Determinations of this protein in urine may be of value in studies of kidney dysfunction that can accompany pancreatitis.
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PMID:Renal handling of beta-2-microglobulin, amylase and albumin in acute pancreatitis. 8 64

Plasma concentrations of bilirubin, alkaline phosphatase (AP), and glutamic oxaloacetic transaminase (GOT) were measured during 122 attacks of acute pancreatitis in 114 patients, on the day of admission to hospital and 2 days after admission. Concentrations in 74 attacks associated with gallstones were compared with concentrations in 31 attacks in which no stones were found. 24 attacks were severe by clinical criteria. On the day of admission plasma GOT concentrations of more than 60 IU/l were found in 88% of attacks associated with gallstones, but in no attacks without gallstones. Plasma concentrations of more than 25 mumol/l bilirubin and more than 14 King-Armstrong units AP were found in 62% and 66% respectively, of attacks associated with gallstones, and 5% and 10%, respectively, of attacks without stones. In attacks associated with gallstones plasma concentrations of GOT and bilirubin usually fell over the first 48 h of admission. No correlation was observed between these biochemical values and the severity of the attack. In the absence of a history of excessive alcohol consumption, increases in plasma GOT on the day of admission to hospital suggest that gallstones are responsible for the pancreatitis.
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PMID:Biochemical prediction of gallstones early in an attack of acute pancreatitis. 8 54

Acute pancreatitis of biliary tract origin and that of alcoholic origin may be difficult to separate on clinical grounds alone. Such separation is important since operation prevents recurrent attacks in gallstone pancreatitis. We examined the records of 78 patients in the first attack of pancreatitis from gallstones or alcohol. The gallstone group were usually women, older, and had a shorter period of abdominal pain. Pancreatic complications occurred more frequently in the alcoholic group and led to two deaths. Amylase values were diagnostically helpful in that a level greater than 1000 units in patients of the proper age and sex, and a level greater than 2000 units by itself indicated gallstone pancreatitis.
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PMID:The first attack of acute pancreatitis: a clinical study. 9 8

Pulmonary edema, cardiac enlargement, and respiratory insufficiency may occur in patients with acute pancreatitis. The mechanisms are complex and incompletely understood, but probable etiologic factors include fluid overload, left ventricular failure, impaired respiratory excursion and microatelectasis, and a nonspecific response of the lung to various types of pulmonary injury including hypotension, intravenous crystalloids, and the effects of circulating pancreatic enzymes. Recognition of the association of pulmonary edema and respiratory insufficiency with pancreatitis is importance because early treatment with positive pressure breathing, careful fluid management and diuretics, and corticosteroids may prevent the development of irreversible respiratory failure.
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PMID:Pulmonary edema and respiratory insufficiency in acute pancreatitis. 12 91

A patient with acute pancreatitis developed subcutaneous fat necrosis of the anterior abdominal wall secondary to leakage of pancreatic enzymes through a rent in the peritoneum following paracentesis. The same patient also had another subcutaneous complication of pancreatitis, namely, nodular liquifying panniculitis of the lower extremities. The diagnosis was made by the typical histological findings of subcutaneous fat necrosis, foci of necrotic cells with a "ghost-like" appearance, and basophilic-staining calcium soaps deposited around the necrotic cells.
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PMID:Subcutaneous fat necrosis after paracentesis: Report of a case in a patient with acute pancreatitis. 13 3


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