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

The practical implications of the new Marseilles classification (1984) of pancreatitis are discussed and the present-day diagnostic methods critically reviewed. The new classification distinguishes between two typical long-term profiles, i.e. acute (reversible) and chronic (progressive) pancreatitis. Modern diagnostic tests such as sonography, CT, ERCP and the secretin-CCK test do not provide a "gold standard" for early chronic pancreatitis. Thus, long-term studies of function and morphology are needed to differentiate chronic pancreatitis (progressive dysfunction, calcification, ERP changes) from acute (reversible) pancreatitis. The etiology is a helpful prognostic guide since gallstone pancreatitis virtually never becomes chronic. However, alcoholic "acute" pancreatitis may not always progress to chronic pancreatitis. Drug or surgical treatment of pain is symptomatic and empirical, since the pathomechanisms of pain are poorly understood. A prerequisite for optimum therapy is exact staging of the disease into: uncomplicated early stages with short, self-limiting episodes of pancreatitis: conservative therapy, persistent pain, mainly due to pseudocysts (diagnosis by morphological tests): surgical therapy, advanced painless forms of chronic pancreatitis associated with diabetes and/or steatorrhea: diet and substitution therapy. After successful surgical drainage persistent pain subsides, but postoperative episodic recurrences of pancreatitis are common in the early stages of the disease and in association with continued alcohol intake. However, spontaneous pain relief occurs in all cases in the late stages of the disease and with progressive pancreatic dysfunction (despite continued alcohol abuse).
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PMID:[Diagnosis and therapy of chronic alcoholic pancreatitis. A critical review of the status]. 390 86

The long-held tenet that a cause and effect relation exists between primary hyperparathyroidism and pancreatitis has recently been questioned. To clarify this association, records of 1475 patients seen with pancreatitis during a 10-year period were reviewed. Five patients (0.4%) were identified with primary hyperparathyroidism. The four men and one woman ranged in age from 31 to 57 years. Four had recurrent pancreatitis over a 2-10 yr period before hyperparathyroidism was diagnosed. One patient had hypercalcemia noted 1 year prior to developing pancreatitis. Four patients had associated potential causes of pancreatitis including alcohol abuse, gallstones, and hypotension. Pancreatitis was severe in each patient. Two patients had more than four admissions for acute pancreatitis, one patient underwent pseudocyst drainage and distal pancreatectomy for chronic pancreatitis, one patient underwent pancreaticojejunostomy for chronic pancreatitis, and one patient died from hemorrhagic pancreatitis. Four patients have undergone successful parathyroidectomy and have had no further attacks of pancreatitis on follow-up ranging from 1 to 4 years. Hyperparathyroidism is rarely associated with pancreatitis, but when this combination occurs, the pancreatitis is likely to be severe. Despite its rarity, a cause and effect relationship is still suggested by the fact that parathyroidectomy seems to prevent recurrence of pancreatitis.
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PMID:The association of primary hyperparathyroidism and pancreatitis. 399 75

Motor disorders of the sphincter of Oddi (SO) may play a role in the pathogenesis of idiopathic recurrent pancreatitis. We have compared manometric records from the SO in 28 patients with idiopathic recurrent pancreatitis with those from 10 control subjects. Patients with idiopathic recurrent pancreatitis had presented with episodes of upper abdominal pain associated with abnormal serum levels of amylase on at least two occasions, in the absence of alcohol abuse and biliary disease. Retrograde pancreatography was either normal or showed only minor changes in pancreatic ducts. A triple lumen low compliance manometric system was used to obtain a 5 min recording of spontaneous SO motor activity. From this recording were determined the SO basal pressure, SO phasic contraction amplitude, SO wave frequency and direction of wave propagation. The SO response to intravenous cholecystokinin-octapeptide (CCK-OP) 20 ng/kg was then recorded for at least 3 min. Twenty-five of the twenty-eight patients demonstrated one or more manometric abnormality when compared with data from the ten controls. The most frequent abnormality was an elevated SO basal pressure in 16 patients. In addition, excess of retrograde contractions in nine patients, high frequency of SO phasic contractions in nine patients, absence of phasic contractions in three patients, and paradoxical response to CCK-OP administration in two patients were recorded. This study has demonstrated a spectrum of sphincter of Oddi manometric disorders in patients with idiopathic recurrent pancreatitis and suggests that motility disorders of the sphincter of Oddi may be associated with episodes of pancreatitis.
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PMID:Sphincter of Oddi motility disorders in patients with idiopathic recurrent pancreatitis. 406 50

Of 311 patients with primary acute pancreatitis, seven revealed major and seven minor lipid abnormalities on hospital admission. One pregnant woman suffered acute pancreatitis associated with Fredrickson type I hyperlipoproteinaemia. Twelve of the 13 men with types IV and V hyperlipoproteinaemia suffered alcohol abuse pancreatitis and represented 13.2 per cent of this aetiological group. However, only one of the 157 patients (0.6 per cent) with biliary disease had lipid abnormalities. Two of the 13 men died--the oldest, who had gallstones, and one with alcohol related disease. The remaining 11 were subject to follow-up (5-10 years). Six, who had improvement of their lipid abnormalities, had abstained from alcohol. The other five had a persistent lipid disorder, and all admitted continuing heavy alcohol ingestion. The clinical diagnosis of acute pancreatitis was supported by serum amylase elevation in only nine of the fourteen patients. Urinary amylase levels were consistent with the diagnosis in 11 of the 12 patients. Estimation of both serum and urinary amylase gave 100 per cent support to the clinical diagnosis of acute pancreatitis. Hyperlipidaemia associated with acute pancreatitis may be secondary to alcohol abuse but the possible role of HLP cannot be discounted. Urinary amylase is useful in diagnosing acute pancreatitis in the presence of hyperlipidaemia.
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PMID:Hyperlipidaemia, alcohol abuse and acute pancreatitis. 620 8

The aetiological associations and proposed pathogenesis of acute pancreatitis have been reviewed. Although 80 per cent of patients have underlying alcohol abuse or gallstones, the precise mechanism of induction and of progression of pancreatic injury remains uncertain. Our current approach to management is summarized in Table 8. At present, no measure designed to limit the severity of pancreatitis or to interrupt the genesis of complications has been of proven benefit. Treatment is therefore primarily supportive. Peritoneal lavage by catheters introduced under local anaesthesia appears to be a valuable adjunct to the treatment of the early cardiovascular and respiratory complications of severe pancreatitis and we continue to recommend this measure. The major unsolved problem in treatment of this disease is the prevention and treatment of infected peripancreatic abscesses.
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PMID:Acute pancreatitis: pathogenesis, outcome and treatment. 638 41

The present investigation defined the pattern of pancreatic, pituitary and adrenal responses after insulin-induced hypoglycemia in chronic calcific pancreatitis (CCP) related to alcohol abuse, and assessed the role of some of these hormones in the counterregulation of blood glucose. We studied 6 Black men with recently diagnosed CCP, all showing radiological evidence of pancreatic calcification and normal glucose tolerance, as well as 7 matched nonobese male controls. After a standard iv insulin tolerance test inducing marked hypoglycemia, patients with CCP showed significantly impaired mean plasma pancreatic glucagon and pancreatic polypeptide responses compared to the controls. Mean basal plasma somatostatin levels tended to be higher in chronic pancreatitis and remained so throughout the test without altering consistently; in the controls somatostatin peaked significantly at 30 min. Concerning extrapancreatic hormonal changes, plasma growth hormone, prolactin and total catecholamines responded normally in CCP, but plasma cortisol rose to significantly higher levels than controls at 60 and 120 min after the injection of insulin. This, coupled with the brisk output of catecholamines, may have prevented the heightened sensitivity to insulin anticipated because of their hypoglucagonemia. We conclude that patients with CCP show impaired pancreatic hormone release after insulin hypoglycemia with the exception of somatostatin; there is also an excessive rise in plasma cortisol, possibly related to the long standing abuse of alcohol in the past.
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PMID:Hormonal profile after insulin-induced hypoglycemia in chronic calcific pancreatitis. Pancreatic, pituitary and adrenal responses. 639 52

Between 1957 and 1977, 95 patients underwent transduodenal pancreatic sphincteroplasty (TPS) for a diagnosis of recurrent pancreatitis. Five to twenty-five year follow-up was obtained for 89 patients (94%) and was analyzed by life-table method. Short-term successful outcome was defined as relief of symptoms (e.g., pain) for one to three years; long-term successful outcome was defined as those patients who remained symptom-free at time of last follow-up. Operative mortality was 4.2% (4 patients). Fifty-six patients (66%) had a successful short-term outcome. Of these, 13 patients had recurrence of symptoms: 7 occurred at 4 years, 5 at 5 years and 1 at 6 years. Preoperative factors associated with poor short-term outcome were previous upper abdominal surgery (X2 = 5.67, p less than 0.05) and frequent diarrhea (X2 = 6.18, p less than 0.05). Preoperative factors associated with poor long-term outcome were previous upper abdominal surgery (X2 = 7.82, p less than 0.01), heavy alcohol intake (X2 = 4.71, p less than 0.05), narcotic use (X2 = 5.68, p less than 0.05) and frequent diarrhea (X2 = 4.8, p less than 0.05). Morphine Prostigmin Test (MPT) was performed preoperatively in 78 patients (82%). A significantly greater proportion of patients with a rise in serum pancreatic enzymes secondary to MPT (MPT+) had a successful long-term outcome compared with those without such a rise (MPT-) (61% v 41%, X2 = 5.13, p less than 0.05). Furthermore, of the patients with a successful short-term outcome, 88% with MPT+ remained long-term symptom-free compared to 38.5% with MPT- (X2 = 8.36, p less than 0.01). We conclude that TPS can be a successful operation for acute recurrent pancreatitis. Previous upper abdominal operations, signs of more advanced pancreatic disease, preoperative narcotic use and alcohol abuse, were associated with a worse outcome and probably associated with chronic recurrent pancreatitis. Preoperative use of MPT, coupled with accurate clinical history, defined groups with different short- and long-term prognosis after TPS.
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PMID:Transduodenal sphincteroplasty. 5-25 year follow-up of 89 patients. 662 16

The authors studied 19 patients with focal inflammatory masses of the pancreas over an 18-month period. In 13 cases, transhepatic cholangiography and/or endoscopic retrograde cholangiopancreatography were unsuccessful in differentiating pancreatitis from carcinoma. Eighteen patients had a history of alcohol abuse, and 12 had had pancreatitis previously. Pre-existing glandular injury appears to be a prerequisite to formation of focal inflammatory pancreatic masses.
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PMID:Inflammatory pancreatic masses. Problems in differentiating focal pancreatitis from carcinoma. 668 84

One hundred and forty patients with undiagnosed severe chronic abdominal pain who had not undergone previous biliary surgery were investigated by ERCP. A diagnosis was achieved in 34 patients (24 per cent) including 8 with previously undiagnosed peptic ulceration and 5 with gallstones. Twenty-five patients (18 per cent) had an abnormal pancreatogram, including 1 with pancreatic cancer. The incidence of pancreatogram abnormalities suggestive or diagnostic of pancreatitis was particularly high (60 per cent) in patients with a history of alcohol abuse. ERCP has a valuable role in the investigation of patients with 'obscure' abdominal pain.
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PMID:The diagnostic yield of ERCP in the investigation of unexplained abdominal pain. 682 2

There is a recognised but poorly understood association between hypothermia and acute pancreatitis. A histological study of the pancreas was made in eight patients with accidental hypothermia who had evidence of pancreatitis at necropsy. From an analysis of the patterns of parenchymal necrosis in the pancreas it was thought that there were at least three possible mechanisms for the relation between hypothermia and pancreatitis. Firstly, that ischaemic pancreatitis may result from the "microcirculatory shock" of hypothermia. Secondly, that both hypothermia and pancreatitis may be secondary to alcohol abuse: and finally, that severe pancreatitis may be the primary disease and that hypothermia results from the patients' social circumstances.
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PMID:Morphological study of the relation between accidental hypothermia and acute pancreatitis. 714 33


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